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High-performance liquid chromatographic determination of pyridinium crosslinks in serum, urine and dialysate of patients in chronic renal failure.
This study describes an isocratic reversed phase high-performance liquid chromatographic method for the analysis of pyridinium crosslinks in serum, urine and dialysates obtained from patients with chronic renal failure on haemodialysis. The mean (SD) urine pyridinoline (PYD) and deoxypyridinoline (DPD) to creatinine (Cr) ratio in 19 healthy volunteers was 28.9 (6.3) and 9.1 (3.6) mumol/mol, respectively. In the 22 patients the PYD/Cr and DPD/Cr ratio was 244.6 (436.5) and 66.5 (116.8) mumol/mol, respectively. The mean serum PYD concentration in 29 patients of 268.5 (334.4) nmol/L was significantly higher than that of 5.9 (1.5) nmol/L found in normal volunteers: the mean DPD concentration was 82.9 (93.7) nmol/L in the patients but was undetectable in the serum from the normal volunteers. The concentration of crosslinks in pre-dialysis serum samples was higher than those found post-dialysis reflecting a significant removal of the crosslinks during dialysis. The assay of pyridinium crosslinks in serum, urine and dialyses fluid could potentially provide evidence of bone collagen turnover in patients in renal failure. Their measurement in serum and dialysate could be particularly useful in anuric patients. |
Colin Galloway. Picture: Sarah Standing
Colin Galloway’s comments are contained in a motion due to be debated at Portsmouth City Council meeting on July 11.
It comes as the number of rough sleepers in the city has ballooned from eight in 2014 to 60 as of this May.
Cllr Galloway’s motion, backed by Cllr Stuart Potter, says Portsmouth ‘is no is no longer a welcoming city to either business or tourist because it seems we prefer to have vagrants’.
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He added: ‘It is time to get our police and crime commissioner to put pressure on his police force to help us clean up this unwelcome detritus.
‘These beggars, vagrants, rough sleepers, homeless, troubled folks or whatever label you want to put on them must be removed from our city and placed in specific care whether they want to or not.
‘We have tried the soft approach and have found it wanting.’
A former member of Cllr Galloway’s party, independent councillor Paul Godier, has been made the council’s homelessness champion.
Speaking to The News, Cllr Godier said people needed to be treated with compassion – and Cllr Galloway needed to be educated on homeless people’s complex needs.
‘The approach must be very soft, it must be compassionate,’ he said.
‘We’re dealing with, in the majority of cases, broken adults, people who have not faith in local authority.’
He added: ‘I’ve listened to Colin Galloway and I asked for him to be on the homeless working group.
‘He even came on a walk with me but I think he needs to sit down and be educated on their complex needs.’ |
Q:
Optimization, asserts and release mode
Consider a function
void f() {
assert(condition);
...
}
In debug mode, where asserts are enabled, the compiler is free to assume condition holds, since the remaining code will not be executed if it does not.
However, in release mode, I believe the compiler will only see
void f() {
...
}
and can no longer assume condition.
Are there any compiler directives or static assert tricks to let compiler know about certain invariants?
A:
This can't be done in portable C or C++.
Some compilers provide intrinsic functions such as __assume (for MSVC) and __builtin_unreachable (for GCC, ICC, and Clang), that can be used for this purpose.
For example:
void f() {
__assume(condition); //For MSVC
/*...*/
}
void f() {
if (!condition) __builtin_unreachable(); //for GCC and Clang
/*...*/
}
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Top 5 Countries Where Cyber Attacks Originate
Cyber attacks have been around as far back as the internet itself. Most countries have fallen victims to the traditional style of cyber attacks originating from other countries and with the rate of information growing exponentially in value and in volume, cyber risks have started to pose serious threats to governments, businesses and economies around the world. It is possible the continuous growth in cyber attacks could result in man-made disasters around the world.
2016 saw some of the most destructive cyber attacks since the dawn of the internet. Looking at the recent trends of the past, we can expect the this pattern to not only continue, but increase in severity.
What are the sources of these cyber attacks?
Most attacks are hatched by unidentified hackers working in groups or individually. The list below identifies the countries in which some of the biggest attacks were sourced from.
China
China continues to wage forward in cyber attacks, stealing intellectual property in the process despite political pressures by the US government. Also, China's cyber espionage campaigns appear to be more streamlined. The purpose of these attacks is to mostly hack the networks of US government and its allies. As per a research, 27.24% of cyber attacks are initiated by China. And according to various estimates, 41% of the world’s cyber attacks trace their genesis back to China.
Last year, ABC news reported that Chinese spies have reportedly stepped up their cyber attacks on networks belonging to Australian government and individuals in Australia. Hundreds of cyber attacks are now carried out every month. Aussies need to be aware of these hacking attempts and must use an Australia VPN to stay anonymous.
United States |
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Uterine cervical cancer is the second most common cancer among women worldwide, with nearly 500,000 new cases per year (Parkin et al., 2005). It caused an estimated 274,000 deaths in the year 2002 and it is one of the leading causes of cancer-related deaths in young women (zur Hausen, 2002). Cervical cancer typically results from cellular transformation after persistent infections with high-risk type human papilloma virus (HPV) (Scheffner et al., 1990). Almost all squamous cell carcinomas and the majority of adenocarcinomas of the stratified epithelium are HPV positive. Although HPV is capable of initiating cancer through the disruption of multiple tumor-suppressor pathways, alone it is not sufficient for the development of the fully transformed cancer phenotype (Burk, 1999). Additional host factors are required for the development of the malignant phenotype.
A precursor of cervical cancer is also called cervical dysplasia, which literally means abnormal cell growth. There are two different systems for classifying cervical dysplasia, the SIL (squamous intraepithelial lesion) system and the CIN (cervical intraepithelial neoplasia) system. Although what the systems describe is similar, they differ in some important respects. The SIL system looks only at individual cells, generally from a Pap test, and these cells are classified according to the degree of cell abnormality. According to the SIL system, cervical dysplasia is divided into AGUS or AGCUS (atypical glandular cells of undetermined significance), LSIL (low grade squamous intraepithelial lesion) and HSIL (high grade squamous intraepithelial lesion). In the CIN system, classification of cervical dysplasia is based both on the degree of dysplasia within the individual cells and the depth below the surface of the cervix to which the dysplasia extends. According to the CIN system, cervical dysplasia is divided into CIN1 (corresponding to mild dysplasia or LSIL), CIN2 (corresponding to moderate dysplasia or HSIL) and CIN3 (corresponding to severe dysplasia or HSIL). Most of CIN1 will regress back to normal tissue over time but about 11% of CIN1 will progress to CIN3. Only a very small percentage of CIN1 leads to cancer. About 43% of CIN2 will regress back to normal and 20% will progress to CIN3. Although some CIN3 will spontaneously regress, this dysplasia is almost always treated since the next step is cancer. CIN3 is sometimes also referred to as carcinoma in situ (CIS).
Three methods are widely used for the screening of cervical cancer and cervical dysplasia, cytology screening, visual inspection with acetic acid application (VIA) and HPV tests. Currently, no method is available to distinguish progressive CIN from that destined to regress. The over-treatment of screen positive women is common.
MicroRNAs (miRNAs) are species of small non-coding single-stranded regulatory RNAs that interact with the 3′-untranslated region (3′-UTR) of target mRNA molecules through partial sequence homology (Yekta et al., 2004). They participate in regulatory networks as controlling elements that direct comprehensive gene expression (Fatica et al., 2006). Bioinformatics analysis has predicted that a single miRNA can regulate hundreds of target genes, contributing to the combinational and subtle regulation of numerous genetic pathways (Hwang and Mendell, 2006; Lewis et al., 2005).
Altered levels of expression of miRNAs correlate with various cancers and the individual controlling elements are thought capable to act as either oncogenes or tumor suppressors (Chen, 2005). A global study on the distribution of miRNAs in human genome revealed that 50% of the annotated miRNA genes are located in the cancer-associated genomic regions known as “fragile sites” (Calin et al., 2004). Furthermore, numerous functional studies indicate that different miRNAs have distinct effects at different stages of cancer progression, from tumorigenesis (He et al., 2007; Voorhoeve et al., 2006) to cancer invasion and metastasis (Budhu et al., 2008; Ma et al., 2007). The deregulation of miRNA levels has been reported in cervical cancer (Lee et al., 2008; Wang et al., 2008), but the effects of individual deregulated miRNA species in cervical cancer are largely unexplored.
Deregulation of miR-133 has also been reported in a number of other diseases, including colorectal carcinoma (Bandres et al., 2006), tongue squamous cell carcinoma (Wong et al., 2008), esophageal squamous cell carcinoma (Guo et al., 2008) and pancreatic ductal adenocarcinoma (Szafranska et al., 2007).
The disclosures of all publications, patents, patent applications and published patent applications referred to herein are hereby incorporated herein by reference in their entireties. |
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A Talk given by Wayne in Santa Ana, CA August, 1997. It's one of the earliest video recordings of Wayne teaching. Those of you familiar with Wayne's current Teaching will be interested to see the origins of some of the concepts he uses regularly today. |
Q:
tag helper to integrate a non-valued attribute
Attempting to generate:
<div data-dropdown-content class="f-dropdown content">
with the tag helper. However there appears to be no syntax for non-valued attributes
<%= tag(:div, :class => "f-dropdown content", data: {dropdown-content: ""}, :'aria-hidden' => true, :'tabindex' => "-1") %>
and different variants all lead to errors.
A:
Try this:
<%= tag(:div, data: {dropdown_content: ""}, class: "f-dropdown content") %>
Your code is failing because dropdown-content is not valid key here.
Tag helper converts dropdown_content to dropdown-content in data.
|
602 So.2d 291 (1992)
STATE of Louisiana, Appellee,
v.
Elijah ALEXANDER, Appellant.
No. 23812-KA.
Court of Appeal of Louisiana, Second Circuit.
June 24, 1992.
*292 Indigent Defender Bd. by Lewis A. Jones, Ruston, for appellant.
Richard P. Ieyoub, Atty. Gen., Robert W. Levy, Dist. Atty., John F.K. Belton, Asst. Dist. Atty., Ruston, for appellee.
Before MARVIN, NORRIS, and STEWART, JJ.
STEWART, Judge.
Defendant, Elijah Alexander, was charged by bill of information with obscenity second offense. After a trial by jury, Alexander was found guilty as charged and subsequently sentenced to serve three years at hard labor, and to pay court costs. *293 In default of paying court costs, Alexander is to serve 60 days concurrent with the three-year sentence.
On appeal, Alexander contends that (1) the trial court erred in refusing to allow him to wear shorts in front of the jury which he averred were identical to those he was wearing at the time of his arrest; (2) the evidence was insufficient to convict him of obscenity second offense; and (3) the trial court imposed an excessive sentence and failed to comply with the sentencing guidelines set forth in LSA-C.Cr.P. Art. 894.1. Finding no merit to these assignments, we affirm the conviction and sentence.
FACTS
On November 30, 1989, Officer Audrey White, the dispatcher at the Grambling State University (Grambling) Police Department, received a telephone call from a female student who complained that a male was exposing his genitals in front of Grambling's cafeteria. The dispatcher contacted the Chief of Police, Edward Adams, who went to investigate the caller's complaint. Upon arrival at the cafeteria, he saw Alexander, who fit the description given by the caller of the male who was exposing his genitals, engaged in conversation with some male companions. Alexander was clothed in a pair of cutoff blue jeans which were mid-thigh length, the shorts were split up along the outer seams all the way up to the waistband which exposed his genitals. Alexander was not wearing any underwear, shoes, socks, or shirt when confronted by Chief Adams. Alexander was arrested and charged with obscenity second offense.
On September 13, 1991, Alexander was tried, convicted as charged, and sentenced. Alexander appeals.
DISCUSSION
Assignment of Error No. 1
Alexander contends the trial court erred in denying his request to wear shorts in front of the jury which he averred were identical to those he was wearing at the time of the arrest. Alexander argues that his demonstration of the shorts would have shown that his genitals were not exposed.
All relevant evidence is admissible except as otherwise provided by the state or federal constitution, by law or by rule of the Supreme Court. State v. Johnson, 453 So.2d 279 (La.App.2d Cir.1984); LSA-C.E. Art. 402. Even if deemed relevant, however, evidence should be excluded if its probative value is outweighed by the danger of unfair prejudice, confusion of the issues or misleading the jury or by consideration of undue delay or waste of time. LSA-C.E. Art. 403.
The use of demonstrative evidence is within the sound discretion of the trial judge and his ruling will not be disturbed on appeal in the absence of an abuse of discretion. State v. Mayberry, 457 So.2d 880 (La.App. 3d Cir.1984), writ denied, 462 So.2d 191 (La.1984).
At trial, defendant conceded that he no longer had the shorts that he was wearing on the date of his arrest approximately one and one-half years prior to trial. Given this long lapse of time, the trial judge was not convinced that the shorts to be demonstrated were sufficiently identical to have probative value. Even if the shorts were identical, the trial judge reasoned that such a demonstration was not in good taste and might result in the commission of another offense in front of the jury.
The testimony of Chief Adams and Officer White established that Alexander was exposed. Therefore, we conclude that a demonstration by Alexander was not necessary to enable the fact-finder to determine whether his genitals were exposed.
Therefore, based on this record, we find no abuse of the trial court's discretion in denying Alexander's request to wear shorts in front of the jury. This assignment of error lacks merit.
Assignment of Error No. 2
Alexander contends that the evidence was insufficient to sustain a verdict of obscenity second offense. He argues that he did not expose himself or, if he did, *294 he lacked the requisite intent because of his religious beliefs.
The proper standard of appellate review for a sufficiency of evidence claim is whether, after viewing the evidence in the light most favorable to the prosecution, any rational trier of fact could have found the essential elements of the crime proven beyond a reasonable doubt. Jackson v. Virginia, 443 U.S. 307, 99 S.Ct. 2781, 61 L.Ed.2d 560 (1979); State v. Doby, 540 So.2d 1008 (La.App.2d Cir.1989), writ denied, 544 So.2d 398 (La.1989).
LSA-R.S. 14:106 A(1), defines obscenity in pertinent part:
Exposure of the genitals, pubic hair, anus, vulva, or female breast nipples in any public place or place open to the public view with the intent of arousing sexual desire or which appeals to prurient interest or is patently offensive.
In the instant case, Police Chief Adams testified that he observed Alexander in front of Grambling's cafeteria and that Alexander's genitals were exposed. Also, Officer White testified that she observed Alexander when he came into the police station and that his genitals were exposed. A victim's or witness's testimony is sufficient to establish that an obscene public exposure occurred. See State v. Magee, 517 So.2d 464 (La.App. 1st Cir.1987); State v. Arabie, 507 So.2d 859 (La.App. 5th Cir.1987). Therefore, the testimony of Adams and White was sufficient to establish that Alexander's genitals were exposed in a public place.
Alexander's arrest was precipitated by the complaint of a female student who found his exposure patently offensive. Further, upon arriving at Grambling's cafeteria to investigate the student's complaint, Chief Adams likewise found Alexander's exposure so patently offensive that he became the complainant. Officer White corroborated the patently offensive nature of Alexander's exposure. The jury, the ultimate fact-finders and a fair representation of the community, found that Alexander's exposure was patently offensive by returning a unanimous verdict of guilty as charged of obscenity second offense.
Based on the record, we find the evidence presented to the jury was sufficient, considered in the light most favorable to the prosecution, for a rational jury to conclude that Alexander was guilty of obscenity second offense.
However, Alexander argues that he did not have the requisite criminal intent. Alexander contends he did not intend to expose himself or offend anyone by wearing the attire which he did, but instead, he believed that his religion dictated that he wear the attire in which he was clothed. Alexander likened his religious habit as to that worn by a priest or nun. However, the jury rejected his contention and we find no error in the jury's conclusion. Therefore, this assignment lacks merit.
Intentional, as used in LSA-R.S. 14:106, refers to general criminal intent as defined in LSA-R.S. 14:10(2), which provides:
General criminal intent is present whenever there is specific intent, and also when the circumstances indicate the offender, in the ordinary course of human experience must have adverted to the prescribed criminal consequences as reasonably certain to result from his act or failure to act.
In reviewing the correctness of a determination of whether requisite intent was present, the court should review the evidence in a light most favorable to the prosecution and must determine if the evidence is sufficient to convince a reasonable trier of fact of the defendant's guilt beyond a reasonable doubt as to every element of the offense. State v. Hunter, (La.App.2d Cir.1984) 454 So.2d 131, writ denied, 456 So.2d 1018.
We conclude that the evidence presented to the jury was sufficient, considered in the light most favorable to the prosecution for a rational jury to reasonably conclude that Alexander was guilty of obscenity second offense.
Assignment of Error No. 3
Alexander contends that the three-year sentence is excessive. The test imposed by the reviewing court in determining *295 the excessiveness of a sentence is two-pronged. First, the record must reflect that the trial court considered the factors set forth in LSA-C.Cr.P. Art. 894.1. The judge is not required to list every aggravating or mitigating circumstance so long as the record reflects that he adequately considered the guidelines of the article. State v. Smith, 433 So.2d 688 (La. 1983). The articulation of the factual basis for a sentence is the goal of LSA-C.Cr.P. Art. 894.1, not rigid or mechanical compliance with its provisions. Where the record clearly shows an adequate factual basis for the sentence imposed, remand is unnecessary even where there has not been full compliance with LSA-C.Cr.P. Art. 894.1. State v. Lanclos, 419 So.2d 475 (La.1982). The important elements which should be considered are the defendant's personal history (age, family ties, marital status, health, employment record), prior criminal record, seriousness of offense and the likelihood of rehabilitation. State v. Jones, 398 So.2d 1049 (La.1981); State v. Mims, 550 So.2d 760 (La.App.2d Cir.1989); State v. Hudgins, 519 So.2d 400 (La.App.2d Cir.), writ denied, 521 So.2d 1143 (La.1988).
The second inquiry made by the reviewing court is whether the sentence imposed is too severe. This depends on the circumstances of the case and the background of the defendant. A sentence violates LSA-Const. Art. 1, § 20 (1974) if it is grossly out of proportion to the seriousness of the offense or nothing more than a purposeless and needless infliction of pain and suffering. State v. Bonanno, 384 So.2d 355 (La.1980). A sentence is considered grossly disproportionate if, when the crime and punishment are considered in light of the harm done to society, it shocks the sense of justice. State v. Hogan, 480 So.2d 288 (La.1985); State v. Richardson, 545 So.2d 714 (La.App.2d Cir.1989). A trial court has wide discretion to sentence within the statutory limits. Absent a showing of manifest abuse of discretion, we do not set aside a sentence as excessive. State v. Square, 433 So.2d 104 (La.1983); State v. Hudgins, supra; State v. Madison, 535 So.2d 1024 (La.App.2d Cir.1988).
In the instant case, the trial court noted that Alexander was 46 years old and was classified as a third felony offender and that he had an extensive prior criminal record which dated back to 1982. The court concluded that Alexander would likely commit another offense based on his prior criminal record and the fact that one of his prior offenses is the same as the instant offense. The court also concluded that Alexander was in need of a custodial environment and correctional treatment which could be best afforded by commitment to an institution.
In imposing sentence, the trial court considered and reviewed the pre-sentence investigation (PSI) report. The PSI indicates that Alexander is single but has been married and divorced twice. Although no children were born of either union, Alexander has four children whom he does not support. The record indicates that Alexander has not been gainfully employed since 1976.
Alexander's criminal history includes 23 separate arrests between 1982 and 1991 with two of those resulting in felony convictions. The first felony was third degree robbery in New York City in which Alexander pled guilty. The second felony was obscenity which occurred at Grambling, for which Alexander was placed on unsupervised probation for two years.
Alexander's other convictions are misdemeanors which include petty larceny, trespassing, criminal trespassing, disobeying a police officer, resisting arrest, and improper dress.
Alexander was also arrested five times after the commission of the instant offense by Grambling Police Department and charged with (1) criminal trespass, (2) failure to obey an officer, (3) disturbing the peace, (4) criminal trespass, and (5) remaining on the premises after being forbidden to stay. All of these charges were still pending at the time of sentencing.
The maximum sentence allowed under the statute for obscenity second offense, is three years without benefit of probation, parole, or suspension of sentence and a fine of five thousand dollars. *296 Maximum sentences are appropriate only in cases involving the most serious violation of the offense and the worst type of offender. State v. Madison, 535 So.2d 1024 (La.App.2d Cir.1988).
In the instant case, the trial judge stated that Alexander was the worst type of offender because he has no regard for the sensitivities of the public and has demonstrated a contumacious and contemptible attitude toward the court, law enforcement and society in general. The trial judge concluded that Alexander's actions demonstrated his antisocial attitude and warrant the maximum sentence. In view of Alexander's third felony offender status and his extensive prior criminal record, we find no abuse of discretion by the trial court in the sentence imposed.
Considering the ample factual support for the conviction and sentence imposed, any less severe sentence would diminish the severity of the offense. The trial judge's articulated reasons for sentence demonstrate adequate compliance with LSA-C.Cr.P. Art. 894.1 and the sentence imposed is not constitutionally excessive. This assignment is without merit.
CONCLUSION
For the above and foregoing reasons, Alexander's conviction and sentence for obscenity second offense is affirmed.
AFFIRMED.
|
This is a scalable context timeline. It contains events related to the event August 1973: Former FBI Director Gray Testifies He Destroyed Evidence. You can narrow or broaden the context of this timeline by adjusting the zoom level. The lower the scale, the more relevant the items on average will be, while the higher the scale, the less relevant the items, on average, will be.
White House counsel John Dean orders the opening of a safe belonging to Watergate burglar E. Howard Hunt (see 2:30 a.m.June 17, 1972). Dean orders that the contents be turned over (six days later, after Dean and other White House officials have had a chance to peruse them) to the FBI. The documents will soon be given to FBI acting director L. Patrick Gray, who keeps them for six months before burning them (see Late December 1972). Gray will later admit to the incident in his testimony before the Senate Watergate Committee (see February 28-29, 1973). [Time, 4/2/1973] Dean finds in the safe, among other things, a loaded .25 caliber pistol; the attache case of burglar James McCord, loaded with electronic surveillance equipment and a tear gas canister; CIA psychological profiles of Pentagon Papers leaker Daniel Ellsberg (see March 1971); pages from the Pentagon Papers; memos to and from Nixon aide Charles Colson; two falsified diplomatic cables implicating former President John F. Kennedy in the 1963 assassination of South Vietnam’s President Ngo Diem Dinh; and a dossier on the personal life of Senator Edward Kennedy (D-MA). Nixon aide John Ehrlichman advises Dean to throw the contents of the safe into the Potomac River. [Reeves, 2001, pp. 501-502] Shortly thereafter, Washington Post reporter Carl Bernstein, in discussions with a young assistant in White House aide Charles Colson’s office, learns that Hunt has been investigating Kennedy’s checkered past, particularly the Chappaquiddick tragedy of 1969, in which an apparently inebriated Kennedy drove his car into a lake, drowning his companion of the evening, Mary Jo Kopechne. Hunt was apparently looking for political ammunition against Kennedy in preparation for a possible presidential run. According to a former Nixon administration official, Colson and fellow Nixon aide H. R. Haldeman were “absolutely paranoid” about a Kennedy campaign run. [Bernstein and Woodward, 1974, pp. 30-31]
Nixon and Haldeman, three days after the June 23 meeting. [Source: Washington Post]With the FBI tracing the Watergate burglars’ $100 bills to GOP fundraiser Kenneth Dahlberg (see August 1-2, 1972), President Nixon orders the CIA to attempt to stop the FBI from investigating the Watergate conspiracy, using the justification of “national security.” One of the areas Nixon specifically does not want investigated is the $89,000 in Mexican checks found in the account of one of the Watergate burglars, Bernard Barker (see April-June 1972). [Reeves, 2001, pp. 508-510; Woodward, 2005, pp. 59-60] Author James Reston Jr. will write in 2007: “The strategy for the CIA to block the FBI’s investigation of the Mexican checks… was devised by Haldeman and Nixon. This was a clear obstruction of justice.” [Reston, 2007, pp. 33-34] The plan, concocted by Nixon campaign chief John Mitchell, is to have deputy CIA director Vernon Walters tell the new FBI Director, L. Patrick Gray, to, in the words of Nixon chief of staff H. R. Haldeman, “stay the hell out of this… this is, ah, business we don’t want you to go any further on it.” Nixon approves the plan. White House aide John Ehrlichman will later testify that he is the one tasked with carrying out Nixon’s command; Nixon tells Ehrlichman and Haldeman to have the CIA “curb the FBI probe.” [O.T. Jacobson, 7/5/1974 ]Nixon: FBI, CIA Should Back out of Investigation - In his discussion with Nixon, Haldeman says that “the FBI is not under control, because Gray doesn’t exactly know how to control them, and they have, their investigation is now leading into some productive areas, because they’ve been able to trace the money… and it goes in some directions we don’t want it to go.” Haldeman also says that the FBI has a witness in Miami who saw film developed from one of the Watergate burglaries (see Mid-June 1972). He tells Nixon that the FBI is not aware yet that the money for the burglars can be traced to Dahlberg, who wrote a $25,000 check that went directly to one of the Watergate burglars. That check is “directly traceable” to the Mexican bank used by the Nixon re-election campaign (CREEP). Haldeman says that he and Ehrlichman should call in both Gray and CIA Director Richard Helms and tell both of them to have their agencies back out of any investigation. Nixon agrees, saying that considering Hunt’s involvement: “that will uncover a lot of things. You open that scab there’s a hell of a lot of things and that we just feel that it would be very detrimental to have this thing go any further. This involves these Cubans, Hunt, and a lot of hanky-panky that we have nothing to do with ourselves.” Haldeman says he believes that Mitchell knew about the burglary as well, but did not know the operational details. “[W]ho was the assh_le who did?” Nixon asks. “Is it [G. Gordon] Liddy? Is that the fellow? He must be nuts.” Haldeman says Mitchell pressured Liddy “to get more information, and as [Liddy] got more pressure, he pushed the people harder to move harder on.…” Both Nixon and Haldeman think that the FBI may believe the CIA, not the White House, is responsible for the burglary; Nixon says: “… when I saw that news summary item, I of course knew it was a bunch of crap, but I thought ah, well it’s good to have them off on this wild hair thing because when they start bugging us, which they have, we’ll know our little boys will not know how to handle it. I hope they will though. You never know. Maybe, you think about it. Good!” A short time later in the conversation, Nixon instructs Haldeman to tell his staffers not to directly lie under oath about their knowledge of the burglary, but to characterize it as “sort of a comedy of errors, bizarre,” and warn the FBI that to continue investigating the burglary would “open the whole Bay of Pigs thing up again. And, ah, because these people are plugging for, for keeps and that they should call the FBI in and say that we wish for the country, don’t go any further into this case.… That’s the way to put it, do it straight.” [AMDOCS Documents for the Study of American History, 6/1993] Later in the day, both Walters and CIA Director Richard Helms visit Haldeman to discuss the situation. Helms says that he has already heard from Gray, who had said, “I think we’ve run right into the middle of a CIA covert operation.” Helms and Walters both agree to pressure Gray to abandon the investigation, but their efforts are ineffective; the assistant US attorney in Washington, Earl Silbert, is driving the investigation, not the FBI. [Reeves, 2001, pp. 508-510]Gray: Improper Use of FBI - Soon after Nixon’s order, acting FBI Director L. Patrick Gray tells Nixon that his administration is improperly using the CIA to interfere in the FBI’s investigation of Watergate. Gray warns Nixon “that people on your staff are trying to mortally wound you.” Gray is himself sharing Watergate investigation files with the White House, but will claim that he is doing so with the approval of the FBI’s general counsel. [New York Times, 7/7/2005] It is unclear whether Gray knows that Nixon personally issued the order to the CIA. Soon after the order is issued, a number of the FBI agents on the case—15 to 20 in all—threaten to resign en masse if the order is carried out. One of the agents, Bob Lill, will later recall: “There was certainly a unanimity among us that we can’t back off. This is ridiculous. This smacks of a cover-up in itself, and we’ve got to pursue this. Let them know in no uncertain terms we’re all together on this. [T]his request from CIA is hollow.” [Woodward, 2005, pp. 189-191] No such mass resignation will take place. Because of evidence being classified and redacted (see July 5, 1974), it will remain unclear as to exactly if and how much the CIA may have interfered in the FBI’s investigation. 'Smoking Gun' - The secret recording of this meeting (see July 13-16, 1973), when revealed in the subsequent Watergate investigation, will become known as the “smoking gun” tape—clear evidence that Nixon knew of and participated in the Watergate cover-up. [Washington Post, 2008]
Acting FBI director L. Patrick Gray calls President Nixon to warn him that some of his White House aides are trying to “mortally wound” him by interfering with the FBI and the CIA in the Watergate investigation (see June 23, 1972). Nixon merely replies, “Pat, you just continue to conduct your aggressive and thorough investigation.” Gray later testifies (see August 1973), “I expected the president to ask me some questions.” When Gray hears nothing for two weeks from Nixon, he concludes that he is just being “alarmist” about the situation. [Time, 8/20/1973]
Acting FBI director L. Patrick Gray burns key documents in the Watergate case. He has had the documents, originally kept in the safe of Watergate burglar E. Howard Hunt, in his possession for about five months. The two Nixon aides who gave him the documents, John Ehrlichman and John Dean, warned Gray that they were “political dynamite” and should never see the light of day. Gray dithers over what to do with the documents for that entire time period before finally burning them with his Christmas trash. The documents include falsified diplomatic cables that implicated former President John F. Kennedy in the assassination of President Ngo Dinh Diem of South Vietnam, and a dossier on Democratic Senator Edward Kennedy’s troubled personal life. Gray will later tell investigators that he destroyed the papers because they had no relation to Watergate, and in 2005 will admit that he destroyed them on direct orders from White House officials. He will say that he had no idea “that these guys are trying to sandbag me,” and will add, “I know it’s hard for people to think somebody could be so stupid, but I believed them.” [New York Times, 7/7/2005] Gray will reveal his destruction of evidence during the Watergate investigation (see April 27-30, 1973).
Attorney General Richard Kleindienst meets with President Nixon to tell him that White House counsel John Dean has testified about the White House’s ordering of the Ellsberg break-in (see September 9, 1971). The biggest problem is not the ties to the Watergate burglary, Kleindienst says, but the trial of Daniel Ellsberg now going on in Santa Monica, California (see May 11, 1973). The prosecution must inform the trial judge about the new information, and the judge must decide whether to inform Ellsberg’s lawyers. Nixon tries to claim that the break-in is a matter of national security and must not be divulged, but Kleindienst says it is too late for that, the information will “be out in the street tomorrow or two days from now, a week, and the law clearly dictates that we have to do—it could be another g_ddamn cover-up, you know.… We can’t have another cover-up, Mr. President.” Nixon says, “I don’t want any cover-ups of anything.” Motive - Dean’s primary motive for divulging this information is his desire for immunity from prosecution, Kleindienst believes. He adds that Deputy Attorney General Henry Peterson has asked about granting Dean immunity: “and he even comes up to the point where a trump card of Dean would be that I’m going to implicate the president—and I told Henry at that point you have to tell Dean to go f_ck himself. You’re not going to blackmail the government of the United States and implicate the president in the Ellsberg matter.” Nixon, depressed and reckless, says that maybe he should just be impeached and removed from office, letting Vice President Spiro Agnew have the presidency. “There’s not going to be anything like that,” Kleindienst assures Nixon. Details of Testimony - Nixon also grills Peterson about Dean’s testimony, and learns that Dean has divulged his knowledge of the destruction of key evidence by FBI chief L. Patrick Gray (see Late December 1972 and April 27-30, 1973)—Gray denies destroying the evidence, claiming Dean is lying. Nixon says Gray has to resign. Peterson says he will not give in to Dean on any attempt to blackmail his way into an immunity agreement; Nixon agrees, comparing it to the stories of paying Watergate burglar E. Howard Hunt “hush money” (see June 20-21, 1972)—“I would never approve the payoff of Hunt,” Nixon assures Peterson. Nixon ends the conversation by asking Peterson for the details of any upcoming case against chief of staff H. R. Haldeman. Peterson agrees to give him that information. [Reeves, 2001, pp. 595-598]
The New York Daily News reports that acting FBI director L. Patrick Gray destroyed potentially incriminating evidence taken from the safe of Watergate burglar E. Howard Hunt (see Late December 1972). Gray, who testified to this days before to the Watergate grand jury, said that he received the material from White House counsel John Dean. “I said early in the game,” Gray testifies, “that Watergate would be a spreading stain that would tarnish everyone with whom it came in contact—and I’m no exception.” Shortly afterwards, Washington Post reporter Bob Woodward learns from his “Deep Throat” source, FBI deputy director W. Mark Felt (see May 31, 2005), that the story is true. Felt informs Woodward that Gray was told by Nixon aides Dean and John Ehrlichman that the files were “political dynamite” that could do more damage to the Nixon administration than Watergate (see June 28, 1972). Woodward realizes that the story means Gray’s career at the FBI is finished. Woodward and his colleague Carl Bernstein write their own report for April 30; the same day, Gray resigns from the FBI (see April 5, 1973). Instead of Felt being named FBI director, as he had hoped, Nixon appoints the head of the Environmental Protection Agency, William Ruckelshaus, to head the bureau. Felt is keenly disappointed. [Time, 8/20/1973; O.T. Jacobson, 7/5/1974 ; Woodward, 2005, pp. 96-98] When he learns of Gray’s actions, Post editor Howard Simons muses: “A director of the FBI destroying evidence? I never thought it could happen.” [Bernstein and Woodward, 1974, pp. 306-307] The FBI’s 1974 report on its Watergate investigation dates Gray’s resignation as April 27, not April 29 [O.T. Jacobson, 7/5/1974 ] , a date supported by reports from Time. [Time, 8/20/1973]
Former acting director of the FBI L. Patrick Gray testifies before the Senate Watergate Committee. He admits to destroying potentially incriminating evidence (see Late December 1972), and testifies that although he improperly cooperated with the White House in providing Nixon aides with FBI files on its Watergate investigation, he never considered himself part of the Watergate conspiracy: “At no time did I feel I was dealing with individuals who were trying to sweep me into the very conspiracy that I was charged with investigating. That’s a madman’s horror.” Gray, a Navy veteran, adds: “In the service of my country, I withstood hours and hours of depth charging, shelling, bombing, but I never expected to run into a Watergate in the service of a president of the United States. And I ran into a buzz saw, obviously.” [New York Times, 7/7/2005]
The Justice Department’s Office of Planning and Evaluation (OPE) submits a report on the role and actions of the FBI in the Watergate investigations. The report finds that, even with the attempts of former Attorneys General John Mitchell and Richard Kleindienst, White House aides John Dean and Jeb Magruder, and others to “mislead and thwart the Bureau’s legitimate line of inquiry,” and the “contrived covers” used to direct attention away from the White House, the FBI investigation was “the ultimate key to the solution of not only the Watergate break-in (see 2:30 a.m.June 17, 1972) but the cover itself.” The report continues: “There can be no question that the actions of former Attorneys General Mitchell and Kleindienst served to thwart and/or impede the Bureau’s investigative effort. The actions of John W. Dean at the White House and Jeb S. Magruder at the Committee to Re-elect the President were purposefully designed to mislead and thwart the Bureau’s legitimate line of inquiry. At every stage of the investigation there were contrived covers placed in order to mislead the investigators.” The OPE notes the following problems in the investigation, and provides explanations of some: Providing information concerning ongoing investigations to the White House, and allowing Dean to actually sit in on interviews of White House personnel (see June 22, 1972). Failing to interview key members of CREEP, the Nixon re-election campaign organization, as well as allowing CREEP attorneys to sit in on interviews of CREEP employees and allowing those attorneys access to FBI investigative materials. The report says that the investigation initially focused on James McCord and E. Howard Hunt, and interviewed CREEP officials tied directly to them. The net was widened later on. However, the report acknowledges that many CREEP employees undoubtedly lied to FBI investigators, “most notably John Mitchell, Jeb Magruder, Bart Porter, Sally Harmony, and Maurice Stans.” Porter and Magruder in particular “lied most convincingly.” Another CREEP employee, Robert Reisner (Magruder’s assistant), was not interviewed because Reisner successfully hid from FBI investigators. The FBI believes it was Reisner who cleaned out the “Operation Gemstone” files from Magruder’s office (see January 29, 1972 and September 29, 1972). Numerous other financial and other files were also destroyed after being requested by the FBI, most notably Alfred Baldwin’s surveillance tapes and logs from the Democratic offices in the Watergate (see May 29, 1972). Many of these files were destroyed by G. Gordon Liddy. “It is apparent that most [CREEP] people in the summer of 1972 were quite willing to lie and/or tell us considerably less than the full truth,” the report notes. An untenable delay in searching and securing Watergate burglar E. Howard Hunt’s desk in the White House, putting the contents of that desk at risk of being removed, and the “[a]lleged activities by former Acting Director [L. Patrick] Gray to limit, contain, or obstruct FBI investigation of Watergate” (see June 22, 1972). Gray is known to have destroyed materials from Hunt’s desk given to him by Dean, and is known to have extensively interfered with the FBI’s investigation (see June 28-29, 1972 and Late December 1972). The report notes that while it cannot find specific evidence that Gray broke any laws in his attempts to impede the FBI’s investigation into the Watergate conspiracy, it is clear that Gray cooperated with the White House, specifically through Dean, to ensure that the White House was always aware of what avenues of investigation were being pursued. The OPE says that Gray’s destruction of files from Hunt’s safe did not necessarily impede the FBI’s investigation, because it has no way of knowing what was in those files. The report says that it is unfortunate that “many people make no distinction between the FBI’s actions and Mr. Gray’s actions.” Failure to interview key individuals with knowledge of the suspicious monies found in the burglars’ bank accounts. Failing to secure and execute search warrants for the burglars’ homes, automobiles, and offices. The OPE says that many of those issuing this criticism “should know better,” and claims that the FBI agents involved did their level best to obtain search warrants within the bounds of the law. The report notes that after the burglary, the assistant district attorney prosecuting the case, Earl Silbert, did not believe there was probable cause to search burglar James McCord’s home or office until after July 10, 1972, when Baldwin told the FBI that he had taken surveillance equipment to McCord’s home (see June 17, 1972). Even then, Silbert decided that because of the amount of time—23 days—that had expired, a search warrant would have been pointless. Failing to identify and interview a number of people listed in the burglars’ address books. The OPE report notes that the decision to interview far less than half of the names in the books was made by FBI agents in the Miami field office, and due to the “fast moving extensive investigation which was then being conducted,” the decision to only track down a selected few from the books was right and proper. The report notes that subsequent interviews by reporters of some of the people in the address books elicited no new information. The report also notes that Gray refused to countenance interviews of the remaining subjects in the address book while the trial of the seven burglars (see January 8-11, 1973) was underway. Failing to find and remove a surveillance device from the Democratic National Committee headquarters (see September 13, 1972). The OPE calls this failure “inexplicable.” Failure to thoroughly investigate CREEP agent Donald Segretti (see June 27, 1971, and Beyond) and other CREEP operatives. The OPE finds that because Segretti was initially uncooperative with FBI investigators, and because an “extensive investigation” turned up nothing to connect Segretti with the Watergate conspiracy, the agents chose not to continue looking into Segretti’s actions. Only after press reports named Segretti as part of a massive, White House-directed attempt to subvert the elections process (see October 7, 1972) did the FBI discuss reopening its investigation into Segretti. After reviewing its information, the FBI decided again not to bother with Segretti. The OPE finds that the decision was valid, because Segretti had not apparently broken any federal laws, and the FBI does not conduct violations of election laws unless specifically requested to do so by the Justice Department. The report also says that politics were a concern: by opening a large, extensive investigation into the Nixon campaign’s “dirty tricks,” that investigation might have impacted the upcoming presidential elections. Media leaks from within the FBI concerning key details about the investigation (see May 31, 2005). The report finds no evidence to pin the blame for the leaks on any particular individual. The report notes that New York Times reporter John Crewdson seemed to have unwarranted access to FBI documents and files, but says it has turned that matter over to another agency inside the bureau. Failing to interview, or adequately interview, key White House officials such as H. R. Haldeman, Charles Colson, Dwight Chapin, and others. The report justifies the decision not to interview Haldeman because the FBI had no information that Haldeman had any knowledge of, or involvement in, the burglary itself. “Alleged attempt on part of Department of Justice officials to limit, contain, or obstruct FBI investigation.” The report is particularly critical of Kleindienst’s concealment of his contact with Liddy about the burglary (see June 17, 1972). “Alleged attempt by CIA officials to interfere, contain, or impede FBI Watergate investigation.” The report notes that during the Senate Watergate Committee hearings, Republican co-chairman Howard Baker (R-TN) tried repeatedly to assert that the CIA was behind the burglary. The report calls Baker’s theory “intriguing” but says no evidence of CIA involvement on any operational level was ever found. The report notes that there is still no explanation for the discussions regarding the CIA paying the burglars (see June 26-29, 1972), or the CIA’s involvement with Hunt before the burglary—loaning him cameras, providing him with materials for a disguise, and helping Hunt get film from the first burglary developed. According to the report, Gray stopped the FBI from pursuing these leads. The FBI report says that the CIA involvement apparently had nothing to do with the Watergate burglary, but was more in support of Hunt’s activities with the Ellsberg break-in (see September 9, 1971). “Alleged activities on part of White House officials to limit, contain, or obstruct FBI Watergate investigation (Dean, Haldeman, Ehrlichman, Colson, et cetera).” The report notes, “There is absolutely no question but that the president’s most senior associates at the White House conspired with great success for nine months to obstruct our investigation.” The report says it was “common knowledge” throughout the investigation that the White House was paying only “lip service” to investigators’ requests for honest, complete answers; the report cites Dean as a specific offender. [O.T. Jacobson, 7/5/1974 ]
In his first interview session with former President Richard Nixon about Watergate (see April 13-15, 1977), David Frost moves from the erased Watergate tape (see November 21, 1973) to Nixon’s damning conversation with Charles Colson about “stonewalling” the Watergate investigation. This time around, Frost is far more prepared and ready to deal with Nixon’s tactics of obfuscation and misdirection than in earlier interviews (see April 6, 1977). Surprise Information - Nixon is unaware that Frost knows about his conversation that same day with Colson (see June 20, 1972). Along with what is known about his conversation with Haldeman, the Colson conversation puts Nixon squarely in the midst of the conspiracy at its outset. More important than Frost’s command of the facts is Frost’s springing of a “surprise card” (Frost researcher James Reston Jr.‘s words) on Nixon at the beginning of the Watergate sessions. Nixon obviously must contend with the questions of what else Frost knows, and how he would ask about it. As Frost details excerpts from the Colson conversation, about “stonewalling” and “hav[ing] our people delay, avoiding depositions,” Reston watches Nixon on the monitor. Reston will later recall: “His jawline seemed to elongate. The corners of his mouth turned down. His eyes seemed more liquid. One could almost see the complicated dials in his head turning feverishly. It was a marvelously expressive face. The range of movement both within the contours of the visage and with the hands was enormous.” Frost concludes with the question, “Now, somewhere you were pretty well informed by this conversation, weren’t you?” After some fumbling and half-hearted admissions of some knowledge, Nixon begins justifying his actions in the conspiracy: “My motive was not to cover up a criminal action, but to be sure that as any slip over—or should I say slop over, a better word—any slop over in a way that would damage innocent people or blow it into political proportions.” [Reston, 2007, pp. 124-126]Pinning Nixon down on CIA Interference - Frost asks about the conversations of June 23 (see June 23, 1972), when Nixon told his aides to have the CIA interfere with the FBI’s investigation of the burglary. Nixon tries dodging the point, emphasizing how busy he was with other matters that day and quibbling about the definition of the phrase “cover-up,” but finally says that he had no criminal motive in ordering the CIA to stop the FBI from investigating the matter of the Mexican checks found in Watergate burglar Bernard Barker’s bank accounts. He was merely engaged in political containment, he says, and besides, two weeks later, the FBI traced the checks to a Mexican bank anyway (see Before April 7, 1972 and August 1-2, 1972). Nixon emphasizes his instructions to then-FBI director L. Patrick Gray to move forward on the investigation (see July 6, 1972). (Later, Nixon staff member Jack Brennan will admit that they had almost convinced Nixon to admit to the illegality of the June 23 orders, but Nixon had demurred.) 'You Joined a Conspiracy that You Never Left' - It now falls to Frost to confront Nixon with the strictures of the law and the evidence that he had broken those laws. Frost says, “But surely, in all you’ve just said, you have proved exactly that that was the case, that there was a cover-up of criminal activity because you’ve already said, and the record shows you knew, that Hunt and Liddy [E. Howard Hunt and G. Gordon Liddy, the leaders of Nixon’s “Plumbers”] were involved… you knew that, in fact, criminals would be protected.” Nixon protests, “Now just a moment,” but Frost says, “Period.” Frost lectures Nixon on obstruction of justice, saying: “The law states that when intent and foreseeable consequences are sufficient, motive is completely irrelevant.… If I try to rob a bank and fail, that’s no defense. I still tried to rob a bank. I would say you tried to obstruct justice and succeeded in that period” between June 23 and July 6. Nixon retorts that he does not believe Frost knows much about the details of the obstruction of justice statutes, but fails to move Frost, who has been carefully instructed in the obstruction statutes all week. Frost eventually says: “Now, after the Gray conversation, the cover-up went on. You would say that you were not aware of it. I was arguing that you were part of it as a result of the June 23 conversation.” Nixon repeats, “You’re gonna say that I was a part of it as a result of the June 23 conversation?” Reston later writes, “It was a crucial moment, a moment that took considerable courage for David Frost.” Frost replies: “Yes.… I would have said that you joined a conspiracy that you never left.” “Then we totally disagree on that,” Nixon retorts. Reston later writes: “No journalist in America, I concluded, would have had the courage of Frost in that vital moment. But therein lay the failing of American journalism. For Frost here was an advocate. He was far beyond the narrow American definition of ‘objective journalism.’” [Time, 5/9/1977; Reston, 2007, pp. 124-126]
Former FBI Director L. Patrick Gray, who resigned under fire during the Watergate investigation (see April 27-30, 1973), appears on ABC’s This Week to respond to the recent revelation that his then-deputy, W. Mark Felt, was the notorious informant “Deep Throat” (see May 31, 2005). Thirty years before, Felt had lied to Gray when asked if he had leaked information to the press (see October 19, 1972). Gray, whose health is in serious decline, airs decades’ worth of pent-up grievances against both Felt and the Nixon administration, which he says left him to “twist slowly, slowly in the wind” (Nixon aide John Ehrlichman’s words—see Late March, 1973) after he admitted giving information about the Watergate investigation to White House staffers (see June 28, 1972 and July 21, 1972). He felt “anger, anger of the fiercest sort” after hearing Ehrlichman’s words, and adds, “I could not believe that those guys were as rotten as they were turning out to be.” He was justified in burning key White House documents instead of turning them over to the FBI (see Late December 1972), he says, because the documents were unrelated to the Watergate investigation. Learning that Felt, his trusted deputy, was “Deep Throat” was, Gray says, “like [being] hit with a tremendous sledgehammer.” Gray says that if he could, he would ask Felt: “Mark, why? Why didn’t you come to me? Why didn’t we work it out together?” Gray says he now realizes that he could not stop the FBI from leaking information to the press because Felt was in charge of stopping the leaks. “I think he fooled me… by being the perfect example of the FBI agent that he was.… He did his job well, he did it thoroughly, and I trusted him all along, and I was, I can’t begin to tell you how deep was my shock and my grief when I found that it was Mark Felt.” Two weeks after the interview, Gray will die of cancer. [New York Times, 6/26/2005; Roberts, 2008, pp. 151] After Gray’s death, his son Ed Gray will call his father “the only wholly honest” man involved in Watergate. [Associated Press, 7/6/2005]
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Traditional U.S. retailers are struggling. Office supply store Staples(SPLS) slumped over 12% on lousy earnings and a warning that results in the current period are likely to fall short of expectations. That news also weighed on rival Office Depot(ODP), which fell 6%.
Dick's Sporting Goods(DKS) tumbled 18% after revealing subpar golf and hunting sales that sparked weaker than expected results. Dick's also spooked investors by dimming its sales and earnings outlook for the entire year. The company needs a new round -- or arsenal -- of ideas.
2. Not so pretty looks at Target, Penney and Urban Outfitters
It wasn't much prettier for regular clothing, either. Shares of Urban Outfitters(URBN) fell 9% after the retailer revealed a profit drop that was driven by higher expenses. T.J. Maxx and Marshalls parent TJX(TJX) slid nearly 8% on an earnings and sales miss.
Another struggling retailer, Target(TGT), announced the departure of Canadian chief Tony Fisher, who will be replaced by Mark Schindele. The move comes just weeks after Target dismissed CEO Gregg Steinhafel and amid concerns about continued losses in the company's Canadian division. Target is set to report results Wednesday morning
One of the lone positive retail stories today is Home Depot(HD), which rallied 2% after upgrading its outlook. The rosier view offset concerns over the home improvement retailer's weak first-quarter profits and sales.
Maybe people really are doing their spring cleaning and summer repairs.
Americans might not be shopping much in brick-and-mortar stores, but they're definitely gobbling up Red Robin(RRGB) burgers. The fast food joint's shares popped 13% on a first-quarter earnings beat fueled by sales and margin growth.
4. Remember momentum stocks?
Growth concerns were triggered by Caterpillar(CAT), which said machine sales slumped 13% in the three months ended in April. The mining equipment maker dropped almost 4%, making it the worst performer on the Dow. Other industrial stocks like United Steel(X) and Alcoa(AA) were also under pressure.
On the heels of Monday's gains, some beat-up momentum stocks continued to make headway despite few major developments. Shares of FireEye(FEYE) climbed 6%, while Pandora Media(P) advanced almost 2%.
Asian markets ended the day on a positive note, though gains were small. Thailand's stock market retreated 1.2% and the country's currency dropped after the Thai army surprised the country by declaring martial law. |
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The opening moments of this week’s “Underground” invites viewers to consider, of all things, the Necco Wafer. A tight shot of a confectioner’s hands shows him meticulously preparing the dough, rolling it into thin sheets and cutting those into small hubs. Arranging these discs in neat cylindrical stacks, they’re wrapped in wax paper and packed into a crate headed South, each package destined to play a silent guest-starring role in the drastically different fates of several children.
Candy is a luxury serving to highlight the division between master and servant in the world of “Underground.” The rich whites always seem to have treats handy, and every now and then, if they’re lucky, a few slaves manage to lay their hands on a piece or two.
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But the choice to feature the Necco Wafer in this new episode, premiering 10 p.m. Wednesday on WGN America, seems particularly intentional, and not just out of a sense of maintaining historical accuracy. Neccos have been around since 1847, having risen in popularity due to their long shelf life and ability to maintain their integrity through even the most adverse conditions. As such, they became a widely-consumed treat in the 1800s and in the early 20th century.
One only needs to eat a Necco Wafer to understand that their relative trendiness wasn’t due to their flavor. Pretty as those little pastel colored discs look, they taste like chalk. In other words – no offense, Necco fans – they are an empty promise and a lure. An edible deception, if you will.
In this week’s episode, titled “Cradle,” the wafers appear in slave cabins and a doctor’s quarters, in candy dishes laying around the luxurious interior of the slave owner’s mansion, and in the elegant sitting parlor of an abolitionist couple. They are given as a gift and a comfort, taken away to prepare a child for hardship, or rejected as would-be peace offerings.
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Until “Cradle,” most of the kids in “Underground” barely had a line or two, largely relegated to the periphery of the action – the exceptions being Ben Pullman (Brady Permenter), who has reluctantly joined his slave-catcher father August to learn the family trade, and Henry (Renwick Scott), the second youngest member of the runaways.
In depicting the action from the viewpoints of Ben, Henry, and the other children, executive producers Misha Green and Joe Pokaski give the drama’s youngest actors the opportunity to fully showcase their talents while lending additional poignancy to a story fueled by the desperation of the runaways and the family they left behind.
When you think about it, sweets and children have played important roles in “Underground” since the show’s beginning. The former is a tool used to reward, placate and manipulate, while the children inspire the adults responsible for them to risk their lives to escape bondage, or twist their moral cores for the sake of financial survival.
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This is true of both the white and African American families featured in the drama. The slave community’s minister and his wife may not have run if not for the opportunity to win freedom for their tiny daughter Boo (Darielle Stewart).
Without molasses candy, head house slave Ernestine (Amirah Vann) couldn’t have bought the compliance and silence of T.R. (Toby Nichols), the young son of slave master Tom Macon (Reed Diamond). T.R. covered for Ernestine’s daughter Rosalee (Jurnee Smollett-Bell) after she stole an important piece of property from the master’s office, for the price of a pocket full of sugar.
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And it was the vision of T.R.’s best friend James (Maceo Smedley) sitting in a cage by the ceiling, listlessly fanning the Southern belles attending a party below him, that lit the fire in a hesitant Elizabeth Hawkes (Jessica De Gouw) to aid the abolitionists running the Underground Railroad. Elizabeth, wife to Tom Macon’s brother John Hawkes (Marc Blucas) witnessed this mundane horror while doing her best to act as if she were enjoying a slice of cake.
Ben, meanwhile, harbors no illusions about his father’s work, and in fact, wonders if August (Christopher Meloni) is a bad person for hunting other people, especially considering that August’s most trusted ally is an African-American man named Jay (Clarke Peters), who is more of a parent to Ben than his largely absent parents.
Director Kate Woods tells each of their stories using plenty of close-ups of the young actors and employing angles that show this world through each child’s point of view, beginning with scenes of James enduring the back-breaking labor of picking for the first time. Filling his bag with cotton bolls bigger than his bleeding hands until the sun sets, James is barely as tall as the plants he’s harvesting, and it’s painful to watch their barbs tear at his flesh.
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In different locales, Boo and Ben are each processing significant trauma – Boo’s perhaps being the more extreme, as the little girl is now alone and being hunted after witnessing a variety of horrors. But their two stories share a commonality as well, in that each learns what dark compromises must be made to ensure survival in this world.
Elsewhere, T.R. doesn’t quite understand why he can’t play with his best friend James anymore, and doesn’t fully have a handle on James’s terrible fate.
Woods and the executive producers highlighting the emotional disconnect between T.R. and James with different versions of “Summertime,” sung by a children’s choir, as a soundtrack running underneath each of their scenes. James’s version is the more forbidding of the two, and for those familiar with the show’s various subplots, the lyric “your daddy's rich, and your ma is good-lookin'” takes on a terrible subtext.
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Scenes like these definitively demonstrate how “Underground” transcends its period setting to sharply resonate with a present day audience. It’s hard to look at James without recognizing parallels to today’s impoverished children, be they American or immigrants — frequently discussed in the abstract during this political season, but not receiving much in the way of tangible empathy.
It is human habit for people who occupy a comfortable status in society to justify unkindness by focusing on what makes the downtrodden, or the foreign, unlike “the rest of us.” But great television makes us see the best and worst of ourselves cloaked in stories that, on the surface, may seem to having nothing to do with our present lives. “Cradle” does this by training its focus on the innocents caught in the net of the slave trade, showing the ways in which both daughters of slaves and sons of slave owners are compromised by widespread injustice.
It brilliantly shows the high price everyone pays to enjoy the sweet luxuries afforded by slavery, a tariff that includes heartbreak, trauma and violence. Indeed, it is a devastating hour of viewing, and one not to be missed. |
No date fixed by US military for withdrawal of troops from Syria
Washington, Mar 8 : US military has not fixed a specific date to withdraw its forces from Syria, General Joseph Votel, head of the US Central Command said.
"We don't withdraw in a manner that increases the risk to our forces. There is no pressure on me to meet a specific date at this particular time," Votel said during a House Armed Services Committee hearing on Thursday.
The US-backed Syrian Democratic Forces (SDF) said that they would launch a final assault on the IS-held enclave of Baghouz in eastern Syria after all civilians have been evacuated, according to media reports.
Votel revealed that the IS militants evacuated from the remaining IS-held territories were largely "unrepentant, unbroken and radicalised," adding that the IS made a calculated decision "to preserve the safety of their families and preservation of their capabilities... and waiting for the right time to resurge."
Declaring victory over the IS, US President Donald Trump announced in December the withdrawal of US troops from Syria, leading to the resignation of then Secretary of Defense James Mattis and wide opposition from home and abroad. UNI |
Books that I have read… / Boeke wat ek al gelees het…
During the holiday, I started to make an inventory of all the books that I have read through the years. The following list includes some of the books that I have read. It is not nearly everyone, but it is a start. As I continue to go through my books, I will be adding the books that I have read. |
We are headed into the heart of the semester and I know you have been busy. Our presses our spinning to prove it!
I’m drinking a large cup of Kroger’s Private Selection Breakfast Blend coffee, which is surprisingly very good. Grab your favorite coffee/tea and dream of some future projects with me. 🙂
This MOTC February Bi-Monthly Update is focused on our recent #HotOffThePress posts and some NEW PRODUCT INTRODUCTIONS. The new products are definitely more on the fashion side of things, so they aren’t for everyone. But I always think it’s good to show you what is out there, even if it’s not quite a good fit right now.
A 3 Color Front print for the beautiful people at Next Step Ministries, an incredible missions trip organization & resource for our Ministry Partners (www.nextstepministries.com):
A 2 Color WINGED Jumbo print for our friends with the North Texas Easter Retreat:
A 1 Color JUMBO for our good friends (old & new) with the Round Rock Area Wide DNow:
A 1 Color WINGED Jumbo print for the ruggedly handsome Ryan Mullins (I totally stole this well made pic from his instagram):
New Product Introductions:
Canvas 3001C Fine Jersey:
This is another great fashion T option. It is most comparable to the Anvil 980 ringspun fashion T, but better. Canvas does a great job making fashion T options that are closer to a standard weight and now they’ve dropped the cost of the 3001C to be competitive with the Anvil 980. I think it’s a better T because it has a better fit and it actually does have a lower price point than the Anvil. So you’ll see it pop up in my product recommendations more and more.
Announcing Alternative Apparel “Fashion Now” Access:
We get some pretty awesome opportunities to bring pieces of the fashion world to you. One of those opportunities is with Alternative Apparel’s “Fashion Now” access. They are offering some pretty wild and pretty exclusive fashion products to us for limited time. Some of the looks include unique stripes, polka dot, bandana floral, and army camo patterns. It’s not for everybody, but if you’re looking for that hipster-chique, then let me know if you would like some more info and we’ll look at the details for you. |
From the makers of The Coverup Film comes “Reefs At Risk”
Set on the beautiful beaches of Hawaii, “Reefs at Risk” explores the harmful effects some sunscreen chemicals have on coral reefs, marine life and people. In order to protect this fragile ecosystem, Hawaii lawmakers pass a bill to ban the sale of sunscreens with oxybenzone and octinoxate, and hope that other states and nations will follow.
“The cinematography! The sound! The editing! Absolutely wonderful! It will shake the world!”
– Dr. Craig Downs, Executive Director Haereticus Environmental Lab
WHAT YOU CAN DO TO HELP:
Protect coral reefs and marine life by choosing to wear sun-protective clothing and sunscreens with non-nano zinc oxide. Many sunscreens are now being labeled as “reef safe” when they are not! If they contain any of the following chemicals they are not reef safe: oxybenzone/benzophenone, octinoxate, octisalate/octocrylene, homosalate, avobenzone, ethylhexl methoxycinnamate, parabens, retinyl palmitate, and fragrance. Read your labels! Download our eco-friendly sunscreen guide to see what brands we recommend and visit your local health food store for good options. Contact your representatives and encourage them to ban sunscreens with oxybenzone and octinoxate (and the other chemicals listed above.) There are many safer alternatives! Help educate others about this issue by sharing Reefs At Risk with your family, friends, clubs and organizations. Tag us on Facebook, Instagram and Twitter @thecoverupfilm and use the hashtag #ReefsAtRisk. Become a sponsor or make a tax-deductible donation to support our outreach and help this film be seen on more airlines, cruise ships, TV stations, at more film festivals, online and at grassroots events.
MAHALO TO OUR REEF SAFE PARTNERS
*These reef safe brands have partnered with us to protect reefs by funding our outreach programs and/or providing sunscreen samples for distribution.
CREATING AN IMPACT: Reefs At Risk has been screened internationally, won awards at several film festivals, and been seen by over two million people online. It has been featured by Upworthy, is currently on all flights on Hawaiian Airlines, and helped get legislation passed in Hawaii to ban sunscreens with oxybenzone and octinoxate from being sold in the state by January 1, 2021. The film was featured in the Washington Post Express, the LA Times, Mother Jones Magazine, EcoWatch, was linked in an article in Vogue, and has been featured in many local newspapers. The filmmakers have done numerous talks and sunscreen swaps at community screenings throughout Hawaii over the past year, presented a webinar with NOAA and have gotten their film shown in classrooms in Belize.
We are currently working to get this film seen by more people both locally and internationally: in schools, on more airlines, TV stations, cruise ships, and in hotels throughout the state. If you are interested in helping us translate Reefs At Risk into another language, get in touch with us! Follow our social media pages to hear about future screenings and sunscreen swaps near you.
It’s going to be a hot summer for our coral and although we may not be able to dial down the ocean’s temperature, we can easily eliminate toxic chemicals in sunscreens that cause coral to bleach at a lower temperature by eight degrees Fahrenheit. The chemicals “oxybenzone” and “octinoxate” harm the reproductive ability of coral and prevent reefs from recovering after a bleaching event has occurred, which threatens many species and the millions of people who depend on reefs for their food and income. We can’t wait for legislation to kick in, we need consumers to become informed and to vote with their dollar!
HELP US SHINE A LIGHT ON MORE TOXIC CHEMICALS! “Reefs At Risk” was made possible with support from The Redford Center and the New York Community Trust. Filmmakers Lynn Pelletier and Malina Fagan, a mother-daughter team from the Big Island of Hawaii, were one of 6 teams chosen from 282 grant applications for their feature film “THE COVERUP,” which explores the personal and environmental effects of the toxic chemicals found in everyday cosmetics and personal care products (like shampoo, deodorant, toothpaste, etc.) They released “Reefs at Risk” to raise awareness of this timely issue and to help influence legislation in Hawaii.
Click below to see a development trailer of our feature film which is currently in production.
Thank you for your support!
Join Our Mailing List And receive a list of the “toxic ten” ingredients to avoid plus updates about the film. Leave this field empty if you're human:
Follow us on Facebook, Instagram and Twitter for updates and information on toxic chemicals in cosmetics and personal care products. |
Wireless Bipolar Nanopore Electrode for Single Small Molecule Detection.
Solid-state nanopore-based techniques have become a promising strategy for diverse single molecule detections. Owing to the challenge in well and rapid fabrication of solid-state nanopores with the diameter less than 2 nm, small molecule detection is hard to be addressed by existing label-free nanopore methods. In this work, we for the first time propose a metal-coated wireless nanopore electrode (WNE) which offers a novel and generally accessible detection method for analyzing small molecules and ions at the single molecule/ion level. Here, a silver-coated WNE is developed as a proof-of-principle model which achieves the detection the self-generated H2, the smallest known molecule, and Ag+ at single molecule/ion level by monitoring the enhanced ionic signatures. Under a bias potential of -800 mV, the WNE could accomplish the distinction of as low as 14 H2 molecules and 28 Ag+ from one spike signal. The finite element simulation is introduced to suggest that the generation of H2 at the orifice of the WNE results in the enhanced spike of ionic current. As a proof-of-concept experiment, the WNE is further utilized to directly detect Hg2+ from 100 pM to 100 nM by monitoring the frequency of the spike signals. This novel nanoelectrode provides a brand new label-free, ultrasensitive, and simple detection mechanism for various small molecules/ions detection, especially for redox analytes. |
Blog
Read the G.I.G Motors blog today and learn about the vehicle launches, deliveries and events that we host all the time.
This blog is also home to our charity of the month initiative, where we choose to highlight a different charity every single
month.
Read our articles below and contact us for more information on any of these posts. |
When it comes to ensuring that its upcoming Juno spacecraft can survive its mission, NASA is surrounding the spacecraft's electronic innards with titanium to ward off radiation.
Juno's so-called radiation vault weighs about 200 kilograms (500 pounds), has walls that measure about a square meter (nearly 9 square feet) in area, are about 1 centimeter (a third of an inch) in thickness, and weigh 18 kilograms (40 pounds). About the size of an SUV's trunk - the vault encloses Juno's command and data handling box, power and data distribution unit and about 20 other electronic assemblies, according to NASA.
NASA telescopes watch cosmic violence, mysteries unravel
"For the 15 months Juno orbits Jupiter, the spacecraft will have to withstand the equivalent of more than 100 million dental X-rays," said Bill McAlpine, Juno's radiation control manager, based at NASA's Jet Propulsion Laboratory in Pasadena, Calif., in a release.
According to NASA Jupiter has sizzling radiation belts surrounding its equatorial region that extend out past one of its moons, Europa, about 650,000 kilometers (400,000 miles). Jupiter has 63 moons.
Juno's handlers are taking it on a path that takes the spacecraft around Jupiter's poles, spending as little time as possible in those radiation belt areas. Engineers also used designs for electronics already approved for the Martian radiation environment, which is harsher than Earth's, though not as harsh as Jupiter's. Parts of the electronics were made from tantalum, or tungsten, another radiation-resistant metal. Some assemblies also have their own mini-vaults for protection, NASA stated.
Packing Juno's innards next to each other allows them to shield their neighbors. In addition, engineers wrapped copper and stainless steel braids like chain mail around wires connecting the electronics to other parts of the spacecraft, NASA stated.
Juno is basically an armored tank going to Jupiter," said Scott Bolton, Juno's principal investigator, based at Southwest Research Institute in San Antonio. "Without its protective shield, or radiation vault, Juno's brain would get fried on the very first pass near Jupiter."
Expected to launch August 2011, NASA has outlined a number of key challenges for Juno:
Juno will determine the global structure and motions of the planet's atmosphere below its colorful cloud tops for the first time, mapping variations in the atmosphere's composition, temperature, clouds and patterns of movement down to unprecedented depths, NASA said.
Deep in Jupiter's atmosphere, under great pressure, hydrogen gas is squeezed into a fluid known as metallic hydrogen. At these great depths, the hydrogen acts like an electrically conducting metal which is believed to be the source of the planet's intense magnetic field. This powerful magnetic environment creates the brightest auroras in our solar system, as charged particles precipitate down into the planet's atmosphere. Juno will directly sample the charged particles and magnetic fields near Jupiter's poles for the first time, while simultaneously observing the auroras in ultraviolet light produced by the extraordinary amounts of energy crashing into the polar regions, NASA said.
NASA's Juno mission is the second spacecraft designed under NASA's New Frontiers Program. The first was the Pluto New Horizons mission. Launched into space in January 2006 and has been hurtling toward Pluto at about 50,000 mph. Even at that rate the 1,054lb satellite will get it close to the dwarf planet sometime around July 2015.
Follow Michael Cooney on Twitter: nwwlayer8
Layer 8 Extra
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Beyond the petaflop - DARPA wants quintillion-speed computers |
Italian entrepreneur Andrea Rossi has surfaced again to restate his claim that his E-Cat low energy nuclear reaction kit puts out more energy than goes in. And so it is that the “cold fusion” debate will be re-ignited – this time with new voices in Rossi's corner.
Giuseppe Levi and Evelyn Foschi (Bologna University, Italy); Torbjörn Hartman, Bo Höistad, Roland Pettersson and Lars Tegnér, all of Uppsala University in Sweden, and Hanno Essén of the Royal Institute of Technology in Stockholm, are claiming that the heat produced in the latest tests of Rossi's E-Cat rig is “one order of magnitude greater than conventional energy sources”.
The report has been released via Arxiv.
Rossi's claim for the E-Cat is that a “low energy nuclear reaction” puts together nickel and hydrogen, with the outputs being copper and heat. He has, however, met with a great deal of scepticism – including on the part of The Register – and has not, to date, been able to have his claims considered to be proven.
One of the chief problems is that nobody has had the opportunity to verify the science behind the claims, because – as noted in the current paper – Rossi continues to regard the insides of the e-Cat as a trade secret:
“As in the original E-Cat, the reaction is fueled by a mixture of nickel, hydrogen, and a catalyst, which is kept as an industrial trade secret. The charge sets off the production of thermal energy after having been activated by heat produced by a set of resistor coils located inside the reactor.” (Emphasis added)
The setup included the system being fed by: “... a TRIAC power regulator device which interrupted each phase periodically, in order to modulate power input with an industrial trade secret waveform.” (Emphasis added)
So the test is probably going to be vulnerable to scientific tooth and claw from the start, since it amounts to researchers being asked to visit the premises of EFA – that is, the company that holds the production rights for the E-Cat – and test a black box whose operations are invisible.
The test claims to have observed power production of 2,034 Watts thermal for an input of 360 Watts.
And that's been received with ecstasy in some unexpected quarters, like Forbes, which got all gushy about E-Cat
“While a few commentators have raised criticisms concerning how the measurements were made and sources of error others have argued that the energy produced is so significant even knocking off an order of magnitude on either axis still portrays a process with insanely valuable output.”
Actually, Mark Gibbs (the Forbes author I've quoted), the “order of magnitude” claim wasn't made by unnamed commentators – it's made in the abstract of the Levi paper we've linked to above.
On the plus side, publication of the test on Arxiv will at least give the rest of the scientific world something to get their teeth into. Articles on Arxiv are not peer reviewed, but may be moderated before inclusion.
It'll also be fascinating to see if this test is strong enough "proof" for Australian philanthropist Dick Smith to fork out the $AUD200,000 he has on the table if the E-Cat works.
Over to you, readers of El Reg; we await your comments with fascination and trepidation. ® |
The Premier League has supplied three of the four semi-finalists for the past three seasons, plus a finalist in each of the last five.
And Ferguson believes they will continue to rule Europe this season, despite competition from Spanish giants Real Madrid and Barcelona.
He said: “The English teams will be involved in the semi-finals again.
“They have been very dominant in the tournament for the last six or seven years. That is shown by the evidence of the latter stages and I think it will be the same this year.”
Manchester United will book their place in the last 16 with two games to spare if they beat CSKA Moscow at Old Trafford tonight.
Chelsea are similarly well placed after their opening three games, while it would be a major surprise if Arsenal did not make it through after collecting seven points so far.
In contrast, Inter Milan and Bayern Munich are currently outside the automatic qualification spots, while AC Milan and Real Madrid have already lost matches in a group they were expected to dominate completely.
Ferguson added: “Obviously Barcelona are one of the favourites. You cannot dismiss them.
“But there is no question in my mind that the English teams will compete for the trophy.” |
using UnityEngine;
using UnityEditor;
using System.Collections.Generic;
using System.Linq;
using com.spacepuppy;
using com.spacepuppy.Utils;
namespace com.spacepuppyeditor.Base
{
[CustomEditor(typeof(VariableStore))]
public class VariableStoreInspector : SPEditor
{
public const string PROP_REFLECTNAMES = "_reflectNamesFromType";
public const string PROP_VARIABLES = "_variables";
private VariantCollectionPropertyDrawer _variablesDrawer = new VariantCollectionPropertyDrawer();
protected override void OnSPInspectorGUI()
{
this.serializedObject.Update();
var propReflect = this.serializedObject.FindProperty(PROP_REFLECTNAMES);
SPEditorGUILayout.PropertyField(propReflect);
var propVars = this.serializedObject.FindProperty(PROP_VARIABLES);
var lbl_Vars = EditorHelper.TempContent("Variables");
_variablesDrawer.ConfigurePropertyList((TypeReferencePropertyDrawer.GetTypeFromTypeReference(propReflect)));
var h = _variablesDrawer.GetPropertyHeight(propVars, lbl_Vars);
var r = EditorGUILayout.GetControlRect(true, _variablesDrawer.GetPropertyHeight(propVars, lbl_Vars));
_variablesDrawer.OnGUI(r, propVars, lbl_Vars);
this.DrawDefaultInspectorExcept(EditorHelper.PROP_SCRIPT, PROP_REFLECTNAMES, PROP_VARIABLES);
this.serializedObject.ApplyModifiedProperties();
}
}
[CustomEditor(typeof(VariableStoreAsset))]
public class VariableStoreAssetInspector : VariableStoreInspector
{
}
}
|
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Rate, Reviews & Complaints about Central Digital Imaging Limited. This is the simplest way to share the experience and review & complaint about Central Digital Imaging Limited. It will not only help you but also save other customer to get cheated by such firms. Without any registration, you can share your feedback but please make sure no abusive or offensive language is used. |
On 6 October 2016 Bird & Bird The Hague co-hosted the seminar Digital Business – Big Data & Cloud Services with the Association of Corporate Counsel (ACC). The seminar took place in Amsterdam at one of Verizon's datacenters. |
# Copyright (C) 2016-2019 The ESPResSo project
# Copyright (C) 2014 Olaf Lenz
#
# This file is part of ESPResSo.
#
# ESPResSo is free software: you can redistribute it and/or modify
# it under the terms of the GNU General Public License as published by
# the Free Software Foundation, either version 3 of the License, or
# (at your option) any later version.
#
# ESPResSo is distributed in the hope that it will be useful,
# but WITHOUT ANY WARRANTY; without even the implied warranty of
# MERCHANTABILITY or FITNESS FOR A PARTICULAR PURPOSE. See the
# GNU General Public License for more details.
#
# You should have received a copy of the GNU General Public License
# along with this program. If not, see <http://www.gnu.org/licenses/>.
#
# This script generates gen_pxiconfig.cpp, which in turn generates myconfig.pxi.
#
import inspect
import sys
import os
# find featuredefs.py
moduledir = os.path.dirname(inspect.getfile(inspect.currentframe()))
sys.path.append(os.path.join(moduledir, '..', '..', 'config'))
import featuredefs
if len(sys.argv) != 3:
print("Usage: {} DEFFILE CPPFILE".format(sys.argv[0]), file=sys.stderr)
exit(2)
deffilename, cfilename = sys.argv[1:3]
print("Reading definitions from " + deffilename + "...")
defs = featuredefs.defs(deffilename)
print("Done.")
# generate cpp-file
print("Writing " + cfilename + "...")
cfile = open(cfilename, 'w')
cfile.write("""
#include "config.hpp"
#include <iostream>
using namespace std;
int main() {
cout << "# This file was autogenerated." << endl
<< "# Do not modify it or your changes will be overwritten!" << endl;
""")
template = """
#ifdef {0}
cout << "DEF {0} = 1" << endl;
#else
cout << "DEF {0} = 0" << endl;
#endif
"""
for feature in defs.allfeatures:
cfile.write(template.format(feature))
cfile.write("""
}
""")
cfile.close()
print("Done.")
|
Frequently Asked Questions
Frequently Asked Questions
FREQUENTLY ASKED QUESTIONS
Chicago Studio FAQs
I've never taken an art class before. Are there classes at Vitruvian that are good for beginners?
Yes. All our classes are open to students of all levels of ability and experience.
Are materials included in the course fee?
No. Since some students already have their own materials, charging a default materials fee can get complicated. It's just simpler if everyone does their own shopping. We do sell "Materials Kits" at the studio for some of our classes, which can be purchased at check-out when you enroll through the website. We offer this as a convenience to our students to save them a trip to the art supply store. Alternatively, a list of recommended materials will be emailed to you when you enroll if you'd prefer to shop elsewhere.
Are model fees extra?
No. The model fee is built into the sticker price of each class.
I'd like to see the studio. When is a good time to drop by?
We're sorry, but we simply can't accommodate studio visits. Our instructors are unavailable to receive visitors because their time here is already occupied with teaching. If you're looking for information about our courses, they're thoroughly described on our website. If you have further questions, we're happy to help via our contact form here.
We'd love to see you, but the best way to see the studio is to take a class!
Does Vitruvian host drop-in drawing and painting sessions with a model?
No. All our studio sessions are for enrolled students only.
I'd like to attend a class on a drop-in basis and just pay-as-I-go. Can I do that?
Sorry, but no. We'd love to have you in the studio, but we ask that everyone commit to the whole class.
Do you ever have daytime classes during the week?
Yes. We have a couple of options for weekdays. Our Weekday Atelier is an ongoing course of study in which students begin with simple drawing exercises that lead to more complicated painting and sculpture work. We also offer 5-Day Intensive Workshops from time to time that are much like their weekly class counterparts, but meet for 5 consecutive days in the studio.
I noticed some different classes that are scheduled to meet at the same time. What’s up with that?
Some classes may feature similar methods and are able to be “piggybacked” in the studio at the same time. For example, we may have Figure Drawing and Grisaille Painting students working at once, since the focus of each is primarily on drawing the figure. An instructor can easily accommodate both, and the cross-pollination of information can make for a richer experience for the students. Bargue Drawing and Cast Drawing is another good example.
Also, we offer “Intensive” versions of some classes that are simply alternative schedulings of existing classes. For example, “Figure Drawing Intensive” meets at the same time as “Figure Drawing”, but lasts all day for 4 weeks instead of a half-day for 8 weeks. This appeals to some students who travel a long distance for class and appreciate a way to minimize their commute.
Does Vitruvian offer classes in Acrylic or Watercolor painting?
Not really. Oil paint is the preferred medium in all our painting classes, although ocassional accommodations are made for students wishing to use other media.
Can I leave my supplies at the studio between class sessions?
We just don't have the space for that. We offer storage racks for work in progress so students don’t have to travel with wet paintings, but if we tried to accommodate the rest of everyone’s stuff we’d soon be over-run with debris. Please be prepared to take your supplies with you at the end of class.
Where can I park?
There are two small parking lots on the north and south sides of our building. Students can park in either lot, but please don’t block the loading dock. For our suburban students, there’s even better news… We’re just a few steps from the Clybourn Metra station, which of course makes parking unnecessary!
I’d like to sign-up, but I’m going to miss a couple of classes. Can I make them up somehow?
Perhaps. For classes that don’t feature a live model, makeup sessions may be scheduled on a case-by-case basis, and must occur within a month of the class completion date. Accommodations for missed class sessions must also be arranged at the time of enrollment. We cannot compensate for unplanned absences.
Our models, however, are booked only for a set number of class sessions, which means makeup sessions are not available for figure or portrait classes.
I’m running a little ahead of schedule today. Is it OK if I come to the studio early and hang out until class time?
Unfortunately, no. Vitruvian isn’t just a classroom space, but is a working studio that we use during the off-class hours. When students arrive too early, it disrupts our workflow and we can get a little cranky. We kindly ask that you don’t arrive more than 30 minutes before the scheduled start time. This should allow plenty of time for students to set up and be ready for when class begins.
I signed-up for a class but I can’t do it after-all. Can I get a refund?
For in-studio classes we offer refunds to students who withdraw from class less the $50 registration deposit, provided they do so before the start of the second class session. Once the second session has begun, however, no refunds will be granted.
Because of the digital nature of our online courses, however, no refunds will be granted. All sales of online courses are final.
I have a question. I called and left a voicemail, but I didn’t hear back. Don’t you guys check your messages?
The studio phone exists for one purpose: as a "doorbell" for the intercom system at the front door of the building. If you're trying to reach us, use the contact form here. We hope to hear from you!
Have a question not listed here? Let us know!
Online Studio FAQs
Our online courses are “asynchronous”, meaning they don’t have a set start-date or end-date. Rather, you can begin an online course at any time, and proceed at your own pace.
How long do I have to complete an online course?
As long as you wish. Once you’ve purchased any of our online courses, your access will never expire. Login to review the material as many times as you wish, for as long as you want.
Can I download the videos from an online course?
The video content of online courses is not downloadable. Instead, the videos “stream” from our server to logged-in students. This means that students must have an active internet connection to watch the videos.
Can I transfer the videos from an online course onto my iPad?
While you can easily login and watch the video content on an iPad – or any device with an internet connection – the video files themselves can’t be “transferred” for offline viewing. As mentioned above, the videos are not downloadable.
Why can’t I order the video content from an online course on DVD?
There are three reasons. First, the videos are just one part of the course content. The great advantage of online courses is that they are multimedia based and interactive. Since the accompanying text, images and Q&A threads are also part of the course, we want students to be engaged with that content, too. Making the videos available on DVD would separate them from the rest of the course and make for a less effective learning experience.
Second, the video content for the portrait drawing course is over 10 hours long, and simply wouldn’t fit on a single DVD, or even two. We’d have to offer more of a boxed set of DVDs that would present production, packaging, storage and shipping challenges that we’re simply not equipped to handle.
Lastly, digital delivery of video content is the future. Support for legacy formats, including DVD, is waning fast and it won’t be long before DVDs have gone the way of VHS tapes. We want our online platform to be forward-looking and demand for DVDs will only diminish with time.
How do I ask questions in an online course?
Each “lesson” includes a Question & Answer area at the bottom of the page where questions are addressed. In-depth, individual feedback – including video critiques – is available to students who purchase a “Critique Extension” as an optional add-on to any course.
Why do in-studio classes at Vitruvian cost more than online courses?
Our in-studio classes offer some advantages over online study, including one-on-one, at-easel instruction for every student included in the price. We offer the same degree of individual attention to our online students, but only with the purchase of a “Critique Extension” as an optional $100 add-on. Including the cost of the extension brings the price of our online courses closer inline with their in-studio counterparts.
Also, in-studio classes cost us more to offer as they require us to maintain a physical studio, and absorb the related costs – rent, utilities, insurance, etc. We also hire models for in-studio classes who are paid by the hour. All these factors contribute to the price difference between in-studio and online study. |
Q:
Pull random 10 entries without duplicating every time when ajax calls
Possible to pull random 10 entries (without duplicating entries) with ajax everytime when scroll to the bottom, right now it loads random 10 entires but it duplicates and some entries never shows up. Any ideas? thanks
index.html:
{exp:channel:entries channel="channel_A|channel_B|channel_C" orderby="random" limit="10"}
{content}
{/exp:channel:entries}
ajax/index.html
{exp:channel:entries channel="channel_A|channel_B|channel_C" orderby="random" limit="10"}
{content}
{paginate}
{pagination_links}
<ul class="lepaginate">
{page}
<li><a href="{pagination_url}" class="page-{pagination_page_number} {if current_page}active{/if}">{pagination_page_number}</a></li>
{/page}
</ul>
{/pagination_links}
{/paginate}
{/exp:channel:entries}
jquery:
var counter = 10;
$(window).scroll(function() {
if($(window).scrollTop() + $(window).height() == $(document).height()) {
var response;
$.ajax({ type: "GET",
url: ""+document.location.origin+"/ajax/P"+counter+"",
async: false,
success : function(text) {
response = text;
}
});
counter += 10 ;
newItems = $(response).appendTo('.grid');
$grid.isotope('appended', newItems );
var $grid = $('.grid').isotope({
masonry: {
columnWidth: 360,
gutter: 30
}
});
}
});
this is using pagination, so it loads like '/ajax/P10' '/ajax/P20' ..., etc
A:
Two approaches come to mind, the first is to load everything (all results) and only show X at a time (JavaScript) based on your own custom pagination or lazy loading effect. But that means you'd still be sending to the browser all the raw html initially, so might have performance issues.
How channel:entries works with the limit parameter in ExpressionEngine is by running a full search and getting all results back as a delimited list of entry id's based on all your search/filtering options. It then runs a second query to extract all the information it needs on the limited subset of entries to then be able to parse and present the data in your template.
So the second approach could actually be done a few ways depending on your skill level, but the principle is that you do a minimal query returning the entry IDs for all results (pipe delimited), then retain that as a JavaScript variable feeding the parts of the total results to match the (paginated) page results you require - feed that to your ajax call which in turn populates the entries to be shown in your final channel:entries tag.
Although initially you could use a channel:entries tag to get the full list, it should be better performance to use the exp:query tag - depending on the complexity of your filtering/search parameters. You could then post the required entries (for next page) to the ajax URL, and on the resulting page/template use the channel:entries parameter dynamic_parameters to use the POST data to automatically populate the entry_id parameter on the channel:entries tag, therefore only showing the limited entries.
Note that by default channel:entries only pulls back 100 results, if you want to pull more, you have to specify the limit parameter. From memory, going over 1000 starts to cause massive performance issues.
|
The Sanctuary of Athena Lindia(Click the image for a full screen view)
The Sanctuary of Athena Lindia
The History of the Excavations
The excavations at the Acropolis
of Lindus were begun systematically by the Danish archaeologists K.F. Kinch
and Chr. Blinkengerg. Their results were published in six volumes published
by the «Foundation Carlsberg» of Denmark. The first two volumes
(1931) deal with the objects, the next two (1941) with inscriptions. All
four are written by Blinkenberg. The architecture was published much later,
in 1960, in two volumes, by E. Dyggve who disagrees with many of the conclusions
drawn by Blinkenberg.
In 1910-1916 and 1929-1932 the Italian
archaeologists Maiuri and Jacopi worked on the site. It should be noted
that the island was under Italian occupation at the time, and the Italians
took an interest in the antiquities. They are responsible for the restoration
of the antiquities of Lindus which contribute to the popularity of the
site today.
The Cult of Lindus
The word Lindia (of Lindus), which
is a constant epithet of the Goddess, is of non-Greek origin etymologically.
Therefore, it seems that a cult existed in Lindus long before the Greeks,
perhaps even before the Mycenaeans, who were Greek-speaking. When the Dorians
brought their Goddess Athena with them, she was assimilated with the older
Goddess, a phenomenon which is very common in the history of religion.
For example, Athena of antiquity has now been assimilated to Virgin Mary
(Panaghia), whose church is to be seen in the village. According to Dyggve,
even the Temple of Athena Lindia was turned into a church of Virgin Mary
in the Christian era.
Apart from the name, another detail
points to an older, pre-existing cult in Lindus before Athena's arrival.
This detail comes from a poem by the 5th cent. BCE poet Pindar, who gives
the following mythical account of the establishment of Athena's cult: Zeus
had a terrible head-ache and asked Hephaestus to split his head. Hephaestus
struck with a brazen hatchet and Athena leapt forth from her father's head
and cried aloud with a mighty shout, while Heaven and Mother Earth, trembled
before her. Then the Sun God, who brings light to men, asked his dear children
to be the first to build an altar for the new Goddess and, by founding
a holy sacrifice, to gladden the heart of the father and daughter. But
sometimes mortals are driven from the right path, and they forgot to take
fire with them. So they performed the sacred rite without fire in the grove
of the Acropolis... (Olympian VII, 35-49).
This is clearly a myth designed to
explain a ritual, namely the custom of performing fireless rites in connection
with the cult of Athena Lindia. This deviated from standard Greek practice,
which demanded fire on the altar and burning of the entrails of the sacrificial
victims. This deviation from standard practice can be explained, if the
cult of Athena was assimilated to an older cult.
Blinkenberg suggested that no sacrifice
was performed at all in the Sanctuary, and that only fruits of the earth,
bloodless offerings, were made. He also stressed that there was no altar.
He concluded that the prehistoric Goddess, venerated before Athena, was
a vegetation Goddess, who did not require animal sacrifice.
Blinkenberg's hypothesis has found
general acceptance, but it may need modification. First, Dyggve identified
architectural evidence of an altar. Second and most important, there is
archaeological evidence of animal bones and ashes from the temenus (enclosure)
area outside the Temple. Third, votive animal figurines, as well as figurines
of men carrying animals, have been found. All this suggests that animals
were sacrificed. Blinkenberg himself was puzzled by the remnants of animal
bones and ashes, but he explained them as remnants of sacred banquets,
which took place in connection with the cult. This makes sense, but it
is difficult to accept that the killing and cooking of the animals was
a ceremony quite separate from the offering ritual.
What is the solution? Can Pindar's
testimony be ignored? Perhaps a close reading of the text will give a clue.
Pindar says that the sons of the Sun God forgot to take fire with them.
Their intention, however, was to perform sacrifice, and Pindar does not
say that they did not perform it; he says that they performed rites without
fire. Perhaps the solution is that they performed the sacrifice and ate
the meat but did not burn the entrails. This would deviate from standard
Greek practice (for sacrificial ritual, see further on) but would allow
the killing of the animal and the eating of the meat by the participants,
a practice which had a very important social function. This is only a hypothesis,
but it reconciles the Pindaric account with the archaeological evidence.
A different solution has been suggested,
Pindar's poem does not refer to Lindus at all but some other city on Rhodes.
The wording of the lines, however, do not support this supposition. Pindar
mentions other cities, but Lindus is mentioned last and the next line begins
with «there it is that...». Thus, the Pindaric account has
to be taken as serious evidence for the cult, whatever interpretation we
give to it.
The Temple Chronicle and the Epiphanies of the Goddess
In the area of Hagios Stephanos (see
map), a marble stele was found with valuable inscription concerning the
history of the Temple and with a list of offerings through the ages. This
is the Temple Chronicle, composed in the 1st cent. BCE. It was compiled
by a certain Timachidas, and its purpose was to advertise the wealth and
importance of the Sanctuary.
Map of Lindus' area, the bays, the Acropolis, the monuments
and the village.(Click the image for a full screen view)
For us it is valuable as a source
of religious belief in the Hellenistic period and as a historical source.
Among the most interesting accounts of the Temple Chronicle are the Epiphanies
(appearances) of Athena to mortals.
Although Athena can appear in person
in the Homeric poems, in the historical period she appeared in men's dreams.
Such forms of epiphany were common in antiquity, and some Greek sanctuaries,
like that of Asclepius at Epidaurus, had special arrangements for people
to sleep in the hope that the God would visit them at night.
One epiphany of Athena occurred at
the time of the Persian invasion in 490 BCE:
"When Darius, King of Persia, sent forth a great army
for the purpose of enslaving Hellas, this island was the first which his
fleet visited. The people in the country were terrified at the approach
of the Persians and fled for safety to all the strongholds, most of them
gathering at Lindus. Thereupon the barbarians set about to besiege them,
until the Lindians, sore-pressed by a water shortage, were minded to hand
over the city to the enemy. Right at this juncture the Goddess stood over
one of the magistrates in his sleep and bade him be of good courage, since
she herself would procure, by intercession with her father, the water they
needed. The one who saw the vision rehearsed to the citizens Athena's command.
So they investigated and found that they had only enough water to last
for five days, and accordingly they asked the barbarians for a truce for
just that number of days, saying that Athena had sent to her father for
help, and that if help did not come in the specified time, they would surrender
the city. When Datis, the admiral of Darius, heard this request, he immediately
burst out laughing. But the next day, when a great cloud gathered about
the Acropolis and a heavy shower fell inside the cloud, so that contrary
to all expectations (paradoxos) the besieged had plenty of water, while
the Persian army suffered for lack of it, the barbarian was struck by the
epiphany of the Goddess. He took off his personal adornment and sent it
as an offering -- his mantle, his necklace, and his bracelets, and in addition
his tiara, his scimitar, and even his chariot, which formerly was preserved
here, but was burned along with most of the offerings when the priest of
Helios was Eucles, son of Astyanactidas (probably soon after 350 BCE),
when the Temple caught fire. As for Datis, he set forth on the business
before him, after establishing peace with the besieged and declaring publicly,
"These men are protected by the Gods".
(From F.G. Grant, Hellenistic Religions, New York 1953)
In this account Athena lives
up to her reputation as a protectress of her city.
The History of the Temple and the Cult Image
Blinkenberg reconstructs the history
of the Temple as follows. At first there was no Temple structure at all,
only a grove to which Pindar refers also. The first structure may have
been built in the 6th cent. BCE. We do not know this; we can infer it only
by analogy from other sites.
A better Temple must have been built
by the tyrant Cleobulus (Kleoboulos) in the 6th cent. BCE. He may also
have strengthened the cult of the Goddess, as other tyrants did with local
Gods of their city-states, in an attempt to foster national religious feeling.
We know that Peisistratus strengthened the cult of Athena at Athens and
Polycrates built a magnificent Temple to Hera on Samos. Tyrants had also
another reason for building Temples: They absorbed the unemployed. The
promotion of national religion strengthened the political base of the tyrant's
power.
The cult image of this Temple has
naturally been lost, but Blinkenberg reconstructs it as a seated figure
with a special hat (polos) wearing necklaces and other jewelry. He infers
that from votive figurines of terra-cotta found in the Sanctuary of a colony
of Lindus which may reproduce the statue.
Figurine possibly representing Athena Lindia.(Click the image for a full screen view)
At the time of Cleobulus there was
also an impressive stairway, 7.5 m. broad, which led up to the Temple and
was used for processions. This stairway went through an enclosure wall
which marked off the temenus from the rest of the Acropolis. The first
built altar was probably erected then. An interesting detail: the Cleobulus
Temple was built above a natural cave in the cliff, which cave must have
been a cult place in prehistoric times. It was perhaps the cave which dictated
the choice of spot for the Temple at the very edge of the cliff. In Byzantine
times, this cave was used for the worship of Virgin Mary.
4th Cent. BCE
Around 342 BCE, the Cleobulus Temple
was burned, and a new one was built in its place in the end of the 4th
cent. BCE or around 300 BCE. The whole temenus area was later reorganized,
the most important addition being the Propylaea, an elaborate gate-structure
leading to the temenus.
The new Temple was in the Doric order.
It had three rooms and two rows of four columns, along the short sides.
(The terminus technicus is amphiprostylos). Its dimensions were 7.75 x
21.65 m.
A new cult image was created for the
new Temple, the type of which we can infer, once more, from votive terra-cotta
figurines. The Goddess was represented standing and carrying a shield,
and the statue almost certainly reflects Pheidian style and the Athena
of the Parthenon at Athens. But on her head she did not wear a helmet,
like the Athenian one, but a polos hat, like that of the older cult image.
An inscription makes some reference to jewelry, so it is quite possible
that this image also was ornated with pectorals and necklaces. The Temple
Chronicle of Lindus gives us some additional information. The statue was
fastened against the short wall of the cella, thus facing the spectator
as he entered from the door. Why was it fastened? Perhaps it was necessary
to secure it in position if it were too big to balance itself effectively
on its own weight, especially since there was always fear of earthquakes.
It must have been over life-size. The materials could have been wood for
the main body and ivory for the extremities, feet, arms, head. The Lindians
could not have afforded a gold and ivory statue as the Athenians did.
The fame of the Temple can be deduced
from the fact that Alexander the Great and many of his successors offered
magnificent sacrifices there, and dedicated weapons after victories. It
can also be inferred from the quality of votive gifts, many of which were
famous in antiquity and are mentioned in the Temple Chronicle. The sculptor
Boethus, the painter Parrhasios of Ephesus and other great artists had
their works exhibited in the Sanctuary.
The Propylaea (Gate)
The Propylaea were built in the first
half of the 3rd cent. BCE. and this involved a radical change in the appearance
of the Sanctuary. Before, the temenus was marked off by a low wall, now
this low wall was replaced by the monumental facade of the Propylaea to
which a very broad stairway gave access.
Reconstruction of the Propylaea after Dyggve.(Click the image for a full screen view)
The Propylaea were in the Doric order
and were U-shaped. The emphasis was on the wings, which looked like the
facades of the Temple. In this way the Temple facade is anticipated before
the visitor enters the temenus. The arrangement was designed to direct
the visitor through a series of surprises and changing views and to prepare
him for a crescendo upon reaching the temenus. We must imagine that the
view changed constantly with gradual ascent by the staircase. When the
visitor reached the top, he had to pass through a hall, which was bordered
by columns on the long sides. He was then confronted with a spectacular
panoramic view on the one hand, on the other he could see the Temple against
this view. The Temple was off the main axis, but the altar stood in the
center of the temenus. This was the sacrificial altar, identified by Dyggve.
Another one, smaller, and destined for bloodless offerings, was placed
inside the Temple in front of the cult image.
The Propylaea were asymmetrical, but
this could be seen only from the inside; from the outside they gave the
illusion of complete symmetry. The rooms of the wings were designed for
banqueting which followed the sacrifice and for display of the most spectacular
votive offerings, the greatest works of art. But the main function of the
whole structure was to isolate the temenus and to screen off unpurified
visitors.
The following prohibitions were effective
regarding entrance to the Sanctuary: Carrying weapons was prohibited. One
had to be decently dressed with the head covered. One had to be barefoot
or else wear white shoes, which could not be made out of horse's skin.
You could not enter at all immediately after loss of virginity; after an
abortion; during menstruation; after you had come into contact with a dead
body; after intercourse, unless a purification bath had taken place, etc.
These instructions shed light on the notions of impurity of the ancients.
The Portico or Stoa
The Hellenistic period was one of
artistic exaggeration. If the early art of the Greeks is characterized
by modesty and simplicity, the late art and architecture, during the Hellenistic
period, delights in dramatic effect. We can seen this in sculpture and
it is valid for architecture as well. By the end of the 3rd cent. BCE,
the monumental Propylaea were no longer considered magnificent enough in
themselves, and another structure had to be added to enhance dramatic effect.
This structure was a Doric portico or stoa which duplicated the facade
of the Propylaea but on a much larger scale.
Reconstruction of the Doric Portico or Stoa.Reconstruction after Dyggve.(Click the image for a full screen view)
The main difference in plan was the
complete symmetry of the Portico. The element of surprise, which was the
principle of the architects of the Propylaea, was repeated here as well.
Most important must have been the interplay of light and shade, as one
passed from the staircase to the columns of the central part. The center
of the long side of the Portico was cut by the stairway which led up to
the Propylaea. In a way the Portico was built as an entrance to this stairway,
just as the Propylaea were built as an entrance to the temenus. The experience
was thus repeated twice, and the visitor's expectations were rising with
each ascent.
It is with purpose that the wings
of the Portico reproduce the facade of the Temple, as was the case in the
Propylaea. The Temple was, after all, the emblem of the Sanctuary and the
culmination of the experience.
The function of the Portico was more
secular. It was outside the temenus and served as an art gallery and as
a shady area, much needed during the hot summer days.
Later Structures
Later additions destroyed rather
than enhanced the effect. The terrace was enlarged in the 1st cent. BCE.
Beneath this terrace there were 10 vaulted cisterns for the collection
of water. In the 2nd cent. CE an Ionic portico was added in the temenus
area, thus blocking the dramatic landscape which acted as a backdrop to
the temenus. Finally, the view from the other side of the acropolis was
blocked by the erection of a Roman Temple in the 3rd cent. CE, presumably
for the cult of a deified emperor. Some think it was for the cult of the
hero Psithyros.
Acropolis reconstruction with later structures.(Click the image for a full screen view)
Votive Offerings
In our times, it is often the case
that votives are placed on an icon of the Greek Orthodox Church as tokens
of gratitude for a difficulty or illness which has been overcome. These
offerings are jewelry or silver/gold limbs representing the healed parts
of the body: Ancient offerings were even more varied. Their value depended
on the economic status of the dedicator. They could range from large-scale
sculptures in stone, or bronze, to small figurines. They could be jewelry,
vases, weapons, and objects of every-day use such as mirrors and spindle
whirls. Most often they had the form of terra-cotta figurines representing
humans or animals. Sometimes the cult image of the divinity was represented,
but more frequently it was the mortal who presented himself as an worshiper
and servant to the God.
In the Sanctuary of Athena Lindia
figurines of musicians, horsemen, men carrying animals (for sacrifice)
have been found, representing different categories of worshippers. It is
female figurines that predominate, however, because of Athena's special
relationship with women as a protectress of the household. Mothers holding
a child are frequently represented; they were placing the child under the
protection of Athena. A special type is the seated boy, which is attested
also in Cyprus. Were these boys rendering services to the Temple for a
period and do the figurines symbolize this? If so, we have an Oriental
custom here. There is also a type of male figurine reclining and holding
a drinking vessel. This must allude to the sacrificial banqueting which
took place in the rooms of the Propylaea. Exotic animals like lions as
well as birds and cats are suggestive of the power of Athena over nature.
There are also objects brought from abroad, gifts from foreigners who visited
the Sanctuary. Egyptian, Near Eastern and Cypriot objects are attested
in significant quantities. A final category of objects represents cult
implements: lamps and torches used in processions, baskets which would
be filled with fruit and offered, wine jars and drinking cups which are
related to the feasting.
Lindus lies 55 km to the S. of the
city of Rhodes and is accessible by bus or even by small boats during the
summer season. The trip by car takes a little less than an hour and the
road is very good. For this reason one can even rent a car and drive without
being apprehensive about the possible mis-fortunes due to the conditions
of some Greek roads.
When you come close to Lindus, there
is a long beach, Vlecha (Vlycha), to your left or N. of the Acropolis which
towers over the landscape. On this beach, there exists the four major hotels
of Lindus: Lindos Bay Hotel, Lindos Royal Hotel, LTI Lindos Royal and Lindos
Mare Hotel. Otherwise, accommodations can be found in the village: there
are rooms to let in pensions or private houses.
The bus, or car, has to stop in the
square of the village; from there one has to go on foot because the village
streets are too narrow. The square is well equipped for the tourist: you
can buy film, souvenirs, refreshments, and there are restaurants as well. |
---
abstract: 'We present a contemporary perspective on the String Landscape and the Multiverse of plausible string, M- and F-theory vacua. In contrast to traditional statistical classifications and capitulation to the anthropic principle, we seek only to demonstrate the existence of a non-zero probability for a universe matching our own observed physics within the solution ensemble. We argue for the importance of No-Scale Supergravity as an essential common underpinning for the spontaneous emergence of a cosmologically flat universe from the quantum “nothingness”. Concretely, we continue to probe the phenomenology of a specific model which is testable at the LHC and Tevatron. Dubbed No-Scale ${\cal F}$-$SU(5)$, it represents the intersection of the Flipped $SU(5)$ Grand Unified Theory (GUT) with extra TeV-Scale vector-like multiplets derived out of F-theory, and the dynamics of No-Scale Supergravity, which in turn imply a very restricted set of high energy boundary conditions. By secondarily minimizing the minimum of the scalar Higgs potential, we dynamically determine the ratio $\tan \beta \simeq 15-20$ of up- to down-type Higgs vacuum expectation values (VEVs), the universal gaugino boundary mass $M_{1/2} \simeq 450$ GeV, and consequently also the total magnitude of the GUT-scale Higgs VEVs, while constraining the low energy Standard Model gauge couplings. In particular, this local [*minimum minimorum*]{} lies within the previously described “golden strip”, satisfying all current experimental constraints. We emphasize, however, that the overarching goal is not to establish why our own particular universe possesses any number of specific characteristics, but rather to tease out what generic principles might govern the superset of all possible universes.'
author:
- Tianjun Li
- 'James A. Maxin'
- 'Dimitri V. Nanopoulos'
- 'Joel W. Walker'
title: ' Blueprints of the No-Scale Multiverse at the LHC '
---
Introduction
============
The number of consistent, meta-stable vacua of string, M- or (predominantly) F-theory flux compactifications which exhibit broadly plausible phenomenology, including moduli stabilization and broken supersymmetry [@Bousso:2000xa; @Giddings:2001yu; @Kachru:2003aw; @Susskind:2003kw; @Denef:2004ze; @Denef:2004cf], is popularly estimated [@Denef:2004dm; @Denef:2007pq] to be of order $10^{500}$. It is moreover currently in vogue to suggest that degeneracy of common features across these many “universes” might statistically isolate the physically realistic universe from the vast “landscape”, much as the entropy function coaxes the singular order of macroscopic thermodynamics from the chaotic duplicity of the entangled quantum microstate. We argue here though the counter point that we are not obliged [*a priori*]{} to live in the likeliest of all universes, but only in one which is possible. The existence merely of a non-zero probability for our existence is sufficient.
We indulge for this effort the fanciful imagination that the “Multiverse” of string vacua might exhibit some literal realization beyond our own physical sphere. A single electron may be said to wander all histories through interfering apertures, though its arrival is ultimately registered at a localized point on the target. The journey to that destination is steered by the full dynamics of the theory, although the isolated spontaneous solution reflects only faintly the richness of the solution ensemble. Whether the Multiverse be reverie or reality, the conceptual superset of our own physics which it embodies must certainly represent the interference of all navigable universal histories.
Surely many times afore has mankind’s notion of the heavens expanded - the Earth dispatched from its central pedestal in our solar system and the Sun rendered one among some hundred billion stars of the Milky Way, itself reduced to one among some hundred billion galaxies. Finally perhaps, we come to the completion of our Odyssey, by realizing that our Universe is one of at least $10^{500}$ so possible, thus rendering the anthropic view of our position in the Universe (environmental coincidences explained away by the availability of $10^{11} \times 10^{11}$ solar systems) functionally equivalent to the anthropic view of the origin of the Universe (coincidences in the form and content of physical laws explained away by the availability, through dynamical phase transitions, of $10^{500}$ universes). Nature’s bounty has anyway invariably trumped our wildest anticipations, and though frugal and equanimous in law, she has spared no extravagance or whimsy in its manifestation.
Our perspective should not be misconstrued, however, as complacent retreat into the tautology of the weak anthropic principle. It is indeed unassailable truism that an observed universe must afford and sustain the life of the observer, including requisite constraints, for example, on the cosmological constant [@Weinberg:1987dv] and gauge hierarchy. Our point of view, though, is sharply different; we should be able to resolve the cosmological constant and gauge hierarchy problems through investigation of the fundamental laws of our (or any single) Universe, its accidental and specific properties notwithstanding, without resorting to the existence of observers. In our view, the observer is the output of, not the [*raison d’être*]{} of, our Universe. Thus, our attention is advance from this base camp of our own physics, as unlikely an appointment as it may be, to the summit goal of the master theory and symmetries which govern all possible universes. In so seeking, our first halting forage must be that of a concrete string model which can describe Nature locally.
The Ensemble Multiverse
=======================
The greatest mystery of Nature is the origin of the Universe itself. Modern cosmology is relatively clear regarding the occurrence of a hot big bang, and subsequent Planck, grand unification, cosmic inflation, lepto- and baryogenesis, and electroweak epochs, followed by nucleosynthesis, radiation decoupling, and large scale structure formation. In particular, cosmic inflation can address the flatness and monopole problems, explain homogeneity, and generate the fractional anisotropy of the cosmic background radiation by quantum fluctuation of the inflaton field [@Guth:1980zm; @Linde:1981mu; @Albrecht:1982wi; @Ellis:1982ws; @Nanopoulos:1982bv]. A key question though, is from whence the energy of the Universe arose. Interestingly, the gravitational field in an inflationary scenario can supply the required positive mass-kinetic energy, since its potential energy becomes negative without bound, allowing that the total energy could be exactly zero.
Perhaps the most striking revelation of the post-WMAP [@Spergel:2003cb; @Spergel:2006hy; @Komatsu:2010fb] era is the decisive determination that our Universe is indeed globally flat, [*i.e.*]{} with the net energy contributions from baryonic matter $\simeq 5\%$, dark matter $\simeq 23\%$, and the cosmological constant (dark energy) $\simeq 72\%$ finely balanced against the gravitational potential. Not long ago, it was possible to imagine the Universe, with all of its physics intact, hosting any arbitrary mass-energy density, such that “$k=+1$” would represent a super-critical cosmology of positive curvature, and “$k=-1$” the sub-critical case of negative curvature. In hindsight, this may come to seem as naïve as the notion of an empty infinite Cartesian space. The observed energy balance is highly suggestive of a fundamental symmetry which protects the “$k=0$” critical solution, such that the physical constants of our Universe may not be divorced from its net content.
This null energy condition licenses the speculative connection [*ex nihilo*]{} of our present universe back to the primordial quantum fluctuation of an external system. Indeed, there is nothing which quantum mechanics abhors more than nothingness. This being the case, an extra universe here or there might rightly be considered no extra trouble at all! Specifically, it has been suggested [@Guth:1980zm; @Linde:1981mu; @Albrecht:1982wi; @Steinhardt; @Vilenkin:1983xq] that the fluctuations of a dynamically evolved expanding universe might spontaneously produce tunneling from a false vacuum into an adjacent (likely also false) meta-stable vacuum of lower energy, driving a local inflationary phase, much as a crystal of ice or a bubble of steam may nucleate and expand in a super-cooled or super-heated fluid during first order transition. In this “eternal inflation” scenario, such patches of space will volumetrically dominate by virtue of their exponential expansion, recursively generating an infinite fractal array of causally disconnected “Russian doll” universes, nesting each within another, and each featuring its own unique physical parameters and physical laws. From just the specific location on the solution “target” where our own Universe landed, it may be impossible to directly reconstruct the full theory. Fundamentally, it may be impossible even in principle to specify why our particular Universe is precisely as it is. However, superstring theory and its generalizations may yet present to us a loftier prize - the theory of the ensemble Multiverse.
The Invariance of Flatness
==========================
More important than any differences between various possible vacua are the properties which might be invariant, protected by basic symmetries of the underlying mechanics. We suppose that one such basic property must be cosmological flatness, so that the seedling universe may transition dynamically across the boundary of its own creation, maintaining a zero balance of some suitably defined energy function. In practice, this implies that gravity must be ubiquitous, its negative potential energy allowing for positive mass and kinetic energy. Within such a universe, quantum fluctuations may not again cause isolated material objects to spring into existence, as their net energy must necessarily be positive. For the example of a particle with mass $m$ on the surface of the Earth, the ratio of gravitational to mass energy is more than nine orders of magnitude too small $$\left| -\frac{G_N M_E m}{R_E} \right| \div m c^2 \simeq 7 \times 10^{-10}~,~$$ where $G_N$ is the gravitational constant, $c$ is the speed of light, and $M_E$ and $R_E$ are the mass and radius of the Earth, respectively. Even in the limiting case of a Schwarzschild black hole of mass $M_{BH}$, a particle of mass $m$ at the horizon $R_{S}=2 G_N M_{BH}/c^2$ has a gravitational potential which is only half of that required. $$\left| -\frac{G_N M_{BH} m}{R_{S}} \right| = \frac{1}{2} m c^2$$ It is important to note that while the energy density for the gravitational field is surely negative in Newtonian mechanics, the global gravitational field energy is not well defined in general relativity. Unique prescriptions for a stress-energy-momentum pseudotensor can be formulated though, notably that of Landau and Lifshitz. Any such stress-energy can, however, be made to vanish locally by general coordinate transformation, and it is not even entirely clear that the pseudotensor so applied is an appropriate general relativistic object. Given though that Newtonian gravity is the classical limit of general relativity, it is reasonable to suspect that the properly defined field energy density will be likewise also negative, and that inflation is indeed consistent with a correctly generalized notion of constant, zero total energy.
A universe would then be in this sense closed, an island unto itself, from the moment of its inception from the quantum froth; only a universe [*in toto*]{} might so originate, emerging as a critically bound structure possessing profound density and minute proportion, each as accorded against intrinsically defined scales (the analogous Newton and Planck parameters and the propagation speed of massless fields), and expanding or inflating henceforth and eternally.
The Invariance of No-Scale SUGRA
================================
Inflation, driven by the scalar inflaton field is itself inherently a quantum field theoretic subject. However, there is tension between quantum mechanics and general relativity. Currently, superstring theory is the best candidate for quantum gravity. The five consistent ten dimensional superstring theories, namely heterotic $E_8 \times E_8$, heterotic $SO(32)$, Type I, Type IIA, Type IIB, can be unified by various duality transformations under an eleven-dimensional M-theory [@Witten:1995ex], and the twelve-dimensional F-theory can be considered as the strongly coupled formulation of the Type IIB string theory with a varying axion-dilaton field [@Vafa:1996xn]. Self consistency of the string (or M-, F-) algebra implies a ten (or eleven, twelve) dimensional master spacetime, some elements of which – six (or seven, eight) to match our observed four large dimensions – may be compactified on a manifold (typically Calabi-Yau manifolds or $G_2$ manifolds) which conserves a requisite portion of supersymmetric charges.
The structure of the curvature within the extra dimensions dictates in no small measure the particular phenomenology of the unfolded dimensions, secreting away the “closet space” to encode the symmetries of all gauged interactions. The physical volume of the internal spatial manifold is directly related to the effective Planck scale and basic gauge coupling strengths in the external space. The compactification is in turn described by fundamental moduli fields which must be stabilized, [*i.e.*]{} given suitable vacuum expectation values (VEVs). The famous example of Kaluza and Klein prototypes the manner in which general covariance in five dimensions is transformed to gravity plus Maxwell theory in four dimensions when the transverse fifth dimension is cycled around a circle. The connection of geometry to particle physics is perhaps nowhere more intuitively clear than in the context of model building with $D6$-branes, where the gauge structure and family replication are related directly to the brane stacking and intersection multiplicities. The Yukawa couplings and Higgs structure are in like manners also specified, leading after radiative symmetry breaking of the chiral gauge sector to low energy masses for the chiral fermions and broken gauge generators, each massless in the symmetric limit.
From a top-down view, Supergravity (SUGRA) is an ubiquitous infrared limit of string theory, and forms the starting point of any two-dimensional world sheet or D-dimensional target space action. The mandatory localization of the Supersymmetry (SUSY) algebra, and thus the momentum-energy (space-time translation) operators, leads to general coordinate invariance of the action and an Einstein field theory limit. Any available flavor of Supergravity will not however suffice. In general, extraneous fine tuning is required to avoid a cosmological constant which scales like a dimensionally suitable power of the Planck mass. Neglecting even the question of whether such a universe might be permitted to appear spontaneously, it would then be doomed to curl upon itself and collapse within the order of the Planck time, for comparison about $10^{-43}$ seconds in our Universe. Expansion and inflation appear to uniquely require properties which arise naturally only in the No-Scale SUGRA formulation [@Cremmer:1983bf; @Ellis:1983sf; @Ellis:1983ei; @Ellis:1984bm; @Lahanas:1986uc].
SUSY is in this case broken while the vacuum energy density vanishes automatically at tree level due to a suitable choice of the Kähler potential, the function which specifies the metric on superspace. At the minimum of the null scalar potential, there are flat directions which leave the compactification moduli VEVs undetermined by the classical equations of motion. We thus receive without additional effort an answer to the deep question of how these moduli are stabilized; they have been transformed into dynamical variables which are to be determined by minimizing corrections to the scalar potential at loop order. In particular, the high energy gravitino mass $M_{3/2}$, and also the proportionally equivalent universal gaugino mass $M_{1/2}$, will be established in this way. Subsequently, all gauge mediated SUSY breaking soft-terms will be dynamically evolved down from this boundary under the renormalization group [@Giudice:1998bp], establishing in large measure the low energy phenomenology, and solving also the Flavour Changing Neutral Current (FCNC) problem. Since the moduli are fixed at a false local minimum, phase transitions by quantum tunneling will naturally occur between discrete vacua.
We conjecture, for the reasons given prior, that the No-Scale SUGRA construction could pervade all universes in the String Landscape with reasonable flux vacua. This being the case, intelligent creatures elsewhere in the Multiverse, though separated from us by a bridge too far, might reasonably so concur after parallel examination of their own physics. Moreover, they might leverage via this insight a deeper knowledge of the underlying Multiverse-invariant master theory, of which our known string, M-, and F-theories may compose some coherently overlapping patch of the garment edge. Perhaps we yet share appreciation, across the cords which bind our 13.7 billion years to their corresponding blink of history, for the common timeless principles under which we are but two isolated condensations upon two particular vacuum solutions among the physical ensemble.
An Archetype Model Universe
===========================
Though we engage in this work lofty and speculative questions of natural philosophy, we balance abstraction against the measured material underpinnings of concrete phenomenological models with direct and specific connection to tested and testable particle physics. If the suggestion is correct that eternal inflation and No-Scale SUGRA models with string origins together describe what is in fact our Multiverse, then we must as a prerequisite settle the issue of whether our own phenomenology can be produced out of such a construction.
In the context of Type II intersecting D-brane models, we have indeed found one realistic Pati-Salam model which might describe Nature as we observe it [@Cvetic:2004ui; @Chen:2007px; @Chen:2007zu]. If only the F-terms of three complex structure moduli are non-zero, we also automatically have vanishing vacuum energy, and obtain a generalized No-Scale SUGRA. It seems to us that the string derived Grand Unified Theories (GUTs), and particularly the Flipped $SU(5)\times U(1)_X$ models [@Barr:1981qv; @Derendinger:1983aj; @Antoniadis:1987dx], are also candidate realistic string models with promising predictions that can be tested at the Large Hadron Collider (LHC), the Tevatron, and other future experiments.
In the latter case, the Flipped $SU(5)\times U(1)_X$ gauge symmetry can be broken down to the SM gauge symmetry by giving VEVs to one pair of the Higgs fields $H$ and $\overline{H}$ with quantum numbers $(\mathbf{10}, \mathbf{1})$ and $(\mathbf{\overline{10}}, \mathbf{-1})$, respectively. The doublet-triplet splitting problem can be solved naturally via the missing partner mechanism [@Antoniadis:1987dx]. Historically, Flipped $SU(5)\times U(1)_X$ models have been constructed systematically in the free fermionic string constructions at Kac-Moody level one [@Antoniadis:1987dx; @Antoniadis:1987tv; @Antoniadis:1988tt; @Antoniadis:1989zy; @Lopez:1992kg]. To address the little hierarchy problem between the unification scale and the string scale, the Testable Flipped $SU(5)\times U(1)_X$ model class was proposed, which introduces extra TeV-scale vector-like particles [@Jiang:2006hf]. Models of this type have been constructed locally as examples of F-theory model building [@Beasley:2008dc; @Beasley:2008kw; @Donagi:2008ca; @Donagi:2008kj; @Jiang:2009zza; @Jiang:2009za], and dubbed ${\cal F}$-$SU(5)$ [@Jiang:2009zza; @Jiang:2009za] within that context.
Most recently, we have studied No-Scale extensions of the prior in detail [@Li:2010ws; @Li:2010mi; @Li:2010uu], emphasizing the essential role of the tripodal foundation formed by the $\mathcal{F}$-lipped $SU(5)$ GUT [@Barr:1981qv; @Derendinger:1983aj; @Antoniadis:1987dx], two pairs of TeV scale vector-like multiplets with origins in $\mathcal{F}$-theory [@Jiang:2006hf; @Jiang:2009zza; @Jiang:2009za; @Li:2010dp] model building, and the boundary conditions of No-Scale Supergravity [@Cremmer:1983bf; @Ellis:1983sf; @Ellis:1983ei; @Ellis:1984bm; @Lahanas:1986uc]. It appears that the No-Scale scenario, particularly vanishing of the Higgs bilinear soft term $B_\mu$, comes into its own only when applied at an elevated scale, approaching the Planck mass. $M_{\cal F} \simeq 7\times 10^{17}$ GeV, the point of the second stage $SU(5)\times U(1)_{\rm X}$ unification, emerges in turn as a suitable candidate scale only when substantially decoupled from the primary GUT scale unification of $SU(3)_C\times SU(2)_L$ via the modification to the renormalization group equations (RGEs) from the extra ${\cal F}$-theory vector multiplets.
In particular, we have systematically established the hyper-surface within the $\tan \beta$, top quark mass $m_{t}$, gaugino mass $M_{1/2}$, and vector-like particle mass $M_{V}$ parameter volume which is compatible with the application of the simplest No-Scale SUGRA boundary conditions [@Cremmer:1983bf; @Ellis:1983sf; @Ellis:1983ei; @Ellis:1984bm; @Lahanas:1986uc], particularly the vanishing of the Higgs bilinear soft term $B_\mu$ at the ultimate ${\cal{F}}$-$SU(5)$ unification scale [@Li:2010ws; @Li:2010mi]. We have demonstrated that simultaneous adherence to all current experimental constraints, most importantly contributions to the muon anomalous magnetic moment $(g-2)_\mu$ [@Bennett:2004pv], the branching ratio limit on $(b \rightarrow s\gamma)$ [@Barberio:2007cr; @Misiak:2006zs], and the 7-year WMAP relic density measurement [@Spergel:2003cb; @Spergel:2006hy; @Komatsu:2010fb], dramatically reduces the allowed solutions to a highly non-trivial “golden strip” with $\tan \beta \simeq 15$, $m_{t} = 173.0-174.4 ~{\rm GeV}$, $M_{1/2} = 455-481 ~{\rm GeV}$, and $M_{V} = 691-1020 ~{\rm GeV}$, effectively eliminating all extraneously tunable model parameters, where the consonance of the theoretically viable $m_{t}$ range with the experimentally established value [@:2009ec] is an independently correlated “postdiction”. Finally, taking a fixed $Z$-boson mass, we have dynamically determined the universal gaugino mass $M_{1/2}$ and fixed $\tan \beta$ via the “Super No-Scale” mechanism [@Li:2010uu], that being the secondary minimization, or [*minimum minimorum*]{}, of the minimum $V_{\rm min}$ of the Higgs potential for the electroweak symmetry breaking (EWSB) vacuum.
These models are moreover quite interesting from a phenomenological point of view [@Jiang:2009zza; @Jiang:2009za]. The predicted vector-like particles can be observed at the Large Hadron Collider, and the partial lifetime for proton decay in the leading ${(e|\mu)}^{+} \pi^0 $ channels falls around $5 \times 10^{34}$ years, testable at the future Hyper-Kamiokande [@Nakamura:2003hk] and Deep Underground Science and Engineering Laboratory (DUSEL) [@Raby:2008pd] experiments [@Li:2009fq; @Li:2010dp]. The lightest CP-even Higgs boson mass can be increased [@HLNT], hybrid inflation can be naturally realized, and the correct cosmic primordial density fluctuations can be generated [@Kyae:2005nv].
No-Scale Foundations of $\cal{F}$-$SU(5)$
=========================================
In the traditional framework, supersymmetry is broken in the hidden sector, and then its breaking effects are mediated to the observable sector via gravity or gauge interactions. In GUTs with gravity mediated supersymmetry breaking, also known as the minimal Supergravity (mSUGRA) model, the supersymmetry breaking soft terms can be parameterized by four universal parameters: the gaugino mass $M_{1/2}$, scalar mass $M_0$, trilinear soft term $A$, and the ratio of Higgs VEVs $\tan \beta$ at low energy, plus the sign of the Higgs bilinear mass term $\mu$. The $\mu$ term and its bilinear soft term $B_{\mu}$ are determined by the $Z$-boson mass $M_Z$ and $\tan \beta$ after the electroweak (EW) symmetry breaking.
To solve the cosmological constant problem, No-Scale Supergravity was proposed [@Cremmer:1983bf; @Ellis:1983sf; @Ellis:1983ei; @Ellis:1984bm; @Lahanas:1986uc]. No-scale Supergravity is defined as the subset of Supergravity models which satisfy the following three constraints [@Cremmer:1983bf; @Ellis:1983sf; @Ellis:1983ei; @Ellis:1984bm; @Lahanas:1986uc]: (i) the vacuum energy vanishes automatically due to the suitable Kähler potential; (ii) at the minimum of the scalar potential, there are flat directions which leave the gravitino mass $M_{3/2}$ undetermined; (iii) the super-trace quantity ${\rm Str} {\cal M}^2$ is zero at the minimum. Without this, the large one-loop corrections would force $M_{3/2}$ to be either zero or of Planck scale. A simple Kähler potential which satisfies the first two conditions is $$\begin{aligned}
K &=& -3 \ln( T+\overline{T}-\sum_i \overline{\Phi}_i
\Phi_i)~,~
\label{NS-Kahler}\end{aligned}$$ where $T$ is a modulus field and $\Phi_i$ are matter fields. The third condition is model dependent and can always be satisfied in principle [@Ferrara:1994kg].
The scalar fields of Eq. (\[NS-Kahler\]) parameterize the coset space $SU(N_C+1, 1)/(SU(N_C+1)\times U(1))$, where $N_C$ is the number of matter fields. Analogous structures appear in the $N\ge 5$ extended Supergravity theories [@Cremmer:1979up], for example, $N_C=4$ for $N=5$, which can be realized in the compactifications of string theory [@Witten:1985xb; @Li:1997sk]. The non-compact structure of the symmetry implies that the potential is not only constant but actually identical to zero. For the simple example Kähler potential given above, one can readily check that the scalar potential is automatically positive semi-definite, and has a flat direction along the $T$ field. Likewise, it may be verified that the simplest No-Scale boundary conditions $M_0=A=B_{\mu}=0$ emerge dynamically, while $M_{1/2}$ may be non-zero at the unification scale, allowing for low energy SUSY breaking.
The specific Kähler potential of Eq. (\[NS-Kahler\]) has been independently derived in both weakly coupled heterotic string theory [@Witten:1985xb] and the leading order compactification of M-theory on $S^1/Z_2$ [@Li:1997sk]. Note that in both cases, the Yang-Mills fields span a ten dimensional space-time. It is not obtained directly out of F-theory, as represented for example by the strong coupling lift from Type IIB intersecting D-brane model building with D7- and D3-branes [@Beasley:2008dc; @Beasley:2008kw; @Donagi:2008ca; @Donagi:2008kj], where the Yang-Mills fields on the D7-branes occupy an eight dimensional space-time. Nevertheless, it is certainly possible in principle to calculate a gauge kinetic function, Kahler potential and superpotential in the context of Type IIB interecting D-brane model building, and the F-theory could thus admit a more general definition of No-Scale Supergravity, as realized by a Kähler potential like $$\begin{aligned}
K &=& -\ln(S + \overline{S}) -\ln(T_1 + \overline{T}_1)
\nonumber \\
&& -\ln(T_2 + \overline{T}_2) -\ln(T_3 + \overline{T}_3) \, ,
\label{Kahler2}\end{aligned}$$ where only three of the moduli fields $S$ and $T_i$ may yield non-zero F-terms.
In Ref. [@Giddings:2001yu], No-Scale Supergravity was obtained in the Type IIB and F-theory compactifications at the leading order. Likewise, the subsequently introduced KKLT [@Kachru:2003aw] constructions also manifest a No-Scale SUGRA structure at the classical level. Indeed, the No-Scale features are generically obtained at the tree-level in string theory compactifications due to the presence of three complex extra dimensions. However, this classical level result is rather precariously balanced, and may be spoiled by quantum corrections to the superpotential including flux contributions, instanton effects, gaugino condensation, and the next order $\alpha'$ corrections. In this sense, we consider the KKLT type SUGRA models as a generalization or extension of the elemental No-Scale form.
The No-Scale ${\cal F}$-$SU(5)$ model under discussion has been constructed locally in F-theory [@Jiang:2009zza; @Jiang:2009za], although the mass of the additional vector-like multiplets, and even the fact of their existence, is not mandated by the F-theory, wherein it is also possible to realize models with only the traditional Flipped (or Standard) $SU(5)$ field content. We claim only an inherent consistency of their conceptual origin out of the F-theoretic construction, and take the manifest phenomenological benefits which accompany the natural elevation of the secondary GUT unification phase to $M_{\cal{F}} \simeq 7 \times 10^{17}$ GeV as justification for the greater esteem which we hold for this particular model above other alternatives. There are, though, also delicate questions of compatibility between the local F-theoretic model building origins and the purely field-theoretic RGE running which we employ up to the presumed high scale. As one approaches the Planck mass $M_{\rm Pl}$, consideration must be given to the role which will be played by Kaluza Klein (KK) and string mode excitations, and also to corrections of order $\alpha^\prime$ from stabilization of the global volume of the six-dimensional internal space in association with the establishment of the string scale $M_{\rm S} \propto (M_{\rm Pl} / R_{\rm global}^3)$.
The most important question is whether our model can in fact be embedded into a globally consistent framework. Without such, we do not know the concrete Kähler potential of the SM fermions and Higgs fields, and cannot by this means explicitly calculate the supersymmetry breaking scalar masses and trilinear soft terms. This construction remains elusive though, and is beyond the reach of the current work. Regardless, one may anticipate that in such a globally consistent model, a string scale of order $10^{17}$ GeV would indeed be realized, as in the weakly coupled heterotic string theory, tying in nicely with our naïvely projected value for $M_{\cal F}$. It seems additionally that a field-theoretic application of the No-Scale boundary conditions might prove to be validated in this case. Moreover, we would not necessarily require the presence of instanton effects or gaugino condensation for stabilization of the modulus $T$ as in the KKLT mechanism. This is crucial, because such effects can have the negative side effect of destroying the leading No-Scale structure. In fact, we could have no gaugino condensation at all, or the superpotential from gaugino condensation might only depend on $S$, as again exemplified in the Type IIB intersecting D-brane models [@Blumenhagen:2005mu].
Such considerations, coupled with the demonstrated testability and phenomenological success of the first order analysis in the simplest No-Scale SUGRA framework, argue for a continuing study of the generalized No-Scale SUGRA picture. It is important to note that there exist several such generalizations, including the previously mentioned Type II intersecting D-brane models [@Cvetic:2004ui; @Chen:2007px; @Chen:2007zu], mirage mediation of flux compactifications [@Choi:2004sx; @Choi:2005ge], and the extraction of SUSY breaking soft terms from the leading order compactification of M-theory on $S^1/Z_2$ [@Nilles:1997cm; @Nilles:1998sx; @Lukas:1997fg; @Lukas:1998yy; @Li:1998rn]; in the latter case we have previously obtained (in a different model context) a generalization employing modulus dominated SUSY breaking [@Li:1998rn].
In this paper, however, we maintain a “first steps first” perspective, concentrating on the simplest No-Scale Supergravity and reserving any such extensions for the future. The potential for stringy modifications duly noted, we then essentially aim to study an F-theory [*inspired*]{} variety of low energy SUSY phenomenology, remaining agnostic as to the details of the Kähler structure. Nevertheless, by studying the simplest No-Scale Supergravity, we may still expect to encapsulate the correct leading order behavior. We likewise maintain the simplicity of a leading order approximation by neglecting consideration of any stringy threshold corrections, the substantive onset of which is anyway expected to be deferred to $M_{\cal F}$, the true GUT scale of this model. It should be added that since the running of the gauge couplings is logarithmically dependent upon the mass scale, the contributions to the RGEs from the string and KK mode excitations are quite small.
The Super No-Scale Mechanism
==============================
The single relevant modulus field in the simplest stringy No-Scale Supergravity is the Kähler modulus $T$, a characteristic of the Calabi-Yau manifold, the dilaton coupling being irrelevant. We consider the gaugino mass $M_{1/2}$ as a useful modulus related to the F-term of $T$, stipulating, in other words, that the gauge kinetic function must depend on $T$. This is realized, for example, in the Type IIB intersecting D-brane models [@Blumenhagen:2005mu] where gauge kinetic functions explicitly depend on both $S$ and $T_i$, as in Eq. (\[Kahler2\]). Again, since the F-theory may be considered as a strongly coupled formulation of the Type IIB string theory, it is natural to believe that the gauge kinetic function under this lift depends on $T$ as well. While the limit is quite suggestive, lacking still a concrete globally consistent embedding, we cannot definitively prove that the superpotential remains unperturbed by $T$.
Proceeding tentatively as such, the F-term of $T$ generates the gravitino mass $M_{3/2}$, which is proportionally equivalent to $M_{1/2}$. Exploiting the simplest No-Scale boundary condition at $M_{\cal F}$ and running from high energy to low energy under the RGEs, there can be a secondary minimization, or [*minimum minimorum*]{}, of the minimum of the Higgs potential $V_{\rm min}$ for the EWSB vacuum. Since $V_{\rm min}$ depends on $M_{1/2}$, the gaugino mass $M_{1/2}$ is consequently dynamically determined by the equation $dV_{\rm min}/dM_{1/2}=0$, aptly referred to as the “Super No-Scale” mechanism [@Li:2010uu].
It could easily have been that in consideration of the above technique, there were: A) too few undetermined parameters, with the $B_{\mu}=0$ condition forming an incompatible over-constraint, and thus demonstrably false, or B) so many undetermined parameters that the dynamic determination possessed many distinct solutions, or was so far separated from experiment that it could not possibly be demonstrated to be true. The actual state of affairs is much more propitious, being specifically as follows. The three parameters $M_0,A,B_{\mu}$ are once again identically zero at the boundary because of the defining Kähler potential, and are thus known at all other scales as well by the RGEs. The minimization of the Higgs scalar potential with respect to the neutral elements of both SUSY Higgs doublets gives two conditions, the first of which fixes the magnitude of $\mu$. The second condition, which would traditionally be used to fix $B_{\mu}$, instead here enforces a consistency relationship on the remaining parameters, being that $B_{\mu}$ is already constrained.
In general, the $B_{\mu} = 0$ condition gives a hypersurface of solutions cut out from a very large parameter space. If we lock all but one parameter, it will give the final value. If we take a slice of two dimensional space, as has been described, it will give a relation between two parameters for all others fixed. In a three-dimensional view with $B_{\mu}$ on the vertical axis, this curve is the “flat direction” line along the bottom of the trench of $B_{\mu}=0$ solutions. In general, we must vary at least two parameters rather than just one in isolation, in order that their mutual compensation may transport the solution along this curve. The most natural first choice is in some sense the pair of prominent unknown inputs $M_{1/2}$ and $\tan \beta$, as was demonstrated in Ref. [@Li:2010uu].
Having come to this point, it is by no means guaranteed that the potential will form a stable minimum. It must be emphasized that the $B_{\mu}=0$ No-Scale boundary condition is the central agent affording this determination, as it is the extraction of the parameterized parabolic curve of solutions in the two compensating variables which allows for a localized, bound nadir point to be isolated by the Super No-Scale condition, dynamically determining [*both*]{} parameters. The background surface of $V_{\rm min}$ for the full parameter space outside the viable $B_{\mu}=0$ subset is, in contrast, a steadily inclined and uninteresting function. In our prior study, the local [*minimum minimorum*]{} of $V_{\rm min}$ for the choices $M_{V}=1000$ GeV and $m_{t}=173.1$ GeV dynamically established $M_{1/2} \simeq 450~{\rm GeV}$, and $\tan \beta \simeq 15-20$. Although we have remarked that $M_{1/2}$ and $\tan \beta$ have no [*directly*]{} established experimental values, they are severely indirectly constrained by phenomenology in the context of this model [@Li:2010ws; @Li:2010mi]. It is highly non-trivial that there should be accord between the top-down and bottom-up perspectives, but this is indeed precisely what has been observed [@Li:2010uu].
The GUT Higgs Modulus
=======================
An alternate pair of parameters for which one may attempt to isolate a $B_{\mu} = 0$ curve, which we consider for the first time in this work, is that of $M_{1/2}$ and the GUT scale $M_{32}$, at which the $SU(3)_C$ and $SU(2)_L$ couplings initially meet. Fundamentally, the latter corresponds to the modulus which sets the total magnitude of the GUT Higgs field’s VEVs. $M_{32}$ could of course in some sense be considered a “known” quantity, taking the low energy couplings as input. Indeed, starting from the measured SM gauge couplings and fermion Yukawa couplings at the standard $91.187$ GeV electroweak scale, we may calculate both $M_{32}$ and the final unification scale $M_{\cal F}$, and subsequently the unified gauge coupling and SM fermion Yukawa couplings at $M_{\cal F}$, via running of the RGEs. However, since the VEVs of the GUT Higgs fields $H$ and $\overline{H}$ are considered here as free parameters, the GUT scale $M_{32}$ must not be fixed either. As a consequence, the low energy SM gauge couplings, and in particular the $SU(2)_L$ gauge coupling $g_2$, will also run freely via this feedback from $M_{32}$.
We consider this conceptual release of a known quantity, in order to establish the nature of the model’s dependence upon it, to be a valid and valuable technique, and have employed it previously with specific regards to “postdiction” of the top quark mass value [@Li:2010mi]. Indeed, forcing the theoretical [*output*]{} of such a parameter is only possible in a model with highly constrained physics, and it may be expected to meet success only by intervention of either grand coincidence or grand conspiracy of Nature. Simultaneous to the recognition of the presence of a second dynamic modulus, we lock down the value of $\mu$, which by contrast is a simple numerical parameter, and ought then to be treated in a manner consistent with the top quark and vector-like mass parameters. For this study, we choose a vector-like particle mass $M_V=1000$ GeV, and use the experimental top quark mass input $m_{t}=173.1$ GeV. We emphasize that the choice of $M_V=1000~{\rm GeV}$ is not an arbitrary one, since a prior analysis [@Li:2010mi] has shown that a $1$ TeV vector-like mass is in compliance with all current experimental data and the No-Scale $B_{\mu}$=0 requirement. The constant parameter $\mu$ is set consistent with its value prior to the variation of the GUT modulus.
In actual practice, the variation of $M_{32}$ is achieved in the reverse by programmatic variation of the Weinberg angle, holding the strong and electromagnetic couplings at their physically measured values. Figure \[fig:sin2T\_MZ\_M32\] demonstrates the scaling between $\sin^2 (\theta_{\rm W})$, $M_{32}$ (logarithmic axis), and the $Z$-boson mass. The variation of $M_Z$ is attributed primarily to the motion of the electroweak couplings, the magnitude of the Higgs VEV being held essentially constant. We ensure also that the unified gauge coupling, SM fermion Yukawa couplings, and specifically also the Higgs bilinear term $\mu \simeq 460$ GeV, are each held stable at the scale $M_{\cal F}$ to correctly mimic the previously described procedure.
![The interrelated variation of $\sin^2 (\theta_{\rm W})$, the GUT scale $M_{32}$ (logarithmic axis), and the $Z$-boson mass $M_Z$ is demonstrated for the parameter strips which preserve $B_{\mu}=0$ and $\mu=460$ GeV at $M_{\cal F}$. The variation in $M_Z$ is linked dominantly to motion of the EW couplings via $\sin^2 (\theta_{\rm W})$. Also shown is the corresponding predicted proton lifetime in the leading ${(e|\mu)}^{+} \pi^0 $ channels, in units of $10^{34}$ years, with the current lower bound of $1.0 \times 10^{34}$ years indicated by the dashed horizontal purple line.[]{data-label="fig:sin2T_MZ_M32"}](sin2T_MZ_M32.eps){width="50.00000%"}
The parameter ranges for the variation depicted in Fig. \[fig:sin2T\_MZ\_M32\] are $M_Z = 91.18 - 92.64$, $\sin^2(\theta_{\rm W}) = 0.2262 - 0.2357$, and $M_{32} = 1.5\times 10^{15} - 1.04 \times 10^{16}$ GeV, and likewise also the same for Figs. (\[fig:dV\_MZ\_tanb\]-\[fig:g\_M12\_MZ\]), which will feature subsequently. The [*minimum minimorum*]{} falls at the boundary of the prior list, dynamically fixing $M_{32} \simeq 1.0 \times 10^{16}$ GeV and placing $M_{1/2}$ again in the vicinity of $450$ GeV. The low energy SM gauge couplings are simultaneously constrained by means of the associated Weinberg angle, with $\sin^2 (\theta_{\rm W}) \simeq 0.236$, in excellent agreement with experiment. The corresponding range of predicted proton lifetimes in the leading ${(e|\mu)}^{+} \pi^0 $ modes is $2.5\times 10^{31} - 5.7\times10^{34}$ years [@Li:2010dp]. If the GUT scale $M_{32}$ becomes excessively light, below about $7 \times 10^{15}$ GeV, then proton decay would be more rapid than allowed by the recently updated lower bound of $1.0 \times 10^{34}$ years from Super-Kamiokande [@:2009gd].
We are cautious against making a claim in precisely the same vein for the dynamic determination of $M_Z \simeq 91.2$ GeV, since again the crucial electroweak Higgs VEV is not a substantial element of the variation. However, in [*conjunction*]{} with the radiative electroweak symmetry breaking [@Ellis:1982wr; @Ellis:1983bp] numerically implemented within the [SuSpect 2.34]{} code base [@Djouadi:2002ze], the fixing of the Higgs VEV and the determination of the electroweak scale may also plausibly be considered legitimate dynamic output, [*if*]{} one posits the $M_{F}$ scale input to be available [*a priori*]{}.
By extracting a constant $\mu$ slice of the $V_{\rm min}$ hyper-surface, the secondary minimization condition on $\tan \beta$ is effectively rotated, albeit quite moderately, relative to the procedure of Ref. ([@Li:2010uu]). The present minimization, referencing $M_{1/2}$, $M_{32}$ and $\tan \beta$, is again dependent upon $M_{V}$ and $m_{t}$, while the previously described [@Li:2010uu] determination of $\tan \beta$ was, by contrast, $M_{V}$ and $m_{t}$ invariant. Recognizing that a minimization with all three parameters simultaneously active is required to declare all three parameters to have been simultaneously dynamically determined, we emphasize the mutual consistency of the results. We again stress that the new [*minimum minimorum*]{} is also consistent with the previously advertised golden strip, satisfying all presently known experimental constraints to our available resolution. It moreover also addresses the problems of the SUSY breaking scale and gauge hierarchy [@Li:2010uu], insomuch as $M_{1/2}$ is determined dynamically.
![Three-dimensional graph of $(M_{Z},\tan \beta,\Delta V_{min}(h)$) space (green curve). The projections onto the three mutually perpendicular planes (red curves) are likewise shown. $M_{Z}$ and $\Delta V_{min}(h)$ are in units of GeV. The dynamically preferred region, allowing for plausible variation, is circled and tipped in gold.[]{data-label="fig:dV_MZ_tanb"}](dV_MZ_tanb.eps){width="50.00000%"}
![Three-dimensional graph of $(M_{Z},M_{1/2},\Delta V_{min}(h))$ space (green curve). The projections onto the three mutually perpendicular planes (red curves) are likewise shown. $M_{Z}$, $M_{1/2}$, and $\Delta V_{min}(h)$ are in units of GeV. The dynamically preferred region, allowing for plausible variation, is circled and tipped in gold.[]{data-label="fig:dV_M12_MZ"}](dV_M12_MZ.eps){width="50.00000%"}
![Three-dimensional graph of $(M_{1/2},\tan \beta,\Delta V_{min}(h)$) space (green curve). The projections onto the three mutually perpendicular planes (red curves) are likewise shown. $M_{1/2}$ and $\Delta V_{min}(h)$ are in units of GeV. The dynamically preferred region, allowing for plausible variation, is circled and tipped in gold.[]{data-label="fig:dV_M12_tanb"}](dV_M12_tanb.eps){width="50.00000%"}
![Three-dimensional graph of $(v,M_{1/2},\Delta V_{min}(h))$ space (green curve). The projections onto the three mutually perpendicular planes (red curves) are likewise shown. $M_{1/2}$, $v$, and $\Delta V_{min}(h)$ are in units of GeV. The dynamically preferred region, allowing for plausible variation, is circled and tipped in gold.[]{data-label="fig:dV_M12_v"}](dV_M12_v.eps){width="50.00000%"}
![Three-dimensional graph of $(M_{Z},M_{1/2},M_{32})$ space (blue curve). The projections onto the three mutually perpendicular planes (red curves) are likewise shown. $M_{Z}$, $M_{1/2}$, and $M_{32}$ are in units of GeV.[]{data-label="fig:M32_M12_MZ"}](M32_M12_MZ.eps){width="50.00000%"}
![Three-dimensional graph of $(M_{Z},M_{1/2},v)$ space (purple curve). The projections onto the three mutually perpendicular planes (red curves) are likewise shown. $M_{Z}$, $M_{1/2}$, and $v$ are in units of GeV.[]{data-label="fig:v_M12_MZ"}](v_M12_MZ.eps){width="50.00000%"}
![Three-dimensional graph of $(M_{Z},M_{1/2},g)$ space (royal blue curve). The projections onto the three mutually perpendicular planes (red curves) are likewise shown. $M_{Z}$ and $M_{1/2}$ are in units of GeV.[]{data-label="fig:g_M12_MZ"}](g_M12_MZ.eps){width="50.00000%"}
The Minimum Minimorum of the Electroweak Higgs Potential
==========================================================
In supersymmetric SMs, there is a pair of Higgs doublets $H_u$ and $H_d$ which give mass to the up-type quarks and down-type quarks/charged leptons, respectively. The one-loop effective Higgs potential in the ’t Hooft-Landau gauge and in the $\overline{\rm DR}$ scheme is given by $$\begin{aligned}
V_{\rm eff} &=& V_0(H_u^0,~H_d^0) + V_1(H_u^0,~H_d^0)~,~\,\end{aligned}$$ where $$\begin{aligned}
V_0&=& (\mu^2 + m_{H_u}^2) (H_u^0)^2 + (\mu^2 + m_{H_d}^2) (H_d^0)^2
\nonumber \\ &&
-2 B_{\mu} \mu H_u^0 H_d^0 + {\frac{g_2^2 + g_Y^2}{8}} \left[(H_u^0)^2-(H_d^0)^2\right]^2
~,~\,\end{aligned}$$ $$\begin{aligned}
V_1 &=& \sum_i {\frac{n_i}{64\pi^2}} m_i^4(\phi)
\left( {\rm ln}{{\frac{m_i^2(\phi)}{Q^2}} -{\frac{3}{2}}} \right) ~,~\,\end{aligned}$$ where $m_{H_u}^2$ and $m_{H_d}^2$ are the supersymmetry breaking soft masses, $g_2$ and $g_Y$ are respectively the gauge couplings of $SU(2)_L$ and $U(1)_Y$, $n_i$ and $m_i^2(\phi)$ are respectively the degree of freedom and mass for $\phi_i$, and $Q$ is the renormalization scale. In our numerical results in the figures, we shall designate differences in the fourth-root of the effective Higgs potential as $\Delta V_{min}(h)\equiv V_{\rm eff}^{1/4}$, measured in units of GeV relative to an arbitrary overall zero-offset.
We have revised the [SuSpect 2.34]{} code base [@Djouadi:2002ze] to incorporate our specialized No-Scale ${\cal F}$-$SU(5)$ with vector-like mass algorithm, and accordingly employ two-loop RGE running for the SM gauge couplings, and one-loop RGE running for the SM fermion Yukawa couplings, $\mu$ term, and SUSY breaking soft terms. For our choice of $M_V=1000$ GeV, $m_t=173.1$ GeV, and $\mu(M_{\cal F}) \simeq 460$ GeV, we present the one-loop effective Higgs potential $\Delta V_{min}(h)$ in terms of $M_{Z}$ and $\tan \beta$ in Fig. \[fig:dV\_MZ\_tanb\], in terms of $M_{Z}$ and $M_{1/2}$ in Fig. \[fig:dV\_M12\_MZ\], in terms of $M_{1/2}$ and tan$\beta$ in Fig. \[fig:dV\_M12\_tanb\], and in terms of $v$ and $M_{1/2}$ in Fig. \[fig:dV\_M12\_v\], where $v=\sqrt{v_{u}^{2}+v_{d}^{2}}$, $v_u=\langle H^0_u \rangle$, and $v_d=\langle H^0_d \rangle$. These figures clearly demonstrate the localization of the [*minimum minimorum*]{} of the Higgs potential, corroborating the dynamical determination of $\tan \beta \simeq 15-20$ and $M_{1/2} \simeq 450$ GeV in [@Li:2010uu].
Additionally, we exhibit the $(M_{Z},M_{1/2},M_{32})$ space in Fig. \[fig:M32\_M12\_MZ\], the $(M_{Z},M_{1/2},v)$ space in Fig. \[fig:v\_M12\_MZ\], and the $(M_{Z},M_{1/2},g)$ space in Fig. \[fig:g\_M12\_MZ\], where $g=\sqrt{g_{2}^{2}+g_{Y}^{2}}$. Fig. \[fig:M32\_M12\_MZ\] demonstrates that $M_{32} \simeq 1.0 \times 10^{16}$ GeV at the [*minimum minimorum*]{}, which correlates to $M_{Z} \simeq 91.2$ GeV, or more directly, $\sin^2 (\theta_{\rm W}) \simeq 0.236$. Together, the alternate perspectives of Figs. \[fig:M32\_M12\_MZ\], \[fig:v\_M12\_MZ\], and \[fig:g\_M12\_MZ\] complete the view given in Figs. \[fig:dV\_MZ\_tanb\], \[fig:dV\_M12\_MZ\], \[fig:dV\_M12\_tanb\], and \[fig:dV\_M12\_v\] to visually tell the story of the dynamic interrelation between the $M_Z$, $M_{1/2}$, and $M_{32}$ scales, as well as the electroweak gauge couplings, and the Higgs VEVs. The curves in each of these figures represent only those points that satisfy the $B_{\mu}$ = 0 requirement, as dictated by No-Scale Supergravity, serving as a crucial constraint on the dynamically determined parameter space. Ultimately, it is the significance of the $B_{\mu} = 0$ requirement that separates the No-Scale ${\cal F}$-$SU(5)$ with vector-like particles from the entire compilation of prospective string theory derived models. By means of the $B_{\mu}$ = 0 vehicle, No-Scale ${\cal
F}$-$SU(5)$ has surmounted the paramount challenge of phenomenology, that of dynamically determining the electroweak scale, the scale of fundamental prominence in particle physics.
We wish to note that recent progress has been made in incorporating more precise numerical calculations into our baseline algorithm for No-Scale ${\cal F}$-$SU(5)$ with vector-like particles. Initially, when we commenced the task of fully developing the phenomenology of this model, the extreme complexity of properly numerically implementing No-Scale ${\cal F}$-$SU(5)$ with vector-like particles compelled a gradual strategy for construction and persistent enhancement of the algorithm. Preliminary findings of a precision improved algorithm indicate that compliance with the 7-year WMAP relic density constraints requires a slight upward shift to $\tan \beta \simeq 19-20$ from the value computed in Ref. [@Li:2010ws], suggesting a potential convergence to even finer resolution of the dynamical determination of $\tan \beta$ given by the Super No-Scale mechanism, and the value demanded by the experimental relic density measurements. We shall furnish a comprehensive analysis of the precision improved algorithm at a later date.
Probing The Blueprints of the No-Scale Multiverse at the Colliders
====================================================================
We offer in closing a brief summary of direct collider, detector, and telescope level tests which may probe the blueprints of the No-Scale Multiverse which we have laid out. As to the deep question of whether the ensemble be literal in manifestation, or merely the conceptual superset of unrealized possibilities of a single island Universe, we pretend no definitive answer. However, we have argued that the emergence [*ex nihilo*]{} of seedling universes which fuel an eternal chaotic inflation scenario is particularly plausible, and even natural, within No-Scale Supergravity, and our goal of probing the specific features of our own Universe which might implicate its origins in this construction are immediately realizable and practicable.
The unified gaugino $M_{1/2}$ at the unification scale $M_{\cal F}$ can be reconstructed from impending LHC events by determining the gauginos $M_{1}$, $M_{2}$, and $M_{3}$ at the electroweak scale, which will in turn require knowledge of the masses for the neutralinos, charginos, and the gluino. Likewise, $\tan \beta$ can be ascertained in principle from a distinctive experimental observable, as was accomplished for mSUGRA in [@Arnowitt:2008bz]. We will not undertake a comprehensive analysis here of the reconstruction of $M_{1/2}$ and $\tan \beta$, but will offer for now a cursory examination of typical events expected at the LHC. We leave the detailed compilation of the experimental observables necessary for validation of the No-Scale ${\cal F}$-$SU(5)$ at the LHC for the future, and we especially encourage those specializing in such research to investigate the No-Scale ${\cal F}$-$SU(5)$.
For the benchmark SUSY spectrum presented in Table \[tab:masses\], we have adopted the specific values $M_{1/2}=453$, $\tan \beta=15$ and $M_Z=91.187$. We expect that higher order corrections will shift the precise location of the [*minimum minimorum*]{} a little bit, for example, within the encircled gold-tipped regions of the diagrams in the prior section. We have selected a ratio for $\tan \beta$ at the lower end of this range for consistency with our previous study [@Li:2010uu], and to avoid stau dark matter.
$\widetilde{\chi}_{1}^{0}$ $94$ $\widetilde{\chi}_{1}^{\pm}$ $184$ $\widetilde{e}_{R}$ $150$ $\widetilde{t}_{1}$ $486$ $\widetilde{u}_{R}$ $947$ $m_{h}$ $120.1$
---------------------------- ------- ------------------------------ ------- ------------------------ ------- --------------------- ------- --------------------- -------- ----------------- ---------
$\widetilde{\chi}_{2}^{0}$ $184$ $\widetilde{\chi}_{2}^{\pm}$ $822$ $\widetilde{e}_{L}$ $504$ $\widetilde{t}_{2}$ $906$ $\widetilde{u}_{L}$ $1032$ $m_{A,H}$ $916$
$\widetilde{\chi}_{3}^{0}$ $817$ $\widetilde{\nu}_{e/\mu}$ $498$ $\widetilde{\tau}_{1}$ $104$ $\widetilde{b}_{1}$ $855$ $\widetilde{d}_{R}$ $988$ $m_{H^{\pm}}$ $921$
$\widetilde{\chi}_{4}^{0}$ $821$ $\widetilde{\nu}_{\tau}$ $491$ $\widetilde{\tau}_{2}$ $499$ $\widetilde{b}_{2}$ $963$ $\widetilde{d}_{L}$ $1035$ $\widetilde{g}$ $617$
: Spectrum (in GeV) for the benchmark point. Here, $M_{1/2}$ = 453 GeV, $M_{V}$ = 1000 GeV, $m_{t}$ = 173.1 GeV, $M_{Z}$ = 91.187 GeV, $\mu (M_{\cal F})$ = 460.3 GeV, $\Delta V_{min}(h)$ = 748 GeV, $\Omega_{\chi}$ = 0.113, $\sigma_{SI} = 2 \times 10^{-10}$ pb, and $\left\langle \sigma v \right\rangle_{\gamma\gamma} = 1.8 \times 10^{-28} ~cm^{3}/s$. The central prediction for the $p \!\rightarrow\! {(e\vert\mu)}^{\!+}\! \pi^0$ proton lifetime is around $4.9 \times 10^{34}$ years. The lightest neutralino is 99.8% Bino.
\[tab:masses\]
At the benchmark point, we calculate $\Omega_{\chi} = 0.113$ for the cold dark matter relic density. The phenomenology is moreover consistent with the LEP limit on the lightest CP-even Higgs boson mass, $m_{h} \geq 114$ GeV [@Barate:2003sz; @Barate:2003sz], the CDMSII [@Ahmed:2008eu] and Xenon100 [@Aprile:2010um] upper limits on the spin-independent cross section $\sigma_{SI}$, and the Fermi-LAT space telescope constraints [@Abdo:2010dk] on the photon-photon annihilation cross section $\left\langle \sigma v \right\rangle_{\gamma\gamma}$. The differential cross-sections and branching ratios have been calculated with [PGS4]{} [@PGS4] executing a call to [PYTHIA 6.411]{} [@Sjostrand:2006za], using our specialized No-Scale algorithm integrated into the [SuSpect 2.34]{} code for initial computation of the sparticle masses.
The benchmark point resides in the region of the experimentally allowed parameter space that generates the relic density through stau-neutralino coannihilation. Hence, the five lightest sparticles for this benchmark point are $\widetilde{\chi}_{1}^{0} < \widetilde{\tau}_{1}^{\pm} < \widetilde{e}_{R} < \widetilde{\chi}_{2}^{0}
\sim \widetilde{\chi}_{1}^{\pm}$. Here, the gluino is lighter than all the squarks with the exception of the lightest stop, so all squarks will predominantly decay to a gluino and hadronic jet, with a small percentage of squarks producing a jet and either a $\widetilde{\chi}_{1}^{\pm}$ or $\widetilde{\chi}_{2}^{0}$. The gluinos will decay via virtual (off-shell) squarks to neutralinos or charginos plus quarks, which will further cascade in their decay. The result is a low-energy tau through the processes $\widetilde{\chi}_{2}^{0} \rightarrow \widetilde{\tau}_{1}^{\mp}
\tau^{\pm} \rightarrow \tau^{\mp}\tau^{\pm} \widetilde{\chi}_{1}^{0}$ and $\widetilde{\chi}_{1}^{\pm}
\rightarrow \widetilde{\tau}_{1}^{\pm} \nu_{\tau} \rightarrow \tau^{\pm}\nu_{\tau} \widetilde{\chi}_{1}^{0}$.
The LHC final states of low-energy tau in the ${\cal F}$-$SU(5)$ stau-neutralino coannihilation region are similar to those same low-energy LHC final states in mSUGRA, however, in the stau-neutralino coannihilation region of mSUGRA, the gluino is typically heavier than the squarks. The strong coupling effects from the additional vector-like particles on the gaugino mass RGE running reduce the physical gluino mass below the squark masses in ${\cal F}$-$SU(5)$. As a consequence, the LHC final low-energy tau states in the stau-neutralino coannihilation regions of ${\cal F}$-$SU(5)$ and mSUGRA will differ in that in ${\cal F}$-$SU(5)$, the low-energy tau states will result largely from neutralinos and charginos produced by gluinos, as opposed to the low-energy tau states in mSUGRA resulting primarily from neutralinos and charginos produced from squarks.
Also notably, the TeV-scale vector-like multiplets are well targeted for observation by the LHC. We have argued [@Li:2010mi] that the eminently feasible near-term detectability of these hypothetical fields in collider experiments, coupled with the distinctive flipped charge assignments within the multiplet structure, represents a smoking gun signature for Flipped $SU(5)$, and have thus coined the term [*flippons*]{} to collectively describe them. Immediately, our curiosity is piqued by the recent announcement [@Abazov:2010ku] of the DØ collaboration that vector-like quarks have been excluded up to a bound of 693 GeV, corresponding to the immediate lower edge of our anticipated range for their discovery [@Li:2010mi].
Conclusion
==========
The advancement of human scientific knowledge and technology is replete with instances of science fiction transitioning to scientific theory and eventually scientific fact. The conceptual notion of a “Multiverse” has long fascinated the human imagination, though this speculation has been largely devoid of a substantive underpinning in physical theory. The modern perspective presented here offers a tangible foundation upon which legitimate discussion and theoretical advancement of the Multiverse may commence, including the prescription of specific experimental tests which could either falsify or enhance the viability of our proposal. Our perspective diverges from the common appeals to statistics and the anthropic principle, suggesting instead that we may seek to establish the character of the master theory, of which our Universe is an isolated vacuum condensation, based on specific observed properties of our own physics which might be reasonably inferred to represent invariant common characteristics of all possible universes. We have focused on the discovery of a model universe consonant with our observable phenomenology, presenting it as confirmation of a non-zero probability of our own Universe transpiring within the larger String Landscape.
The archetype model universe which we advance in this work implicates No-Scale Supergravity as the ubiquitous supporting structure which pervades the vacua of the Multiverse, being the crucial ingredient in the emanation of a cosmologically flat universe from the quantum “nothingness”. In particular, the model dubbed No-Scale ${\cal F}$-$SU(5)$ has demonstrated remarkable consistency between parameters determined dynamically (the top-down approach) and parameters determined through the application of current experimental constraints (the bottom-up approach). This enticing convergence of theory with experiment elevates No-Scale ${\cal F}$-$SU(5)$, in our estimation, to a position as the current leading GUT candidate. The longer term viability of this suggestion is likely to be greatly clarified in the next few years, based upon the wealth of forthcoming experimental data.
Building on the results presented in prior works [@Li:2010ws; @Li:2010mi; @Li:2010uu], we have presented a dynamic determination of the penultimate Flipped $SU(5)$ unification scale $M_{32}$, or more fundamentally, the GUT Higgs VEV moduli. We have demonstrated that the $B_{\mu}$ = 0 No-Scale boundary condition is again vital in dynamically determining the model parameters. Procedurally, we have fixed the unified gauge coupling, SM fermion Yukawa couplings, and Higgs bilinear term $\mu\simeq 460~{\rm GeV}$ at the final unification scale $M_{\cal F}$, while concurrently allowing the VEVs of the GUT Higgs fields $H$ and $\overline{H}$ to float freely, as driven by $M_{32}$ and the low energy SM gauge couplings, via variation of the Weinberg angle. Employing the “Super No-Scale” condition to secondarily minimize the effective Higgs potential, we have obtained $M_{32}\simeq 1.0 \times 10^{16}$ GeV, $\sin^2 (\theta_{\rm W}) \simeq 0.236$, and $\tan \beta \simeq 15-20$.
The blueprints which we have outlined here, integrating precision phenomenology with prevailing experimental data and a fresh interpretation of the Multiverse and the Landscape of String vacua, offer a logically connected point of view from which additional investigation may be mounted. As we anticipate the impending stream of new experimental data which is likely to be revealed in ensuing years, we look forward to serious discussion and investigation of the perspective presented in this work. Though the mind boggles to contemplate the implications of this speculation, so it must also reel at even the undisputed realities of the Universe, these acknowledged facts alone being manifestly sufficient to humble our provincial notions of longevity, extent, and largess.
Acknowledgments {#acknowledgments .unnumbered}
===============
This research was supported in part by the DOE grant DE-FG03-95-Er-40917 (TL and DVN), by the Natural Science Foundation of China under grant No. 10821504 (TL), and by the Mitchell-Heep Chair in High Energy Physics (TL).
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Only a few precious Sundays stand between us and 'The Walking Dead' season 4's 2014 premiere "After," but while most will be busy with the big game this coming Sunday, AMC has yet another chilling new trailer for its horror smash's winter return. Rick looks worse than ever, while Daryl races around a graveyard in the latest spot for 'The Walking Dead''s 2014 return, but has another promo revealed a major character return?
Earlier today we caught a fresh look at 'The Walking Dead' season 4's latter half before the big February 9 premiere, but why stop there? A fresh batch of photos has emerged from the 2014 premiere installment "After," and considering how splintered everyone became by the big prison showdown of midseason finale "Too Far Gone," the survivors we pick up with aren't looking too good...
Much as we love 'The Walking Dead' and the brutal finish that capped off the first half of season 4, we have to admit a bit of disappointment with the most recent trailers for the AMC horror drama's 2014 return. Thankfully, the latest 4-minute preview for the back half of season 4 has loads of new footage, and insight from the cast and crew into what might be the darkest and deepest episodes yet!
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# More Praise for
## _On Edge_
"This remarkable and beautifully written description of Andrea Petersen's lifelong journey with anxiety combines an account of her personal experience with a description of up-to-the-minute research describing what we know about anxiety and its treatment. Everyone dealing with anxiety—the common cold of mental disorders—will benefit from the important information in this entertaining and erudite reflection on coping with the burden of anxiety."
—David H. Barlow, professor of psychology and psychiatry emeritus, Boston University, and founder and director emeritus, Center for Anxiety and Related Disorders
"This story of resilience in the face of enormous challenge powerfully illustrates Andrea Petersen's pathway to recovery from mental illness. Eminently readable and at times controversial, Andrea's story is a beacon in the darkness for those living with anxiety disorders in silence. Stories like hers, shared openly, can change lives by reducing the stigma and discrimination that still surrounds mental illness."
—Former First Lady Rosalynn Carter, cofounder, The Carter Center
"Andrea Petersen raises the bar for anyone attempting to explain the complex science of the anxious brain. I was fascinated by the candid, painful, often humorous account of her own struggle and her quest for the best information about anxiety."
—Karen Cassiday, president, Anxiety and Depression Association of America
Copyright © 2017 by Andrea Petersen
All rights reserved.
Published in the United States by Crown, an imprint of the Crown Publishing Group, a division of Penguin Random House LLC, New York.
crownpublishing.com
CROWN is a registered trademark and the Crown colophon is a trademark of Penguin Random House LLC.
Library of Congress Cataloging-in-Publication Data
Names: Petersen, Andrea.
Title: On edge : a journey through anxiety / Andrea Petersen.
Description: First edition. | New York : Crown, [2017] | Includes bibliographical references and index.
Identifiers: LCCN 2016050111 (print) | LCCN 2016059341 (ebook) | ISBN 9780553418576 (hardcover) | ISBN 9780553418590 (pbk.) | ISBN 9780553418583 (ebook)
Subjects: LCSH: Petersen, Andrea—Mental health. | Anxiety disorders—Treatment. | Anxiety—Patients—Biography.
Classification: LCC RC531 .P4227 2017 (print) | LCC RC531 (ebook) | DDC 616.85/22—dc23
LC record available at https://lccn.loc.gov/2016050111
ISBN 9780553418576
Ebook ISBN 9780553418583
_Cover design by Na Kim_
v4.1
ep
# Contents
Cover
Title Page
Copyright
Dedication
Author's Note
Prologue
[Chapter 1: The Anticipation of Pain
_Defining Anxiety_](Pete_9780553418583_epub3_c002_r1.xhtml)
[Chapter 2: Scary Clowns and the End of Days
_Anxiety in Childhood_](Pete_9780553418583_epub3_c003_r1.xhtml)
[Chapter 3: My Grandmother's Madness
_The Genetics of Anxiety_](Pete_9780553418583_epub3_c004_r1.xhtml)
[Chapter 4: From CBT to Karaoke
_Nondrug Therapies for Anxiety_](Pete_9780553418583_epub3_c005_r1.xhtml)
[Chapter 5: May Cause Dizziness
_Medications for Anxiety_](Pete_9780553418583_epub3_c006_r1.xhtml)
[Chapter 6: Cold Calls, Airplanes, and Indecision
_Anxiety at Work and on the Road_](Pete_9780553418583_epub3_c007_r1.xhtml)
[Chapter 7: The Isolation Chamber
_Anxiety in Love and Friendship_](Pete_9780553418583_epub3_c008_r1.xhtml)
[Chapter 8: Worries About My Daughter
_The Education of an Anxious Parent_](Pete_9780553418583_epub3_c009_r1.xhtml)
[Chapter 9: Staying Grounded
_Learning to Live with Anxiety_](Pete_9780553418583_epub3_c010_r1.xhtml)
Notes
Acknowledgments
About the Author
For my parents
This is a work of nonfiction. Although Kate, Scott, Brad, Alice, and Michael are pseudonyms, all others who appear in the book are identified by their real names, and none are composites. I have made every effort to be accurate, but memory is fallible and some of the events I and others recall here happened decades ago. Whenever possible, I have corroborated events through medical records and interviews with people who were there.
Fear ambushes me.
It is early on the morning of December 5, 1989. At least early for a college student, which is what I am. A sophomore at the University of Michigan in Ann Arbor, a bucolic campus of creaky A-frame houses, earnest politics, fraternity sweatshirts, and dollar pitchers of beer.
I am in the basement of a 1940s academic building staring at a wall covered in long sheets of dot-matrix printer paper detailing which classes have slots for the upcoming semester: Economics 101, Introduction to Buddhism, a Jane Austen seminar. Other sleepy students, jeans-clad and tousle-headed, are scribbling in notebooks nearby.
I feel fine. Groggy from a late night of studying, yes. Touched by a bit of that midwestern late-fall dread, anticipating another long winter of fierce winds and sleeping-bag-shaped coats. But I'm fine.
And then, a second later, I'm not.
A knot of fear erupts at the base of my spine and travels upward. My stomach flips, and I break out in a thin film of sweat. My heart rate shoots up—I feel the erratic _thump thump_ banging against my ears, my stomach, my eyes. My breathing turns shallow and fast. Fuzzy gray blotches appear before my eyes. The letters before me warp, words dip and buckle.
There is no warning, no prodrome. The onset is as sudden as a car crash. Something in my body or brain has gone dramatically and irrevocably wrong. My noisy internal monologue—usually flitting from school to boys to a laundry list of insecurities—coalesces around one certain refrain: _I'm dying. I'm dying. I'm dying._
I flee the building and somehow make it home, crawling into my bottom bunk in the room I share with two other girls. I hug my knees into my chest and huddle against the cinder-block wall—my breathing still shallow, my heart still racing, the hot terror still there. Remarkably, it seems, I am alive. Any relief that gives me, however, is short-lived: _If I'm not dying, I must be going crazy._
Crazy like my grandmother.
Like the woman who clutched knives and thought Catholics were trying to kill her. Like the woman who spent three years in a mental institution, had electroshock therapy, and tried to burn the house down with my nine-year-old father and his brother and sister in it. Like the woman who died in my grandfather's arms when I was two years old. She had suffered a heart attack but was too terrified to go with paramedics to the hospital.
Crazy like that.
I lie still. Perhaps if I cease all movement, even the tiniest shudder, become frozen, waxlike, I can quiet the torment. My insides feel noisy, in flux. Everything is revved up—as if the blood in my veins were running faster and the synapses in my brain were firing, or misfiring, at warp speed. I can feel the loud, frantic presence of every organ—liver, intestines, spleen. The cells in my body are vibrating, it seems, knocking awkwardly against one another. If I move at all, I will shatter, scattering bits of blood and bone all across the salmon-hued sorority house. I am sure of that.
Later that afternoon my boyfriend drives me to my parents' house, all windows and suburban beige, about ninety minutes away. Over the next five weeks, I barely move from the living room sofa. I spend the days with my fingers pressed against my neck, feeling my pulse, counting the beats, reassuring myself at any given second that I'm alive. I keep still, trying to will my frenzied molecules to quiet. At night I have vivid, violent dreams. I develop weird new symptoms: tingling in my face and feet, chest pain, constant vertigo. The world is flat and out of focus, as if I'm wearing someone else's glasses. My thoughts careen toward heart attacks, stroke, insanity.
I see a doctor. He listens to my story of how I've been transformed from a slightly silly sorority girl to a terrorized shut-in in just a few weeks' time. He examines me, takes blood, does an EKG, and orders an echocardiogram, which details the chambers of my heart. His diagnosis: mitral valve prolapse, an anomaly of the heart that can cause palpitations but is generally benign. He prescribes a beta blocker, which he says will stop my heart from racing.
Except that it doesn't.
This doctor is only the first of more than a dozen I will see over the next year. During that time, I will have several more EKGs, countless blood tests, another echocardiogram, a CAT scan and an MRI of my brain, and an EEG to check my brain's electrical activity. I will take multiple trips to the emergency room, each time leaving without a diagnosis. This medical odyssey will cost my parents thousands of dollars. Doctors will suspect multiple sclerosis, a brain tumor, Epstein-Barr virus, and chronic fatigue syndrome. I will be told that I am fine. One doctor will fire me. I will drop most of my classes and barely leave my room. I will peer over the banister of a rooftop parking garage and think of jumping. I will go to a psychiatric emergency room and be sent home. I will have six sessions of psychotherapy, in which I'm asked whether I'm angry with my father. I'll largely stop eating.
And still no one will know what is wrong with me.
Fast-forward to the beginning of the next school year. I am sitting in a psychiatrist's office at the campus health center, telling the doctor that I won't—I can't—leave until she does something. She says she can prescribe Prozac, an antidepressant, or she can refer me to the anxiety disorders program at the University of Michigan hospital.
_Anxiety disorder_. It is the first time anyone has spoken the words.
Eleven different anxiety disorders are listed in the fifth edition of the _Diagnostic and Statistical Manual of Mental Disorders_ , commonly referred to as the diagnostic bible. I had symptoms of four. I was having panic attacks—sudden, intense periods of blinding terror, rapid breathing, and chest pain—several times a day (diagnosis: panic disorder). The rest of the time I worried, living with the nervous expectation of imminent disaster (diagnosis: generalized anxiety disorder, or GAD). I had developed a long list of particular fears, too: dentists, flying, driving on highways, taking medication, touching dirt, using a new tube of toothpaste, and licking envelopes. I did my best to avoid them all (diagnosis: specific phobia). My world was becoming smaller and smaller as more places became no-go zones: movie theaters, stadiums, lines. The potential for panic attacks—and the difficulty of escape—was too great (diagnosis: agoraphobia).
I had symptoms of a couple of cousin disorders, too. A twisted perfectionism turned the smallest decision into a colossal obstacle; I felt a sense of sinister foreboding if I didn't choose the "right" dress to wear, the "right" water glass (diagnosis: obsessive-compulsive disorder). I agonized over every odd sensation or twinge of physical pain. A headache was clearly an aneurysm; a bruise, leukemia (diagnosis: illness anxiety disorder, previously called hypochondriasis).
The estimated number of people who will have at least one anxiety disorder during the course of their lives is staggering: one in three Americans ages thirteen or older. If we look only at women, the number is even higher—about 40 percent. In any given year, about 40 million American adults have an anxiety disorder. And those numbers do not include the millions of garden-variety worriers and insomniacs whose anxiety, though not debilitating, leaches joy and steals peace of mind.
A certain amount of anxiety is good. It motivates us to study for tests, prepare for presentations, and save for retirement. It spurs us to get a physical or check the gas gauge. Too much anxiety, however, can be incapacitating and costly. In a 1999 study, the most recent estimate available, anxiety disorders cost the United States about $63 billion a year, more than half of it attributed to doctor and hospital visits. Other costs included psychiatric treatment, prescription drugs, and the value of lost productivity at work. There's also mounting evidence that out-of-control anxiety wreaks havoc on the body, increasing the risk of heart disease and weakening the immune system. Ironically, being a hypochondriac may actually make you sick.
It is tempting to think of our era—with its wars, terrorist attacks, rising sea levels, and economic insecurity—as, to borrow the poet W. H. Auden's phrase, "the age of anxiety." But cultural commentators throughout history have viewed their own times as equally fraught. In the 1880s, the telegraph, the steam engine, and even women's intellectual pursuits were blamed for the nation's unease. In the 1950s, it was the atomic bomb. Our world, it seems, always provides ample fodder for fear.
What is disconcerting is that rates of anxiety disorders—and depression—seem to be increasing among young people, particularly college students. According to a spring 2016 survey by the American College Health Association, 17 percent of students were diagnosed with or treated for anxiety problems during the previous year, and nearly 14 percent were diagnosed with or treated for depression. That is up from about 10 percent each for anxiety and depression in the fall 2008 survey. Parents and professionals are perplexed. While some of the rise may be because of increased prevalence, it could also be that more people are comfortable asking for help and admitting their troubles to researchers.
Depression may get most of the headlines and the research dollars, but anxiety is more prevalent. In people with a history of both an anxiety and a mood disorder, anxiety usually makes an appearance first. Anxiety disorders strike young, too: They have a median age of onset of fifteen, compared with twenty-six for mood disorders. And while anxiety disorders are pretty miserable in and of themselves, they are increasingly being thought of as gateway illnesses that can lead to a host of other problems, such as depression, substance use, and even suicide.
In fact, anxiety can be deadly. Depression is the mental illness most strongly associated with suicidal thoughts, but it doesn't often lead to suicidal acts. Recent research has found that it is anxiety disorders and other illnesses, like problems with impulse control and addiction, that are more likely to lead to suicide attempts.
In most cases, the consequences aren't fatal. Still, anxiety disorders can derail lives. Someone who develops an anxiety disorder at a young age is less likely to attend college. Anxious people who work have lower incomes. They are less likely to marry and, if they do, more likely to divorce. Anxious women face a greater risk of getting into unhealthy relationships and being the victim of domestic abuse.
That, thankfully, is not my story. If you met me now, you probably wouldn't even notice my anxiety. (When I began telling acquaintances the topic of this book, they almost uniformly said, "I would never have guessed you're anxious.") I have a career I love, as a reporter writing stories for the _Wall Street Journal_. I'm happily married, with an adorable seven-year-old daughter. I have friends, laugh a lot, go to parties, and bake pies. My affliction is often invisible.
I have had many advantages. I grew up in a loving home, lived in safe neighborhoods, and went to good schools. I have almost always had health insurance and the ability to pay for therapy and medication. While these privileges didn't prevent me from falling apart, I know they were critical in putting me back together.
But it has been a struggle. In tough years, I take medication and cycle through new therapies. In easy years, I still have to be diligent: Sleep eight hours. Do yoga. Take it easy on the wine. Pare down my responsibilities. And still I grapple with worry-induced insomnia. I tend to procrastinate, terrified of making the wrong choices. I have odd, unexplained physical symptoms—a tingling arm, chest pain. I can't drive on highways. Anxiety affects how I work, how I love, and how I parent.
So what is anxiety?
The _DSM_ calls it "anticipation of future threat." Søren Kierkegaard, the nineteenth-century Danish philosopher, called it "the dizziness of freedom." But the most cogent definition I've heard comes from Christian Grillon, a neuroscientist at the National Institute of Mental Health (NIMH). "Anxiety is the anticipation of pain," he told me. "It could be physical pain or emotional pain."
Anxiety is related to fear but is distinct. Whereas fear is concrete and imminent, anxiety is, as Grillon says, "sustained uncertainty." It's a chronic sense of uneasiness about a vague future, a gnawing worry about what may or may not happen.
Anxiety is universal, but the language we use to talk about it varies by culture, and so do its symptoms. The word _anxiety_ comes from the Latin _angere_ , which means "to choke or throttle." In Cambodia, _khyâl_ ("wind") attacks involve neck pain, dizziness, and ringing in the ears. In Vietnam, _trúng gió_ ("wind-related") attacks are characterized by headaches. In Latin America, _ataques de nervios_ ("attacks of nerves") can include uncontrollable screaming and crying.
Differing cultural perceptions of anxiety make it difficult to accurately compare rates of anxiety disorders in countries around the world. Yes, studies show that, in Japan, only about 4 percent of the population has an anxiety disorder in a given year, and that the French have a rate (13.7 percent) more than double that of the Spanish (6.6 percent). But these statistics are influenced by everything from how researchers define the word _worry_ to who responds to surveys. (You could argue that the most anxious people are the least likely to answer a stranger's probing questions.)
Anxiety also exists on a continuum. There is no sharp boundary between mental health and mental illness, and no doubt other cultures draw the boundary differently than we do. When I asked Ron Kessler of Harvard Medical School, the country's leading mental health epidemiologist, why so many people have anxiety problems, he said it was because "we have decided it is a disorder." Still, even if we have become alert to the idea that everyday anxieties can be symptoms of a disorder, a formal psychiatric diagnosis requires that the person suffer from "clinically significant distress or impairment" in functioning. No matter the symptoms or the name you give it, anxiety is a problem if it keeps you from living—and enjoying—your life the way you want to.
—
I've tangled with severe anxiety for more than twenty-five years. Looking back, my troubles didn't actually begin that December day in college, though it wasn't until then that it spiraled out of control. I had been having strange "spells" for months. They started when I was living at home the summer after my freshman year. During the day, I was working as a receptionist at a company that made steel forgings, the kind of place where the women were called by their first names while the men were all Mister So-and-so. At night, I waitressed at an Irish bar in East Lansing, where I checked fake IDs, dodged the advances of horny Michigan State guys, and learned to perfect the head on a pint of Miller Light. Between jobs, I took step aerobics classes.
One night I was at the apartment of my boyfriend, Scott, a Michigan State student and Christopher Reeve doppelgänger I had begun dating in high school. The evening's goal was, to paraphrase him, to get me high. I had tried smoking pot once or twice before but very tentatively. (I, seriously, tried not to inhale.) Frankly, I was afraid of it. I had been around enough of the stuff when I was a kid at my parents' and my friends' parents' parties, the blue sheen of bongs glinting off Pledge-buffed coffee tables. Pot always seemed to make people silly and stupid. But Scott, an enthusiastic stoner, had been touting its effects for month. I was in.
We started smoking a joint and waited.
Nothing.
"Take another hit," Scott said.
I did. And when Scott took one, he grabbed me and kissed me, blowing smoke into my mouth.
Several more minutes went by.
Then it hit me.
My heart beat faster. My mouth went dry. I felt breathless. My equilibrium and vision contorted; it was as if I were on a roller coaster the moment before the big plummet. I lay down on Scott's bed, trying to take deep breaths and calm down. My legs felt like they were stretching, _Alice in Wonderland_ style. I looked down and could have sworn I saw my feet on the other side of the room.
Desperate for distraction and wanting to feel grounded in some way, I reached for Scott and we started having sex. But I could barely feel him. My body was numb, deadened. I panicked.
"I can't breathe," I cried, sitting bolt upright.
"Sure you can," Scott said, taking my hand. "Just relax."
"I can't. And my heart is beating so fast, too fast," I said. "Something must have been in that pot. It must have been laced with something."
I darted around the room, pacing and gulping air. "Or maybe I'm having an allergic reaction. Something is really wrong. I think I need to go to a hospital." I threw on sandals, a T-shirt, and a pair of Scott's boxer shorts. He scrambled to get dressed, too. I was already turning the doorknob to leave. Scott grabbed his car keys and followed.
At the ER, the bright lights, shiny linoleum, and bureaucratic questions sobered me up fairly quickly. I was not the only college student whose visit was spurred by chemical overindulgence. One drunken kid threw up on the waiting room floor. Another sobbed incoherently. In the exam room, a technician hooked me up to a heart monitor. A few hours later I was told I could go. A doctor scribbled my discharge instructions: "Avoid THC," he wrote of the active chemical in marijuana.
I did that easily. That one episode was more effective than an entire adolescence of antidrug After School Specials. But the spells of breathlessness, racing heart, and, increasingly, fear, recurred every month or so. They seemed to come from nowhere. I had one while eating fried cheese sticks at Bennigan's. I had another in the middle of a women's studies class. I feigned a bathroom emergency and spent the rest of the class crouched in a ladies' room stall. The attacks subsided after twenty or thirty minutes but left me jelly-legged and shaky for hours.
I don't remember thinking much about the episodes during the intervals between them. I brushed them off, telling no one but Scott and hoping they'd vanish as abruptly as they'd begun.
According to the _DSM_ , a panic attack is "an abrupt surge of intense fear or intense discomfort that reaches a peak within minutes." After that, it usually subsides. But when I landed on my parents' sofa that December, it felt as though I were having a monthlong panic attack. Sure, my fear had peaks and valleys, but it was always there. Soon I was nearly immobile, a pajama-clad heap with greasy hair, one hand checking my galloping pulse, the other on the TV remote control, switching from MTV videos to _Love Boat_ reruns and back again. I couldn't read. I wasn't actually watching the TV either. The noise was just a soundtrack for my fear.
My parents were bewildered and scared. My fourteen-year-old sister, Dana, would sometimes sit next to me, but mostly she tried to stay out of the way. "Nobody really told me what was going on," she said recently. "I just knew that you were sick and needed some time off from school to get better. Everybody was tiptoeing around. I felt like I should not be trouble because Mom and Dad were clearly worried about you."
It was only a few weeks before final exams, but I didn't make it back to school. I took incompletes in my classes and planned to take my tests after winter break, when, I hoped, I'd feel better.
My dad was alarmed to see me transform overnight from an energetic young adult into a listless lump. "It scared the shit out of us," he recently recalled. "The next thing you know you're rolled up in a fricking ball in bed."
My parents took me to a doctor. I was terrified that something was wrong with my heart. "You thought it was going to explode," my dad says. I started having strange neurological symptoms, too. Once, when I'd gathered the courage to venture to the mall with my mother, my peripheral vision vanished next to an Orange Julius. I had vertigo, too. The floor would rise up and the walls would tilt at odd angles. But the only diagnosis I was given was a fluttery heart valve, the mitral valve prolapse.
Nights were increasingly difficult. I was exhausted but had a tough time falling asleep. When I did, I had terrifying nightmares that became increasingly gory. Sometimes I was being chased by an unknown assailant. I dreamed I was shot in the head. Other times my face was being torn apart by an electric drill. The violence had a Tarantino vividness, but without the humor and gloss. I'd wake up shaking, with tears running down my face.
Rules crumbled. My boyfriend started spending the night with me in my high school bed, an almost life-size poster of Morrissey and his pompadour looking over us. Nothing sexual happened. Scott was more of a nocturnal life raft. I'd clutch his arm, hoping the warmth of his healthy twenty-year-old body would somehow heal me.
After a couple of weeks of infirmity, and with no real answers from the doctor, my parents began losing patience. It was right before Christmas, and we had plans to drive to the small southern Illinois town where my grandparents, aunts and uncles, and a mess of cousins lived, but I couldn't imagine moving from my sofa. I begged them to let me stay home. They refused. I said I wouldn't leave. They could go without me.
I didn't win that fight. Instead, I ended up in the backseat of our blue Ford Thunderbird for the seven-hour drive to Salem, Illinois, a town of dried-up industry and oil wells, chain fast-food joints, and vast starlit skies. I don't recall much from that trip. Did I eat my grandmother's famous divinity—white sugary blobs topped with a single half walnut? Did I make small talk with cousins? Could anyone tell how scared and screwed up I was? Terror has a way of blacking out the details.
I do know that I took my pulse a lot, trying to will it back down to double-digit-per-minute territory. The vertigo and a growing exhaustion made it difficult for me to stay upright. I leaned against walls and car doors. And I soon found a spot on another sofa, this one in my grandparents' house, and spent most of the time quaking under the orange and brown afghan my grandmother had crocheted. I spoke little and smiled wanly at the parade of relatives.
Back at home in Michigan, winter break was coming to an end. The new semester would be starting soon. The arguing with my parents intensified. I didn't see how I could go back to school. I was too fragile. I still didn't know what was wrong with me. I wanted to stay on that ridiculous beige-striped sofa (who knew there were so many shades of beige?) until I was better.
"You have to go back," my parents said, unified in their decision.
"This is tough love," said my father.
I was furious with them. I felt tossed out. Abandoned.
"We were concerned that if you stayed in your bedroom much longer, you would never go back to school," my mom recalled recently.
"We wanted to get you off the couch. We wanted you to be normal," my dad said. "Maybe it was a sink-or-swim move on our part."
It took me years to forgive them. Now, after all my research, I know that they did the right thing. If I had stayed on that sofa, I would probably never have risen from it. Avoiding experiences that make you anxious just reinforces your anxiety.
—
I had to move rooms when I returned to school. I had been living with two other women, but now I would be living with three in a single room, a so-called quad. There were two sets of bunk beds, four dressers, four desks, a hodgepodge of sweatshirt-filled milk crates, and all the drama that four nineteen-year-old women can conjure.
It is awfully difficult to fall apart with no privacy, and I was almost never alone. The four of us lived in a stately, white-columned sorority house with close to a hundred other young women. We ate meals together, cooked by a surly, spice-averse man. We had weekly meetings where we'd debate which fraternities to party with and honor women who'd been "lavaliered," given necklaces graced with the Greek letters of their boyfriends' fraternities, a "going steady" move that was only one step away from engagement. It was hard for me to feign the required gushing.
I wasn't alone even in the shower. The house had communal bathrooms, and the shower was a three-person affair, a white-ceramic-tile-covered stall with three metal showerheads. Fear had stolen my appetite, and I had lost fifteen pounds over the previous month. I had started to become afraid of food itself, worrying about unknown allergies or food poisoning. In that shower, I felt so fragile and ashamed as I compared my skeletal nakedness to the spirited curves of my sorority sisters. I did my best to shower at off-peak times—in the very early morning or during happy hour.
Trying to hide my terror and appear "normal" was exhausting, so I came up with a cover story. I told my roommates and others I was recovering from mono, the quintessential college "kissing" disease. That was meant to explain why I skipped parties, stayed in bed a lot, and escaped to my parents' house on weekends. And to a certain extent, I faked it.
In pictures from that semester, I don't look haunted or timorous. In fact, apart from the awkwardly layered bangs, I look surprisingly okay. The extra-large men's sweatshirts that were in fashion then hide my skinniness. I pose perched on bunk beds and smile widely with my arms flung around other girls. Flipping through the photos, I'm reminded of something Ned Kalin, a psychiatrist at the University of Wisconsin, told me, that patients with anxiety fascinated him because they often seemed so together, even when they were plagued by intense worry and fear.
I had seemingly normal conversations with friends about boys they liked, about the fall of the Berlin Wall. I attended classes and did some schoolwork. (But only a minimal amount. I completed only two courses that semester.) Yet these efforts were undertaken, it seemed, by no more than a tiny sliver of my brain. The rest was stuffed with a litany of fears: my heart, my breathing, never being well again.
I had always been a quick, voracious reader, but ever since my spell on the couch, I found that I read pages, then had no recollection of their contents. My eyes skipped around, missing entire paragraphs. I'd finish a passage feeling inadequate and confused.
I still had to make up my final exams from the previous semester. I met with the dean in his office, and he explained the process of taking the exams, when and where they would happen. I nodded my head. After we had wrapped up, almost as an afterthought, he asked, "So what do you have?"
"Mitral valve prolapse," I said. It was the only diagnosis I had been given, and I didn't want to trot out my mono lie to an authority figure.
"Really? My wife has that," he said, clearly unimpressed.
"It makes my heart race," I mumbled weakly as I left, cheeks burning with shame.
Getting through each day was becoming harder and harder. My heart raced, my fear spiked, and I had difficulty breathing (these were clearly panic attacks, though I still didn't know it at the time) when I stood in a line or went to a movie theater. So I stopped standing in line. Stopped going to see movies. Even more nonsensical things started to scare me, too. I became terrified of contamination, of dirt, of being infected by some ferocious bacterium. Using something new—a bottle of shampoo, a toothbrush—took major effort. (Perhaps it had been tampered with, my paranoia whispered.) I'd panic for a good hour or so afterward, waiting for some dire physical reaction. Choosing a plate or glass at dinner turned into a ten-minute struggle. I'd check carefully for dried food, lipstick marks, chips. Even if I found a pristine cup, it still might not "feel right." Sometimes the easiest thing was not to drink or eat at all.
New fears cropped up everywhere. I licked an envelope, then recalled reading that LSD was sometimes delivered via paper. _Was there LSD on that envelope?_ I thought. I knew the thought was ridiculous, yet I couldn't shake it. (I haven't licked an envelope since. I heartily thank the inventor of self-sticking ones.) I didn't know it, but I had turned a corner in my anxiety disorder. No longer was anxiety merely rattling around my brain and body; I was now exhibiting multiple "avoidance behaviors." I could no longer do the things I wanted to do when I wanted to do them.
Avoidance behaviors are associated with more serious, harder-to-treat illnesses. Avoidance fuels anxiety in a vicious cycle. By steering clear of the things I was afraid of, I never got a chance to learn that what I feared most—dying, going crazy—wouldn't actually happen. The not knowing made me even more anxious.
I saw many more doctors in the ensuing months in search of a real diagnosis, my mother often making the hour-long drive to Ann Arbor to accompany me to assorted specialists. I also ended up at the ER several times—driven by my ever-patient college friend Susie—when my symptoms became particularly intense. I was convinced I was having a heart attack. My heart beat like an avant-garde jazz number, cacophonous and herky-jerky. It would speed up, slow down, skip. In the waiting room, Susie would try to make me laugh. She had asthma and knew what it was like to feel fragile and breathless. But after each visit, I was sent home without any answers. I think a doctor or nurse or two might have said something about avoiding stress.
I continued to have neurological issues, too: tunnel vision, vertigo, freaky depth perception. My hands and feet were often numb and tingly. A neurologist suspected multiple sclerosis, and I had an MRI of my brain. In the middle of it, I began having trouble breathing, and my heart beat so rapidly and loudly, it seemed to strain my ribs. Spots danced in front of my eyes, and I thought I would pass out. Crying, I had to be pulled out of the clanking, vibrating tube.
They did a CAT scan instead. The machine was less tomblike so I gave it a go. My mother held my hand, her body shrouded in a lead apron to protect her from the radiation bathing my brain. That scan was "inconclusive," with some vague shadow possibly suggesting a brain tumor. After a completely sleepless night picturing my slow and awful death from brain cancer, back into the MRI machine I went, this time with several milligrams of Valium in my bloodstream. The MRI was fine. My brain, I was told, was normal.
My dad now says that the scariest thing about that time was that nobody had a clue as to what was wrong with me. With no definitive diagnosis, the expanse of possibilities and prognoses was terrifying.
I was tired all the time, a bone-deep torpor. For a few weeks, I was actually excited to think that I might have chronic fatigue syndrome, a disorder that had suddenly emerged in the zeitgeist. Sure, it didn't sound like fun, there weren't really any effective treatments, and some doctors didn't believe it existed. But at least it had a name.
—
I like to think that none of this would happen now. Today there's a much better chance that a doctor would properly diagnose me, that the school would refer me to the counseling center, or that I would look up my symptoms online and figure it out on my own. But all this happened in an era before large-scale mental health awareness campaigns, when there was greater stigma around psychiatric disorders. In the 1980s, organizations like the National Alliance on Mental Illness and the Anxiety Disorders Association of America (now the Anxiety and Depression Association of America) mailed out their newsletters in plain envelopes. Active Minds, a robust advocacy and support organization with chapters at more than four hundred college campuses, wasn't founded until 2003. I didn't know anyone who had been to a therapist or was taking psychotropic medication.
Anxiety disorders didn't even exist as a category in the _DSM_ until 1980, and it wasn't until 1987 that Prozac was released in the United States. Then in 1989 the World Wide Web was born. The internet and Prozac would dramatically change the diagnosis and treatment of mental illness. Prozac, a new selective serotonin reuptake inhibitor, had far fewer and less onerous side effects than earlier medications. And the internet made a torrent of health information available to anyone with a keyboard and made it possible to anonymously join online support groups. In 1990, the Americans with Disabilities Act spurred colleges to open disability offices that now field requests for academic accommodations like quiet rooms for test taking and extra time for assignments for students with all types of disabilities, including psychiatric ones.
Without these new supports, I had to tough it out. I did my best to play the role of the free-spirited college student, even heading to Cancún for spring break with my roommates. Although I was barely hanging on to my student status, my parents were happy to fund the trip. Maybe doing something fun and frivolous would bring me back to health.
It was a disaster.
The days were all right. We spent them sunbathing and swimming. But at night my friends headed out to bars, and despite having been an enthusiastic binge drinker my freshman year, I hadn't had a drink since I got sick. My body and brain already felt so haywire, I couldn't imagine doing anything to make it more so. (My reaction was not typical. Many people with anxiety disorders drink to relax, a way of self-medicating.) But I wasn't open about my abstinence. So there I was at Señor Frogs, a bar crammed with sunburned spring breakers, with a tequila shot in one hand, desperately trying to figure out how to surreptitiously ditch it. I lowered my hand and poured it down the leg of my chair, figuring it would blend in with the sticky sludge already on the floor.
I managed to dance a little that night, but later on, back at our hotel, I felt a pain in my neck, and my hands and feet went numb. What if I somehow had broken my neck? It was an absurd thought. I hadn't fallen. I could walk. I knew my fear was ridiculous, but I couldn't get logic to prevail. On some primitive, emotional level, I was convinced I must have fractured a vertebra.
I called the front desk and asked for a doctor. They sent someone up. The doctor examined me and said I needed an X-ray. So I got into a taxi with him and rode through the chaotic Cancún streets to an all-night medical clinic. (Why this didn't freak me out more than a completely hypothetical injury, I have no idea.) Several X-rays revealed—surprise—that I was fine. For a second I was relieved. Then I started worrying about the thyroid cancer I would most likely get because of the radiation from the X-rays.
The next day I stayed at the hotel while my friends went to the beach. I furtively called my mother, begging her to buy me a plane ticket so I could come home early. As in, that day. She did. Then I left my friends a weird, rambling note, packed my bags, and left. I was back in my parents' house by late evening.
As the weeks wore on, I became lonelier and increasingly hopeless. Upon waking, I'd have a moment of sunny optimism— _this_ would be the day I'd feel normal again. But then I'd prop myself up on an elbow, and the heart palpitations and vertigo would return, and the fears would gnaw at me again.
I began to think it would be easier to not wake up at all. I didn't want to die. I'd spent months terrified of dying. But I couldn't see any other way to escape how I felt. The doctors couldn't help me. Nor could my parents or friends. And I increasingly didn't feel strong enough to continue to slog through the days and nights.
Finally, when these dark, desperate thoughts scared the hell out of me enough to share them, I called my father and asked him to come to Ann Arbor and take me to the hospital. This time he didn't tell me to buck up or that things would be better if I got some sleep. He came and got me right away.
We parked the car in a high-rise parking garage. As we walked to the stairwell, I glanced over the railing to the ground far below and had a sudden, strong impulse to jump. To erase everything. But self-preservation and a slim hope won out. I grabbed my father's hand.
At the hospital, we bypassed the regular ER and instead went to the psychiatric emergency room. It was a small, quiet waiting room, and I was the only patient in it. I remember giving someone, a psychiatrist or psychologist, a short synopsis of the last three months and my new despondency. The doctors considered admitting me but decided that I wasn't at acute risk of harming myself. (I had no actual suicide plan.) What I needed, they said, was outpatient counseling. The therapist handed me a small card with the words PSYCHIATRIC EMERGENCY SERVICES in all caps and my appointment time written in black pen. A twenty-four-hour emergency phone number was on the back.
I had several therapy sessions, but the treatment seemed irrelevant. The therapist asked me about my childhood and how I felt about my parents, but I wanted to know why my heart raced and why I was always terrified. Scratch that. I had stopped caring why. I only wanted it to stop.
—
For centuries, excessive anxiety was considered more of a moral failing than a medical problem. The stories of the ancient Greeks and Romans are filled with negative depictions of people who don't cope well with fear. "The skin of the coward changes color all the time, he can't get a grip on himself, he can't sit still," writes Homer in the _Iliad_ , about an anxious man preparing for battle. "He squats and rocks, shifting his weight from foot to foot, his heart racing, pounding inside the fellow's ribs, his teeth chattering—he dreads some grisly death."
Specific phobias pop up in ancient writings, too. In the third century B.C., Andreas of Charystos described aerophobia, a fear of open spaces. He also defined the apex of all phobias: pantophobia, the fear of everything. In the Classical period, anxiety was considered a component of melancholia, a mental state marked by fear and despondency. The Hippocratic physicians of ancient Greece thought all illness was caused by an imbalance among the four "humors," or bodily liquids: phlegm, blood, yellow bile, and black bile. Melancholy was thought to arise from a surfeit of black bile. Practitioners treated melancholy with everything from special diets and exercise to enemas and bloodletting. The belief in humors persisted for centuries.
Religion tackled anxiety, too. Faith in God was the cure. "It was as if a light of relief from all anxiety flooded into my heart. All the shadows of doubt were dispelled," wrote Saint Augustine in the fourth century A.D. of his experience reading the teachings of Jesus Christ.
By the seventeenth century, the belief in humors as the cause of melancholia and its attendant anxiety was supplanted by the emerging concept of nervous disorders. Dysfunction in the brain and nerves was now thought to be the cause of a host of mental and physical symptoms. The nervous disorders were generally treated by neurologists and general physicians. In 1869, George Miller Beard, a neurologist from New York, coined the word _neurasthenia_ , literally "tired nerves," to describe a constellation of physical and emotional symptoms, including headaches, rashes, fatigue, insomnia, and phobias. This weakness of the nervous system was caused, Beard thought, by the fast-paced lifestyle of nineteenth-century America. In particular, he blamed the stress of technological advances like the telegraph and steam power, as well as the "mental activity of women."
Anxious women who weren't diagnosed with neurasthenia were likely to be slapped with the label of hysteria. The Greek physician Hippocrates named the disease in the fifth century B.C.; he believed it was caused by the uterus wandering around the body. In Victorian-era women, hysteria was characterized by nervousness, insomnia, "excessive" sexual desire (or the complete lack of it), and a panoply of psychosomatic symptoms from headaches to fainting. It was commonly treated with "pelvic massage," with orgasm as the goal. (The development of the vibrator was heralded as a major treatment advance.)
Just two years after Beard introduced the idea of neurasthenia, Jacob Da Costa wrote about a peculiar syndrome he had seen while working as an army doctor during the Civil War. He relayed the story of WWH, a young Union soldier who had survived the bloody battle of Fredericksburg. After the battle, WWH "was seized with lancinating pains in the cardiac region, so intense that he was obliged to throw himself down upon the ground, and with palpitation. The symptoms frequently returned while on the march, were attended with dimness of vision and giddiness, and obliged him to fall out of his company and ride in the ambulance."
Da Costa saw similar symptoms in hundreds of other soldiers, too. The young men complained of chest pain and heart palpitation, difficulty sleeping, dizziness, shortness of breath, and upset stomachs. Finding the soldiers otherwise healthy, Da Costa chalked up their symptoms to an overactive heart. He called the illness "irritable heart syndrome." Today we might call it panic disorder or post-traumatic stress disorder (PTSD). Da Costa treated irritable heart with various drugs, including opium, digitalis (derived from the foxglove plant and not dissimilar to medicines used to treat heart failure today), and lead acetate.
It's impossible to talk about the history of anxiety without mentioning Sigmund Freud. In 1894, he wrote a groundbreaking paper with a cumbersome name, "The Justification for Detaching from Neurasthenia a Particular Syndrome: The Anxiety-Neurosis." Out of the broad bucket of neurasthenia, Freud adroitly defined what we now know as the anxiety disorders. His descriptions of panic attacks (which he called anxiety attacks), generalized anxiety, phobias, and even obsessive-compulsive disorder are vivid and sound incredibly modern. Freud, then working as a neurologist in Vienna, grouped all these symptoms under the diagnosis of "anxiety neurosis," a disorder that existed in the _DSM_ until 1980.
Here's Freud's pitch-perfect characterization of generalized anxiety, or what he calls "anxious expectation": "A woman who suffers from anxious expectation will imagine every time her husband coughs, when he has a cold, that he is going to have influenzal pneumonia, and will at once see his funeral in her mind's eye. If when she is coming towards the house she sees two people standing by her front door, she cannot avoid the thought that one of her children has fallen out of the window; if the bell rings, then someone is bringing news of a death, and so on; whereas on all these occasions there is no particular ground for exaggerating a mere possibility."
Freud goes off the rails, however, when he describes the cause of anxiety neurosis. It arises, he asserts, from an accumulation of sexual energy that is inadequately released. Abstinence, premature ejaculation, and coitus interruptus are primarily to blame for anxiety neurosis in both men and women, Freud says. In later works, he abandoned this theory. Eventually, he came to believe that anxiety arose from unconscious threats and conflicts. This view would hold sway for decades.
—
We've come a long way from bloodletting and opium. Advances in brain imaging and genetics are yielding new insights into the origins of anxiety disorders and what can go awry in the brain. Groundbreaking treatments are on the horizon. Pioneering scientists are experimenting with programs intended to prevent anxiety disorders in children as young as three.
We now know that the foundation of anxiety is the defense system that nearly every organism has to detect and react to threats. That's what trips off the racing heart, the shallow breathing, and the urge to escape—a response that makes clear sense if you're being chased by a bear. The fight-or-flight response is critical to survival.
When that response is initiated, the adrenal glands release the hormone epinephrine. Blood pressure rises and senses become sharper. The hypothalamus, a part of the brain that acts as the control center for the autonomic nervous system, releases corticotropin-releasing hormone (CRH), which in turn tells the pituitary gland and the adrenal glands to release the stress hormones adrenocorticotropic hormone (ACTH) and cortisol. This activation of the so-called HPA axis works together with the sympathetic nervous system to keep the body on high alert for danger. (Some studies have found a range of HPA axis abnormalities in people with anxiety disorders.)
At the root of this threat detection system is the amygdala, an almond-shaped structure in the brain that has been called its fear center. Probably no one knows more about the amygdala than Joseph LeDoux, a sixty-six-year-old neuroscientist at New York University and a genuine rock star in the world of anxiety disorders. (He fronts a band called the Amygdaloids.) In the 1980s, he successfully mapped the neurocircuitry of the defensive mechanism in rats.
People had speculated before that the amygdala was involved with fear. In the 1930s, Heinrich Klüver, a German-American psychologist, and Paul Bucy, an American neurosurgeon, conducted a series of experiments on monkeys. They found that removing both temporal lobes (which include the amygdala) caused monkeys to exhibit bizarre behaviors, including eating anomalies, hypersexuality, and fearlessness. Later scientists noticed similar behavior in people who had sustained damage to the amygdala and nearby brain structures due to strokes, infections, or other ailments. This came to be known as Klüver-Bucy syndrome.
Building on this work, LeDoux used a common experimental model called fear conditioning to teach his rats to react to an audible tone. When rats are threatened, say by a predator or by an electrical shock to the feet, they freeze, their hair stands on end, and their blood pressure and heart rate shoot up. In his experiments, LeDoux played a tone to the rats and followed it with a shock. After several rounds of this, the animals began to freeze as soon as they heard the tone. They had been conditioned to perceive the sound itself as a threat.
LeDoux's goal was to trace the path in the rats' brains from tone to rodent freak-out. To do this, he damaged different regions of the brain and then fear-conditioned the animals, noting what effect the various lesions had on the rats' behavior. He started with the auditory cortex, which directly receives sensory information, and worked downward to more primitive brain structures. Lesions to the auditory cortex didn't do much; the rats still froze to the tone. Lesions to the caudate-putamen, which is involved in movement and learning, also didn't affect freezing behavior. But when LeDoux made lesions in the amygdala, the rats stopped freezing. No amygdala, no threat response. The locus of fear, it seemed, had been found.
The tone takes one of two routes to the amygdala, LeDoux found. The more direct route, which he dubs the "low road," sends the stimulus right from the sensory thalamus, which relays sensory and motor information, to the amygdala, a journey that takes 10 to 12 milliseconds. The "high road," by contrast, where the stimulus travels from the sensory thalamus to the sensory cortex and then to the amygdala, takes about twice as long. The low road is a "quick and dirty processing system," LeDoux says. It unleashes the defense system almost instantly, even before a threat is consciously registered. He gives an example of a prairie dog spotting a bobcat. "The sight or sound of the bobcat goes straight to your amygdala and out comes the freezing response. If you had to make a deliberate decision about what to do...you could get so bogged down in decision making that you might be eaten before you made a choice."
The amygdala itself has different regions that serve different functions. The lateral nucleus, for example, is the part that receives the information. The central nucleus sends that information to the parts of the brain that control the physical responses associated with fear—freezing, respiration, heart rate, and the release of stress hormones. The hippocampus is the region that processes the context of the threat experience. This cage is where you got the shock, it tells the rat.
LeDoux then tackled the question of how animals can shake fear. Rats that have been fear-conditioned by the pairing of a tone with a shock can override that learning when the tone is repeatedly presented without the shock. Eventually they cease to freeze. This process is called extinction. In experiments in the 1990s, LeDoux found that another part of the brain, the medial prefrontal cortex, is critical to extinction. It acts, he says, by dampening the amygdala's action. "The medial prefrontal cortex is clamping down the amygdala, sort of like the brakes. The amygdala is the accelerator." Stress, however, can undo extinction. "The brake comes off," he says.
LeDoux says that in people, anxiety happens when thoughts interact with this threat-defense mechanism. While our body is going into fight-or-flight mode, our mind conjures catastrophe and dredges up memories of prior peril. The result, LeDoux says, is the conscious experience of anxiety.
On an October afternoon, I visited LeDoux at his office on the eleventh floor of the Center for Neural Science at NYU, a block from Washington Square Park in Greenwich Village. His office has a view of the Empire State Building. His desk is cluttered with books, unopened mail, and a baseball cap adorned with the image of a brain. LeDoux is the hippest-looking neuroscientist I've met, sporting dark jeans, a checked shirt, and a gray-blond soul patch. He speaks slowly, with a bit of a Louisiana drawl; he grew up in Eunice, the son of a butcher. (The part of the cow that most intrigued him? "The slimy, wiggly, wrinkled brain," of course.) He played in rock bands throughout high school and college, including one presciently named Cerebellum and the Medullas.
LeDoux takes me on a tour of his lab. We stop in a room lined with shelves, each piled with stacks of slim white boxes. "Here we have thirty years of rat brains," he says, gesturing with an arm. He takes a box down, opening it to reveal dozens of slides, each with a thin slice of brain stained a brilliant cerulean blue.
In another room, we see an apparatus designed for rodent neurosurgery, a silver bracelike contraption with various arms, knobs, and grooves indicating measurements. Brain lesions, he tells me, are usually made with an electric current. The rats themselves (two hundred or so) are out of sight, in a room that is off-limits to visitors. (After several more interviews with scientists who work with animals, I discover that it's standard policy not to let visitors see their subjects. Scientists are afraid of becoming the targets of animal rights activists.)
At one point, LeDoux confesses that he has a phobia of snakes. He traces the fear back to a traumatic childhood experience. "I remember as a kid being taken craw fishing on the bank of a bayou," he recalls. "It seemed like there were thousands of slithering black snakes everywhere. It was so disgusting." After that, he did everything he could to avoid them—a challenge given that he was an avid water-skier. "I would never get in the water ever. I'd be able to jump off the pier as the rope tightened and ski and then ski back up onto the landing."
After I visited LeDoux, I watched a video of one of his band's songs, "Fearing," based on a poem by Emily Dickinson. The Amygdaloids, which LeDoux formed with other NYU scientists, write and perform songs about emotions and the mind. In the video, LeDoux appears in the dark, ominous attic of a ruined house, wearing opaque black sunglasses and singing these words:
> But recollecting is not forgetting
>
> It's vivid rehearsal of pain
>
> It reminds me of that day
>
> It keeps fear in my brain
—
Studies have found that the amygdala and prefrontal cortex are involved in fear conditioning and extinction in people, too. Our fear response can be measured in a variety of ways, including skin conductance (a method of measuring sweating using electrodes) and fear-potentiated startle, an eyeblink reflex. Tiny sensors are placed under the eye to record the magnitude and intensity of the eyeblink. Researchers have found that people with anxiety disorders have a larger startle response than healthy people to conditioned stimuli—the colored light or tone that precedes an unconditioned stimulus, like an electric shock. And during extinction, the startle response tends to remain elevated. Simply put, anxious people catch fear easily and have a hard time letting go of it, even when there's mounting evidence they're safe. The amygdalae of anxious subjects also tend to be hyperactive even when they are not facing a potential threat. It is as if the anxious brain were always scanning the horizon for danger.
Anxious people aren't just constantly on guard; they actually see more peril in the world. If a situation is ambiguous, they are more likely to perceive it as negative or threatening. That's why when I have a headache, I think of brain tumors. And if my husband, Sean, is being quiet, I don't consider that he might be tired—I think he's mad at me. (Okay. Sometimes he is.) Scientists call this "attention bias to threat," and they think that, like lightning-quick fear conditioning, the bias is linked to a hyperactive amygdala and dampened prefrontal cortex activity.
Scientists often use the dot probe task to measure attention bias. It generally works like this: Subjects are shown photos of two human faces side by side, one angry or fearful, the other neutral. The faces disappear, and a small dot or cross (the probe) is shown in place of one of the faces. Subjects need to respond as quickly as possible (often by pushing a button) to the probe. A subject is considered to have an attention bias toward threat if they respond more quickly to the probes that replace the threatening faces versus the neutral ones. In many studies, those with anxiety disorders are shown to have this bias. This is true even when the faces are flashed so quickly that they can't be processed consciously. Nonanxious people, however, don't show this bias.
Besides being constantly ready for crisis, anxious people have a hard time with uncertainty. _What if? What if? What if?_ is the endless refrain of the anxious mind. Uncertainty far too easily morphs into inescapable catastrophe. Scientists call this "intolerance of uncertainty," and it actually makes parts of the brain light up on a functional magnetic resonance imaging (fMRI) scan. Researchers at the University of California, San Diego, found that intolerance of uncertainty was linked to activity in the insula, part of the cerebral cortex that plays a role in emotion processing and body awareness. In a small experiment published in 2008, the scientists gave fourteen young adults a task called the Wall of Faces. The study subjects saw a series of pictures of thirty-two faces against a black background. Some faces had ambiguous expressions. Others were clearly happy or sad. The subjects who scored higher on a measure of intolerance of uncertainty had greater activity in the insula when they saw more faces with ambiguous expressions. Other studies have found that people with PTSD, social phobia, and GAD have increased activity in the insula when they anticipate seeing negative pictures.
Interestingly, scientists are finding that fear and anxiety may originate in different parts of the brain. The amygdala, it seems, is more closely tied to fear. It generates the raw, immediate response to an imminent threat. Anxiety, however—longer-lasting, amorphous uneasiness—may be rooted in an adjacent structure with an ungainly name: the bed nucleus of the stria terminalis, or BNST.
Michael Davis, a neuroscientist who recently retired from Emory University, has been exploring the BNST for decades. During the 1980s, he and LeDoux were in something of a race to map the neurocircuitry of fear conditioning in rats. At that time, he noticed that the BNST was connected to the same structures as the amygdala: the parts of the brain stem that control blood pressure, heart rate, and freezing. Why, he wondered, would there be a second area of the brain that appeared to serve the same function as the amygdala? Nature didn't usually duplicate itself like that.
While LeDoux was measuring fear conditioning by looking at freezing behavior, Davis began studying the startle reflex—specifically, fear-potentiated startle. Rats have a whole-body response when startled: Electrical activity can be detected in the rodent's neck muscles 5 milliseconds after a loud sound. In Davis's lab, first at Yale and then at Emory, rats were fear-conditioned by being exposed to a light followed by a shock. Then researchers elicited the startle response with a series of loud noises. Sometimes sounds followed the light that predicted the shock; other times there was no light, only sound. Not surprisingly, the startle response to the loud noise was bigger when the rats were also exposed to the light. This amplified response is known as fear-potentiated startle.
It was during these experiments that Davis stumbled on a potential role of the BNST. Over the years, he and his colleagues tested a host of compounds to see how they worked on fear-potentiated startle and, by extension, anxiety disorders. But there is a problem with fear conditioning. It involves learning: The rats have to learn that the light precedes the shock. So if a substance reduces fear-potentiated startle, you don't know whether it is because the substance is actually reducing the fear response or whether it is simply causing amnesia. It's possible, in other words, that the substance caused the rats to forget the link between the light and the shock.
With that in mind, the lab searched for a way to elicit an amplified startle without learning. Davis's colleague David Walker discovered that exposing rats to bright light for twenty minutes also enhanced startle. No learning was required. (Rats naturally avoid bright light and open spaces, which to a rodent signal danger.) "When the bright light is on for a long time, you don't know when something bad is going to happen," Davis says. Davis and Walker assumed that the amygdala was key for this extended fear conditioning, but it turned out that inactivating the amygdala didn't block the increase in startle after the twenty minutes of light. Deactivating the BNST, however, did.
The amygdala, it seemed, controlled the lightning-quick response. The BNST was switched on by longer-lasting apprehension—the expectation of pain without any certainty as to when it would occur. Scientists aren't certain when the shift from amygdala to BNST activity occurs in the face of danger, but it seems to be somewhere between four seconds and a minute.
In the 1990s, Christian Grillon, who was collaborating with Davis at Yale, began doing similar experiments in people. Humans have a whole-body startle reflex, too, but the eyeblink part of it is the most consistent and easiest to measure. Sustained uncertainty, Grillon found, makes people jumpy for a sustained period of time. In one critical experiment, Grillon and Davis recruited fifty-eight Yale students. Most of the subjects underwent repeated rounds where they saw a blue light and received a shock to the left wrist. The students were divided into three groups. In the first group, the shock was predictably delivered a few seconds after the light. In the second, shocks were delivered randomly, with no relation to when the light was shown. (A third group saw the blue light but didn't receive any shocks.) Startle was elicited with a loud sound. Four days later the students underwent the same experiment. After being fear-conditioned, the first group startled more after hearing the sound—despite the four-day break. That wasn't surprising. But the second group had a bigger so-called baseline startle, the startle scientists elicited even before the subjects began this round of the experiment. The unpredictability of the shocks had made them on guard and ready to jump as soon as they were back in the same environment.
"In a way, anxiety is the opposite of fear. Fear is about something that is in front of you that is predictable and imminent. Anxiety is the opposite. It is worrying about something that is in the future that may or may not happen," Grillon says.
Based on the animal data, Grillon is pretty sure that the BNST is behind uncertainty-driven apprehension. One challenge for researchers is that the structure is small and hard to see on an fMRI scan. Grillon is excited about a powerful new scanner that his lab, now at NIMH, has procured. Using the new equipment, Grillon and colleagues have recently mapped the human BNST and its connections to other brain structures. It is a step toward understanding the area and its role in human anxiety. "Where is the anxious thought of a shock?" he says. "It may not be at the same place as the anxious thought of my kid not going to college or losing my job or fear of God." Perhaps the BNST will prove to be a fruitful target for new drugs or psychotherapies.
Neuroscientists caution that this kind of imaging work is still in its infancy. Other brain regions are being explored, too, and it's unlikely that there's any single route to an anxiety disorder. Also, developing anxiety is likely a dynamic process, with anxious thoughts and behaviors reinforcing the underlying neurobiology. As researchers Dan Grupe and Jack Nitschke write, "A patient with an anxiety disorder probably builds up neural pathways of anxiety just as a concert pianist strengthens neural pathways of musicianship—through hours of daily practice."
I wonder when things started to go awry in my brain. When did my amygdala go into overdrive? When did my prefrontal cortex cease to keep my body's fight-or-flight response in check? Neuroscientists are starting to see anxiety disorders as disorders of brain development that begin in childhood. And as with other neurological diseases—such as Alzheimer's disease with its telltale plaques and tangles—the brain likely shows signs of the illness long before the first panic attack or paralyzing bout of worry. The trick will be to locate those signs.
I am seven years old, sitting at my desk at school. I have a blank piece of notebook paper in front of me and a number-two pencil at the ready. My teacher, a stony-faced young woman wearing orange kneesocks and brown loafers, is standing in front of the class.
"What's five times four?" she says.
Barely a second passes before she opens her mouth again.
"Nine times six."
"Three times four."
"Eight times two."
She's barking out math problems in an unrelenting monotone. Everyone around me is scribbling down answers. Except me. I'm frozen. My mind is blank. My mouth is dry. My hands are sweaty, tightly gripping the pencil. A hot blush rushes up my cheeks. My heart feels like it is doing penny drops, the flips I love to do on the monkey bars during recess.
I look down at my paper and see a few halfhearted numbers, a stray pencil mark, and lots of blanks.
But here's the thing. I know all the answers.
I've choked. This happens during every one of these oral math quizzes. I fail them all. So I wasn't that surprised when my first second-grade report card came home with a big U for "unsatisfactory achievement" in mathematics. In fact, I even traced over the U in black pen, as if to highlight my shame. My parents, however, were stunned. My math homework and written tests had come home nearly errorless, and I hadn't told them about those awful oral quizzes.
My father called the teacher, who told him to get me flash cards. (In my parents' telling, the teacher was snippy and unsympathetic. My dad got angry, and the teacher hung up on him.) So he got flash cards. Every evening after dinner, my father would sit in his chair while I sat on the floor in front of him. "What's eight times nine? What's three times eleven?" he'd quiz. I swear he mimicked that teacher's impatient bark and pinched, irritated expression, too.
Although I dreaded those flash card sessions, the constant repetition boosted my confidence. We didn't know it at the time, but those sessions were very similar to exposure therapy, one of the most effective treatments for anxiety disorders. Little by little I began to dread the school tests less, and my terror subsided. I started passing the quizzes. Then I started acing them.
On my next report card, I received an S for "satisfactory achievement" in math. I got an S on the one after that. And by the last report card of second grade, I was fully vindicated, with an O for "outstanding achievement."
Many childhood events and experiences—from illness to trauma to certain styles of parenting—can contribute to the development of anxiety. Although I'm not sure those mini panic attacks—what scientists call "fearful spells"—were the beginning of my anxiety, they were certainly a red flag. Having a panic attack or even several isn't a disorder in and of itself. About one-quarter of the U.S. population will have a panic attack during their lifetime. But scientists are finding that panic attacks are often a harbinger of future mental health problems. In a study that followed more than three thousand young people ages fourteen to twenty-four, German researchers discovered that those who reported having had panic attacks before joining the study were much more likely to develop a wide range of disorders, including specific phobias and social phobia, during the four years that followed. They also had more than double the risk of an alcohol-use disorder and more than ten times the risk of GAD.
Full-blown panic attacks are less common in kids. An adult with a panic attack has to manifest at least four out of thirteen possible symptoms, which include feelings of choking, chest pain, nausea, and fear of dying. Children, however, often experience less severe or more circumscribed attacks, like my fearful spells. A fearful spell is "a sudden experience of fear and anxiety but it does not have to be associated with all these panic symptoms like heart racing, sweating, feeling that you're losing control," says Katja Beesdo-Baum, a coauthor of the German panic attack study and a professor of behavioral epidemiology at the Technische Universität Dresden. Children who experience fearful spells have a higher risk of developing major depression and are more than three times more likely to develop panic disorder, agoraphobia, and GAD within the ten years following the spells. "Fearful spells might be an early indicator and you can assess it quite easily," Beesdo-Baum says.
But maybe my anxiety took root even earlier.
At age four, I developed an intense fear of clowns. (Yes, I realize this isn't a particularly original phobia. Clowns are creepy.) At first I was as fascinated as I was afraid—I actually dressed up as a clown for Halloween. My mother sewed the outfit herself, a turquoise suit with fluffy white pom-poms and a conical hat. I also had a deep affection for Ronald McDonald, and when I heard that he was visiting a local McDonald's, I begged my parents to take me. They did, grudgingly, even though my mother was a health nut who tried to pass carob off as chocolate and put wheat germ on just about everything. But when we arrived on that much-anticipated day, I was too scared to get out of the car. My parents cajoled, bribed, and threatened to try to get me to go meet the smiley, yellow-suited guy. I wouldn't budge. Finally, my father turned the car toward home, grumbling.
Clown-induced terror was waiting for me at home, too. From the ages of about three to five, I was hooked on _Sesame Street_ , often watching it twice a day. In the 1970s, one recurring segment featured a clown with a curly red wig and painted white face with an oversize red mouth and black triangles above and below his eyes.
"I don't always look like a clown, you know," he would say, sounding sad and stoned. "I have an everyday face, too."
He'd yank off his nose and wig. Then, accompanied by a frenetic soundtrack of horns, whistles, and a panicked piano, they'd run the tape of him putting on his clown face in reverse. The triangles below his eyes and the red around his mouth were sucked back into their respective makeup pencils. The white of his face disappeared back into a small tube. At the end he was revealed to be a pasty, dour, thin-faced man.
"This is my everyday face. Which do you like best?" he would ask in a slow, dispirited voice. The screen split, barefaced man on left, clown on right. The man looked to his clown face and dejectedly said, with a small shrug, "Me, too."
The frenzied music, the aggressive unmasking, the clown's obvious depression, all of it terrified me. I'd watch _Sesame Street_ in a state of nervous anticipation, one foot literally out the door as each new segment began. As soon as I saw a glimpse of that painted white face or heard the first honk of his red nose, I'd run out of the living room, yelling. I wouldn't go back in until my mother had assured me that the segment was over.
I found the clip of that _Sesame Street_ segment on YouTube recently. Watching it, I wanted to give the guy a hug and hand him some Prozac.
Various fears, of course, are normal in childhood and adolescence. Separation anxiety in one-year-olds and fear of thunderstorms and the dark in toddlers. Fear of monsters and ghosts in five-year-olds and fear of social rejection in teenagers. These are all typical. According to the _DSM_ , in order for a fear to be classified as a phobia, it should last at least six months and impair a person's life. For example, if you can't go to school because you're terrified of the bus getting into an accident, that's an impairment.
Specific phobia is one of the earliest of all the anxiety disorders to appear, with an age of onset generally between seven and fourteen years old. It is also the most common of the anxiety disorders, affecting 15.6 percent of Americans ages thirteen and older during their lifetime. People can develop phobias to almost anything. (I came across a case report of a nine-year-old boy who had a phobia of buttons.) The most common involve animals (dogs, spiders, bears), the natural world (heights, water, storms, earthquakes), blood, or situations like flying or being in enclosed places (claustrophobia). There are some gender differences in phobias. For example, phobias of bugs and snakes are more common among women. Both men and women are equally afraid of heights and closed spaces.
The most common phobias make a lot of evolutionary sense because they can involve real peril. The psychiatrist Randolph M. Nesse argues that these fears developed over millennia with the purpose of keeping people safe. Even modern phobias, like those of flying or driving, are primed by the age-old dangers posed by heights, speed, and being stuck in small spaces. "Our emotions are adaptations shaped by natural selection," Nesse writes.
Anyone with a phobia knows that it can be crippling. (My driving-on-highways phobia would be a serious problem if I lived in Los Angeles, for example.) They also can foreshadow even more serious mental health problems. A 2010 study of about fifteen hundred young German women, for example, found that those with specific phobia were twice as likely to develop GAD, depression, or a somatoform disorder (mental illnesses that cause unexplained physical symptoms, including pain and distress) during the next seventeen months compared with those who didn't have a phobia.
My clown phobia was quickly surpassed by something much more overwhelming and unavoidable: a colossal fear of death. I was terrified of it—the pain, the fear, the blank blackness. I could not handle any depiction, or even mention, of death in books or movies. _Charlotte's Web_ was a horror. If any creature seemed in peril, I would ask my mother, "Does he die? Does she die?" I soon became more demanding: "Promise me she doesn't die." The no death edict eliminated many children's classics: No _Bambi_. No _Wizard of Oz_. No _Snow White_.
I became increasingly alarmed by the breathless descriptions of hell—the eternal fires, the screams of the damned—delivered many Sundays by the pastor at our Baptist church. My mother had grown up Southern Baptist, which meant that my sister and I did, too. (For years, my father, who drank beer, cursed, and smoked, didn't accompany us to church, declaring that he wasn't "good enough" for it.)
According to our church, the only way you could avoid hell was to be "born again" or "saved" and to accept Jesus Christ as your Lord and Savior. At the end of every church service, while the congregation sang the hymn "Just As I Am," the pastor would invite people to come up to pray and be saved. This became my favorite part of the service. Who would escape hell's clutches this week? The pastor, in a dark suit with his hands clasped behind him, would wait expectantly in front of the wooden pulpit, his eyes scanning the congregation. Sometimes one verse, then two, would go by, and no one would stir. The singing would take on more urgency. There were days when someone would scurry up just before the choir started singing the last "Oh Lamb of God, I Come, I Come."
My favorite Bible verse became John 3:16: "For God so loved the world, that he gave his only begotten Son, that whosoever believeth in him should not perish, but have everlasting life." Not perish. Woo-hoo!
I became fixated on being born again, not because of true religious fervor but because of its get-out-of-eternal-damnation-free card. But there seemed to be some unspoken rule that you had to wait until a certain age. Nine seemed to be the magic number. That's how old I was when I finally strode down the church aisle. A few weeks later I was baptized in the hidden pool behind the pulpit. It was actually more like a big bathtub. I wore a brand-new baby-blue sundress. The pastor wore black rubber waders under his suit jacket and put a white handkerchief over my mouth and nose as he dunked me under three times: one for the Father, one for the Son, and one for the Holy Ghost.
I was elated. Salvation, however, didn't seem to let you escape this whole death thing. Sure, your spirit would live on. But your body would still conk out. Then I found a loophole: the Rapture. From church services, I gleaned that Jesus was supposed to return to Earth and that those who were alive at his second coming would be taken directly up to heaven, bypassing death altogether. What a neat trick!
Every night before I went to sleep, a stuffed animal menagerie surrounding me, I'd pray for the second coming of Jesus so I wouldn't have to die. "Please come soon. Please don't let me die, get hurt, get killed, or get scared," I'd say, making sure to leave no wiggle room in my request.
A couple of years after that, I learned that the world was supposed to end on March 10, 1982, when I would be eleven. At least that was the prediction set forth by John Gribbin and Stephen Plagemann, two Cambridge-educated astrophysicists, in their 1974 book, _The Jupiter Effect_. On that date, major planets would align on the same side of the sun. The gravitational pull of those planets, especially Jupiter, would supposedly cause all sorts of mayhem, from altering Earth's rotation to generating earthquakes, one of which would level Los Angeles.
I never read _The Jupiter Effect._ I was too busy warping my mind—and my future view of romance—with my mother's Danielle Steel novels and with V. C. Andrews's books (arsenic poisoning! incest!), surreptitiously purchased with my allowance money. But I was aware of the apocalyptic date. The prediction and the response to it were being covered by the local news. I recall seeing TV segments and newspaper articles about people—even teachers and their classes—throwing weirdly ebullient "End of the World" parties, complete with balloons and Carvel ice cream cakes.
As the date edged closer, I became more and more nervous. What would it feel like to die in an earthquake? Would I be knocked out immediately by a falling ceiling? Or would my demise be slow and agonizing? Would I be trapped under debris, calling weakly for help until I finally starved? I spent hours mulling over various outcomes, all tragic. There were no world-saving superheroes in my anxious imaginings.
March 10 was a Wednesday, so I must have gone to school that day. But what I remember is sitting immobilized in my dad's tan corduroy La-Z-Boy chair with the pop-out footrest that evening, pretending to watch _The Facts of Life_ while monitoring the passing minutes on the clock, trying to will the hour hand past midnight. Then it would be March 11, and I—and the world—would be safe.
—
Trauma during childhood is a strong predictor of psychiatric disorders, including depression, drug and alcohol abuse, ADHD, and anxiety disorders. Researchers at Harvard Medical School and the University of Michigan analyzed data from 5,692 adults, examining the association between a host of childhood adversities—from physical abuse, sexual abuse, and neglect to divorce, poverty, and the death of a parent—and the onset of a psychiatric disorder. They found that these experiences are remarkably common: More than half of respondents had experienced at least one, with divorce, violence in the family, and the mental illness of a parent among the most typical. The most serious traumas, what researchers dubbed maladaptive family functioning (including mental illness of or substance abuse by a parent, criminal behavior, violence within the family, physical and sexual abuse, and neglect), most strongly predicted psychiatric disorders.
Scientists are trying to figure out exactly how childhood trauma can lead to mental health problems. Some studies show that early maltreatment can alter the HPA axis and cause long-term dysfunction in the body's stress response. Childhood stress affects the brain. When researchers at the University of Wisconsin gave sixty-four adolescents MRI scans, they found that a history of abuse and neglect during childhood was associated with altered connections between the hippocampus and the subgenual anterior cingulate cortex. And the adolescents who had these altered connections had more symptoms of anxiety and depression.
Interestingly, the traumas specifically linked to anxiety disorders are childhood physical illness and economic adversity. A study that surveyed nearly seven hundred high school students and their parents found that a serious illness or infection during the first year of life strongly predicted anxiety disorders by the teenage years. The risk of anxiety disorders was also higher among teens whose mothers had a history of pregnancy problems, particularly miscarriages and stillbirths.
My mother says that when I got a cold, it almost always turned into a nasty bout of bronchitis. Once when I was not quite one year old, I was coughing and then suddenly stopped breathing. My mother tells me that she was holding me and patting me on the back and that I just went limp. For a minute she thought I was dead. My father grabbed my ankles, hung me upside down, and started whacking me on the back. I finally started crying. Later the doctor said that I had nearly drowned on phlegm.
A similar thing happened when I was four, while I was recovering from another spell of bronchitis. I was playing with my Barbie dolls in my room when I started feeling funny, compelled to take deep breaths and hold them. I sat on my pink comforter, hands on knees, arms rigid, focused on pushing the air in and out of a space that soon felt no bigger than a coffee stirrer. I tried to distract myself from the sensation of breathlessness by bundling Barbie and Skipper into their RV camper. (I was never a big fan of Ken, with his suspect intentions and immovable hair.) It didn't help; I felt increasingly desperate, each breath a struggle. Panicked, I ran into the kitchen, where my parents were sitting at the table, and was able to croak out "I can't breathe" before passing out on the linoleum floor.
I woke in a car hurtling toward the nearest hospital emergency room, curled on my mother's lap in the front seat. Suddenly I looked up and said, "Where are we going?" "You popped right out of it," my father recalls.
In high school, I was diagnosed with exercise-induced asthma. In college, when I began having panic attacks, the feeling was instantly familiar. Even though I didn't have bronchitis and there was no lung-clogging phlegm, the terror and struggle to breathe were no less real. Anxiety is a fantastic mimic.
Research today is showing a link between respiratory illnesses and anxiety. A study of nearly one thousand young people by researchers from UCLA and New Zealand revealed that a history of asthma increases the risk of panic disorder in young women. Other studies have found that adults with asthma, emphysema, and bronchitis have higher rates of both anxiety disorders and depression. There's also evidence that lung problems in kids are associated with a greater risk of anxiety disorders by young adulthood. A 2008 study showed that those who had pneumonia, asthma, croup, or bronchiolitis—or a history of it—at age one were nearly three times more likely to be treated for an anxiety disorder by age thirty-four. Those who had respiratory diseases at both age one and age seven were nearly twenty times more likely to have received treatment for an anxiety disorder by thirty-four. The risk was evident even in infants. Babies with a higher breathing rate at just four months old had more than double the odds of being treated for anxiety by thirty-four.
Still, these studies show only an association; they don't prove that breathing disorders _cause_ anxiety. Some scientists speculate that breathing problems and mental disorders could both be at least partly caused by immune system issues. Another hypothesis is that they share an underlying genetic or environmental source. There's evidence that people with anxiety disorders, particularly panic disorder, have an overly sensitive "suffocation alarm system," a mechanism that evolved to help people survive. Recently, scientists have located a gene that creates a protein that acts as a sensor for carbon dioxide (rising CO2 levels can indicate impending suffocation). The gene has been linked to a risk for panic disorder.
It is not only being ill as a child that can lead to anxiety disorders. Witnessing the serious illness of a parent also increases the risk. In the UCLA and New Zealand study mentioned earlier, young women whose parents had had a stroke, heart attack, or high blood pressure during the women's childhood or early teenage years had an increased risk of panic disorder. It could be that being sick as a child or growing up in close proximity to illness elicited fears about bodily sensations. Perhaps these children were more likely to misinterpret mild shortness of breath or a fluttery heartbeat as impending catastrophe. It's also possible that the parents' ill health and fragility spurred them to become overprotective.
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Of course, parents do not have to be in ill health to be overly controlling of their children. Overprotective and controlling parenting—telling kids what to think and feel and micromanaging their activities—sends the message that children aren't capable, a belief that can fuel anxiety. But scientists haven't been able to tease out which comes first—the kids' anxiety or the controlling, overprotecting parenting. It could be that moms and dads are molding their parenting style to their already anxious kids rather than shaping their kids' temperaments.
If a child is anxious from an early age, parental hovering is understandable. Kids who are genetically vulnerable to anxiety disorders may be skittish and sensitive. Parents, in turn, tend to respond to these kids by being overinvolved and overprotecting in an attempt to ease their children's distress. The trouble is, this sends the message that the world is a dangerous place and that kids can't cope on their own. Also, when parents allow their children to avoid scary or distressing situations, the kids have fewer opportunities to learn to master their fear. Thus the fear-overprotection-fear cycle goes on and on. There's also some evidence that parents who are colder, more critical, and less responsive—what researchers call rejecting—are more likely to have anxious kids.
Researchers in Australia wanted to see if and how this played out in real time. They watched 95 children ages seven to fifteen and their mothers in two five-minute experiments: 43 kids had anxiety disorders, 20 had oppositional defiant disorder (characterized by behavioral problems and anger, defiance, and vindictiveness), and 32 had no psychiatric diagnosis. Children were asked to complete two difficult tasks: a tangram puzzle, where geometric shapes need to be arranged to form particular larger shapes, and a Scrabble-type game where kids were given letters and told to form as many words as possible. The mothers were given the answers to the first task and extra letters—which would make the game easier—for the Scrabble task. Moms were told they could help their kids when they felt the children needed assistance.
A researcher rated the mothers' interactions with their children to assess the level of controlling and rejecting parental behavior. Measures included things like "degree of unsolicited help," "touching of the tangram/Scrabble pieces," "mother's tension," and "mother's degree of verbal and non-verbal encouragement/criticism." Mothers of anxious children were significantly more controlling than mothers of children without a psychiatric diagnosis. They were also more negative. Mothers of oppositional children were about equally as controlling and negative as the mothers of anxious kids. The researchers speculated that this style of parenting might be a reaction to not just anxiety but psychiatric problems in kids in general.
On the whole, though, the effect of parenting on the development of anxiety is thought to be relatively modest. In a big 2007 review of the scientific literature looking at the link between parenting and anxiety in kids, researchers found that parenting explained only about 4 percent of the variation in anxiety issues among children. Controlling parenting behaviors fueled anxiety slightly more than rejection did. The one parenting behavior that did appear to have a strong impact on a child's anxiety was "granting autonomy," which explained 18 percent of the variance in childhood anxiety. "When parents fail to provide children with the opportunity to experience control in age-appropriate contexts, it is possible that children may not develop a strong sense of self-efficacy, thereby increasing their sense of vulnerability to threat and heightening anxiety," the scientists wrote.
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I'm apt to buy that parenting doesn't contribute much to anxiety because my parents weren't controlling or overprotective at all.
My mother was twenty, my father twenty-one when I was born. They had gone to high school together in Salem, Illinois, but didn't get to know each other until 1969, as students at Kaskaskia College. My mother was pretty, studious, and very shy. My father was a cutup, boisterous and popular. He had long hair and lamb-chop sideburns, and he carried a beat-up leather briefcase to classes. (This was exotic. Hippie style had yet to hit Salem.) He strode up to my mother's table in the library while she was studying, sat across from her, stared at her, and declared, "If you don't talk to me, I'm going to play with your leg." She talked to him. They fell in love. She got pregnant. And then they eloped. My mother didn't tell her parents about the pregnancy or the marriage until months later.
During the first few months of my life, I lived with my mother, her parents, and five of her six siblings in her childhood home, an old converted schoolhouse where chalkboards still lined the walls. My father lived a few hours away at the University of Illinois, in a fraternity for engineering students—then a hotbed of loud music, marijuana, and geekdom. On weekends, my mom and I took a bus there. During one visit, my parents ran out of diapers. The fraternity's housemother wrapped me in an old dishcloth.
My parents eventually landed a two-bedroom apartment in a married-student housing complex. Still, they were young and broke. One night while my father was watching me and my mother was working her job at a pharmacy, he and a friend were high on hash. My dad turned around to find me, about a year old, with a mouth full of the stuff. He force-fed me mayonnaise to make me vomit. More than once we had no food in the apartment except for baby formula and a jar of peanut butter. For my first birthday, my mother broke a piggy bank and took five hundred pennies to the bank, swapping it for a crisp bill. She had just enough to buy a cake mix and party hats.
After my dad graduated from Illinois, we bounced around the country as my father built a career as an industrial engineer: to Neenah, Wisconsin; Scranton, Pennsylvania; Appleton, Wisconsin; and Danbury, Connecticut, all by the time I was ten.
My childhood was warm and loving. I have fond memories of family sing-alongs and camping trips. But Mom and Dad's parenting style was decidedly laissez-faire. In Pennsylvania, at age seven or so, I spent weekends riding bikes and playing Red Rover with a pack of other kids. We'd stop home for dinner, then dash back outside to play Flashlight Tag until long after dark. As a teenager in Connecticut, I'd break curfew to drive around with friends in my silver Chevy Sprint, go skinny-dipping in Candlewood Lake, or head to Images, a teen dance club where kids slam-danced to Big Audio Dynamite and the Jesus and Mary Chain and gave each other Mohawks in the parking lot. I don't remember ever getting grounded.
My dad was transferred to Michigan the summer before my senior year of high school. My parents let me move in with my best friend, Kate, her mother, and their cat for the rest of the school year so I could graduate with my class. Kate and I were both obsessed with books and music. As preteens, we had spent hours making up dances to the songs we loved like Joan Jett's "I Love Rock and Roll" and Queen's "Another One Bites the Dust."
But the new living arrangement was difficult from the start. Kate's mother was dating a ringer for Moses who blared organ music through the T-top of his red Camaro Z-28. The couple practiced jujitsu in the living room and left violent, pornographic comic books on the coffee tables. Kate's mom read my mail, listened in on my phone conversations, and called my boyfriend's mother when he cut baseball practice to hang out with me. My best friend and I fought. I was allergic to the cat. At Thanksgiving, my boyfriend and I drove my Chevy to Okemos, Michigan, where my parents had moved. A week later I sent him back to Connecticut on a Greyhound bus. I stayed.
After the chaos and intrusiveness of my friend's home, I was thrilled to be back with my family, even though it meant starting over in a new school and making new friends a third of the way through senior year. The truth was that I craved a bit more parental guidance and a few more rules. I felt like I was winging it too often. And I felt unmoored by typical teen feelings of anger and sadness.
I didn't have much of a model for dealing with negative emotions. My family didn't talk about them, or even acknowledge that such feelings existed. My father was usually jovial and a goof, my mother sunny and optimistic. They almost never fought. The only time I saw my father yell at my mother was after she drove our Oldsmobile through the garage door. The maddest I saw my mother was once when my sister and I were arguing; she jumped up and down and yelled, "Stupid, stupid kids," and slammed a cabinet door, which broke off the hinges and clattered to the ground. (The three of us laughed for a long time afterward.) Her most serious curse was "gosh darn it." When I was mopey or sad, she would tell me to "just be happy."
So I learned to bury bad feelings. And I didn't divulge teen friend and boyfriend dramas, like the time a friend was kicked out of her house and we stuffed her belongings in my hatchback. Or the times when one early high school boyfriend became psychologically manipulative ("You would if you loved me," he actually said) and even physically scary, pushing me and blocking doors when we fought.
I don't have the scientific studies to back this up, but now—after years of therapy—I think my college breakdown was, in part, my body's way of saying, _Enough already! You have to pay attention to how you feel. And that means the tough stuff, too._
—
Some of the most promising research is looking into what goes on in the brains of anxious kids. About half of kids with anxiety disorders won't go on to have anxiety problems as adults. But half will. So scientists are trying to identify markers in the brain that might reveal which kids will remain anxious.
Daniel Pine, chief of the section on development and affective neuroscience in the Intramural Research Program at the National Institute of Mental Health, believes that the key to tackling anxiety is to start early in the lifespan. "If we think of mental disorders as disorders of brain development, most of the keys are going to be found by working with kids," Pine says.
Studying kids will also help scientists overcome a problem inherent in looking at the brains of anxious adults: untangling whether the dysfunctions that have been identified in mature brains are evidence of the disease or simply the brain's way of compensating for the disorders.
"Anxiety is a normal part of childhood," Pine observes. "But among that large mass of normal anxiety, hidden in there somewhere, are the seeds of most chronic emotional problems in adults. Most adult emotional problems—anxiety disorders definitely, but also depression and even bipolar disorder—will start as elevated levels of anxiety." But because anxiety is a normal part of being human, the line between illness and health is fuzzy. "The thing that keeps me up at night," he says, "is how do you sort out what's normal and what's not normal?"
Pine is perhaps the most influential person in the world when it comes to pediatric anxiety disorders and their development. His lab has scanned the brains of hundreds of anxious children and launched the careers of many anxiety experts. His arm of the NIMH has partnered with scientific institutions all over the world and funded hundreds of studies.
I visit Pine on a balmy June day. The NIMH building looks like a strange, small afterthought on the sprawling NIH campus in Bethesda, Maryland. It is tucked away on a tree-covered hill, a cream-colored house with a brown roof and accents, looking vaguely like a Swiss chalet. A flimsy, curling piece of copy paper with NIMH printed on it is taped to the door—the only indication I see of what's inside.
Danny (everyone calls him Danny) Pine's office is on the first floor, a spacious corner spot filled with beige-striped furniture that looks like castoffs from a conference room at a Sheraton. Chicago Cubs and Bruce Springsteen memorabilia dot the room; a framed _Darkness on the Edge of Town_ album, a poster from _Magic_. Pine is wearing khakis, a blue polo shirt, and gold wire-rimmed glasses. He is a fifty-three-year-old father of three and has a full reddish beard. He's enthusiastic and informal, with the demeanor of a beloved professor. "That's a great question," he says, often.
Pine and his colleagues are finding that many areas of brain dysfunction are similar in anxious adults and kids. As in an anxious adult, in an anxious kid something is often amiss in the connection between the amygdala and the prefrontal cortex. The amygdala of an anxious child tends to be overactive, the prefrontal cortex underactive. One of Pine's major areas of research is on the relationship between anxiety and attention. He uses the dot probe task with kids to measure attention bias. "Attention is very tightly related to anxiety," Pine says. But the relationship is fuzzy. "In some situations, anxious people pay more attention to threat. In other situations, they pay less attention."
While we talk, Pine walks me over to the NIH's clinical building, where his research studies are conducted. Two young NIMH research fellows take me to a room where they conduct a fear-conditioning task using the "screaming lady" paradigm. It is a way to fear-condition kids without using electric shocks (used with adults but not kids, for ethical reasons). Children are presented with two different female faces—one blonde, the other brunette—via a black-and-white video screen and are told that one of the faces will be accompanied by a loud sound. "The scream happens 80 percent of the time," says Liz Ivie, one of the fellows. "The uncertainty makes the arousal higher." Various physiological measures are taken, including heart rate, skin conductance, eyeblinks, and startle response.
Ivie and Laurie Russell, another fellow, demonstrate the experiment.
As they set things up, we debate which woman is creepier. Honestly, neither one looks very pleasant even with their faces resting, but we settle on the brunette. Russell says she "looks like she's plotting someone's demise." As I await the scream, I can feel myself getting anxious; my heart rate jumps, and my stomach feels buzzy. "Just get it over with. The anticipation is horrifying," says Russell, who, like me, will be hearing the scream for the first time. When it finally accompanies the blonde, I jump. It sounds slightly strangled, and the face contorts into a twisted shriek. (NIMH has had a problem with the screaming lady being too terrifying, so much so that they lost about a third of the studies' participants. They are now working on a new paradigm that uses bells.)
In some studies, participants are also shown merged images of the two faces. After the kids are conditioned, they undergo extinction, which entails being shown the faces without the scream.
In a small study using this paradigm published in 2008, adolescents with anxiety disorders developed more fear of both women's faces, whether they were coupled with the scream or not. This speaks to the tendency of anxious people to generalize threat; fear of a situation that is genuinely scary can spill over to one that is safe, too.
Another larger study published in 2013 used fMRI scans to see what happened to two parts of the prefrontal cortex, the subgenual anterior cingulate and the ventromedial prefrontal cortex (vmPFC), three weeks after anxious adults and adolescents underwent fear conditioning and extinction with the screaming women. These parts of the brain are critical for extinction and dampen the activity of the amygdala. Both anxious adolescents and adults had less activity in the subgenual anterior cingulate than healthy people when they were asked whether or not they were afraid while viewing the women's faces during the three-week follow-up, so this pattern may be a common feature of both adolescent and adult anxiety disorders. But anxious adolescents and adults differed in the activity of the vmPFC. The researchers conjecture that certain patterns of activity in this brain region might help identify those young people most at risk of remaining anxious in adulthood.
Children tend to classify more things as dangerous, but "when kids mature they get better at recognizing the nuanced boundaries between things that are safe and things that are dangerous," says Pine. It is the prefrontal cortex that helps us do that. Pine thinks that the development of anxiety has something to do with prefrontal maturation. He explains that one of the things that separates healthy from unhealthy development is learning how to appropriately classify things that are ambiguous.
After I've been spooked by the screaming blonde, Russell takes me to a room with a fake MRI machine designed to acclimate kids to being in an actual scanner. There she shows me one of the newest research paradigms, dubbed "Virtual School." Virtual School "enrolls" subjects aged eight to seventeen and tries to replicate the treacherous social waters they have to navigate, which are particularly terrifying for children with social anxiety disorder.
Social anxiety disorder (SAD) or social phobia is one of the most common anxiety disorders, affecting more than 10 percent of the U.S. population during their lifetime. Children and adults with SAD fear meeting new people, being at parties, and other situations where they are expected to interact with strangers. Terrified of embarrassment, they often avoid such situations entirely. Some evidence shows that the brain dysfunction in social anxiety disorder may be different than in other anxiety disorders.
In Virtual School, kids are told that they will be chatting online with six other kids in a virtual school. In preparation for that, they make an avatar and answer questions about their favorite subject, color, actor, and type of music, among others. Once the experiment starts, they "attend" the virtual school while in an fMRI scanner, as their brain is being scanned. They are told that two of the other kids are mean, two are nice, and two are sometimes mean and sometimes nice. (In reality, there are no other children in the experiment. A computer generates the responses.)
Kids see an electronic rendering of a schoolroom, with various avatars sitting at desks. Bubbles appear above the avatars' heads when they are about to chat. Some of the other kids taunt them, and the information they provided about their personal likes and dislikes is used to make the teasing more pointed. A mean kid might say something like, "You like Miley Cyrus? Wow, you're such a loser."
The researchers are particularly interested in what happens in anxious kids' brains as they anticipate comments from the kids who are sometimes mean and sometimes nice, which is known as ambiguous social feedback. Other studies have shown that kids with SAD tend to interpret ambiguous social feedback as negative.
Afterward kids are debriefed and told that they weren't chatting with real kids after all. "The anxious kids are usually pretty sad," says Russell. "They usually say, 'I can't believe I didn't figure it out.' That they weren't smart enough to know that we were tricking them.
"Some of the kids come out of the scanner really upset because they got bullied." Other kids are relieved when they find out they weren't actually talking to real kids. "It actually makes a lot of them feel better," says Russell. "Some say, 'I'm glad kids aren't that mean in real life.' "
The goal of these NIMH experiments is to figure out the "neural signature" of nascent anxiety disorders. Identifying the signature could allow doctors to identify at-risk children and develop treatments to prevent the anxiety from becoming entrenched.
It was in the middle of the night sometime in the fall of 1958 when my grandmother Gladys Schneidervin Petersen, a thirty-nine-year-old Wisconsin housewife, tried to kill her family.
She began by crumpling some papers and putting them under the beds of her two sleeping sons, nine-year-old Gary, my father, and eleven-year-old Bill. Next, she crumpled more papers, placed them between the stove and the refrigerator, and arranged a tower of garbage in a back storage room. Then she collected her thirteen-year-old daughter Susan's schoolbooks and stacked them at the bottom of the sleeping girl's bed. Finally, she moved through the house and set each spot aflame.
"I woke up and the bottom of my bed was on fire," my aunt Susan recalls. She ran to wake up her father and then her brothers; my grandfather screamed for them to leave the house. "Mom just kept saying she needed to protect us and if we were dead nobody could hurt us. That made sense to her."
"That's when Dad took her to the hospital, and she didn't come back for a long, long time," my father said recently. Gladys would spend the next three years at Mendota State Hospital, a mental institution in Madison that opened in 1860 as the Wisconsin State Hospital for the Insane.
—
Throughout my childhood, my grandmother was a specter. She died when I was two, and I have no memory of her. But I heard bits of stories—of the fire, of the mental hospital, of how my mother was afraid of the knives Gladys carried. While my parents were dating, my father told my mother that the only thing she could do to make him leave her would be to "go crazy."
When I got sick in college, I was terrified that I was following in my grandmother's footsteps—beginning my own descent into psychosis. My father was worried, too. "It got stuck in my head that somehow you ended up with a little bit of the wrong Petersen DNA," he said.
Mental illness is at least partly genetic. Studies of twins have found that genes are responsible for 30 to 40 percent of the variation in the individual risk for anxiety disorders. For schizophrenia, Gladys's diagnosis, the genetic toll is much higher: Genes contribute close to 80 percent of the variation in risk. Having a first-degree relative—a parent, sibling, or child—with an anxiety disorder bumps a person's risk of developing one up to five times that of the general population.
New research is showing that some of the same genes underlie different mental disorders. In a 2013 study, genetic overlap was found between five different illnesses: schizophrenia, bipolar disorder, depression, autism, and ADHD. The overlap was highest (about 15 percent) between schizophrenia and bipolar disorder and lowest (about 3 percent) between schizophrenia and autism. Researchers suspect that the genes implicated in anxiety disorders also overlap.
Scientists believe that a set of genes crucial to brain development can go wrong in many different ways, says Francis McMahon, chief of the Genetics Basis of Mood and Anxiety Disorders Section of the Human Genetics Branch at the NIMH Intramural Research Program. "The more severe mutations are more likely to be seen in cases of autism, the less severe in cases of schizophrenia, and perhaps the more subtle defects we'll see in the mood disorders and the anxiety disorders." So some of the same genes may be behind both Gladys's breakdown and my own struggles.
Genetic research into anxiety disorders has been hampered by small sample sizes, says McMahon. Some scientists believe this is because of inadequate funding. Also, anxiety disorders often coexist with other mental illnesses, such as depression, which muddies the waters. A further complication is that patients with the same diagnosis can show great variation in symptoms and severity, which means that scientists risk comparing apples to oranges. And since anxiety is a normal human emotion, it can be difficult to ascertain where disorder begins.
McMahon believes that the number of genes involved in anxiety disorders is "probably going to be in the many hundreds." Each one likely contributes a tiny amount to the overall risk.
Gladys had been deteriorating for years before the fire. Indeed, her children can't remember a time when she was healthy. However, old friends of my grandmother told my aunt Susan that, in her youth and when she first married, Gladys was "a wonderful woman. She cared about people, taught Sunday school, was active in church, and was there to help anybody that needed it." In my favorite photo of my grandparents, from the early 1940s, my grandfather Pete Petersen is dashing in his army uniform. (He was a fighter pilot in the Pacific during World War II.) My grandmother, wearing a chic white suit and dark blouse, her brown hair lustrous and curled, leans tenderly into him. They look joyous and hopeful.
In 1950, when the children were five, three, and one, my grandfather had a tragic accident. He had become a carpenter after the war and was making repairs on a church roof when he fell thirty feet and punctured a lung. Then, while recuperating in the hospital, he caught polio. He spent several months in an iron lung, a cylindrical respirator that did the work of his paralyzed chest muscles, and was not expected to survive. Although he ultimately recovered, he used crutches because of his weakened legs until his death in 1979.
Even before the accident, the family's lifestyle was hardly luxurious. The family lived in a one-bedroom home (the boys slept in a screened-in porch and Susan slept in the living room) on the banks of Eagle Spring Lake in Eagleville, Wisconsin. There was no indoor plumbing, and my grandmother hauled water down from the lake so that she could wash clothes and the family could bathe. "Mom would do the laundry, then she'd do us," my dad recalls. As the youngest, he went last and "got the grimiest stuff" at bath time. There was an outhouse and a jerry-rigged contraption to fall back on during the cold Wisconsin winters—a wicker chair with a hole and a bucket under it. But on idyllic summer days they swam in the lake and picked wild black raspberries, asparagus, and rhubarb.
Because of Pete's polio, the whole family was under quarantine for weeks. "There was a big colored piece of paper on our front door that boldly said QUARANTINED and warned people not to approach us or the property," my aunt Susan relays in a life history she wrote for her daughter. My aunt was barred from attending first grade for several weeks. Food was dropped off outside the fence surrounding the yard, including a piece of birthday cake left over from a party she had to miss. Money dried up. "Our relatives called us the 'poor Petersen kids,' " my dad says.
Pete's illness seems to have been the catalyst for Gladys's decline. "It kind of ripped her to shreds. She was never the same again," my dad recalls.
Gladys spent two months at Waukesha County Hospital near her home, where she underwent insulin coma therapy (ICT), a widely used psychiatric treatment from the 1930s to the 1950s. Patients were injected with large doses of insulin that sent blood sugar levels plummeting, inducing temporary comas. The comas—characterized by profuse sweating, muscle twitching, and sometimes seizures—were ended with infusions of glucose. Higher doses of insulin were used for schizophrenia, lower doses for "nervousness." ICT would not be discredited until the 1960s, when it was supplanted by new antipsychotic drugs and electroconvulsive shock therapy.
The records are sketchy, but it's likely that doctors saw little improvement, because she was transferred to Mendota on July 12, 1955, and stayed there for more than a month. In her medical records from that stay, under "present illness," it says: "Symptoms she recalls are loss of memory, of articles just read and program [ _sic_ ] just seen on T.V. and crying herself to sleep at night after working continuously day after day....She also remembered being alarmed about reading an article in a newspaper in which the names, Sharon [ _sic_ ], Gary and Bill, appeared being killed by a truck backing over them, the names being those of her children." The notes give two potential diagnoses: "schizophrenic reaction, paranoid type" and "SIMPLE SCHIZOPHRENIC or REACTIVE DEPRESSION." On August 3, doctors wrote that she "went into remission." She was released on August 17.
Reading the records from her first Mendota admission, I feel like I'm trespassing. There are weirdly intimate details: when she learned about sex and how many sanitary pads she used during her period. At times I sense a tone of disapproval, as in the first line of the case summary: "The patient [is] a dependent individual with little self-confidence."
It is eerie how similar my grandmother's early symptoms were to some of mine: fuzzy memory, strange superstitions, and a fixation on catastrophe. My own doctors have hypothesized that, if she were treated today, Gladys might have initially been diagnosed with severe obsessive-compulsive disorder and GAD.
In the 1950s, schizophrenia was a bit of a catchall diagnosis. In Mendota's 1955 annual report to the State Board of Public Welfare, patients are given only a handful of diagnoses, such as schizophrenia, syphilis, alcoholism, "senility," and "psychoneuroses." Until 1960, Mendota patients were divided into "quiet" and "disturbed" groups.
After my grandmother's first hospitalization, she declined further. She was so afraid of something terrible befalling her children that she had trouble letting them out of her sight. She forbade Susan to see friends and followed her to the school bus stop. Then the fear curdled into psychosis. She became terrified of Catholics and "bad spirits." (My grandparents were Lutheran. My aunt says my grandfather told her that Gladys had been raped by a boyfriend who was Catholic.) She was afraid of being poisoned. She tucked a screwdriver into her purse for self-defense. She also carried a pocket mirror and would tilt it to catch the sunlight, a habit she thought would protect her family. Once she tried to force Susan to take the pills she had been prescribed at Mendota.
"I was afraid to go to sleep," Susan says. "I would lie on my stomach with my face to the wall and the covers over my head so I couldn't see her. I knew she was going to come and kill me."
Then Gladys set the fires.
"She was trying to save us from all the terrible things that were going through her mind. She was going to send us to heaven. She thought that's what needed to be done to protect us," my dad says.
My grandfather put out the fires, and it seems that no authorities were notified. Pete took Gladys back to Waukesha County Hospital, and she was transferred to Mendota on November 28, 1958. In the admissions report from her second stay, under "mental status," it says: "Heard rumblings under floor, threatening voices, both male and female. Became doubled over in the middle—'they were putting the screws on me' and believed her 'insides were empty.'...Has expressed fears about being placed in a pinball machine." This time the diagnosis is more definitive: "SCHIZOPHRENIC REACTION, CHRONIC UNDIFFERENTIATED IN TYPE."
In 1958, my grandmother was one of 936 patients at Mendota. The most common diagnoses that year were "schizophrenic reactions" and alcoholism. About 28 percent of patients had been at Mendota for less than three months; 8 percent had been there for a decade or more. Space was tight, and resources were taxed. The original main building had become a drafty firetrap, and there were plans to abandon it. Goodland Hall, a new building for "chronic disturbed patients," opened that year.
The year of her admission marked the beginning of a movement to provide more freedom for Mendota patients. Six locked wards were now unlocked during the day, and the administration gave some say to an advisory board made up of patients. There was swimming, archery, and field trips to sporting events at the University of Wisconsin. The hospital received a new 35-millimeter projector for watching movies. Attendance at the Sunday worship service reached nearly two hundred, and communion was given every twelve weeks. A volunteer group, the Gray Ladies, came each week to visit patients and write letters for them.
During her time in the hospital, Gladys was treated with psychotherapy. In her records are several notations about her level of "insight" into her problems, a reflection of the supremacy of Freudian psychoanalysis at the time. My grandmother was also prescribed a few of the new antipsychotic medications just coming to market. At various times, she was on Thorazine, first synthesized in 1950, and Mellaril, a medication that largely disappeared from the market in 2005 over concerns about cardiac arrhythmias. During at least one period, the medication seemed to be helping her. The records say her thinking was better "organized" after the dose of one drug was raised.
Antipsychotic drugs were instant hits at mental hospitals like Mendota. In February 1955, 147 patients were being treated with the new "tranquilizing" medications. Less than a year later, by May 1956, four hundred patients were on the drugs. By 1960, staff members were complaining that some patients whom the hospital relied on to work in the facility—particularly in food service and the laundry—were "so heavily sedated that their work output is limited."
Gladys herself worked in Mendota's kitchen. But at some point, she developed paranoid fears about the job and refused to continue. Later hospital staff encouraged her to do a shift in the laundry, but she refused to go, saying she was worried about her heart. At least one staffer was downright grumpy about her noncompliance, noting in her records that "she always uses her health as an excuse for not doing something."
In May 1961, doctors noted that my grandmother had begun to experience a disturbing new hallucination and decided that shock therapy, also referred to as ECT or EST, was imperative. "Her hallucinations stem from the fact that she feels that her son is someplace in the hospital. She takes walks around the grounds hoping to find him. It is recommended that the patient have EST. If we do not obtain permission for shock therapy it is recommended that the patient be transferred to the county hospital." The message was clear: Undergo shock therapy or be kicked out of the hospital. Gladys was terrified of ECT, but she did ultimately have the treatments.
Electroconvulsive therapy was first employed in Rome in 1938. Ugo Cerletti, a psychiatry professor, had been tinkering with electricity in his research on epilepsy, using it to induce seizures in dogs. (About half the dogs died; their hearts stopped.) Cerletti became intrigued by the use of insulin and other compounds to induce convulsions in psychiatric patients and wanted to see whether electricity could be safely applied to people to similar therapeutic effect. His assistant, Lucio Bini, built the first ECT machine for humans, which delivered 80 to 100 volts of electricity via electrodes placed on the temples. The first patient was a thirty-nine-year-old engineer with hallucinations. Not only did the patient survive the treatment, he seemed to get better. ECT spread rapidly to mental hospitals around the world, used primarily to treat patients diagnosed with schizophrenia and depression.
In its early years, ECT caused violent convulsions, and it was not uncommon for patients to fracture their spines as they thrashed about. Soon doctors began using muscle relaxants and short-acting anesthesia to keep patients still and prevent broken bones. By the time my grandmother underwent ECT, the treatment was considerably safer, although some patients were troubled by aftereffects such as headaches and short-term memory loss. (Today ECT has been largely redeemed: It is one of the most effective therapies for treatment-resistant depression and suicidal ideation.)
According to my grandmother's doctors, the treatment was effective. A note from September 26, 1961, says: "The patient has also completed a series of 18 EST Treatments" and states that she is hallucinating less and seems less suspicious and paranoid.
During Gladys's time at Mendota, my grandfather made the hour-and-a-half trip every weekend to visit her. Often he would take their children. "All I remember is people screaming," Susan says. "That just frightened the heck out of me. Mom didn't [scare me]. But in the background you could hear the screaming." On the way home, as a reward, my grandfather would stop and buy the kids Neapolitan ice cream.
—
It's a chilly October night, and Aunt Susan and I are going through hundreds of family photos in her office at home in Waukesha. We stop at a haunting picture of my grandmother shot during a weeklong visit home from Mendota in the fall of 1960. Gladys is staring at the camera, grim-faced and weirdly vacant, her dark hair tightly curled. She's wearing a checked dress and a black cardigan and holding a white stuffed dog she made at the hospital. "What a sad face," my aunt says.
My grandmother was released from Mendota on January 3, 1962. During the 1960s, a movement arose to shift treatment away from inpatient psychiatric facilities to outpatient programs, and Mendota, like many other mental hospitals, was aggressively looking to discharge patients. The final note in her medical records reads, "The patient shows some improvement over her status previously, but she is not well by any means." She was transferred to the county hospital and then sent home. She didn't take medication or have any outpatient treatment after her release.
For the first six months or so after she was back, Gladys seemed better, but soon enough the intense fear and paranoia returned. By then Susan had graduated high school and studied keypunch, an early form of computer data entry. She moved to Racine and married. "I wanted out," she recalls. The rest of the family moved to Salem, Illinois, where my grandfather, an actuary at an insurance company, had been transferred.
My grandmother never recovered. "She talked to herself all day," my dad says. "She'd rail against the Catholics and just crazy shit." As a teenager, my father never invited friends over. Still, Gladys made rhubarb pies and sticky buns that my father still raves about, and she was able to take care of the house. She also liked to walk to downtown Salem and visit the shops. Her favorite was one that sold yarn, thread, and material.
Despite her delusions, my father was always able to make my grandmother laugh. She loved it when my father would come up behind her while she was washing dishes and give her bear hugs. He would talk in silly voices, make up nonsense words, and snap a towel on her behind. "She was usually so serious because she was so worried," my mom recalls. "But when your dad was around, she really brightened up."
When I was a baby, my grandmother doted on me. She would sit next to whoever was holding me and coo and smile. She was particularly delighted when I began walking, dragging a Raggedy Ann doll around by its tuft of red hair. But my grandfather never allowed Gladys to hold me. She had started carrying knives again. No matter where she was in the house, no matter what she was doing, she kept a large kitchen knife nearby.
Gladys died in 1972, when she was fifty-two years old. She had long had heart problems, perhaps caused by the rheumatic fever she'd had as a child. On the night she died, she had chest pains, and my grandfather called an ambulance. When it arrived, however, she wouldn't let EMS take her to the hospital. My grandfather pleaded with her, and so did the emergency responders. No. She wouldn't go. She was terrified of doctors and of being confined to a hospital again. Terrified of more shock treatments.
My grandfather stayed with her to the end. "He loved what she was and she loved him, too," my father says. "But she was living in a whole different world."
—
I visit what is now called Mendota Mental Health Institute for the first time on a sunny fall afternoon. Because of my panic around driving on highways, I take the back roads from my sister Dana's house in nearby Janesville. I drive past dairy farms and drying cornfields, ignoring the incessant "recalculating" pleas from the GPS trying to nudge me back on the highway. I had originally planned on asking Dana to be my driver, but she had scheduling issues. And, it turns out, in the last few years she's started to panic on expressways, too. Genes indeed.
The street leading up to Mendota's entrance is lined with modest vinyl-sided homes that look to be from the 1940s and 1950s—many probably built during the time period when my grandmother was inside. Mendota isn't what I expected. I'm not sure what I thought it would be like, exactly—something more foreboding, perhaps, that portended the human misery inside. But the original building was razed in the 1960s, and nothing of it remains but a stately line of trees. Now Mendota looks like a graceful college campus. I can see Wisconsin's capitol building across Lake Mendota, which abuts the four-hundred-acre campus. Sunlight glints off the water and dapples the gold and orange leaves overhead. Burial mounds from the Ho-Chunk Indians dot the grounds, graceful green hills in the shape of a deer, panther, and eagle. Banners proclaiming HEAL, RESPECT, HELP, and HOPE line the roads.
Mendota now has 315 inpatients and 825 staff members. Almost all are so-called forensic patients, part of the criminal justice system. People are taken here so that clinicians can assess whether they are competent to stand trial. If they are found not to be, Mendota treats them until they are deemed competent. About 150 residents are long-term patients who have been acquitted of their crimes—almost all violent—by reason of insanity. (The vast majority of people with mental illnesses are not violent. In fact, those with psychiatric disorders are far more likely to be the _victims_ of violence than the perpetrators.) There's also a small geriatric ward for patients with dementia and an innovative juvenile treatment program housing twenty-nine teenagers. Most patients in the facility are men; female forensic patients are sent to a different state hospital.
I'm here to meet with Gregory Van Rybroek, Mendota's director. Van Rybroek is fifty-nine years old with close-cropped gray-blond hair and small, rimless rectangular glasses. He's dressed in a gray polo shirt featuring the word MENDOTA and an image of an eagle. His baseball cap also sports an eagle and the word MENDOTA, along with 1860, the year the hospital was founded. The employee badge around his neck says HOW CAN I HELP YOU? He looks like a college athletic director and is both self-deprecating ("I'm not that smart," he jokes periodically and very unconvincingly) and profane. He has a Ph.D. in psychology and a law degree and started working at Mendota as a student in 1980.
We get into Van Rybroek's decade-old silver Acura, and he gives me a tour of the grounds. Mendota divides its facilities into maximum security, medium security, minimum security, and "minimum plus." Patients are assigned to a facility based not on the severity of their crimes but on how well they are recovering. (You're just as likely to find a killer in minimum plus, where residents have jobs mowing the lawn, are allowed to make excursions into town, and can attend college, as you are in maximum security.) Most patients come in with psychotic symptoms and are diagnosed with disorders such as schizophrenia, bipolar disorder, and major depression.
Van Rybroek points out a new greenhouse where some patients work and that provides flowers to the governor's mansion. He tells me about plans to build a new "skilled learning center" that will include a house where patients can practice the skills they'll need to live independently. "You should be able to make a bed and fry an egg," he says.
We drive by Goodland Hall, a beige brick building that houses maximum and medium security wings. There are bars on its windows. In a grassy courtyard hemmed in by a barbed-wire fence, a young bearded guy in jeans and a tie-dyed shirt runs around a track. Other men sit at picnic tables near an unused volleyball net. One man in a blue short-sleeved shirt leans back to catch the sun on his upturned face.
We move on to Stovall Hall, which houses minimum-security and geriatric psychiatric patients. In its courtyard, there's an incongruous white gazebo and red flowers. Men play basketball and sit in lounge chairs. The "minimum plus" facility is a low-slung brown and white building that looks faintly Swiss. RECOVERY THROUGH INDEPENDENCE says a plaque above its front door. The perky language and bucolic setting should not lead to any misperceptions, though, Van Rybroek says. "You try to help people who are sick. These people can be dangerous. It is not Disney here."
Contrary to the perception (which, I admit, was mine) that criminals who enter a psychiatric facility are never released, Van Rybroek says that currently four hundred former inpatients have been released "on conditions"—meaning that their housing, medication, and future treatment have been planned in detail. Those who have been acquitted of their crimes because of insanity have the right to petition the court for release every six months. Van Rybroek says the recidivism rate of those released is just .25 percent.
We stop at a building that houses an employee conference center and a cafeteria for employees and minimum-security patients. In the hallway, Van Rybroek stops to congratulate a pleasant white-haired man who looks to be in his sixties. I take him for an employee who is moving to a new job, but after the man walks away, Van Rybroek says, "He killed his mother twenty years ago." After about a dozen years at Mendota and successful treatment, the man is about to be released. Van Rybroek was congratulating him on overcoming a hurdle to his release by finding a place to live near a sister who was willing to check in on him.
In the employee conference center, where staffers are participating in a "leadership seminar," historical photos and maps of Mendota line the walls: The grand 1860 main building with its striking cupola and white terraces. A steam yacht outing to a Norwegian Sunday school picnic in 1879, complete with boat schedule. Boats "to asylum for insane and maple buff" depart at one, three, and five, it says. Rows of nurses in starched white hats and cat-eye glasses, circa 1960.
A glass cabinet in a corner holds artifacts: A photo of the "1901 Wisconsin Hospital for the Insane Band," a group of grim-faced men with natty ties, tubas, and trombones. A prescription dated 1927. A photo of the "dayroom" in 1870 with rocking chairs, upright piano, easel, and chandelier. My eyes fix on a foot-long brown box with black knobs and gray plastic tubing: a vintage Medcraft Mark II ECT machine. So this is the device my grandmother was so afraid of. It looks no more sophisticated than my childhood Lite-Brite.
"In college I spent a lot of time holding people down" while they were getting electroshock, Van Rybroek says. He says he would hold one arm and one leg of a patient. Someone else would pin down the patient's other arm and leg, and a third person would hold the patient's head still. (The first time, Van Rybroek didn't hold tight enough and when the electric current was switched on the patient socked him on the side of the head.) Afterward, ECT patients often had short-term memory problems. "They didn't remember who I was or where they were," Van Rybroek says. Gradually, their memories returned and some patients got better, though he's not certain it was solely because of the shock treatments.
We drive past a boarded-up brown brick building constructed in 1922 for World War I vets with "shell shock," or what we now call PTSD. Van Rybroek wants to turn it into a drug and alcohol treatment facility. As we drive around more, with Van Rybroek pointing out some of the burial mounds and the view to the calm, shimmering surface of Lake Mendota, he sighs and says, "All the terrible tragedy all mixed up with the beauty."
My grandmother's records don't reveal where she lived while she was here. But Van Rybroek thinks she most likely was in Stovall Hall or Lorenz Hall. Lorenz was built in 1953 and housed adult civil patients until the 1970s. I'm not allowed into any of the occupied patient zones, but one wing is empty. It is being transformed into a forensic wing, so security must be added before patients can move in. Lorenz is yet another low-slung beige brick building, but there's a chic Mad Men–like concrete entrance and steel-rimmed walls of windows. Van Rybroek takes me inside.
We head down a series of hallways, through two sets of doors. The ceiling is low, with white perforated squares. Fluorescent lights illuminate a floor made up of yellowish-green tiles. The hallway opens into a dayroom filled with tables and modular chairs like those in an airport terminal, where patients relaxed between treatment sessions. Big windows offer views of the autumn trees. An enclosed nurses' station—shrouded in steel and tempered glass—sits in the center. There's also a smaller "secure" dayroom with a locking door for patients who couldn't handle being around so many other people. Along one wall are five "seclusion" rooms for patients who behaved violently—nine-by-twelve-feet cinder-block cells (stained with a slight green tinge) illuminated by fluorescent lights. Each has a steel door with a small window. A camera beamed video to the nurses' station.
One of the seclusion rooms has a "restraint" bed, a low silver metal platform with small circular holes punched into it that's used to prevent self-harm. The bed is bolted to the floor. Green, blue, and purple leather straps lie across it, the cheerful colors incongruous given their function.
We walk down another hallway with patient rooms, small cinder-block spaces with dressers bolted to the walls. A bulletin board offers suggestions for things patients can do when they're bored. Among them: Draw pictures. Play Yahtzee. Clean your room. Make paper airplanes.
—
In the days after my visit to Mendota, I often think about the march of mental illness across my family tree. Gladys's brother, Harold, spent years at a psychiatric hospital in Utah; he died there in the late 1980s, of lung cancer. Susan thinks that he, too, was diagnosed with schizophrenia. Susan herself has bipolar disorder. Her daughter, my cousin Renee, has GAD and for years self-medicated with alcohol. My father struggles with depression. About fifteen years ago he asked his doctor for Zoloft because "maybe I've just never been happy," he says.
Susan muses hopefully that as time has passed, the illnesses have become less severe—that in three generations we've gone from psychosis to anxiety. Maybe my daughter and Renee's three children will be even more lightly touched.
My mother's side isn't completely even-keeled. My mother is a worrier with frequent insomnia and an anxiety-fueled cleaning compulsion. Growing up, Dana and I knew that if we heard the vacuum cleaner running before seven a.m., we needed to tread carefully. My mom's siblings can be tightly wound, too. Their group texts are a constant volley of concerns and comfort. Two of my cousins deal with recurrent panic attacks.
Over time anxiety has become an issue for my sister Dana, too. She's always been introverted and shy, more comfortable one on one than in big groups, and she's dealt with a bit of social anxiety, but none of these things ever impaired her life in a significant way. She always had friends and boyfriends. And I still remember her, age seven or so, decked out in a red satin and silver-sequined outfit, shaking it onstage to Prince's "Little Red Corvette" at one of our yearly dance recitals. Then, during her twenties, Dana had a handful of panic attacks while driving. Bridges and interstates were the triggers. More recently, she says that anxiety has taken up permanent residence.
"I feel like my nervous system is on overload compared to normal people," she says. "Sometimes I just don't feel calm, don't feel present or as able to interact. I feel like I just drank coffee even when I haven't." She's started to avoid highways (not an easy thing to do in Wisconsin) and driving at night. She's afraid of flying.
At the time Dana and I have this conversation, she knows that I've been dealing with a serious set of anxiety disorders for more than twenty-five years and that I've been working on this book for the last three. Yet this is the first time she's ever talked to me about her own anxiety. She hasn't told her husband about it either. And she's had a hard time even admitting it to herself. "For a long time, I didn't think about anxiety in terms of myself. You were always the one who had that, and I didn't," she says. "I think it kind of crept up on me. It's scary to talk about because that means admitting you have an issue. I was in denial."
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Scientists have been searching for the genes behind anxiety disorders for at least twenty years. For the first decade or so, researchers focused on individual "candidate genes."
One of the most extensively researched is the SLC6A4 gene, which makes a protein called the serotonin transporter. The protein's job is to pick up excess serotonin from the space between neurons (the synapse) and suck it back into the neuron. It isn't particularly surprising that scientists landed on this gene: SSRI drugs like Prozac, which alleviate depression and anxiety, block the serotonin transporter so more serotonin remains in the synapses. This extra serotonin is thought to account for the drugs' therapeutic effects. So for scientists trying to home in on the genes that might confer risk for anxiety disorders, zeroing in on the serotonin transporter gene was as good a guess as any.
The SLC6A4 gene has a "promoter region" that regulates how active it is and how much serotonin transporter protein it makes. Some studies found that people who had one or two copies of the "short" version (or allele) of this region were more likely to have anxiety symptoms than those who had two copies of the "long" allele. Researchers also discovered that when people with at least one short allele were put into an fMRI scanner, their amygdalae had stronger responses to angry and fearful faces than those with two long alleles.
Unfortunately, the science isn't consistent. Other studies haven't shown an association between the variation of short and long alleles and anxiety disorders.
Many other individual genes have been implicated in anxiety disorders, too. Indeed, there's a veritable alphabet soup of genes that have been explored, some with a heftier body of evidence behind them than others. However, geneticists say that much of the research on candidate genes isn't that useful. Even in the best-case scenario, it just confirms preexisting hypotheses.
Thankfully, about a decade ago technology evolved to enable genetic research that is likely to be more fruitful. Genome-wide association (GWA) studies let scientists cast a wide net and scan across the genome. GWA studies are leading researchers to genes they never even suspected might contribute to anxiety disorders. The hitch is that very large sample sizes are needed for this research. Groups of scientists are now collaborating to build these big data sets.
Still, genetic research on anxiety disorders lags behind other psychiatric illnesses.
"There's been very little funding for anxiety genetics despite the fact that it is a massive public health problem," says Jordan Smoller, a professor of psychiatry at Harvard Medical School and a leading genetic researcher. "Anxiety disorders don't quite have the visibility" of schizophrenia, bipolar disorder, and autism. "People underrecognize the toll that [anxiety] takes on people's lives."
One of the most exciting areas of research is the interaction of genes and the environment. We already know that childhood trauma increases the risk of anxiety disorders, but it turns out that the level of that risk depends, at least in part, on your genes. Some scientists are focusing on the gene FKBP5, which makes a protein that regulates the cellular response to stress hormones like cortisol. People with a certain version of the gene—the T allele—who are exposed to trauma during childhood, may be more likely to later develop PTSD and major depression than those with a different version of the gene.
The hope is that genetics will be able to guide patients to the most appropriate treatments. One person's genetic profile might make her responsive to CBT, for example, while another person might be more responsive to an SSRI. Also, genetic research could lead to entirely new ways of understanding the biology of anxiety disorders, which could lead to better treatments.
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There is no greater risk factor for anxiety disorders than being born female. Women are about twice as likely as men to develop one, and women's illnesses generally last longer, have more severe symptoms, and are more disabling. The bad news doesn't stop there. Anxious women are also more likely to develop an additional anxiety disorder, an eating disorder, or depression. In general, women worry and ruminate more than men.
What is it about being female that makes women vulnerable to anxiety? Are women born anxious, or are we raised to be that way? Scientists are looking at how gender differences in upbringing can fuel anxiety. Intriguingly, as newborns, it is boys who are more fussy and irritable. Michelle Craske, director of the Anxiety and Depression Research Center at UCLA, says that boys' cantankerous early temperaments may actually protect them from developing anxiety later on. Several studies have noted that mothers are more likely to match their sons' facial expressions and the direction of their gazes, which makes them more in sync with sons than with daughters. Craske conjectures that irritable baby boys may be better able to harness their mothers' attention than more placid baby girls. Mothers' greater harmony with sons may give boys the sense that the world is a predictable place, one over which they have some degree of control.
By the time babies are a few months old, however, the temperaments of boys and girls don't differ as much. And when girls hit age two, they start to show more "negative affect," expressing more fear and acting more inhibited than boys. Researchers note that two is also the age when kids begin to exhibit traditional gender role behaviors—stereotypically, boys gravitate to trucks and soccer balls, girls to dolls and dress-up clothes. By this age, parents have also begun encouraging their daughters—more than their sons—to exhibit empathy and help others; they urge their daughters to share toys with other children and consider others' points of view more often than they do their sons.
It could be that instilling empathy in very young girls has a downside. There's evidence as early as toddlerhood that girls "catch" fear more easily. Girls and women are better able to identify facial expressions, so scientists conjecture that they may be more vulnerable to internalizing the threats they see reflected on others' faces.
In one study, mothers presented two toys—a rubber snake and spider—one at a time to their toddlers. In one trial, the mothers were instructed to make fearful or disgusted faces and describe the toy as "horrible, scary, or yucky." In the other trial, they made positive, joyful expressions and described the toy as "fun, cute, and nice." Ten minutes after completing both rounds, mothers showed their children the spider and snake again. (This time moms were told to hold a neutral expression.) Both boys and girls were warier of the toys in the trials when mothers made frightened expressions and used negative words. And the effects of the moms' words also stuck: The kids continued to be fearful and avoided the toys even after the ten-minute delay. Girls generally had more extreme avoidant responses and seemed more afraid of the toys than the boys did.
People—particularly parents—respond to children's fears in markedly different ways, too, depending on gender. When girls are anxious, adults are more likely to be protective and allow them to avoid scary situations. Boys are told to suck it up. "There's an assumption that boys should be courageous and they should overcome their fears and face their fears. With girls, we are a little bit more accommodating, and we permit this sort of reluctance or avoidance of situations," says Carmen McLean, an assistant professor of psychology in psychiatry at the University of Pennsylvania School of Medicine who has studied gender and anxiety. But this protection, she says, has lasting consequences. "You are teaching the girl, 'If I feel a little bit nervous, that means I should not do something.' A boy learns, 'If I feel this way, I should act anyway.' He learns, 'I can do it, and my anxiety goes down.' He feels more confident and has more efficacy. A little girl doesn't learn that lesson." It is as if boys are engaged in continual exposure therapy. Perhaps this inoculates them from future anxiety disorders.
A large body of dispiriting research shows just how much boys are encouraged to be independent and brave while girls are dissuaded from the same behavior. Parents have been found to be more controlling with daughters than with sons, which puts girls at greater risk of an anxiety disorder. In a University of California, Berkeley study, researchers videotaped ten-minute interactions of mothers and fathers with their preschool-age children. The families were told to "create a world" out of a sand tray and small toys. When boys asserted themselves by, for example, telling their parents where to put a toy, parents were more likely to praise them. When girls were assertive, parents were more likely to interrupt, talk over, or disregard them. This gives girls the message that they don't have control over their environment. Feeling out of control is, of course, a core belief in the anxious mind.
I take some solace from the fact that this particular study was conducted in 1993. Surely we must be more enlightened now?
I pose that hopeful question to McLean, and she quickly shuts it down. She tells me about a conversation she recently had with the father of a newborn daughter and an older son. "He was telling me how having a girl is so different than having a little boy. He said he felt a lot more protective, like his daughter was more fragile," she recalls.
Barbara Morrongiello, a professor of psychology at the University of Guelph, has conducted a fascinating series of studies looking at how parenting interacts with gender to affect children's risk-taking behaviors. When Morrongiello was on maternity leave in the early 1990s, after her oldest son was born, she spent a lot of time at playgrounds and noticed huge differences in what boys and girls were encouraged to do—and not to do. In the sandbox and on the jungle gym, "I saw much more encouragement [expressed] to boys and caution to girls," she says. Morrongiello had a hunch that these different messages might be contributing to high injury rates for boys: After age two, boys have two to four times more injuries than girls. Their injuries also tend to be more serious.
Although Morrongiello isn't an anxiety researcher, her findings may be critical for understanding the gender disparity in rates of anxiety disorders. Morrongiello and her colleague Theresa Dawber conducted a study that observed forty-eight sets of parents and toddlers on a playground. Parents and kids first played freely on a slide, swings, and jungle gym for ten minutes. Then the grown-ups were instructed to teach their children how to slide down a pole similar to what you'd see at a fire station.
Both boys and girls were just as skilled at navigating the playground equipment. Still, parents more often warned girls about safety and the risk of getting hurt, whereas they tended to encourage independence in boys. They also were more likely to physically help girls, even when girls didn't ask for assistance. For example, parents spontaneously helped girls during 67 percent of their attempts to slide down the pole. By contrast, they physically helped boys only 17 percent of the time. Incredibly, even when boys requested help, parents often initially denied their requests and urged them to try again on their own. Parents were so hands-off with their sons that several boys tumbled off the pole and onto the ground.
Indeed, by school age, girls seem to have learned to be vigilant to threat. In other research, Morrongiello and colleagues found that when six-to-ten-year-old girls and boys assessed the same potentially dangerous scenario—such as riding a bicycle without a helmet—girls tended to see it as riskier than boys.
Parents also have different emotional reactions when sons and daughters do things that could get them hurt. When girls engage in risky behaviors, mothers, in particular, respond with disappointment and surprise. When boys do it, mothers react with anger. Parents are also more likely to chalk up their sons' injuries to personality, a "boys will be boys" mentality. When girls are injured, however, parents are more likely to blame the child. They are more likely to think that if only their daughters were more careful or listened better, they wouldn't get hurt.
While these messages may protect girls from physical injury, Morrongiello conjectures that they could pave the way for feelings of vulnerability and self-blame. Boys are told that being a daredevil is just part of being a boy, whereas girls are taught that if something bad happens, it is their fault. "To the extent you're telling girls you are responsible for your own negative outcomes, you can see girls being more anxious and more self-evaluative and self-critical," she says.
By late elementary school, girls are less likely to expect that they will succeed and more anxious about the prospect of failing. When facing stressful events, boys are more likely to problem solve on their own. Girls are more likely to seek support from their friends.
There is, however, one "equal opportunity" type of anxiety: social anxiety disorder. McLean tells me that this makes sense given how boys and girls are socialized. Girls are expected to master small talk, be charming, and make friends. Parents may consider it socially acceptable for a daughter to be afraid of snakes or dogs and avoid them, but they likely communicate that it's _not_ all right to refuse to say hi to a teacher or withdraw during a playdate.
Surprisingly, men's _physiological_ reactions to stressful events are stronger than women's. Levels of the stress hormones epinephrine and norepinephrine tend to spike higher in men when they undergo stress-inducing laboratory experiments, like taking a difficult test. Researchers say this makes evolutionary sense since a hair-trigger fight-or-flight response would have been adaptive when hunting or fighting adversaries. Women, on the other hand, have a more muted fight-or-flight response, which scientists have dubbed "tend and befriend." According to this model, women respond to stress by producing more oxytocin, a hormone thought to promote attachment, which spurs them to tend to their young and befriend other members of their group. The disadvantage to the tend-and-befriend response is that it could fuel anxiety by reinforcing worry and a pattern of avoiding threats.
Men and women also often try to ease their anxiety in different ways. Anxious men, for example, are more likely to self-medicate with alcohol or drugs and develop a substance-use disorder. For years my friend Mike, a fellow journalist, turned to alcohol and drugs to try to ease his anxiety and depression. Mike is handsome, smart, and wickedly funny, but when his anxiety is full throttle, he constantly churns over conversations with editors and friends, worrying that he's offended someone or said something stupid. The physical symptoms of anxiety are even more debilitating: His stomach churns, his skin tingles, and he feels constantly light-headed.
For Mike, marijuana and narcotics like Vicodin were a revelation. They took away the worrying. They calmed his twitchy body. "When you find something that makes that go away, you'll do anything," he says. But after a while, the marijuana turned on Mike. It started making him more anxious. His drinking and use of narcotics slid into addiction. He went to rehab. He relapsed. He kicked the drugs and alcohol again. Now he combats anxiety with an SSRI, daily exercise, and a strong spiritual practice.
There's evidence that estrogen and other sex hormones affect how women learn fears and how they override them. Women with anxiety disorders often say their symptoms worsen before their periods. Fluctuating estrogen levels could be partly to blame. Some studies show that when estrogen is high, fear responses are lower and vice versa. In one study, thirty-four women underwent a fear-conditioning procedure in which a picture of a lamp was paired with a shock to the hand. The women later underwent extinction, where the lamp picture was followed by no shock. Level of fear was measured by skin conductance. Women with higher levels of estradiol, a form of estrogen, had stronger extinction recall (meaning that they maintained a lower level of fear) than women with lower levels of estradiol. The women with high estrogen also had greater activation in the brain network implicated in fear extinction, the vmPFC, and amygdala.
It isn't just genes, hormones, and socialization that contribute to women's greater vulnerability to anxiety disorders. The risk of sexual assault and abuse does, too. Men generally encounter more traumatic events—such as serious accidents and experiencing or witnessing violence—in their lives than women. Women, however, are more likely to be the victims of sexual abuse and assault. Because sexual trauma is so uncontrollable and unpredictable, Craske argues, it is more likely to lead to PTSD and other anxiety disorders.
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Scientists can identify some people at increased risk for anxiety disorders when they are infants. Researchers do it by assessing temperament, that unique, innate fingerprint of personality.
Temperament is a "biologically-based bias, usually inherited, that affects the chemistry of the brain," Jerome Kagan, a professor emeritus of psychology at Harvard University, tells me. "It is analogous to the behavior and mood of a dog breed. You know the difference between a laid-back Labrador and a Pekingese or a pit bull?"
Kagan, who is now eighty-seven, has spent his career studying two particular temperaments—what he calls high-reactive and low-reactive—that relate to how we respond to new objects, situations, or sounds. High-reactive babies thrash their arms and legs, arch their backs, and cry when confronted with novelty. Low-reactive babies remain relatively quiet and relaxed. Kagan has found that, as toddlers, high-reactive babies tend to be shy, quiet, socially reticent, and fearful, or what he calls behaviorally inhibited. Low-reactive babies, by contrast, generally become more boisterous, outgoing, and daring. Kagan calls them uninhibited. Studies by Kagan and others have found that inhibited children are much more likely than uninhibited kids to develop anxiety disorders. About one-third to one-half of inhibited kids develop anxiety disorders—most often social anxiety disorder—by adolescence. Behavioral inhibition (BI) is largely genetic. Twin studies have found that the heritability of BI is anywhere from 40 to 75 percent.
Kagan started his temperament work in 1957 at the Fels Research Institute at Antioch College in Ohio. At the time, the institute was conducting a longitudinal study of children born between 1929 and 1939. The researchers noticed that a small group of participants who were very fearful as small children remained cautious and introverted into adulthood. Kagan, along with colleagues at Harvard, where he began teaching in 1964, hypothesized that the root of our differing reactions to novelty lay in the amygdala. Since the amygdala projects to brain regions that control motor activity and the autonomic nervous system, the theory was that babies with more excitable amygdalae would thrash and cry more and have higher heart rates and blood pressure. In 1989, Kagan and colleagues recruited five hundred four-month-old infants. The researchers conducted a series of experiments (what scientists now call the Kagan paradigm) to assess how the infants reacted to new things.
Each baby was put in an infant seat for the forty-five-minute assessment. First, the mother was told to look at her baby and smile but not talk, while researchers took the infant's resting heart rate via electrodes. The baby was then presented with a series of noises, including a taped female voice reading sentences and nonsense syllables and a balloon popping behind the child's head. Mobiles with colorful toys were dangled in front of the baby's face. A researcher placed a cotton swab dipped in alcohol in front of the baby's nose.
The researchers characterized about 20 percent of the babies as high-reactive, meaning they cried and moved their arms and legs around during at least 40 percent of the experiments. About 40 percent were low-reactive. (The rest were a mix of the two.)
Kagan and colleagues continued to assess the children every few years.
When the babies were two years old, each toddler was asked to put a finger in a glass of black liquid and to let a researcher put a drop of water on his or her tongue. The child was approached by a stranger wearing a white lab coat and gas mask, a moving toy robot, and a person dressed as a clown. Toddlers who were fearful, cried, and avoided at least four of the objects or situations were tagged as behaviorally inhibited (BI).
About 46 percent of the high-reactive infants went on to become inhibited four-year-olds. Two-thirds of the low-reactive infants became uninhibited kids. When the kids were seven, they were assessed for anxiety symptoms. About 45 percent of high-reactive babies developed anxiety problems by age seven. Only 15 percent of low-reactive babies, however, became anxious. Kagan also discovered that blond, blue-eyed, fair-skinned children were more likely to be inhibited, a finding that, he believed, may indicate that the same genes influence both eye color and temperament.
Of course, if nearly half of BI kids will go on to have problems with anxiety, it means that half won't. Nathan Fox, a developmental psychologist at the University of Maryland and a former graduate student of Kagan's, is trying to discern which kids are most at risk. Fox notes that BI kids can still be shy without developing a disorder. "They are not your cheerleaders and football captains. But they end up being professors or computer scientists."
Fox is leading two longitudinal studies of behavioral inhibition. The first began in 1991 with 156 four-month-old babies. By the time they were fifteen, he discovered that about half the BI babies had developed an anxiety disorder; 40 percent had developed social anxiety disorder. By age twenty-three, about 19 percent had a mood disorder.
One October morning, I head to College Park, Maryland, to see Fox. Meeting me in his office, he looks professorial, with a graying mustache and wire-rimmed glasses. A toy Oscar the Grouch, complete with garbage can, sits on his desk, a relic from his years as a consultant for _Sesame Street_. Idyllic photos of Lake Como, Italy, are blown up on his walls, souvenirs of a trip he took while writing a book about his work in Romania with orphan children.
Fox brings a laptop over to a table and shows me a video. A little blond boy I'll call Michael, fourteen months old, leans against the legs of his mother, who sits behind him in a chair. The boy, Fox tells me, was a high-reactive baby. Meanwhile a research assistant, off camera, plays with blocks and tries to entice the child to join her. The toddler rebuffs the advances, clutching his mother's legs and burrowing his head in her lap. While this is happening, we can hear the mother telling the researcher about the boy's first birthday party. "We had a bunch of people over. He wouldn't open his presents. He wouldn't eat his cake. He cried the whole time. That was a fiasco." He's scared, she says, of most adults but is fine around children.
Fox shows the next video, which features Michael at age four. The study paradigm is a "play quartet" with the target child and three unfamiliar children. I see three boys playing in a room strewn with action figures, cars, and dolls, but no Michael. Then I hear crying and then a loud, plaintive "Nooooo!" coming from off camera. A woman, his mother, then carries a flailing Michael into the room. He tries to run out the door, but she drags him back in. He sobs and sobs. After a few minutes, he stops crying and slumps in a corner, defeated.
"He's just going to watch the other three kids for the rest of the time. He's not going to play by himself," Fox says. At one point, a little boy comes over to Michael and says, "You don't like being here."
The third video Fox shows me is of Michael at age seven. The paradigm is again a play quartet that includes the target child and three unfamiliar peers. Three of the boys walk into the room and immediately start exploring the toys on the floor (Legos, action figures). Michael, on the other hand, simply looks around and doesn't pick up any of the toys. "He's going to go and stand in the corner of the room for the entire fifteen minutes," Fox tells me. Indeed, Michael does just that. He looks miserable, as if he's hoping the floor will swallow him up. At one point, a boy walks over to Michael and puts his arm around him, but Michael shrugs the arm off. The other boy walks away.
I ask Fox if he knows what became of Michael, who now must be about twenty-three. Michael, he says, did develop an anxiety disorder and, later, depression. Fortunately, he got treatment and was prescribed medication. He graduated college and seems to be coping reasonably well.
Fox and colleagues have found that, while parenting may not contribute much to the development of anxiety disorders for children who aren't inhibited, it matters a lot for BI kids. In one study, the researchers found that only those BI kids whose mothers were overcontrolling developed greater social anxiety symptoms by adolescence. They cited various examples of this kind of parenting behavior during playtime including mothers dominating the conversation, giving frequent and unnecessary instructions, interrupting the child, or taking away a toy. In other studies, the researchers found that BI kids who are put in day care during the first few years of life became less inhibited. Being exposed to new people and experiences at day care—and possibly getting a break from controlling parenting at home—helps kids become less fearful.
Fox and his fellow researchers are finding that particular cognitive processes of some BI kids raise the risk of anxiety disorders. They have found that behaviorally inhibited toddlers who have an attention bias to threat are more socially withdrawn at five years old and are more anxious in adolescence. BI kids who don't have an attention bias to threat don't end up socially withdrawn and anxious. "We find that BI kids way before they show any signs of anxiety are showing this attention bias to threat," Fox says. "So it is not a symptom of an anxiety disorder. It is an underlying mechanism which facilitated the emergence of anxiety."
Fox and his colleagues have found that some cognitive processes protect BI kids from developing anxiety disorders. Kids with BI who are adept at attention shifting (being able to shift one's attention in order to complete a task or to achieve a goal) are less likely to develop anxiety disorders. This skill could help kids divert their attention away from threatening stimuli.
BI kids who have higher levels of inhibitory control, however, are more likely to develop anxiety disorders. Inhibitory control is the ability to override an ingrained response that is maladaptive and respond in a more beneficial way. For kids without BI, this is thought to be adaptive, but it doesn't seem to be for BI kids. Scientists aren't quite sure why. One hypothesis is that, because BI kids already have a trigger-happy fear system (that twitchy amygdala), having a strong voluntary control system on top of it leads to overcontrol and inflexibility. In other words, researchers say, such kids "may be better able to monitor their response and reflect on past errors, leading to increased levels of rumination and increased anxiety symptoms."
In one study, Fox and colleagues assessed inhibitory control by asking behaviorally inhibited four-year-olds to say the word _day_ when shown a picture of a white moon and stars with a black background and _night_ when shown a picture of a yellow sun on a white background. This is known as a Stroop task, and it requires participants to override a powerful response. Kids who were more accurate in the task were considered higher in inhibitory control. Researchers assessed attention shifting by asking the children to sort a set of cards based on a given rule by color. Then they were asked to sort the cards according to a new rule, by shape. The greater a child's accuracy, the greater their ability to attention shift. The study found that BI kids who had lower levels of attention shifting and higher levels of inhibitory control had anxiety problems. But BI kids who had higher levels of attention shifting and lower levels of inhibitory control seemed to be protected from excess anxiety. The hope is that this research might lead to new interventions for BI children that could prevent anxiety disorders from developing. A therapy that increases attention shifting and decreases inhibitory control is one possibility.
I ask Fox what his personal temperament is. "I don't think I was highly inhibited, but I think I was somewhat inhibited," he says. "I think I was—more so than I needed to be—an overly sensitive kid, just in terms of friendships and entering into peer groups and all that. High school was not a pleasant time as I remember." What helped him was having a best friend. "I had one very good friend, and I think that was a very important anchor for me." Not all BI kids have this. In his studies, when the children come in for their nine-year-old assessments, researchers ask them to bring in their best friend. "We had some kids where the mom said, 'Can he bring his cousin?' "
I was not an inhibited child. I made friends easily, was independent, and could be a bit of a show-off, dancing and making up skits for any audience I could find. My mother says that once, at age two, I walked by myself from our house to the park—a distance of several blocks. My father, who was supposed to be keeping an eye on me, was washing his lemon-yellow Ford Torino in the driveway and didn't see me leave. "I just wanted to go to the park," I said calmly when my parents found me after a frantic search.
A couple of years later I got lost in a department store while shopping with my mother. "There's a little lost girl named Andrea," my mother heard over the loudspeaker, with directions on where to collect me. She found me sitting happily on top of a checkout counter, a lollipop in my mouth, being fawned over by a group of young saleswomen. We continued shopping and I quickly vanished again, this time deliberately, in search of more sweets and attention.
In doing this research, I have realized that my temperament is probably not the root of my anxiety disorders. It is doubtful that I'll ever find a single smoking gun, although genes most likely play a part. Mental illness isn't like tuberculosis, which is always caused by one particular bacterium. Anxiety disorders almost certainly have multiple causes—from genetics to childhood trauma to how your parents interact with you. And for any given person, the mix of these factors will be as singular as a fingerprint.
> Anxiety Disorders Program, Evaluation Summary, November 20, 1990
>
> Ms. Peterson [ _sic_ ] is a 20-year-old single student who is a junior at the University of Michigan who was referred to the anxiety disorders clinic by Dr. Pitt. She comes with a chief complaint of a one-year history of panic attacks....The patient presented as an attractive young women [ _sic_ ] who was appropriately dressed and presented as mildly anxious. Thoughts were fluid and coherent, affect was appropriate to the content of discussion. There was no evidence of impairment of memory or judgment. Our conclusions are as follows: Panic Disorder with Agoraphobia. OCD (mild).
It is the fall of 1990, nearly one year since that December day I fell apart, and I'm sitting in a small, nondescript conference room with about ten other people—all women, all anxious. We are in a group therapy session in the Anxiety Disorders Program at the University of Michigan Health System. At twenty, I'm decades younger than most of the other participants. Looking around the room, I glimpse the sad progression of my own life if I let anxiety control me. Plagued by panic attacks, several of the women have been practically homebound for years, their trips to "group" one of their few (white-knuckled) outings each week.
We go around the room and talk about our "homework" for the next week. One of the homebound women has an assignment to leave the house each day and walk to the mailbox. Mine is to buy multiple travel-size tubes of toothpaste and open a new one every day. This is exposure therapy, the most effective—and most excruciating—treatment for anxiety problems. The idea is for us to actively face our fears by eliciting anxiety symptoms and gathering evidence that experiencing them won't lead to whatever catastrophe we've conjured. Gradually, week by week, the assignments become more difficult. The goal is to scale our emotional Everests.
Exposure therapy is the workhorse of what is known as cognitive behavioral therapy (CBT). Remember the fear-conditioned rats that stopped freezing when the tone was no longer followed by the shock? Learning that the tone was safe overrode the association of the tone with the shock. Some scientists think exposure therapy does the same thing in people. Each time I used a new tube of toothpaste and didn't drop dead reinforced the reality that it wasn't, in fact, dangerous.
The toothpaste was item one on the "fear hierarchy" my therapist had me create, a list of things and situations I avoided because of anxiety. As the weeks went by, I tackled each one. Standing in line at a coffee shop. (Lines made me feel trapped.) Taking a vitamin. (I was afraid it would make me sick.) Running up a flight of stairs. (I panicked when my heart rate went up.) My therapist even had me breathe rapidly to induce hyperventilating, one of the classic symptoms of my panic attacks.
My therapist also helped me tackle my catastrophic thoughts. This was called cognitive reappraisal. Each time I had a calamitous thought, I was to challenge my negative beliefs by amassing evidence and then calculating the actual odds of disaster on a scale from 0 to 100. For example, say my heart rate kicked up suddenly. Typically, my first thought was: "Maybe I'm having a heart attack." Cognitive reappraisal went something like this: "This has happened before, and I've never had a heart attack. I'm only twenty years old, and I've had several tests to rule out heart disease. The symptoms I'm having are also the same as a panic attack. What is the actual likelihood that I'm having a heart attack? Maybe 3 percent."
I can't say I was always persuaded by these arguments. The tiny voice of rationality was often drowned out by the loud, demanding symptoms of my body. In the battle between my racing heart and logic, the heart usually won.
But as time went on, as I exposed myself to more scary situations and continued not to die, the symptoms became slightly less urgent, the rational thoughts a little sturdier. By the end of the group sessions, I certainly wasn't back to my old self, but I was more functional. My world—which had pretty much narrowed to a few classes and my room—expanded. I took on a full course load. I ventured out for pizza. I remembered more of what I read. I even made it to a fraternity party and had an energetic dance-off to Madonna with my friend Lisa.
CBT, which usually involves twelve to fifteen weekly sessions with a therapist plus daily homework, is effective: About half of anxiety disorder patients experience clinically significant improvement. In a meta-analysis of twenty-seven studies comparing CBT for adult anxiety disorders to a placebo, CBT was found to have a "medium to large" effect on the severity of anxiety symptoms. Neuroimaging studies show that successful CBT treatment changes the brain—some reveal reduced activity in the hyperactive amygdala and increased activity in the listless prefrontal cortex. In one 2016 study, CBT actually shrank the amygdala.
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Nondrug treatments for anxiety have a colorful history. In the nineteenth century, people flocked to spas to ease their anxiety, a practice that had begun earlier but was now booming. Hydrotherapy was used to treat all manner of chronic illnesses, including psychological ones. Charles Darwin, for example, frequented Malvern in England for his hypochondriasis. The Italian and French Rivieras were recommended for the treatment of nervous problems. In the major cities, "hydros," private mini-spas, cropped up. Paris had dozens. Depending on the diagnosis, patients were sprayed with water, alternately hot and cold, and then dunked into arctic swimming pools. Massage and electrotherapy were on offer, too. Hydros competed with private "nervous clinics," which were overseen by a growing cadre of "nerve doctors," usually neurologists or general physicians. Psychiatrists, by contrast, who were called alienists, worked almost exclusively in asylums, grim places that housed the psychotic and the criminal. Treatment there was generally limited.
One of the most popular therapies for neurasthenia, the "tired nerve" disease of the late 1800s, was the rest cure. In 1875, Silas Weir Mitchell, a nerve doctor in Philadelphia, popularized a souped-up rest cure: a stringent regimen of bed rest, massage, and a high-fat diet rich in milk. Patients often took the cure in spa clinics, staying for as long as three months. (Needless to say, this was a therapy available only to the well-off.)
Some found the cure more harrowing than the illness. The writer Charlotte Perkins Gilman described her experience with the rest cure in the autobiographical short story _The Yellow Wallpaper_ , published in 1892. In the story, the heroine is separated from her baby and mostly confined to a room in a rented summerhouse. She is forbidden to write or do housework and is admonished not to even think or imagine too much. "So I take phosphates or phosphites—whichever it is, and tonics, and journeys, and air, and exercise, and am absolutely forbidden to 'work' until I am well again," Gilman writes. "Personally I believe that congenial work, with excitement and change, would do me good. But what is one to do?" Deprived of distraction and any intellectual life, the heroine spends hours staring at the yellow wallpaper in her room, gradually descending into madness, her unraveling revealed through her hallucinatory descriptions of the wallpaper.
The rest cure was primarily prescribed to women. When Theodore Roosevelt was diagnosed with neurasthenia, his doctor sent him to a dude ranch in the Dakotas for a spell of riding and hunting.
The seeds of CBT were also planted around this time. The origins of the treatment go back to the Russian physiologist Ivan Pavlov and his concept of the conditioned reflex, an automatic form of learning. In his famous experiments with dogs in the 1890s, Pavlov found that if the sound of a buzzer was followed by food, the animals eventually learned to associate the buzzer with food and would salivate as soon as they heard the sound, even before they saw the food.
John Watson, an American psychologist, expanded upon Pavlov's ideas. In 1913, he published a paper delineating his belief that psychology must be rooted in observable behavior. In the 1920s and 1930s, pioneering psychologists like Hans Eysenck and B. F. Skinner fleshed out the approach. Skinner asserted that people act to gain a reward or avoid pain and behavior changes through either reinforcement or discouragement. Eysenck said people become neurotic through learning experiences undertaken to avoid anxiety. Healing happens when these experiences are "unlearned." The behaviorist school of psychology was born.
Meanwhile psychiatrists continued their love affair with Freud, who had trained as a neurologist and studied hysteria with Josef Breuer. Working with Breuer, Freud claimed he was able to bring relief to hysterical patients by hypnotizing them and having them zero in on the psychological origins of their symptoms, a process the duo called "catharsis." Over time, his psychoanalytic method evolved. Instead of relying on hypnosis, patients—with the help of their analysts—could supposedly uncover the unconscious conflicts that were the origin of their distress simply by talking, saying whatever came to mind. Psychiatrists throughout Europe and the United States adopted his "talking cure" to treat people with anxiety problems and other mental illnesses.
In the 1950s, while Freudian psychoanalysis reigned, therapy for anxiety disorders took a huge step forward with Joseph Wolpe, a South African psychiatrist. Wolpe began his career as a staunch follower of Freud. But when he began working with soldiers suffering from "war neurosis" (what we now know as PTSD), he was disillusioned to discover that the treatments he had been trained to provide—talk therapy and medication—didn't seem to work. He began exploring alternatives. Eventually Wolpe developed a treatment called "systematic desensitization," an early form of exposure therapy. The treatment rested on his belief that it was impossible to simultaneously feel anxious and relaxed. It entailed teaching people with phobias relaxation techniques, then gradually exposing them to the things they feared while they employed the relaxation tools they had learned. Soon Wolpe's teachings spread to psychologists around the world.
In the 1960s, Aaron T. Beck, a psychiatrist at the University of Pennsylvania, developed cognitive therapy, initially as a treatment for depression. Beck said that psychopathology was largely the result of distorted thinking. Treatment focused on identifying maladaptive thoughts, challenging them, and replacing them with more realistic ones.
Frustrated at the dismal success rates of traditional analysis and psychotherapy, a handful of renegade psychiatrists and psychologists took the behaviorist and cognitive theories and began to experiment further with new ways of treating anxiety. Like Wolpe, they largely abandoned the idea of trying to uncover the root cause of a patient's anxiety, focusing instead on relieving the symptoms. In the 1960s, they were dismissed as quacks and charlatans by the psychiatric establishment.
In 1971, psychiatrist Manuel Zane opened the country's first phobia treatment center at White Plains Hospital in New York. He treated his patients in the community, driving over bridges with those with bridge phobias, riding elevators with those with elevator phobias, and tape recording every panicky pronouncement. Soon he began sending patients out to tackle their fears with "phobia aides," trained people who had recovered from their own phobias.
Meanwhile in California, psychiatrist Arthur Hardy was taking a similar approach. He developed a behavioral treatment for agoraphobia (which he dubbed territorial apprehension) and generated a huge amount of press coverage.
These iconoclasts and others eventually banded together and formed an organization to educate other clinicians and raise money for research. In 1977, about three hundred patients, psychiatrists, and psychologists convened in an auditorium at White Plains Hospital for the first meeting of the Phobia Society. Since renamed the Anxiety and Depression Association of America, the group now publishes one of the field's key scholarly journals and holds a yearly research conference that attracts more than a thousand scientists and clinicians from around the world. Neuroimaging experts mingle with CBT trainees. Geneticists chat with mindfulness experts. All are focused on improving the lives of the chronically anxious.
—
It took nearly a year and numerous doctors for me to be diagnosed and treated. I'm unusual, however, in that I sought help from the medical system at all. People with panic disorder wait an average of ten years before discussing their symptoms with a doctor, psychologist, or other professional (including an acupuncturist or "spiritual advisor"). Those with social phobia delay sixteen years; those with generalized anxiety disorder, nine years. With specific phobia, the wait is twenty years. And when they do seek help, patients may not receive appropriate treatment. This is particularly true of African Americans. Though they have lower rates of anxiety disorders than whites, studies have found, their illnesses are more chronic and severe and the quality of care they receive is generally lower.
In the months after my stint in group therapy, I continued to get better. The panic attacks and overall anxiety abated. I went to class and started working part time at a funky clothing store called Splash where our manager judged employees' success not by how much we sold but by how much we flirted with customers. Scott and I broke up. During spring break in South Padre Island, Texas, I met Joel, a sweet, goofy MBA student. I stayed in Ann Arbor for most of the summer to spend time with my new boyfriend before he moved to San Francisco. Throughout the fall of my senior year, I felt pretty good. I was taking a full load of classes again, going dancing with friends, and flying to visit Joel when time—and cash—allowed.
Then the day after Christmas, I relapsed.
I am in my parents' car, sitting in the backseat. It is the middle of the night. My sister is sleeping next to me, my mother nodding off in the passenger seat. My father is driving, blasting Led Zeppelin on a classic rock radio station to keep himself awake. We are in the middle of the fourteen-hour drive from San Antonio, Texas, where my parents had moved more than a year earlier, to Salem, Illinois, on our way to visit family.
Suddenly I feel a slight pressure on my chest. I try to ignore it, silently singing along to the radio: "Oh oh oh oh oh oh. You don't have to go oh oh oh oh oh." It quickly becomes a weight. The air in my lungs seems to have turned from a gas to something more solid. Breathing starts to feel like a struggle or at least a conscious action. If I stop paying attention, I think, it will stop. And I will die.
I try to use some of the techniques I learned in group therapy. _I'm okay_ , I tell myself. _I'm still breathing. This is just a panic attack._ But my puny thoughts are no match for the powerful, catastrophic sensations. For the rest of the ride, I huddle against the car door and focus on moving the air in and out of my lungs. When we arrive at my grandparents' house, I head right for the afghan-strewn sofa. The terror abates enough—or I am able to mask it enough—for me to get through the trip without a visit to the ER, but when we get back to San Antonio, I crumble.
The weight on my chest is constant. Sometimes it feels like my ribs have shrunk a few sizes. Other times I imagine the pressure as the anvil that eternally drops on Wile E. Coyote. I am too scared to sleep. If I sleep, I can't concentrate on breathing. In my mixed-up mind, sleep equals death. All night I lie on the sofa in my parents' living room, the TV turned to Nick at Nite's _My Three Sons_ marathon. At times my mother stumbles half-asleep out of her bedroom, sits next to me, and silently strokes my hair. I nod off for a half hour, an hour, and wake up with a heart-racing start. The weight on my chest is always there.
I see my mother's doctor, who thinks I might be having an asthma flare-up. She puts me on an oral steroid, which makes me jittery and does nothing to lift the burden on my chest. That doctor sends me to a pulmonologist and a cardiologist. They find nothing wrong. When I tell the cardiologist that I have had perhaps ten hours of sleep over the entire week, he prescribes Xanax. I'm still afraid of taking medication, but I'm so desperate that I swallow half a tablet and zonk out for fourteen hours.
My parents call my therapist back in Ann Arbor.
> # ANXIETY DISORDERS PROGRAM: Progress Note
>
> ## PETERSON [ _sic_ ], Andrea
>
> ### January 16, 1992
>
> Andrea comes in after a 6-month absence from the clinic....She comes complaining of difficulty breathing, shortness of breath, light-headedness, dizziness, occasionally experiences derealization, depersonalization, and describes anxiety over many catastrophic thoughts that she has about her physical well being. We reviewed her symptoms and again reviewed the behavioral and cognitive interventions that have helped her in the past.
Back in Ann Arbor for the winter term, I resumed weekly therapy. Because the fears of food and contamination had reappeared, causing me to lose ten pounds, my first homework was to eat four to six small meals and drink eight glasses of water a day. I was also to take a vitamin pill.
I also embarked on another medical odyssey, looking for some reason other than anxiety—and the mild asthma I already knew I had—for my shortness of breath and weight on my chest. Through the winter and spring, I was a regular at the Pulmonary Function Laboratory at the University of Michigan Hospital. I had multiple spirometry tests to see how much air I could quickly blow in and out of my lungs and a methacholine challenge test, where I had to breathe in a substance that makes the airways constrict in people with asthma. I had a test to measure my blood gases during exercise: I jogged on a treadmill while blood was taken from an artery in my wrist. The diagnosis? Mild asthma.
The fatigue and constant fear returned, along with weird new physical symptoms. The tingling in my feet that I had felt off and on before settled into a constant throb. It slowly crept up from the soles to the tops of my feet, to my ankles, then licked the bottoms of my shins. I had a test to assess the nerves in my feet and legs using pinpricks, electric currents, and vibrations. I visited the Chronic Fatigue Clinic and even the Infectious Disease Clinic. I was convinced that I had some rare fatal disease the doctors just couldn't identify. I started to sneak around. I'd make an appointment with a new doctor without telling the previous one. (I was mortified when my doctor at the University Health Service received a detailed letter from a doctor I had seen at the Infectious Disease Clinic.)
Why didn't the CBT techniques prevent this? Maybe it was because, after two years, the major physical symptom of my anxiety had changed from a racing heart to chest pressure. Or maybe it was simply because the effects of CBT can wear off. One study followed sixty-three panic disorder patients, most of whom had responded well to a course of CBT; nine of them relapsed during the following two years. And more than one in four participants sought additional treatment within those two years because of persistent symptoms.
Psychologists are tweaking CBT to boost its performance. Very simple adjustments, such as scheduling appointments in the morning or asking that patients nap or run after therapy, may make it more effective. A 2016 study found that exposure therapy appointments in the morning were more helpful than those later in the day. Higher levels of the stress hormone cortisol occur naturally in the morning, and researchers concluded that they were responsible for at least part of the benefit of the earlier sessions. A surge in cortisol can facilitate learning, they said.
Napping after therapy was shown to be beneficial in a 2014 study of people with spider phobias. The subjects did a session of exposure therapy using virtual reality: Using a head-mounted display, they moved through simulated rooms containing virtual spiders. After the session, some subjects were given ninety minutes to nap. Others watched a video. Then they were asked to approach a live tarantula in a cage. At that point, there were no significant differences in anxiety symptoms between the groups. However, an appointment a week later yielded different results. Compared to those who didn't sleep after exposure therapy, the people who had napped had a greater reduction in anxiety and catastrophic thoughts about spiders as they moved toward the tarantula. Scientists believe that sleep can strengthen the memories of new learning that occurs during therapy.
Psychologists are also adding other components to improve CBT. In a 2016 study of patients with severe GAD, CBT was augmented by motivational interviewing, an approach where therapists focus on expressing empathy and validating patients' feelings. Those who got the combined therapy saw a greater reduction in worry and distress over the one-year period after the treatment ended, compared to those who got only CBT. In addition, far fewer patients who had the combined therapy—about half as many—dropped out of treatment. David H. Barlow, a CBT pioneer and founder of the Center for Anxiety and Related Disorders at Boston University, has, along with colleagues, developed a treatment called the Unified Protocol that they are using to treat a range of anxiety disorders and depression. It builds on CBT and includes sessions to teach patients to fully experience their emotions. Barlow says the dropout rate is much lower than traditional CBT.
Michelle Craske and colleagues at UCLA are finding that asking patients to vividly imagine happy scenes before therapy may improve learning during exposure and make the treatment work better. Craske is also finding success in modifying exposure therapy. Modifications include varying where and how patients do the therapy and intensifying exposure to the feared object or situation. For example, a person with a dog phobia might encounter two dogs at one time.
Craske will soon launch a study to see whether exercise after exposure therapy boosts its effectiveness, since exercise increases the level of a protein that is critical for the consolidation of memories.
Anne Marie Albano, director of the Columbia University Clinic for Anxiety and Related Disorders, says that it is important to do periodic booster sessions of CBT, particularly during times of stress and big life changes, like getting married, getting divorced, having a child, or losing a parent. "Demands become different over time. The person's ability to adapt to that is challenged," she says.
Psychologists have also developed a number of other therapies for anxiety disorders. The most heavily researched is acceptance and commitment therapy (ACT). Whereas in CBT you're taught to challenge your anxious thoughts, weigh the evidence, and modify them so that they are more realistic, in ACT you're taught to accept your thoughts and feelings. "Trying to get rid of your pain only amplifies it, entangles you further in it, and transforms it into something traumatic," writes clinical psychologist Steven Hayes, one of the creators of ACT.
Acceptance doesn't mean succumbing to anxiety, though. Rather, you're taught to distance yourself from your anxious thoughts and feelings, to see them more objectively. This is known as cognitive defusion or a way, as Hayes writes, to "look _at_ thought, rather than _from_ thought." ACT therapists use dozens of different defusion techniques, including having clients say one word over and over for twenty to forty-five seconds until it seems stripped of its meaning. Patients do this for benign words like _milk_ and then move on to emotionally charged words like _weak_ or _stupid_. Other exercises include visualizing thoughts as leaves floating by on a stream or stating fears in a silly voice or as lyrics to a song.
ACT involves a variety of mindfulness techniques. Derived from ideas from Zen Buddhism and yoga, mindfulness, says Hayes, is the "nonattached, accepting, nonjudgmental, deliberate awareness of experiential events as they happen in the moment." ACT includes meditations on bodily sensations, walking meditation, and such exercises as mindfully eating a raisin or drinking a cup of tea.
Like CBT, ACT also includes exposure. But in ACT, exposure is presented as a way to achieve personal goals. Therapists have patients identify core values through exercises such as writing their own eulogies and epitaphs. Clients are encouraged to see exposure as helping them move toward what they find personally meaningful.
Hayes was already working with anxiety patients when he had his own first panic attack in 1978. He was in a contentious meeting with colleagues at the University of North Carolina at Greensboro when he moved to ask his coworkers to "stop fighting and to start cooperating." "I couldn't make sound come out of my mouth," he told me. "My heart rate was going so fast." Over the next three years, the panic attacks worsened. He tried relaxation tapes and exposure therapy, but nothing worked, and he felt himself spiraling downward.
It was only when he went back to the influences of his hippie youth, he says, that he started feeling better. He had dabbled in meditation, lived in a spiritual commune, and gotten involved in the so-called human potential movement that came out of the Esalen Institute in California. He began combining what he had learned from these experiences with the behavioral therapies he had studied and, with like-minded colleagues, launched the research that would lead to the development of ACT.
A 2012 study revealed that twelve sessions of ACT or CBT were about equally effective at reducing the symptoms of anxiety disorders. Another 2012 paper found that ACT was more effective for anxiety patients who also suffered from depression, while CBT was better for those without depression and those with "moderate levels" of anxiety sensitivity. Anxiety sensitivity is the belief that anxiety symptoms like a fast heartbeat and dizziness are dangerous.
—
Anxiety is a future-oriented state, so it's not surprising that learning to focus on the present would help to subdue it. Not only ACT but mindfulness practices of all kinds are increasingly being used to treat anxiety disorders. Mindfulness-based stress reduction (MBSR) focuses on meditation and yoga. Applied relaxation (AR) teaches people to identify early symptoms of anxiety and quell them using fast-acting relaxation techniques. Mindfulness-based cognitive therapy (MBCT) and emotion regulation therapy (ERT) combine meditation with practices from CBT.
These treatments are effective for many patients. In a meta-analysis of thirty-nine studies involving more than a thousand people in total, mindfulness-based therapies significantly reduced symptoms in patients with anxiety disorders.
Knowing what a magic bullet they can be for some people with anxiety disorders, I've tried meditation. _How hard can it be?_ I asked myself. It's incredibly popular. Kids learn it in school. You can download meditation apps on your smartphone. There's even a book that teaches you to meditate with your dog.
It is very unfashionable to say that you suck at meditation.
I suck at meditation.
I know that one can't really be awful at meditation. It is, devotees tell me, all about the practice. Still, I can't get into it. I've tried. But my mind jumps around so much, from worries to the ache in my hip to the dust on the carpet. I usually abandon the practice after a few days.
I decided to visit Jeffrey Rossman, a clinical psychologist and the "director of life management" at Canyon Ranch, a luxury spa and health resort in Lenox, Massachusetts. Rossman treats anxiety with mindfulness and a range of other alternative therapies including biofeedback and EMDR (eye movement desensitization and reprocessing), which entails having clients recall traumatic memories while moving their eyes rapidly back and forth. The treatment is supposed to ease the intensity of the memories and reduce anxiety.
Rossman is trim and youthful with a wide, toothy smile and voluminous salt-and-pepper hair. He tells me that anxiety (and its cousin, stress) is what brings most people to Canyon Ranch. "You would think people are coming to lose weight," he says, "but we have more people coming to deal with stress in their lives than any other reason. People working seventy, eighty hours a week, commuting two hours a day, sleeping four hours a night. That's an extreme version, but I see it."
After chatting for a while, Rossman does a biofeedback session with me. With biofeedback, you're hooked up to sensors that monitor functions like heart rate, skin temperature, and muscle tension, and you're then taught strategies to modify those functions. Rossman attaches a sensor to my ear, and a digital chart of my heart rate shows up on his computer screen. He has me close my eyes and guides me through a brief meditation. "Breathe peacefulness in," he says over and over.
After a few minutes, he says "good" and tells me to open my eyes. He points to a line on my chart that is sharp and jagged with abrupt peaks and deep valleys. That is my heart rate before the meditation, when it was jumping from one hundred beats a minute down to sixty and all points in between. The good news, according to him, is that my heart rate variability means that my heart is "very dynamic. You've got a healthy young heart," he says. "My guess is you have a lot of adrenaline in your system." Then he shows me a different part of my chart, where the jagged peaks become rolling hills. If this were a ski run, it would go from black diamond to easy green. This, he says, is my heart rate during meditation. "You need some of this," he says, pointing to the smooth hills. "People need recovery time." As soon as I open my eyes and begin asking questions again, the jagged peaks have returned. Rossman points to them and says, "If somebody stays in this state for a long period of time..." His voice trails off. I know that whatever he left unsaid isn't good.
Rossman advises people to "punctuate the day with many moments of mindfulness" so that over time they can rewire their nervous system. "There are some people who are on medication who don't need to be," he assures me. "If they practiced mindfulness, yoga, and meditation, they could train their brains."
Yoga and massage: They help tremendously when I'm relatively healthy. They keep me on an even keel and make relapses less likely. However, when anxiety has a tight hold on me, I turn to CBT and medication. These other things don't help at all. In fact, they seem to make things worse. I've had panic attacks while having my shoulders kneaded and while in Downward Dog. I've had to clamber off massage tables while mumbling apologies to a surprised therapist, slink off to the locker room, and down some Klonopin.
I've had mixed results with other "alternative" therapies as well. I'm still traumatized from my first acupuncture treatment, with a doctor who practiced "integrated medicine," which combines Western approaches with mindfulness, herbs, and acupuncture. (There's emerging research that acupuncture can ease anxiety before surgery and reduce the symptoms of GAD.) My amygdala feels like it has been on overdrive for months. Brad, the man I'm living with, is emotionally distant and critical, and the stress of the relationship is taking a toll. I'm having trouble sleeping and experiencing near-daily episodes of a racing heart. I've lost ten pounds.
That's why I'm lying on a table in a dark room with needles in my ankles, arms, and face.
"I've had great success helping people with anxiety with acupuncture," the doctor says as he works. I barely feel a pinch as the needles pierce my skin.
"Don't put too many needles in. I've never done this before, and I'm pretty nervous," I say.
"We'll go slowly. You'll be fine," he says. "You should start to feel very relaxed." Then he leaves the room.
I close my eyes and scan my body. I notice that my heart rate has slowed; the beats feel more regular and even. The tension in my muscles eases slightly. I sink lower into the table.
My mind, however, is whirring just as swiftly. The worries mount and collide, interrupting one another like rude dinner guests.
_Where is the doctor? Is he ever coming back? Am I stuck here? I'm alone. I'm alone and I'm trapped._
The mismatch between my torpid body and my frenetic mind makes me even more freaked. It is as if the telephone wire between body and mind has been severed. I feel completely out of control.
"Excuse me. Excuse me!" I call.
No answer.
"Excuse me! Excuse _me_!" I yell.
The doctor comes back into the room.
"Are you okay?" he asks.
"No. Please take the needles out. This isn't working for me," I say. As soon as they're out, I hurry off the table. Needless to say, I don't make another appointment.
It turns out that I'm not the only anxious person who loses it while trying to chill out. A phenomenon called relaxation-induced anxiety appears in the scientific literature at least as far back as the 1980s. In one admittedly tiny study of fourteen people with chronic anxiety, four felt increased tension during progressive relaxation, a technique where people tense and then relax various muscle groups in the body. Seven became more tense during a meditation exercise. Another small study of college students who said they felt anxious at least half the time incorporated similar relaxation techniques. Again the findings were counterintuitive: A handful of subjects felt increased anxiety during the relaxation exercises, and their heart rates jumped by ten to twelve beats per minute.
Researchers have various theories about relaxation-induced panic. The physical changes caused by relaxation, such as floating sensations and muscle twitches, can be jarring for anxious people. It can feel like a loss of control. Practices like meditation and muscle relaxation encourage people to focus on their bodies and breath, which can make anxious people overly aware of their revved-up thoughts and distressing bodily sensations. And calming the body and mind can, paradoxically, open up more mental space for worrying.
There's been a flurry of research activity recently around yoga in particular. A 2016 meta-analysis of seventeen studies found that yoga had a medium effect on anxiety symptoms. Stefan Hofmann, a professor of psychology at Boston University, is in the middle of a $4 million NIH-funded study of yoga as a treatment for GAD. The study compares the effectiveness of CBT to Kundalini yoga and a stress-education program. Kundalini, sometimes called "the yoga of awareness," focuses on breathing techniques and mindfulness. Hofmann says that the results from a pilot study are encouraging. "The effects we observe with Kundalini are actually quite strong," he tells me. The deep, slow breathing that is a hallmark of Kundalini can modify the level of CO2 in the blood and kick-start the parasympathetic nervous system, and mindfulness counteracts the excessive worrying that plagues those with GAD.
"GAD is a disorder where people are overly focused on the future, on what could go wrong. They are in this loop that is the essence of worrying—what could happen?" says Hofmann. "Mindfulness encourages individuals to stay in the here and now. The present-moment awareness at the heart of mindfulness works directly against these worrisome cognitive tendencies." Hofmann's study will measure changes in how focused the mind is on the current moment and on "respiratory sinus arrhythmia," or variation in the heart rate that occurs with breathing. Hofmann says certain heart rate patterns are linked to GAD; they are one of the few biomarkers scientists have associated with worry.
For me, attending yoga classes sounds definitely more palatable than slogging through sessions of CBT and daily exposure therapy homework. I've done yoga fairly regularly for more than fifteen years. I stumbled onto it when I was in my twenties, living in Manhattan's Chelsea neighborhood. I used to walk by the local Sivananda yoga studio and see relaxed-looking, clear-eyed patrons milling about after their classes, yoga mats tucked under their arms. I started going to beginner classes and immediately liked the low-key vibe and the emphasis on strength and stretching.
The habit took, and I soon began exploring other studios. I went to midnight yoga, where class was accompanied by live drumming and frantic flirting. I went to packed popular classes frequented by models and got used to being splashed with other people's sweat. I went to my first ashram in upstate New York, where I was awakened by a gong at five-thirty a.m. and shoveled manure as part of "karma yoga." I went to a conference filled with celebrity yogis: One teacher autographed students' mats after class. Taking a challenging yoga class grounds me in the present moment. If I don't concentrate on what I'm doing, I might literally fall over. There's a reason many teachers call yoga a "moving meditation."
There are only a handful of Kundalini studios in New York. Online reviews of one of them mentioned the dirty light-blue carpet and cultlike environment, with most participants wearing white. One reviewer even said she'd had a panic attack midclass! I passed on that one. Instead I went to Golden Bridge Yoga in Nolita one bright and balmy fall afternoon. Until then my yoga experience had been mostly secular, the only nod to the spiritual practice a few _oms_ chanted at the beginning and end of class and maybe a photo of a guru stashed in the corner. From that vantage point, Kundalini seems pretty eccentric. The name _Kundalini_ refers to a coiled-up energy shaped like a serpent that is housed in the base of the spine. The yoga practice is supposed to unwind this energy along the chakras, energy centers in the body.
When I peeked into the studio, I saw a woman sitting cross-legged on a platform flanked by several photos of serene-looking elderly men. She was wearing a white scarf over her long curly dark hair and had her eyes closed while chanting in Sanskrit. She opened her eyes and welcomed me, saying I might be the only student that day. Thankfully, five others soon arrived.
Many yoga classes include some kind of breath work, called _pranayama_ in Sanskrit. Kundalini takes this to the extreme. We did seven minutes of "breath of fire": You suck in your belly sharply while you exhale audibly through your nose. After only a couple of minutes, my hands and the skin around my mouth began tingling, and I felt light-headed. No way was I going to make it. I stopped, then started again. It went on and on. Everyone around me seemed fine. I, however, felt as if I were going to pass out. The sound of everyone exhaling puffs of air was accompanied by a recording of a woman singing "Guru Ram Dass" over and over at high volume. Very trippy. This is what a yoga rave would be like, I thought.
We followed that with some deep breathing, then countless leg lifts and stomach crunches. Chakras were mentioned several times. During one move, the teacher said we were going to "make our auras all shiny." Next we sat on our heels, raised our arms, clasped our hands behind our head, elbows pointing outward, and chanted _HUD_ (the acronym for the Department of Housing and Urban Development, I thought) over and over, thrusting our elbows back with each _HUD_. The music (still Guru Ram Dass) seemed to swell and fill the room. After a couple of minutes, my arms started aching; a few minutes more, and they were throbbing. The muscled, heavily tattooed guy on the mat in front of me lowered his arms and massaged them. I dropped mine, too. I felt a faint euphoria.
As I was leaving, thrust back into the reality of a downtown New York City afternoon (a guy was slurping soup on the front stoop next door), I realized that my mind had not wandered once during the class. Despite the ridiculously sore muscles I knew were in store, I felt genuinely peaceful.
—
I'm lying on a mat with a tennis ball under my butt trying to learn to relax. I'm in Lenox, just a few minutes away from Canyon Ranch, at the Kripalu Center for Yoga & Health for a weekend Yoga for the Nervous System workshop with Bo Forbes, a Boston-based clinical psychologist who has developed a yoga practice that she says can heal anxiety and depression.
"This is a release," says Forbes, as I and about ninety other anxious people roll around on our tennis balls, attempting to massage our piriformis, a muscle deep in the hip. The woman on the mat next to me and I look at each other and giggle.
Later we're all walking around the room trying to find a particular spot on the scalene muscles in our neck. "This is a direct release valve, a direct pathway to our nervous system," says Forbes, clad in snakeskin-print yoga pants and a red top adorned with a silver lotus flower. (Sunday's pants feature an image of a cow skull.) Three gold earrings dangle from each ear. Three gold necklaces encircle her neck. Her long, straight red hair is pulled back in a black scrunchie. She's wearing a headset microphone, a black foam ball a few inches from her mouth, like Lady Gaga.
I'm confused, and I must look it, because Forbes strides over to me, puts her fingers on my neck, and pushes. I gasp. It hurts!
The workshop takes place in what must have been the church of this former Jesuit seminary, with soaring ceilings, eight modern chandeliers, and a grand piano on a dais. Instead of a cross, there is a screen to project Forbes's PowerPoint presentation and a fabric scrim in soothing pink, orange, and gold. A metal statue of Shiva, standing on one leg, four arms outstretched, stands by it. We're in the middle of an early September heat wave (upper eighties and high humidity), and the room has no air-conditioning. An industrial fan and several white boxy models have been brought in. A few participants were savvy enough to bring paper fans and are waving them wanly.
Forbes is thin and punctuates her sentences with big smiles. She tells the story of a woman who recently attended the workshop and said that her husband had sent her there with an ultimatum: She must learn to be calm, or he would divorce her. Yikes! As she talks, I start to get her quirky Bo-isms. When she wants us to explain something, she asks us to "language it." She's going to "curate" some tools to help with our anxiety. She speaks a lot of the various "boxes" she says we put ourselves in.
Forbes began her career doing traditional talk therapy. After she became a yoga teacher, she started integrating yoga poses, fascia release, and breath work into her sessions. She soon realized, she says, that it was the yoga, not the talk, that was making her patients better. Now she believes that the body, not the mind, is the key to relieving anxiety and depression. "Breath and simple restorative poses are most effective in our clinic for anxiety and depression," she says. Telling our "stories" too often, she says, can exacerbate anxiety. She's critical of current mindfulness practices, too, saying they have become too removed from the body. No clinical trials have been published to assess Forbes's specific methods, though she makes several references during the weekend to neuroscience and to others' scientific studies.
In one exercise, she has us pair off and tell our partner a difficult story from our life. A fashion designer from Manhattan tells me of the engagement she regrets breaking off several years ago. I tell her about an awful fight my husband and I had in the presence of our baby daughter—one that made her cry. Forbes has us notice how our bodies feel after telling our stories. My stomach feels tight, my heart beats faster.
Then she has us use one of our new tools. I lie in Child's Pose, head resting on a block, breathing slowly through my nose. I do feel better. She teaches us about interoception, our sense of the physiological condition of our body. "Being with the changes in our bodies moment to moment is most calming to the nervous system," she says.
At Kripalu, breakfast in the main dining room is a silent meal. (When I forget that one morning, I get a stern lecture from one of the volunteer staff members.) We wear name tags and collect our food from metal vats, piling it onto too-small, scuffed black plastic trays. It is a cross between grade school and _Orange Is the New Black_ , except with delicious food and middle-aged women in lululemon yoga pants and tank tops. During dinner—when we're allowed to speak—I meet a neurologist and several therapists, all of whom struggle with anxiety. I debate the merits of Klonopin versus Xanax with a massage therapist from Nyack.
Forbes doesn't teach typical yoga here, the very physical vinyasa classes that are popular in most gyms and yoga studios, the ones that can lead to taut arms and tight abs. Her approach is subtle. In one exercise, she has us count our pulse for one minute. Mine is galloping along at ninety-six. Then she has us clasp our hands together and press them to our forehead, stimulating our vagus nerve, she says, while we breathe slowly. After a few minutes, she has us check our pulse again. Mine has slowed to a more respectable eighty-three.
After the weekend, when I feel twitchy or sleepless at one a.m., I find myself doing this, and it seems to have a calming effect. While the workshop didn't hand me any cures, I did learn a few useful tricks. And it felt freeing to be surrounded by so many of my fellow anxiety sufferers. Every so often, I wonder what became of the woman whose husband gave her the ultimatum. Did she learn enough to save her marriage?
—
CBT and ACT were developed decades before the latest advances in neuroimaging and genetics. New technologies are spawning treatments that aim to directly target the brain dysfunctions that underlie anxiety disorders. One such approach is called attention bias modification (ABM). It often uses a simple—actually quite boring—computer task to try to normalize the attention bias toward threat that many anxious people have.
One version of ABM is a variation on the dot probe task that scientists use to assess attention bias. In this version, however, subjects are trained to attend to _non_ threatening stimuli. In the task, participants might see two faces side by side—one with a neutral expression, the other with an angry or scared expression. There are also two buttons, one corresponding to each face. The faces vanish, and a probe (it could be one dot or two) appears in the same position as one of the faces. Participants must then push the button that corresponds to the placement of the probe. In ABM the probe always appears in the same spot as the nonthreatening face. Sometimes, instead of faces, ABM uses threatening words (such as _explosion_ or _humiliation_ ) and neutral ones.
Treatment varies, but participants often spend ten to fifteen minutes doing the task twice a week for a month, says Yair Bar-Haim, a professor of psychology and neuroscience at Tel Aviv University in Israel and a leading researcher on attention bias modification in anxiety disorders.
In a small study with GAD patients, half the patients no longer met _DSM_ criteria for their disorder after eight sessions of ABM. By comparison, only 13 percent of patients who had the control treatment no longer met criteria for GAD. A study with social phobia patients yielded similar results: Half the patients who got ABM treatment no longer met criteria for social phobia, compared with 14 percent of those who got the control treatment.
I spent a week playing with one ABM app called Personal Zen, a free download available at the Apple iTunes app store. On a field of green grass, two little blue heads pop up: One creature wears a cheerful expression while the other has an angry scowl. The heads appear for only a second, but a trail of waving grass lingers where the happy creature was. Players have to trace the trail of grass with a finger as quickly as possible. After using the app, I didn't feel noticeably more relaxed, but I did get quicker at the game. And I was better able to ignore the grumpy guy.
ABM doesn't seem to work as well as CBT or ACT, although some evidence shows that combining ABM and CBT has benefits. In a 2015 meta-analysis, ABM had a "medium effect" in reducing anxiety symptoms. ABM appears to be most beneficial for GAD, social anxiety disorder, and PTSD. The meta-analysis also found that the treatment didn't work well when participants used it online on their own. Instead, ABM seems to ease anxiety primarily when mental health professionals oversee the treatment.
"You don't know how the people on the internet were doing the treatment," Bar-Haim, one of the authors of the meta-analysis, told me. He speculates that they might have been "sitting on the bus and paying half of their attention to doing the task and half on 'where's the next bus stop and where do I get off?' "
Bar-Haim also notes that not all anxious people have attention bias to threat, so the treatment isn't likely to work for everyone. Researchers are also trying to figure out the appropriate "dose." Could a person overdose on ABM? And what would overdosing mean—becoming too blasé in the face of real danger? Bar-Haim reminds me that our threat-detection system is critical to survival.
There's also the issue of boredom. Bar-Haim's group is collaborating with others to try to jazz up the ABM tasks. "We have color versions, but it doesn't help with the boredom," he says. "It would be great if we could create a Candy Crush version."
Another relatively new technology is transcranial magnetic stimulation (TMS), which has been approved by the FDA as a treatment for migraines and for treatment-resistant major depression. Now researchers are exploring whether it could effectively treat anxiety disorders. TMS is noninvasive; a device that generates a magnetic field is placed above the scalp directly over the part of the brain researchers want to stimulate. While the science is preliminary, TMS has shown benefits for people with GAD, PTSD, and panic disorder. It can cause some transient side effects like headaches and light-headedness.
Probably the coolest, most sci-fi-sounding new treatment is fMRI neurofeedback. Patients can see the workings of their own brains and then—in real time—modify the dysfunctions. In neurofeedback's newest iterations, patients lie in a functional magnetic resonance imaging scanner. (Older methods use EEG, a test that records electrical activity in the brain, but EEG cannot target brain structures as precisely as fMRI.) They're told to conjure memories or look at pictures while their brains are being scanned, and a computer analyzes the activity of the relevant brain regions. Patients see real-time feedback from their brain activity, often presented in the form of a thermometer or colored bar. Depending on what their brain is doing, the subject is told to enhance or suppress that activity. Patients "need to train their brain like they train their muscles when they want to be fit," says Anna Zilverstand, a postdoctoral researcher at the Icahn School of Medicine at Mount Sinai in New York.
In a 2015 study, Zilverstand and colleagues used neurofeedback to treat women with a phobia of spiders. Patients in the scanner saw a series of spider images. The pictures got progressively scarier—from a tiny spider on a green leaf, to a larger, hairier one on a computer keyboard, to a giant iridescent spider crawling on a man's face. The subjects in the active treatment group were also shown an image of two thermometers: a blue one that reflected the activity of the dorsolateral prefrontal cortex (dlPFC), which helps to regulate emotions, and a red one that signified activity in the insula, which is implicated in sustained anxiety. They were told to enhance the activity of the dlPFC and dampen the activity of the insula by using cognitive strategies, such as describing the physical attributes of the spider or imagining it as small and powerless. The control group saw the same spider photos and were told to use the same reappraisal strategies but didn't get the neurofeedback. At the end of the treatment, the women who received the active training had lower anxiety scores. They also had lower insula activity during the treatment.
In another study, researchers at Yale tested two sessions of neurofeedback in people with high levels of contamination anxiety. (Now this is a study I wish I could have joined!) The scientists focused on activity in the orbitofrontal cortex, a part of the brain implicated in emotion regulation. Participants saw a series of images meant to induce contamination anxiety: pictures of cockroaches, feces, blood, and dirty needles. "It had to be something where you'd think, 'I could get sick from that, or somebody could get sick from that,' " says Michelle Hampson, an assistant professor of radiology and biomedical imaging at Yale University School of Medicine and a coauthor of the study. The subjects in the active arm of the study got neurofeedback in the form of a line graph. The control group saw so-called sham feedback—activity from another person's brain rather than their own.
Several days after the study ended, the subjects who received active neurofeedback had reduced contamination anxiety. They also showed increased connections in regions of the brain linked to the regulation of emotion and decreased connections in regions linked to the processing of emotions, such as the quick appraisal of whether something is threatening. One exciting message of this study is that the effects of neurofeedback persist, perhaps causing lasting changes in the brain.
The science on neurofeedback for psychiatric disorders is still in its early days. So far studies are very small, and researchers are still figuring out which brain areas to target and how many sessions will be needed. Results are modest, and it is unclear how long the effects of the treatment will last. Also, fMRI scans are expensive, costing hundreds of dollars. Because of this, some researchers believe that neurofeedback will most often be used as an adjunct to medication and talk therapy.
—
Therapy doesn't only happen with a therapist.
The New York Shyness and Social Anxiety Meetup Group has more than eight thousand registered members. Founded in 2006, the group arranges a dizzying array of activities—from hikes and museum outings to game nights. The events give socially anxious people a safe space in which to pursue friendships and practice social skills. Basically, it is a support group and exposure therapy wrapped together.
I have a tinge of social anxiety, mostly when I'm around someone in authority or someone who I perceive as "cooler" than me. I also consider myself an introvert in that I prefer to spend time with friends one on one instead of in large groups, and I can feel drained by big social gatherings. That said, I'm generally gregarious and comfortable meeting new people, and I don't fit the criteria for social anxiety disorder. Still, I want to understand it better. It is one of the most prevalent of the anxiety disorders and the only one that affects men and women in equal numbers. I'm also intrigued by the idea of anxious people taking charge of their own exposure treatment.
So on a frigid February evening, I join one of Meetup's social anxiety (SA) support groups. When I arrive at the Sony Atrium, an indoor public space in Manhattan filled with metal tables and chairs, about twenty-five people have gathered for the meeting. Nearby a few homeless people, weighed down with bags of belongings, doze.
Most of the SA group participants on this night are in their twenties and thirties, and all but five are men. The organizer, a slightly harried but friendly guy named Steven, divides us into small groups. We go around the table, introduce ourselves, and say a bit about what brought us to the meeting. One aspiring computer programmer says he's "anxious all the time" about making money and someday having to support his parents. A clean-cut young man who works in finance says he's looking to make friends. He tells a sad story about lunchtime during his middle school days. "I would stand in the lunch line, and when I got to the register, I'd pretend that I forgot my wallet in my locker," he says. "I'd go to my locker and then have to wait in line again. It killed time and hid the fact that I was always alone." A veteran of the group, a guy in his forties, says that during his travels around the city, he looks for groups of tourists who appear to be lost and asks if they need directions. "It is a way for me to practice approaching people," he says. "They're usually really grateful, so it makes me feel good."
I'm perplexed as to why one older man is here. He dominates the conversation and repeatedly pounds the table when making a point. "I used to be shy, but I overcame it," he says. I wonder if he's shouting to drown out his anxiety.
We pass around a pile of notecards and are instructed to write down a fear related to social anxiety. Then we share them. The guy who talks to lost tourists says he's afraid of conflict. The aspiring computer programmer says he's afraid of looking incompetent. I write that I'm afraid of saying something stupid.
I'm heartened to see these people bravely sharing their vulnerabilities. There's a real sense of warmth and camaraderie in the room. But I'm also struck by how much pain there is, and how much anxiety has robbed them of.
For months afterward, I receive emails from the SA group about its activities. Then an invitation lands in my inbox that I can't ignore. It comes with a disclaimer: "WARNING: This is high-level exposure, so if you're not ready to be thrown into the pool of sharks then please reconsider coming."
The SA group is doing karaoke.
I'd never visited a karaoke bar. I can carry a tune and like to sing; I was in an a cappella show choir in high school. But I loathed doing solos. The one time I did—during a performance at a senior center—I was so nervous that my voice came out in thin, breathy puffs. But if I am ever going to do karaoke, doing it with a bunch of other anxious people seems like the way to go.
A few days later I'm belting out Madonna's "Holiday" at Planet Rose, a karaoke joint in the East Village. I have a microphone in one hand and a bottle of Brooklyn Lager in the other. "It's time for the good times. Forget about the bad times," I sing, and do a little dance, stamping my boots on the leopard-patterned rug. Members of the SA group lounge on zebra-print couches. The room is mercifully dark, and strings of Christmas lights ring the walls. During the chorus, two guys jump in and sing backup. "Celebrate," we wail.
I feel ridiculous. And exhilarated.
When I'm finished, an SA member, a thin blond man who has spent most of the evening nursing a beer by himself, steps up and sings a Metallica song. Ultimately, about half the group ends up singing. Everyone is friendly and welcoming. "People here are really nonjudgmental," says one woman. While the support group I attended was made up of a lot of new members, this night is dominated by veterans. Several have been coming to SA Meetups for years and have made their closest friends in the group. Steven, the organizer, says the group has been life-changing for him.
I think about the guy I met at the Sony Atrium, the one who pretended to forget his wallet at lunch. In a year or two—after more support group meetings and other outings—maybe he'll be ready for a karaoke outing, too.
After I relapsed during my senior year of college, my therapist encouraged me to take Prozac.
Well, at first she encouraged. But after I kept saying no, she outright begged.
"I'll meet you on campus every day and watch you take it," she said.
No, I told her.
"I'll take it, too," she offered. (In retrospect this seems pretty strange, but maybe she was already taking it.)
Still no, though I let her give me the prescription.
My resistance was largely part of my illness. I still had a tough time eating. I avoided anything that looked or tasted slightly weird (and weird was a very broad category). I was gripped by fears of salmonella, _E. coli_ , listeria, or some other nameless bacterium. I worried about out-of-the-blue allergic reactions. When the fear was too strong, I didn't eat at all. More often the fear would surge after I'd swallowed a bite. Then I'd rush to a bathroom, scan for feet under the other stalls to ensure I was alone, and make myself throw up.
There was no way I was going to be okay with taking a psychotropic drug. Whatever grip on reality I had, whatever fragile equilibrium I had found, would never withstand the manipulation of my brain's neurotransmitters. I never even filled the prescription.
Prozac (or its generic equivalent, fluoxetine) is a selective serotonin reuptake inhibitor (SSRI), a class of drugs that also includes Paxil (paroxetine), Zoloft (sertraline), Celexa (citalopram), and Lexapro (escitalopram). Although the SSRIs are best known as antidepressants, if you complain to a doctor about excessive anxiety, you'll almost certainly be given a prescription for one of them. Serotonin is a neurotransmitter, a chemical that transmits signals between neurons in the brain and is believed to play an important role in mood and anxiety. SSRIs block the reabsorption of serotonin. That leaves more of the chemical hanging around the synapses, the spaces between neurons. That action is thought to account for SSRIs' mood-boosting and anxiety-reducing effects.
Serotonin-norepinephrine reuptake inhibitors (SNRIs) like Effexor (venlafaxine) are also used in anxiety disorders. These drugs act on serotonin and on norepinephrine, a neurotransmitter that is involved in the stress response.
Doctors call SSRIs a "first line" treatment, and reams of studies have shown them to be at least modestly effective in treating the various anxiety disorders. But there's one wrinkle: Placebos have been shown to work almost as well. In a 1998 study of panic disorder patients who took either sertraline (Zoloft) or a placebo for ten weeks, those on the drug saw their mean number of panic attacks per week drop by 88 percent. Those taking the placebo had a 53 percent fall in their number of attacks. In a 2004 study looking at escitalopram (Lexapro) for GAD, patients on the drug saw their scores on an anxiety symptom scale drop by about 29 percent after eight weeks. The scores of those on placebo fell by about 19 percent.
Even the relatively lackluster effects of antidepressants are likely overstated. Research on the efficacy of medications is often paid for by the pharmaceutical companies that stand to profit from their drugs' sales. Studies that reveal that a drug _isn't_ beneficial—so-called negative clinical trials—are frequently not published. Also, in some positive trials, research results are written up in a way that inflates a treatment's benefits. This reporting bias is evident in write-ups of studies on both depression and anxiety disorders.
If placebos work almost as well as the drugs, and if even those modest effects are embellished, what's the point of taking an SSRI? The real benefit, it turns out, may be not in treating acute illness but in preventing relapses, says Robert Temple, deputy director for clinical science at the Center for Drug Evaluation and Research at the U.S. Food and Drug Administration (FDA). He is a coauthor of a review paper that found that, for people with a history of major depression, continuing on antidepressants cut the risk of relapse in half. Temple says the FDA has unpublished data showing similar results for GAD.
In college, I eventually recovered without medication. CBT, and maybe just the passage of time, got me to some sort of stability. After graduation, I moved to Washington, D.C., and spent a little more than two years working in politics, writing speeches and press releases for a U.S. senator. Then I moved to New York City to take a job as an administrative assistant at the _Wall Street Journal_ —answering phones, fetching faxes, and in my spare time, writing brief articles, focused on the dream of becoming a full-fledged reporter there. I worked hard, had eccentric roommates, traveled, dated both appropriate and inappropriate men, and spent lots of time drinking red wine and dancing in dark velvet-walled bars. I was doing the things you're supposed to do in your twenties.
My anxiety didn't disappear. I still had frequent chest pain and episodic fears of heart attacks. I occasionally visited a cardiologist, a family friend of my college boyfriend. He would hook me up to an EKG and tell me I was fine. I'd be reassured until a few months later, when pain and doubt would land me back in his office. I fretted more than most about dating disasters and setbacks at work. But I remember those first six years after graduation as a period of relative health and equanimity.
By the summer of 1998, I had landed a junior reporter position at the _Journal_ , writing, ironically, about the pharmaceutical industry. The big story then was the launch of Viagra, the little blue pill to treat impotence. It became a huge seller for Pfizer, its manufacturer, and a controversial cultural story as well. Why were insurance companies paying for an anti-impotence pill when many didn't pay for birth control? Would it unravel marriages? I spent my days talking to Wall Street analysts, urologists, and formerly impotent men, asking them about their new and improved erections. For a story on the burgeoning recreational Viagra market, I visited clubs with names like Hell and the Tunnel and bought rounds of cosmopolitans for groups of men. I was on the lookout for recreational users and for stories of the drug dealers I had heard were peddling Viagra alongside cocaine and ecstasy, the former used to counteract the erection-deflating effects of the latter.
I loved asking people questions and hearing their stories. I did an actual jig each time I saw my name in print followed by the words "Staff Reporter of the _Wall Street Journal_."
I had a new boyfriend, too. Alan was also a journalist, tall, lanky, and adorable with a lack of style and a social awkwardness that was boldly—and refreshingly—out of step with most men I had met in New York. He was a terrific writer and had a background that I greatly admired, having worked as a freelance reporter in Africa covering the aftermath of the genocide in Rwanda. We were in that giddy stage of new love, just five or so months in, and deep in the emotional striptease of joyful declarations and new confidences. And then I began to unravel.
—
It is a brilliant warm Saturday in June. I am walking down Seventh Avenue in Greenwich Village, tired and a little exhilarated, heading to a deli to grab a snack. I have just left the gym where I have taken a class in capoeira, a Brazilian martial art, an intense ninety minutes of kicks and spins, and my legs are already starting to ache. I am looking straight ahead at the pavement and pedestrians in front of me. In my peripheral vision I see a whizzing blur of yellow as the taxis head down Seventh Avenue, tender green splotches of early summer leaves on the trees above, and the architectural lines of nearby buildings.
Suddenly a chunk of the landscape disappears. A black smudge with jagged edges appears in my field of vision, blocking out the taxis, leaves, and buildings. I stop in the middle of the sidewalk and rub my eyes. Close them tightly and open them. The smudge is still there, blocking the upper-right quadrant of my field of vision.
Did I get something in my eye? I put a palm over one eye and look up. I change eyes. The splotch is in both eyes.
I know what that means. Something is wrong with my brain. I am having a stroke.
_I am having a stroke. And I have to get to a hospital._
St. Vincent's, thankfully, is only a few blocks away. But I can't get there on my own. I may be seconds away from losing the ability to walk. I'll crumble onto the sidewalk. Baffled tourists will dodge the heap of me. A twenty-seven-year-old woman in yoga pants and a ponytail collapses in the middle of the day? She must be drunk.
In a panic, I scan the sidewalk around me and grab the nearest forearm. It is smooth and sinewy and pale. It belongs to a tall, freckled blond guy about my age. He looks surprised but doesn't blanch or shake me off.
My explanation comes out in a rush: "I think I'm having a stroke. I can't see. There's a hospital two blocks away. Can you please walk me there?"
He says okay.
I grip his forearm the entire way there. He deposits me in St. Vincent's ER and disappears. I hope I remembered to say thank you. (I'll say it now: thank you.)
I go up to a man doing intake. "A huge chunk of my vision just vanished. I can't see," I say.
He tells me to sit down in the waiting room. I sit for five minutes, closing and opening my eyes, trying to will the black smudge away.
I rush back to the man. "I need to see someone now. I think I'm having a stroke."
Either my urgency or the word _stroke_ sets things in motion. I'm taken inside and put into a bed: White sheets hang from a metal rod to offer some semblance of privacy. A nurse hooks me up to a heart monitor.
Then all hell breaks loose. The nurse starts pulling my shirt apart. She yells for assistance. Someone else rushes in.
"What is it? What's happening?" I plead.
"You're having a hypertensive episode," the nurse says.
The next few minutes are a blur of hands and movement. _This is it. I really am dying._
Then, abruptly, the activity stops. The nurse begins pulling the cardiac leads off my body. Her helper disappears behind the white sheet.
"What's going on?" I say.
"Your blood pressure is normal. When we measured it again, it was fine," she says.
"So I'm _not_ having a hypertensive episode?"
"No."
The initial high reading, the nurse says, must have been an error. It is then that I realize that I can see perfectly again. The black smudge is gone.
I'm discharged from the ER a little while later, with no explanation for the sudden blind spot or its speedy resolution.
Later that day, when I talk to my regular doctor, he says I must have had an ocular migraine, a type of headache where funky visual changes are the primary symptom. "You should have called me instead of going to the ER," he scolds. "I would have told you you were fine." I feel chastised and a bit sheepish but also a little angry. It seems like losing your vision should be an acceptable reason to go to the ER, even by the standards of a nonanxious person.
—
The migraine episode triggers a swift slide into constant worry about my health—and everything else. What if something really is wrong with my brain? My mind feels sluggish. I think I can feel the neurons stalling. I handwring about my memory and start writing down conversations for fear I'll forget. I feel cut off from my boyfriend and my friends. My body may be at a museum or at a party, but my mind is elsewhere, caught in a loop of dread.
I worry that my worry will scare away those I love.
Unlike in college, I can't retreat to my parents' sofa or drop a few classes until I feel better. I will lose my job. I will lose my boyfriend. I will have to leave New York.
_No. I will not hit the pause button on my life._
I call my therapist, Dr. D, and tell her what is going on. I have been seeing her for about a year now. She's a psychologist who practices psychodynamic therapy, which aims to help people understand how their past history and relationships influence their current behavior. I started therapy with the goal of figuring out why I had the breakdowns in college and why I'm so anxious. Now she gives me the name and number of a psychiatrist. It's time for medication.
The psychiatrist, Dr. I, has frizzy, haphazard gray hair and wears colorful ankle-dusting skirts and macramé necklaces. While she speaks with authority about psychotropic drugs, she looks as if she should run a feminist bookstore in Seattle. I'm relieved when she prescribes Zoloft. After years of fear and trepidation, the little pill doesn't look quite so dangerous anymore. Besides, I feel like I have no choice but to take it. The only other option I see is months of infirmity.
So I start taking Zoloft. My head doesn't explode. I don't instantly feel different, but I know better than to hope for that. SSRIs can take anywhere from four to six weeks to work. When they work at all, that is.
I feel the side effects, however, almost immediately.
It is a few days after I've taken my first pill. I'm sitting in the Bubble Lounge, a silly, expensive champagne bar in Tribeca, with friends from work. We're surrounded by finance types, groups of clean-cut men in dark suits and a handful of serious-looking women. Our group of journalists is a bit scruffy in comparison. I'm chatting with friends, a champagne flute in my hand, when I feel a chill run up and down my forearms. I rub my arms with my hands and pull on a sweater, but the chill doesn't stop. It's not a chill exactly. No, it feels like something is moving up and down my arms. Soon it reaches farther, dancing up the back of my neck and across my scalp.
My skin is crawling.
The medical term for this is _formication_. It is a type of paresthesia, a sensation on the skin that can also include tingling, numbness, and itching. In clinical trials by Pfizer, Zoloft's manufacturer, about 2 percent of people who took the drug experienced it. (Oddly, 1 percent of those taking a placebo did, too.)
The next day I call my psychiatrist and tell her what I'm feeling. According to her, it's my anxiety and not the drug that is making my skin crawl. She recommends that I double the dose of Zoloft. I do what I'm told and pop two tablets.
Within a few hours, my entire body erupts in waves of sensation—tingling, crawling, and something almost electric. The tiny hairs on my body feel charged, as though they're standing on end. My skin seems to move. It is as if an ant farm has been let loose on my body. My anxiety has never felt like this. Those are the last Zoloft pills I'll ever take.
I try Paxil next. Even though the SSRIs are all similar, individual patients often react differently to each drug. With Paxil, my skin doesn't crawl. I don't, in fact, feel much of anything. But slowly, over several weeks, some space seems to open up in my brain. Instead of the worry occupying, say, 70 percent of my mind, it now seems to take up 40 percent. And the volume of my anxiety is turned down a bit, too. I'm better able to set it aside. I'll come home from dinner with friends and realize that I was able to concentrate on a conversation for several hours, that I was truly present.
If I miss a pill, however, I am light-headed and dizzy. I get a woozy feeling even if I take my dose a few hours later than I did the day before. It is a daily reminder that the drug is playing with my brain chemistry. Though I have ample evidence that this is a good thing, it makes me uneasy. Other side effects sneak up on me, taking several months to make themselves known. My sex drive plummets. Having an orgasm requires Herculean effort. I become ravenously hungry. It is a needy, demanding hunger, impossible to ignore. Sometimes I wake up in the middle of the night, starving, and clandestinely scarf down a bowl of cereal. My weight inches upward. (Both "increased appetite" and "decreased appetite" are among the long list of Paxil's potential side effects.)
Still, I'm lucky that I've found a medication that works for me. At least a third of people with anxiety disorders don't get much relief from the available drugs. Even when drugs do help, there's the lag time before they alleviate symptoms, and patients often have to cycle through multiple drugs before they find the right one.
This may change soon. A flurry of research is looking at whether brain scans or other tests can predict which patients will respond to a particular treatment. The hope is to uncover biomarkers, such as patterns of activity in the brain or levels of hormones in the blood, that can direct patients to the medication or therapy that will help the most. However, the research is still in its early stages, and it could be years before such tests are available. But if it shakes out, biomarkers could save patients time, money, and a lot of misery.
Scientists have homed in on a number of potential biomarkers for a range of disorders, including PTSD, social anxiety disorder, and OCD. Many studies have found distinct patterns of brain activity that can predict how well someone will do with a specific treatment. In one study, fourteen people with GAD underwent fMRI scans while looking at pictures. Some pictures were revolting, showing mutilated bodies or violent scenes; others were benign. Subjects were warned as to whether they were about to see a disturbing or benign picture. The participants then took the SNRI Effexor for eight weeks. The people who had higher levels of activity in the anterior cingulate cortex when they were anticipating seeing either kind of picture had a better response to Effexor. The anterior cingulate cortex is thought to be involved in detecting and resolving emotional conflict.
In another study, researchers in Oxford, England, gave MRI scans to fourteen patients with panic disorder while they viewed anxiety-provoking pictures of accidents, funerals, and hospitals. The subjects then had four sessions of CBT. The study found that those who had increased gray matter volume in the hippocampus and increased activity in the insula and dorsolateral prefrontal cortex while viewing the disturbing pictures before their treatment had greater reductions in their symptoms.
I was on Paxil for about two years. Since then I've cycled on and off SSRIs. I had another year's stint on Paxil. A few years on Prozac. Most recently I've taken a daily dose of five milligrams of Lexapro, one of the newer SSRIs. They've all worked similarly well for me, but I've switched in a search for the fewest side effects. Paxil, for me, was the worst. Prozac was a huge improvement. Lexapro has gone down the easiest, although I still feel dizzy when I miss a dose. Hopping off and on medication has been fairly easy for me. I know I'm lucky in that regard. The internet is full of horror stories of immediate relapses and awful withdrawal symptoms.
I've been on SSRIs for eight of the past eighteen years. I've usually gone on them during crises, when the anxiety is unrelenting and prevents me from experiencing much else. But they have never cured my out-of-whack anxiety. Even on medication, I'll get the occasional panic attack. And when things are very stressful, drugs seem to be no match for my amped-up amygdala. What they do, however, is give me space and opportunity. They are like an air pocket for a drowning woman. They aren't the solution, but they keep me conscious long enough to figure out my next move.
—
I keep my childproof bottle of Lexapro in a silver bowl on top of my dresser, but there's another orange-hued bottle I keep much closer. This one I have with me always, tucked into my handbag. It is my security blanket, my good luck charm, my talisman.
The bottle is slapped with three warning stickers.
> May Cause Drowsiness and Dizziness. Alcohol May Intensity This Effect. Use Care When Operating A Car Or Dangerous Machines.
>
> If You Are Pregnant Or Considering Becoming Pregnant You Should Discuss The Use of This Medicine With Your Doctor Or Pharmacist.
And this one, in bright, traffic-cone orange:
> CONTROLLED SUBSTANCE. DANGEROUS UNLESS USED AS DIRECTED. CAUTION: Federal law prohibits the transfer of this drug to any person other than the patient for whom it was prescribed.
The bottle is filled with pale orange pills with the letter K cut out of the center. It's Klonopin. And it's fantastic.
Klonopin can melt my anxiety and many of its annoying accoutrements—racing heart, shallow breathing, twisted thoughts—in about thirty minutes. It can even derail a full-blown panic attack if I take enough. When I wake at four a.m. with a churning litany of what-ifs and must-dos, half of a .5 milligram tablet eases me back to blank sleep. It is literally a chill pill.
Klonopin (or the generic clonazepam) is a benzodiazepine, one of the class of drugs that also includes Valium and Xanax. Benzos enhance the activity of the central nervous system's main inhibitory neurotransmitter, GABA (gamma-aminobutyric acid). Its primary function is to reduce the activity of neurons. Benzos are used not only for anxiety and panic attacks but also to treat seizure disorders and insomnia. Doctors wrote more than ninety-three million prescriptions for benzodiazepines in 2015, according to QuintilesIMS, which tracks pharmaceutical sales. That is up 16 percent since 2006.
Weirdly, I don't remember taking my first Klonopin. I had tried other benzos a handful of times—a Xanax that knocked me out after a nearly sleepless week, a Valium before an MRI. But my life "before K" and "after K" is starkly delineated. Klonopin is a safety net, a panic button. The difference between having it in my purse and not is like the difference between rock climbing with a harness and ropes and free climbing, an insane practice in which climbers use no safety equipment whatsoever.
My dose of Klonopin has always been "p.r.n." or "as needed." Over the years, "as needed" has meant different things. Some instances are clear-cut, like the time I had a terrifying panic attack on an airplane. (Hands down, a metal tube hurtling through space thirty thousand feet above the ground is the absolute worst place to have a panic attack. No escape. Dozens of onlookers.) I fled to the galley near the back of the plane and clutched the arm of a surprised flight attendant. She gave me a cup of water, and we sat in side-by-side jump seats while I tried, pitifully, to breathe deeply and ride the panic out. I gulped down two full Ks, four times my usual dose, and within an hour I was sprawled across three seats and slept until touchdown.
I've used it as a prophylaxis. I'll pop half of a .5 milligram tablet before I go into a high-anxiety situation: a big meeting or interview at work, or a daunting party, or when getting behind the wheel of a car. (A twenty-year resident of New York City, I rarely drive. I'm nearly assured of a panic attack when I have to take a highway.) Many CBT therapists would _tsk tsk_ at this approach, saying that I'm not allowing myself to master my anxiety. But hell, sometimes I just need to get through the day—or the next hour.
I've used K to play medical detective. When I'm plagued by weird physical symptoms, I'll take a benzo to see if the feeling—an odd pain or numb limb—goes away. If it does, I'll chalk it up to anxiety.
During times of sky-high anxiety, I've taken K daily for weeks. Sometimes this means I'm headed for a relapse, and it's a sign that I need to return to therapy and go back on an SSRI. Other times there's a clear, time-limited cause. For a few weeks two winters ago, my husband and I thought our daughter might have a brain tumor. She had been complaining of headaches, smacking her hand against her forehead, and whimpering pitifully. A round of antibiotics for a potential sinus infection didn't help. We were sent to a neurologist who saw something worrying in our daughter's exam. (There aren't many things sadder than the waiting room of a pediatric neurologist's office.) The doctor scheduled our daughter for an MRI. During those two weeks of awful uncertainty—until the neurologist called and said the only thing abnormal on the MRI was, in fact, a tenacious sinus infection—I took Klonopin twice, sometimes three times, a day.
Still, it was no match for my terror. I had vivid images of a grim future. I worried constantly and formulated elaborate plans. How I'd take a leave from my job to care for my ailing child. How I'd cope with the divorce that would be the result of my husband's and my eventual grief. I took videos of my daughter chatting, so I could remember her healthy. I had trouble sleeping. How much worse would it have been if my brain weren't being bathed in benzos?
At other times I've used K more casually, even under questionable circumstances. I'll sometimes take it when I have trouble sleeping and have a big day of work ahead. I'll (very rarely) use it as a chaser after a glass or two of red wine, though not for fun. After I turned forty, I found that if I drank a glass of wine, my heart rate would rise, and that night my sleep would be unsettled. A teensy bit of Klonopin counteracts that.
Klonopin can cause a daunting list of side effects: depression, coordination problems, dizziness, and my favorite, "intellectual ability reduced," according to the manufacturer, Genentech. But what makes some doctors skittish about prescribing benzos is the potential for addiction and abuse. Combined with enough alcohol and other drugs, they can be lethal. People can just stop breathing. Benzos were implicated in the deaths of the actor Heath Ledger, the singer Whitney Houston, and the model Anna Nicole Smith.
Benzos can also be hell to withdraw from, especially for people who have taken them regularly for years. Entire workbook programs have been designed to ease benzo withdrawal, with names like "Stopping Anxiety Medication: Panic Control Therapy for Benzodiazepine Discontinuation." The forums on BenzoBuddies.org, one of several online withdrawal support groups, contain desperate descriptions of horror show symptoms: nausea, a burning tongue, ringing ears, crying jags, depression. People's sign-offs are often long litanies of their benzo use and their slow, agonizing attempts to get off them. Some people posting have been on the drugs for more than twenty-five years. There are chronicles of lost jobs and lost relationships because of addiction.
"Absolute hell on Earth" is the title of one recent post from a BenzoBuddies member who had stopped Xanax cold turkey after taking it daily for three years. She says the withdrawal left her with no energy, no appetite, headaches, and a racing heart. She lost fifteen pounds in two weeks. The anxiety has come roaring back, too. "Talk about wanting and feeling DEATH....I could barely take 10 steps without feeling like my heart was going to beat out of my chest," she writes. "I had depersonalization, insomnia, constant tremors, pain in my limbs, tingling in my limbs, felt detached from my body, I couldn't cry or laugh, I couldn't form complete sentences. I was truly a walking zombie."
The number of American adults who filled prescriptions for benzos jumped 67 percent between 1996 and 2013, up from 8.1 million to 13.5 million people. During that same period, the quantity of medication doled out per person more than doubled and overdose deaths involving benzos quadrupled. The most lethal combination is benzos and opioids: About three-quarters of the deaths involving benzos also involved drugs like OxyContin and Percocet.
I've never felt addicted to Klonopin. I often go months without taking it. And most people on benzos for anxiety disorders don't abuse them or develop a tolerance.
However, lately I've become much more conflicted about my Klonopin use. In the last few years, several studies have found an alarming link between benzos and Alzheimer's disease and dementia. One study published in the journal _BMJ_ in 2014 found that older people who had taken benzos daily for more than three months were 32 percent more likely to develop Alzheimer's disease. Not only that, the greater the exposure, the greater the risk. Those who took daily doses for more than six months had an 84 percent greater risk. The risk was greater for benzos with a longer half-life, like Klonopin, than for those with a shorter one, like Xanax and Ativan.
I'm reassured by a more recent study, published in the same journal in 2016, that does not support the hypothesis that benzo use causes dementia. Researchers followed more than 3,400 people older than sixty-five. Over approximately seven years, about 800 subjects developed dementia. People who had used benzos lightly (defined as about 120 or fewer daily doses) during a ten-year period before the study were slightly more likely to be diagnosed with dementia in the follow-up period. Surprisingly, those who had the heaviest use during the ten-year period were no more likely to develop dementia than those who didn't take the drugs at all. The researchers conjecture that the slight risk associated with light use may simply reflect the fact that people with early symptoms of dementia, which include anxiety and insomnia, are more likely to be prescribed benzos. But these results, at least, suggest that benzos don't lead to dementia.
So the science is mixed. Which is why, lately, I pause before opening my bottle of Klonopin and do a silent cost-benefit analysis. Is my anxiety that bad? Is easing my mind now worth ruining it later on? Sometimes—though not as often as I wish I did—I put the bottle away.
—
A range of pharmacological treatments for anxiety was available in the nineteenth century, particularly bromides and chloral hydrate, a popular sedative introduced in 1869. Lily Bart, the tragic heroine of Edith Wharton's _The House of Mirth_ , dies from an overdose of chloral hydrate. Just before nodding off for her final sleep, Lily describes the sedative's initial effects, "the gradual sensation of the inner throb, the soft approach of passiveness, as though an invisible hand made magic passes over her in the darkness."
In 1903, the first barbiturate, barbital, was launched in the United States under the brand name Veronal. Barbiturates were safer than the earlier bromides and were primarily prescribed for insomnia and anxiety. In the first half of the twentieth century, sales soared, and dozens of variations flooded the market. The pills' many colors earned them nicknames like blue angels, pink ladies, and yellow jackets. On the street, they were dubbed goofballs, explains medical historian Andrea Tone.
Barbiturates were dangerous and addictive. It was easy to overdose: The same amount of medication that was sleep-inducing and safe for one person could kill another. And you could build up a tolerance; over time people often needed more of the drug to get the same effect. It was tough to get off barbiturates, too. Stopping them suddenly could lead to a host of awful side effects like rapid pulse, high blood pressure, sweating, and convulsions. Marilyn Monroe was found dead in her Brentwood, California, home with an empty bottle of barbiturates by her side. Judy Garland also died of an overdose of barbiturates.
It was not until 1955 that a safer—and revolutionary—anti-anxiety drug came to market: Miltown.
Miltown was developed by Frank Berger, a scientist from Czechoslovakia. In 1938, he and his new wife fled the Nazis and settled in England, where he began working on methods to boost the production of penicillin, which was desperately needed on the battlefields of World War II. Berger was testing compounds that might serve as a preservative for penicillin and noted something striking about mephenesin, a substance that was typically used, in modified form, as a disinfectant. When he injected mice with mephenesin, their muscles went limp, but the animals remained conscious and alert. Unlike barbiturates, mephenesin didn't induce a zoned-out state.
In 1949, Berger took a job at Wallace Laboratories, a division of Carter Products, in New Jersey. Carter's cash cow was Carter's Little Liver Pills, a laxative. (It also made Arid deodorant and Nair, the hair-dissolving cream.) But Carter wanted to push forcefully into the prescription drug business. Berger's first project at Wallace was to create a version of mephenesin that was long-lasting and could be taken in pill form. He and his colleagues synthesized five hundred compounds and tested a dozen on animals. One of them, meprobamate, made the muscles of mice go limp and made rhesus and Java monkeys docile. Normally the monkeys were vicious and violent, so much so that "you've got to wear thick gloves and a face guard when you handle them," Berger said. But after a shot of meprobamate, they became "very nice monkeys—friendly and alert."
After a few studies in humans found that meprobamate was safe, eased anxiety, and promoted sleep, Berger submitted an application to the FDA to authorize its sale. The new drug, now named Miltown after a sleepy little town not far from Wallace's headquarters, came to market in May 1955. The pharmaceutical behemoth Wyeth bought a license to manufacture meprobamate, too, and a few months later started selling the drug under the name Equanil. It was the first of what are known as the minor tranquilizers. By 1957, a full third of all prescriptions filled in the United States were tranquilizers.
Miltown became a Hollywood sensation. Lucille Ball was a fan, and so was Tennessee Williams. Milton Berle was so enamored of it that he sometimes called himself Uncle Miltown. "Movie stars and television personalities gushed about Miltown," writes Tone, "gossip reporters wrote treatises on it, and at celebrity galas, illicit Miltown was passed around as casually as canapés." People drank Miltinis, a martini garnished with a Miltown pill instead of an olive. The drug was invoked in ads for everything from ice cream to vacations. It was nicknamed "Executive Excedrin" for its popularity among overworked businessmen. Athletes used it to calm precompetition jitters. The team doctors for the Philadelphia Phillies and the Cincinnati Redlegs (as the Reds were known for a time in the 1950s) prescribed it.
Carter and Wyeth aggressively courted doctors, too. One ad published in the _American Journal of Psychiatry_ touted Miltown for a broad swath of people, including "the tense, nervous patient," "the agitated, senile patient," "the alcoholic," and "the problem child." Carter hired the surrealist painter Salvador Dalí to create an installation for the 1958 annual meeting of the American Medical Association depicting the experience of being on Miltown. (Dalí's wife took the drug.) The work, titled _Crisalida,_ was a silk-walled tunnel weighing two and a half tons and adorned with murals representing the journey from anxiety (depicted as a twisted hollow figure) to tranquillity (a diaphanously dressed woman with a crown of flowers).
With this success, pharmaceutical companies scrambled to find new anxiety-lifting blockbusters. At Hoffmann–La Roche, Leo Sternbach was a Jewish scientist from Eastern Europe who had left Switzerland in 1941 to escape the growing Nazi threat. Instead of creating a me-too drug like Miltown and its ilk, Sternbach wanted to develop an entirely new tranquilizer. He started tinkering with substances called benzheptoxdiazines, which, years earlier, he had explored while searching for new dyes, creating dozens of derivatives. But when he tested them, none worked as tranquilizers. Disappointed, Hoffmann–La Roche tasked Sternbach with researching antibiotics instead. That could have been the end of the story, but a year later a colleague found a sample that Sternbach had failed to test, numbered Ro 5-0690.
Ro 5-0690 was tested in mice and cats. Mice given the drug hung limply when researchers held them by the ear. When medicated mice were put at the bottom of a tilted screen, they slid down. (Normally mice can easily run to the top.) Cats held by the nape of the neck were relaxed and placid. The animals weren't zonked, however, but remained aware and were able to walk normally. Sternbach even tested it on himself. About an hour and a half after taking fifty milligrams (a bit higher than a therapeutic dose today), Sternbach felt, as he wrote in his journal, "slightly soft in the knees." Later that day he felt sleepy, but by dinnertime he was back to normal. Ro 5-0690 seemed to be the holy grail of tranquilizers—less deadly, more powerful, and not as sedating as competitors. The drug was named Librium (for equilibrium). Within three months of its introduction in 1960, it became the bestselling tranquilizer on the market.
—
While tranquilizers and benzos generated most of the excitement, the drug treatment of anxiety disorders took another, quieter leap forward in the 1960s, too.
In 1961, Donald Klein was working at Hillside Hospital in Queens, New York, which was then a two-hundred-bed long-term psychiatric facility. He worked with Max Fink, who was an expert in shock therapy. Imipramine, the first of the tricyclic antidepressants, had just recently become available for research, and Fink was eager to experiment with it. Hillside began giving imipramine to some of the depressed patients. "You give it to patients, and they slept a little better, they started eating, and three or four weeks into the treatment, some would come into the office and say, 'Doc, the veil is lifted. I'm okay,' " Klein recalls. Some of the depressed patients were also anxious. Klein noticed that imipramine seemed to be easing the anxiety, too. So Hillside started an experiment, giving imipramine to patients with anxiety, including those who were not depressed.
Klein recalls one pivotal case. The man had been staying at the hospital nearly a year, but he was still terrified of being alone. He wouldn't walk anywhere without a chaperone, and about three or four times a day he ran to the nurses' station in a panic, convinced that he was dying. Klein offered the man the new drug.
Each week Klein increased the patient's dose. For a while, things were status quo. The patient kept having several panic attacks each day. During their appointments, the man would tell Klein what a "lousy" doctor he was. After a few weeks, though, one of the nurses remarked that the patient seemed better. He had made no dramatic appearances at the nurses' station that week. Not one. The patient was as shocked as Klein.
The man wasn't totally cured. He was still afraid to be alone, and his amorphous, free-floating anxiety remained. But the imipramine did block his panic attacks.
Klein and Fink published a paper on their work in 1962 in the _American Journal of Psychiatry_. "It became apparent that anxiety was at least two different things," Klein said. "You had these terrible crises of anxiety which drove him to the nurse's station and this anticipatory anxiety that everything is lousy and is going to get worse. And the drug had dissected those things out."
Today Klein lives in a grand building across the street from the Metropolitan Museum of Art in Manhattan. He greets me at the door of his apartment, accompanied by his small, energetic dog, Koko. He has a shock of white hair and is wearing a blue-and-white-checked dress shirt and navy corduroys. His stocking feet are covered in Koko's hair. At eighty-eight, he is still working. Though he retired from the psychiatry department at Columbia in 2003, he still sees private patients one day a week, publishes papers, and consults on grant proposals.
Klein's imipramine discovery revolutionized psychiatric thinking. It showed that anxiety wasn't a single, amorphous disorder and that patients' responses to medication could help science define the boundaries of illnesses. Of his breakthrough, Klein says, "Pasteur had it right. He says for discovery, it is chance and a prepared mind."
Klein's success with imipramine prompted Robert Spitzer, chairman of the task force working on the _DSM_ -III, to invite him to join the group.
Today the _DSM_ is arguably the most powerful book in the field of psychiatry. Insurance companies use it to determine coverage. The government uses it to allocate benefits. Scientists use it to plan their research studies. Lawyers use it to defend their clients.
But it was not always so influential. The first edition of the _DSM_ was published in 1952, primarily so that doctors in state mental hospitals could more easily compile statistics about their patients. It was firmly under the sway of Freudian ideas. In that edition, anxiety was the star. It was thought to fuel all of the so-called psychoneurotic disorders, comprising what we now consider the various anxiety disorders, depression, and somatoform disorders. "The chief characteristic of these disorders is 'anxiety' which may be directly felt and expressed or which may be unconsciously and automatically controlled by the utilization of various psychological defense mechanisms (depression, conversion, displacement, etc.)," it reads. Disorders included anxiety reaction, obsessive-compulsive reaction, depressive reaction, and phobia reaction, among others.
_DSM_ -II, published in 1968, didn't depart dramatically from the original version. The term _reaction_ was dropped, and certain historical terms, like _anxiety neurosis_ , _hysterical neurosis_ , and _neurasthenic neurosis_ , came back. But these were largely semantic changes. The illnesses were still considered to be the result of anxiety produced by unconscious conflicts.
Overseen by Spitzer, the _DSM_ -III, published in 1980, was revolutionary. Spitzer was a psychiatrist at Columbia. Although trained as a psychoanalyst, he wanted the new edition of the _DSM_ to be based as much as possible on empirical data and to include detailed inclusion and exclusion criteria that would be more useful to clinicians than the vague soup of the two earlier editions. The new book jettisoned the idea that disease had its origins in unconscious conflicts.
Klein was part of both the task force and the working group on "anxiety and dissociative disorders." His experiments with imipramine had convinced him that panic attacks were a distinct disorder. With that in mind, he pushed to create a separate entry for panic disorder, which had previously been lumped in with anxiety neurosis. Anxious expectation became generalized anxiety disorder. Social phobia and post-traumatic stress disorder made their first appearances in _DSM_ -III, too.
Psychoanalysts pushed back, deriding the new approach as simplistic and dismissive of their work. A heated controversy erupted over the category of "neurotic disorders." Spitzer wanted it gone, saying it was too tied up with the psychoanalytic views on the origin of mental disorders. But for many psychiatrists, neurosis was their bread and butter. It encompassed their most common diagnoses. They worried that if it disappeared from the _DSM_ , insurance companies might stop paying for their services. In the end, the task force compromised, keeping neurosis but demoting it to a few parenthetical phrases, such as "phobic disorders (or phobic neuroses)."
Psychoanalysis was under attack elsewhere in the scientific community, too. One study compared two groups of anxious patients: one that underwent psychoanalysis and another that was kept on a waiting list and did not. The rates of improvement for the two groups were the same. It did not help that psychoanalysis was costly and time-consuming and that there weren't enough practitioners for every anxious person. Of course, medications, which offered the potential of a quicker fix, also hastened its decline.
—
Despite the runaway success of Librium, Sternbach was not satisfied. He was determined to create a stronger benzodiazepine with even fewer side effects. Valium, from the Latin _valere_ , "health," was unveiled in 1963, followed by several others. (I have Sternbach to thank for my Klonopin.) In 1968, Librium, the most frequently prescribed medication in the United States, was dethroned by Valium. From 1968 to 1981, Valium was the most popular drug in the Western world.
By the late 1960s, the market for tranquilizers was overwhelmingly composed of women. A 1968 study, for example, found that women were twice as likely as men to use them. In the 1970s, women made up two-thirds of tranquilizer users. A Valium ad published in 1970 in the _Archives of General Psychiatry_ introduces a woman named Jan, "35, single, and psychoneurotic." "You probably see many Jans in your practice," the ad tells doctors. "The unmarried with low self-esteem. Jan never found a man to measure up to her father. Valium (diazepam) can be a useful adjunct in the therapy of the tense, over anxious patient who has a neurotic sense of failure, guilt or loss."
It was not long, however, until benzodiazepines were revealed to have a dark side. Throughout the 1970s, scientific research and stories mounted—in complaints to the FDA and articles in the press—of benzo addiction and patients who suffered awful side effects when going off the drugs. In 1978, former first lady Betty Ford went to rehab for her addiction to alcohol and medications, including Valium. The following year Barbara Gordon released a memoir, _I'm Dancing As Fast As I Can_ , about her panic disorder and her horrific withdrawal from Valium. In 1979, Senator Edward Kennedy convened Senate hearings on the dangers of benzodiazepines. Federal and state regulations were changed to rein in refills of benzos and stiffen the penalties for illegal use. Sales slid: Valium prescriptions fell from 61.3 million in 1975 to 33.6 million in 1980. Some people returned to older, even more dangerous drugs, like barbiturates, for relief.
Meanwhile pharmaceutical companies kept churning out new drugs. In 1981, Upjohn introduced Xanax, touting it as safer than Valium, in part because of its shorter half-life. Xanax also benefited from being FDA-approved for panic disorder, which _DSM_ -III had recognized as a separate disorder a year earlier. Soon sales of Xanax overtook those of Valium.
Then came the SSRIs. While the drugs, including Prozac, Paxil, and Zoloft, were initially approved for depression, manufacturers quickly sponsored trials showcasing the drugs' efficacy in treating anxiety, too. By 1998, major organizations like the American Psychiatric Association began recommending the SSRIs as first-line medications for anxiety disorders.
In the 1990s, consumer advertising of prescription drugs exploded. GlaxoSmithKline won FDA approval for Paxil as a treatment for social anxiety disorder in 1999. The company spent more than $92 million in one year on a marketing campaign to educate consumers about the disorder and sell them on the new drug to treat it. "Imagine Being Allergic to People," ads said. One TV spot featured a businessman leaning against a wall in despair; a student watching TV alone, bathed in blue light; and a woman gazing forlornly out a window. After Paxil, needless to say, the sun was always shining. The student is playing football with friends and graduating from college. The woman is smiling and joining a party. The businessman is being feted at a dinner while his father smiles proudly. "Paxil, Your Life Is Waiting," the ad proclaimed.
—
In recent years, traditional pharmaceutical companies have scaled back their development of drugs for psychiatric illnesses. In 2009, GlaxoSmithKline said it was shutting down its neuroscientific research into depression and pain. That same year AstraZeneca said it would stop trying to develop medications for anxiety, depression, schizophrenia, and bipolar disorder. With so many patients getting little relief from current drugs, the market—and potential profits—for new medicines for anxiety and depression would seem to be huge. So why the retreat?
It turns out that new psychiatric drugs take a lot more time and money to bring to market than other medications, for a number of reasons. Symptoms of mental illness can be incredibly heterogeneous, and many people have more than one disorder. Early scientific work is usually done on animals such as rats, but rat brains do not mirror the complexity of the human mind. Also, despite advances in imaging, the human brain usually can't be directly observed. In cancer research, for example, scientists can work directly on tumor cells removed from living patients. No one, thankfully, is going to be slicing into an anxious person's brain.
The next hurdle after development is gaining approval from the FDA. Between 1993 and 2004, however, only 8 percent of medicines developed for the central nervous system passed muster. Potential psychiatric drugs have sometimes failed because of toxic side effects, but usually they've been doomed because they didn't work well enough.
A few years ago scientists and drug companies thought they were on the verge of a breakthrough. A new class of medications for patients with depression and a variety of anxiety disorders was being studied in large-scale clinical trials. The drugs worked completely differently from existing ones, offering hope to people who didn't respond to SSRIs and other available antidepressants. The new medications acted on a receptor in the brain named corticotropin-releasing factor (CRF) receptor 1. CRF is an amino acid peptide that is involved in the body's response to stress: It activates the HPA axis and spurs the release of adrenocorticotropic hormone (ACTH), kicking off the fight-or-flight response. It made sense that blocking the CRF1 receptor could alleviate anxiety, and in a series of animal studies, it seemed to do just that. Rats injected with the CRF1 antagonists spent more time in open spaces, froze less during fear conditioning, and when subjected to shocks, were less likely to try to bury themselves in the wood shavings and fluffy bedding in their cages.
Early studies with people were encouraging, too. But in larger trials, the kind needed to secure FDA approval and bring the medications to market, the drugs faltered. One medication, saddled with the name Pexacerfont, was no better at treating GAD than a placebo. Another, Verucerfont, didn't help patients with depression. Two others were abandoned when they were found to dangerously raise the levels of subjects' liver enzymes.
The book isn't completely closed on CRF1 antagonists. Some scientists think that perhaps the drugs may be better suited to PTSD, panic disorder, and alcohol and drug addiction. In these disorders, anxiety spikes and dips as opposed to being more chronic, as with GAD.
In the hope of jump-starting drug development, the NIMH launched a program dubbed "Fast-Fail." The federal government is funding small trials to test new compounds as well as existing drugs that scientists think could be repurposed for use in psychiatric illnesses. Instead of starting with studies in animals, Fast-Fail will go straight to human trials.
—
Researchers are also exploring medications that might boost the efficacy of nondrug therapies. In the early 1990s, Michael Davis (the same neuroscientist who had been engaged in a friendly competition with Joe LeDoux, whom we met in chapter 1), then at Yale, found that NMDA (N-methyl-D-aspartate) receptors were critical for extinction, which some scientists believe underlies exposure therapy. NMDA receptors are activated when glutamate, the main excitatory neurotransmitter in the brain, binds to them. In a pivotal study, Davis and colleagues discovered that when they injected an NMDA antagonist, which blocked the receptor's activity, into the amygdalae of rats, extinction learning didn't occur. The rats continued to freeze and startle even when there was no shock.
If blocking NMDA activity prevented learning, then scientists theorized that perhaps something that enhanced NMDA activity would propel learning, recalls Kerry Ressler, a neuroscientist who was a fellow in Davis's lab at the time. The group considered a host of NMDA agonists and partial agonists and quickly zeroed in on D-cycloserine (DCS). Long used to treat tuberculosis, the drug was safe for humans. At low doses, it sticks to the NMDA receptor, changes its shape, and allows more calcium into the cells so that "a little bit more learning happens," says Stefan Hofmann of Boston University.
In 2002, Davis, Ressler, and colleagues published their first study using DCS in rats. They found that injections of DCS indeed enhanced extinction learning. The higher the dose, the greater the effect.
Davis and Ressler then teamed up with Barbara Rothbaum, a pioneer in using virtual reality to treat psychiatric disorders, to test the drug in people with a fear of heights (acrophobia). Two to four hours before each of two exposure sessions, the researchers gave one group DCS and another a placebo. The participants then donned a virtual reality helmet and spent thirty-five to forty-five minutes in a simulated glass elevator gazing over a railing. Every few minutes, the virtual elevator rose. The subjects could control how high it went. After two sessions, the people who got DCS were "much better, as if they'd had six or seven sessions [of exposure therapy] relative to placebo," says Ressler. The improvement was evident even three months later, when researchers put the participants through a battery of tests. Those who had taken DCS said their fear of heights was dramatically diminished. And compared to those who had gotten the placebo, they willingly exposed themselves to heights more readily in their daily life.
When Davis presented preliminary findings of the study during a NIMH meeting on extinction learning, Hofmann was in the room. "Everybody was speechless," he recalled. A drug that dramatically boosted the effectiveness of exposure therapy could slash the cost of treatment and transform the lives of patients. Many people drop out of therapy after just a few sessions because they find it too difficult or don't see the benefits. DCS may bring relief to those people, too.
Hofmann went back to Boston and started a trial with his social anxiety disorder patients. Other scientists tested DCS in panic disorder, PTSD, and obsessive-compulsive disorder (OCD). Davis and Ressler also obtained a patent for the use of DCS in psychotherapy.
But although the results of the early trials were promising, later studies were disappointing. In one trial, DCS failed to help OCD patients. A larger study of people with social anxiety disorder found that DCS sped up improvement with exposure therapy, without boosting the rates of treatment response or remission. One study of veterans who returned from Iraq and Afghanistan with PTSD found that those who got DCS fared worse than those who got the placebo.
Hofmann, who had done the trials in social anxiety, tried to make sense of these results. He went back through his data and found that a patient's experience during exposure therapy was critical to whether DCS helped. DCS worked when participants had a "good" exposure, meaning that their fear rose initially then plummeted during the task. It didn't work, however, when people had a "bad" exposure, meaning that their fear didn't fall during the sessions, or fell only slightly. In some cases, the anxiety got worse with DCS. The timing and dosing of DCS is critical to its efficacy as well. If given in too big of a dose or too long before exposure therapy, it is less likely to work. Now Hofmann is experimenting with administering DCS after therapy, rather than before, and only to patients who had a "good" session.
Scientists are studying other substances that, like DCS, seem to act as cognitive enhancers when combined with therapy. Yohimbine is derived from the bark of a tree typically found in parts of central and western Africa. (It is also used for erectile dysfunction and weight loss.) In a few small trials, it has been found to reduce fear in patients who have undergone exposure therapy. Hydrocortisone, better known as an anti-itch cream, has been shown to boost fear extinction in people with a spider phobia when used in pill form before exposure therapy.
Another promising drug is ketamine, most commonly used as an anesthetic but also known as the street drug Special K, which acts on NMDA receptors as well. Ketamine has been shown to relieve symptoms of depression within hours, and there have already been small positive trials with PTSD and OCD patients. A few scientists are even starting to look at MDMA, better known as ecstasy, as a way to augment treatment, particularly for PTSD. The euphoria and disinhibition the drug induces seem to help people process terrifying memories. In a few small studies, people have taken MDMA and then had daylong therapy sessions. In a small study with PTSD patients, two MDMA-enhanced therapy sessions were much more effective than a placebo, and the benefit was still evident three years later.
—
Almost as fraught as the decision to go on psychiatric medication is the decision to go off it. There are no fixed rules for when to stop. Psychiatrists I've spoken to generally suggest that people with anxiety disorders stay on an SSRI for at least one year after their anxiety has remitted. That gives patients time to get through one full cycle of stressors: the holidays, the anniversary of a divorce or the death of a loved one, the start of their children's school year. After that "you almost have a muscle memory" of how to handle those experiences without anxiety exerting control, says Beth Salcedo, a psychiatrist in Washington, D.C. She also recommends doing a course of CBT either before or while going off medication.
I had planned to stop taking my daily 5 milligrams of Lexapro almost a year ago, after I finished the first draft of this book. But then I had to write a second draft. And a third. I was also juggling the book writing with my job at the _Journal_. My daughter started a new school. My father's health faltered. Our bank balances dipped. And my to-do list seemed endless. Little things—like picking up a birthday present or deciding what to make for dinner—made me panicky.
I simply felt too stressed out. The waters of my life were too choppy to travel without my chemical life vest. I kept refilling my prescription.
Stopping an SSRI is always a leap of faith. Without that excess serotonin floating around my synapses, will I fall apart? And if I do, and I need to reach for medication again, will it work? There is no guarantee.
It may seem strange that I've chosen to be a reporter, a profession characterized by deadlines, not to mention one that requires cold-calling sometimes hostile strangers. My job often makes me anxious. During my years covering technology news, I lived in fear of being beaten on a story by competitors. I opened the _New York Times_ with dread.
But this kind of anxiety is rooted in reality. And it has helped me to cope with the amorphous anxiety that doesn't seem to have a good reason.
Looking through the data on anxiety disorders and the workplace, I feel extraordinarily lucky. Many people don't fare so well. A 2005 study by Australian researchers found that a staggering 47 percent of those aged fifteen to sixty-four with anxiety disorders were not working. By comparison, about 20 percent of those in a control group (people without disabilities or chronic health problems) weren't in the labor force. People with anxiety disorders were also more likely to work from home, to be self-employed, or to be employed by the government. They also more often said that they "accomplished less" and "took less care than usual" in their jobs during the previous month.
Maybe that study is an outlier. While both anxiety disorders and depression are associated with short-term and long-term absences from work, once people get better, only past depression is still linked to absenteeism. After people's anxiety disorders remit, they don't miss more work than healthy people do. (Of course, many people suffer from both depression and anxiety.)
This reality is reflected in data on disability benefits. Of the more than ten million Americans receiving disability benefits in 2015, less than 3 percent got them because of an anxiety disorder, whereas about 14 percent received them because of mood disorders, and about 29 percent (the biggest chunk by far) for musculoskeletal and connective tissue problems.
In a lot of ways, my work has been like constant exposure therapy. I've used it to get close to what scares me the most: illness, madness, and death. I've sought out stories about hospice patients and spent many hours with the dying. There have been ridiculous episodes, too: me, working on a story about carbon monoxide poisoning, conducting an interview with my head between my knees. It was via phone, thankfully. During the conversation, I could have sworn that I felt every symptom the doctor I was talking to described.
When I was younger, anxiety sometimes flat-out crippled my ability to work. In second grade that took the form of those math-fueled panic attacks. In college, I had to drop classes when I had my breakdown and relapse. The only reason I was able to graduate on time was because I took a couple of classes during the summer and received college credit for AP courses I'd taken in high school.
Anxiety has also had subtler, more insidious effects on my work. During my school years, it fueled procrastination. For me, procrastination seems tied up with perfectionism. Scientists define perfectionism as the will to achieve high standards combined with excessive self-criticism. Perfectionists expect, well, perfection. Anything less won't do. In their minds, a mistake equals failure. Perfectionists also tend to doubt their actions.
It isn't tough to see similarities between perfectionism and anxiety: the self-doubt, the self-criticism, the fears of catastrophe. Indeed, people with panic disorder, OCD, and social phobia all score higher on certain measures of perfectionist thinking than do people without those disorders. Research shows, however, that anxiety is linked to some aspects of perfectionism but not others. Specifically, while anxious people are concerned about mistakes and doubt their actions, they don't necessarily have superhigh personal standards. Worriers actually tend to lower their standards when stressed out. It isn't that they want to be the best. They just don't want to mess up.
Perfectionism, in my case, is really just the fear of screwing up. And until I get started on something, I can't fail at it. This is not a useful way to go about life.
In eighth grade, my history class had a series of assignments due. I didn't turn them in on time. I don't think I had even started the project by the deadline. A day went by. Then two. Then a week. Every morning I said I would start the assignment, and every morning I made some excuse to myself. I didn't yet know how to tackle it. I was too tired. I was too anxious. I was too ashamed. I didn't tell my parents about my predicament or ask my teacher for an extension. Instead, I quickly slunk out of class each day to avoid an awkward encounter.
One day at the end of class, the teacher announced that he would leave his grade book open on his desk and we could all take a look to see how our projects had fared. "There were a handful of A's," he said. "And one F." My humiliation was on display for the entire class. As my fellow students crowded around his desk, I busied myself putting my books in my backpack. My heart raced, and hot shame rushed to my cheeks. There was no need for me to join the scrum.
As my friend Mark walked by, he said with a bewildered shake of his head, "Congratulations. You got an F."
I wish I could say that this experience cured my problem, but I continued to struggle with it. Although I never outright didn't do an assignment again, I became a crammer, an extreme deadline student. I finished papers in the car on the way to school, desperately trying to steady a shaking pen as my mother drove up the steep hill that was home to Danbury High. I was a good, but not stellar, student, earning A's and B's.
Procrastination is often defined as voluntarily delaying action despite the knowledge of future negative consequences. A review of more than two hundred journal articles and other scientific sources found that one feature of anxiety—fear of failure—was slightly associated with procrastination. And one aspect of perfectionism—the belief that loved ones have high standards for you—was tied to procrastination. Procrastination was much more strongly linked, however, with impulsiveness. Depression also fueled procrastination.
Maybe I was just a typical student. After all, about 75 percent of college students say they are procrastinators. Half say their procrastination is chronic and problematic. Students say they spend about one-third of their day procrastinating (by, say, sleeping and eating instead of studying). Fortunately, procrastination tends to wane with age: Only about 15 to 20 percent of adults say they chronically procrastinate.
Indeed, procrastination became much less of an issue when I hit the working world. Letting myself down was one thing. But letting other people down—bosses, colleagues—was quite another. I couldn't do it.
I still am a deadline writer. I turn in my stories for the _Journal_ pretty much exactly when they're due. I need the urgency of a deadline, the clock ticking down, the specter of a disappointed editor or a blank space in the paper's lineup of stories. It is a duel between anxieties, and only my fears of judgment or failure surmount my fears of writing imperfect words and clumsy sentences.
—
I've loved reading, writing, telling, and hearing stories since I was a child. I was that kid who always had her nose in a book, oblivious to the world. My mother would call from the kitchen, summoning me to get ready for school, to come for dinner, her voice rising until finally I'd tear myself away from _A Wrinkle in Time_ or the latest _Sweet Valley High_ and answer her with a mumbled monosyllable. I'd walk down hallways holding a book in front of me, once slamming into a concrete pole at the Danbury Fair Mall. My childhood best friend, Kate, and I would call each other and say, "Want to come over and read?" Our play dates consisted of both of us splayed on a sofa, books in hand and boxes of cookies within reach.
I wrote earnestly in diaries, thrived in English classes, and scribbled short stories and poems, but I knew nothing about journalism. Some of my _Wall Street Journal_ colleagues idolized Woodward and Bernstein and had quoted _All the President's Men_ in junior high. I didn't regularly read a newspaper until college.
By the time of college graduation, my ambitions were still fuzzy. I had a degree in political science and wanted to do something with "writing" and "politics," but what? Sidelined by anxiety, unpreparedness, and the need to earn money, my résumé was skimpy. No fancy internships in D.C. or New York, let alone overseas—just babysitting and waitressing, summers working at a day care center, and filing and answering phones in offices.
My good friend Vanessa was already living in D.C. and had an extra bedroom. It was 1992, and a presidential campaign was going on. That was good enough for me. I piled my books, sorority sweatshirts, and diploma into my red Honda Civic and drove from Ann Arbor to Washington, fending off panic attacks all through Ohio, Pennsylvania, and into Maryland. I'd pull over at rest stops and call my dad from roadside pay phones, crying over the din of eighteen-wheelers. "I'm so scared. I can't do this," I'd say. He'd give me pep talks. "Just breathe. You're doing great," he'd say. I'd be bolstered enough to get back in the driver's seat for another half hour, maybe an hour. And then I'd find another pay phone. The eight-hour drive took me more than fifteen hours.
I found an internship in an office that handled direct mail for political campaigns—those pamphlets of smiling candidates and their families and their promises that flood people's mailboxes at election time. Through connections I made there, I landed a job in the press office for Senator Harris Wofford, an inspiring liberal Democrat from Pennsylvania who had advised Martin Luther King, Jr., and JFK and cofounded the Peace Corps. I worked twelve-hour days, writing press releases and speeches and traveling to little towns all over Pennsylvania—meetings with former steelworkers in Johnstown, rallies with teachers in Altoona. I went to one of Bill Clinton's inaugural balls and watched Bill and Hillary groove to Fleetwood Mac. (You couldn't escape "Don't Stop" during the campaign.) I rode the underground train that whisked senators from their office buildings to the Capitol: Yes, that was Ted Kennedy sitting across from me. In this age of political cynicism, my excitement might sound ridiculous and naïve. But I was twenty-two, and those were my words being quoted in newspapers, my words—one exhilarating time—the senator was speaking on the Senate floor.
I wrote constantly. I loved to experiment with words and phrases, loved the challenge of crafting something clear and compelling. But I quickly realized a truth about political writing. You have to cover the same topics—using essentially the same words—over and over again. It's called "being on message." I was also becoming more intrigued by journalism. I spoke to reporters every day as part of my job. They called for comments from Senator Wofford. I met them at political events in Pennsylvania and saw their bylines in newspapers—the _Pittsburgh Post-Gazette_ , the _Harrisburg Patriot-News_. They jumped from topic to topic: They might write about health care reform one day, the State of the Union Address the next. But what really awed me was the simple fact that if they were curious about something—anything—they could call someone on the phone, and most likely that person would talk to them. A job where you got to satisfy an insatiable curiosity and write was, I decided, the job for me.
In November 1994, Senator Wofford was voted out of office, and I was out of a job. I decided to look for a journalism job in earnest. There was just one problem: I had zero experience. I had written reams of press releases and speeches, but I'd never written a news article. Blogs barely existed. Serendipity arrived in the form of a phone call. My boss from Wofford's office had a friend who was an executive at the _Wall Street Journal_ in New York. He was looking for an assistant. The job wouldn't be glamorous. I would be answering phones and picking up faxes. I'd even have to take a pay cut. But I'd at least be in the same building with people who were doing the jobs I wanted. Maybe I would get an opportunity to write.
I was offered the job and moved to New York two weeks later. I rented a U-Haul with the boyfriend I was leaving back in D.C., and we argued the entire trip there. I didn't know anyone in New York and had no place to live, so I bounced around on the couches at friends' parents' places until I found a room in Chelsea. My new roommates were a New England prep school boy turned composer and a drugged-out Minnesota girl who worked in a SoHo shop during the day and danced on a box at the Limelight nightclub at night. She often got home just as I was waking to get ready for work.
—
In many ways, anxiety has fueled my work. Fear of hurting my career was what finally drove me to take medication in my twenties. In college, I could drop classes and make up tests, but there are no time-outs in the working world. Fear of messing up is what drives me to triple-check that spelling and do one last interview. Many reporters are dilettantes, bouncing between disparate topics. We often have to learn new subjects quickly, synthesize the information, and make it understandable to readers. Mistakes are all too easy to make. (For one of my first feature stories as a cub reporter, I thought someone I interviewed had said his name was Kurt. Alas, it was Knut.) Twitter and Facebook have amplified the reach of our stories—but social media also means that a screw-up can be very public. Insecurity and paranoia can be useful qualities.
Anxiety has made me braver and more tenacious. Fear of not getting the story has overridden my other anxieties—about rejection, about bothering people. One story in particular sticks with me. I was still an administrative assistant at the _Journal_ , writing stories after my other duties were done, when an editor gave me an idea for an article. His Sunday _New York Times_ had included a packet of salad dressing, a promotional giveaway. But the weight of the paper slamming against his front porch had caused the packet to burst, leaving his paper dripping with dressing. Maybe, he said, there was a story in this advertising message gone awry.
I called the circulation department at the _Times_ , and a clerk confirmed that the exploding dressing was not an isolated incident. She herself had received several complaints. Now I just needed to find a subscriber with a sticky paper. With the help of our librarian, I got a list of addresses and phone numbers of people who lived near the editor. The salad dressing promotion had gone only to certain subscribers, so I figured the editor's neighbors were likely suspects. Then I proceeded to cold-call strangers, during dinnertime.
"Do you get the _New York Times_?" I asked.
"Did you get a package of salad dressing in your paper last Sunday?"
"Did it explode?"
I was nervous. I knew how absurd this sounded. As I dialed, my hands shook, and my stomach did flip-flops. I recalled prank calls that friends and I had made during preteen slumber parties: "Is your refrigerator running? You better go get it," we'd giggle.
For four hours, I was hung up on and yelled at. Finally, at nearly nine p.m., someone said yes. After I hung up the phone, I did a little dance in my chair.
My story ran on May 7, 1996. "Greg Kauger would like to try the new Hellmann's salad dressing. If only he could scrape it off his newspaper," it began. "Mr. Kauger, of Short Hills, New Jersey, was among the lucky recipients of 170,000 packets of Hellmann's salad dressing tucked into _New York Times_ home deliveries last week. And one of the unlucky ones whose samples exploded when the paper landed on the driveway."
—
Psychologists have long asserted that a certain amount of anxiety can be helpful. More than a century ago, in 1908, the Harvard psychologists Robert Yerkes and John Dodson published the results of an experiment showing that performance on a difficult task is enhanced by anxiety (often referred to as arousal by researchers) but only up to a certain point. Too much anxiety causes performance to suffer. The so-called Yerkes-Dodson law is portrayed as a bell-shaped curve: As arousal increases, so does performance. Until it hits the peak, that is. If arousal continues to rise beyond this point, performance slides.
Yerkes and Dodson's experiments were with mice, but a range of studies in people has supported their conclusions, finding that memory and learning are best achieved when the levels of stress hormones are neither too high nor too low.
But the relationship between anxiety and success remains murky. Some scientific studies show that anxiety interferes with achievement. Others show the opposite. A study of beginning nursing students in Canada, for example, found that those who had more anxious temperaments had higher first-semester grade point averages.
There's an enduring stereotype of the addled, anxious intellectual, but the research into the relationship between anxiety and intelligence is also quite contradictory. Canadian researchers, for example, have found that people who worry and ruminate have higher scores on a verbal intelligence test. Those who tend to process past social events, however—a hallmark of social anxiety disorder—score lower on a test of nonverbal intelligence. A small 2012 study looked at the intelligence of people with GAD compared with controls. Among GAD patients, those with the most severe symptoms had the highest IQs. But among the controls, those with the least anxiety had the highest IQs. The researchers argue that this may make evolutionary sense. Society needs smart, relaxed people, but it needs intelligent, high-strung ones, too.
The high-strung people are the sentinels, says Israeli psychologist Tsachi Ein-Dor, the ones constantly scanning the horizon for danger. They'll sound a warning or mobilize a retreat, thus saving the hides of their more Zen-like neighbors. Ein-Dor and his colleague Orgad Tal conducted an experiment that revealed the role of the sentinel in action. First, the scientists had the subjects fill out surveys that assessed various psychological measures. The subjects, eighty undergraduate students, were then told that they would be rating how much they liked a series of artworks displayed on a computer screen. Each subject was given instructions and left alone in a room with the computer. After a few minutes, the subject was prompted to press "okay." Then a series of frantic error messages flashed on the screen, warning of a virus and stating that the files on the computer's hard drive were being erased. When the subject told a study staffer—a trained actress in on the ruse—about the virus, the staffer pretended to panic and told the subject to go get help from another employee.
During their trek to get help, the subjects encountered several obstacles. A person asked them to complete a survey. Someone else asked for help photocopying a document. Another person dropped a big pile of papers at their feet. This series of events was intended to test how well subjects remained focused on the original goal: to deliver the news about the dangerous computer virus. The researchers found that subjects who scored higher on measures of anxiety were less likely to let themselves be delayed by the obstacles (i.e., they didn't take the survey or help pick up papers). Anxious people were "eager to spread the word of a troubling, socially threatening incident, a tendency that, in many real world situations, might save others from serious threat," the researchers wrote.
It takes a lot of creativity to envision vivid catastrophes and spin doomsday narratives. Worriers often fashion elaborate contingency plans to avoid disaster. They may create cover stories to hide their anxiety. It isn't hard to see that this requires some smarts.
—
For many of my years at the _Journal_ , our offices were in the World Financial Center, a warren of buildings in Manhattan's financial district directly across the street from the twin towers of the World Trade Center. On the morning of September 11, 2001, I was leaving for work, heading down the stairs of the Cobble Hill, Brooklyn, brownstone where I rented an apartment on the top floor. My landlords, a couple of documentary filmmakers, were heading up the stairs, looking for me.
"Where are you going?" the woman asked.
"To work," I said.
"Haven't you heard the news?" the man asked. "A plane crashed into the Trade Center. You can probably see it from your window."
The three of us raced up the stairs to my apartment. Indeed, the twin towers were perfectly visible from my living room window on that bright, clear day. Thick gray smoke encircled both towers.
I flipped on the television. The next half hour or so was surreal; our heads whipped back and forth between the news coverage and the real thing. Then we heard a rumble, like slow rolling thunder, and one of the towers crumbled, the whole edifice sliding down with a billowing roar. The newscaster's voice turned shrill, unbelieving. It was a weekday morning, and those buildings were filled with offices. How many hundreds, thousands were dead? Then the second tower fell.
I received three phone calls in quick succession. My mother. My ex-boyfriend Alan, phoning from Mexico City. And a new guy I was dating, a photojournalist named Brad who lived in Manhattan, on the Upper West Side. He was already heading downtown on his bicycle to see what he could shoot.
Brad's phone call jarred me. I was a journalist, too, and here was a huge, tragic story. There was actually something I could do. So why the hell was I still sitting in my apartment?
My BlackBerry was buzzing nonstop with emails from my colleagues in the _Journal_ 's technology group. I covered wireless telecommunications. Our team started planning stories on how New York's technological infrastructure was holding up during the crisis. It was clear that cell phone service was crippled. I hadn't been able to make a call in hours. I grabbed a notebook and a pen and headed outside.
By then the sky had darkened. The air around me was thick with smoke, ash, and millions of tiny bits of paper. The winds had blown Trade Center debris across the East River and over to Brooklyn. I ran back inside to grab an old T-shirt to cover my face, then walked toward the Brooklyn Bridge. I interviewed a few people lined up at pay phones, asking them when they lost cell phone service and who they had been calling. Then, approaching the bridge, I saw a couple of dazed people covered in gray soot. Then tens more. The Brooklyn Bridge, usually a joyful, cacophonous parade of cyclists, stroller-pushing locals, and tourists, was now a solemn march away from destruction. Volunteers handed out cups of water. One man yelled at me, "You're walking the wrong way." The twin towers were now just a smoky blot on the Manhattan skyline.
I didn't get far into Manhattan. By then police and firefighters had cordoned off the Trade Center site and the surrounding blocks. So I walked back to my apartment, wrote up my interviews, and sent them to my editor. Only hours later did I find out that the _Journal_ 's offices were now a toxic crime scene. Weeks later we would learn that more than 2,600 people died in the towers that day.
In the days after the towers fell, I threw myself into work. I wrote a story about New Yorkers who had heard from old lovers, schoolteachers, and even therapists on 9/11. I wrote another about local businesses that weren't sure whether they should remove the Trade Center from their logos. I wrote about residents of the financial district who, having lost access to their apartments, were being put up in fancy boutique hotels. One man had hotel employees remove a picture above the bed that reminded him of the desperate men and women he had seen jumping from the burning towers.
We set up a temporary newsroom in SoHo, and I was asked to join a group of reporters who would continue writing about the aftermath of 9/11. One of my first assignments was to cover the anthrax attacks in New Jersey. I can't think of a story more tailor-made to unhinge an anxious person: an unknown assailant sending white powder through the mail that could be lethal when inhaled.
I spent several days camped out front of one of the target post offices in Trenton in a scrum of other reporters. Periodically a spokesman would appear to deliver a bit of news. There was a 7-Eleven across the street, and one day I picked up a bottle of orange Gatorade, took a swig, and put the rest in my purse. I must not have closed the cap securely because the bottle leaked, sending sticky liquid all over the lip balms, crumpled receipts, and other detritus at the bottom of my bag. And my cell phone. When I pulled it out, it was drenched and dead. A little wave of orange sloshed back and forth within the display like a mini lava lamp. To file my story that day, I had to run back and forth across the busy road between the post office and a pay phone, dictating the words to my editor in New York.
Sometimes I spent the night at a hotel in New Jersey, but usually I'd drive the ninety minutes or so back to my apartment in Brooklyn. I wanted to see Brad. He was also becoming irritated by my constant absence. I'd spend the night in Brooklyn or at Brad's apartment and then drive back to Trenton in my rental car in the morning.
The stresses were mounting. Brad. The driving. Long hours pursuing stories. Anthrax.
It is late at night, after eleven p.m., and I'm driving from Trenton to my hotel in a nearby town after a long day of reporting, when I start to feel breathless. A slight pressure builds in my chest. My heart beats quickly. Spots dance in front of my eyes. My grip on the steering wheel tightens.
I try to breathe slowly, deeply. _You're just having a panic attack,_ I say to myself. I keep driving down the dark highway, but the symptoms are getting worse. My hands sweat. The edges of my vision are fuzzy. Every muscle tenses. Then I see a sign with a capital H and an arrow. There's a hospital nearby.
I drive straight to the emergency room, leave the car in the driveway, and race up to the triage nurse on duty. "I'm a journalist, and I've been writing about anthrax," I say in a rush. "I've been at the post office where the letters came through, the ones with anthrax in them. I'm scared that I could have it."
"You think you have anthrax?" the nurse says, looking alarmed. "I'm sorry, but you'll have to wait outside. Someone will meet you there."
I'm hustled out of the hospital and dumped in the driveway. Standing there alone, bathed in the spotlight of the red and white EMERGENCY ROOM sign, I start to feel ridiculous. I haven't actually been inside the post office. I haven't touched any anthrax-laced letters. I haven't touched anyone who has touched an anthrax-laced letter. There's really no way I could have contracted it. I'm just having a panic attack about the very _idea_ of having anthrax.
A few minutes later an ambulance appears, and a guy in an orange hazmat suit jumps out. I sheepishly explain that I've been reporting a story on anthrax but don't have it myself. The man gets back in, and the ambulance drives away.
After that I hit a wall. I was working on a feature story about a small-town New Jersey mayor who had become an unlikely force in the anthrax attack response. It was slated for page one, for the coveted "A-hed" center column. (The name _A-hed_ has to do with the stars and dashes around the headline.) The A-hed and the "leders" were the most sought-after slots in the paper, reserved for the best stories, and competition was fierce. I had only a couple of days to turn the story around.
For the first time in my career, I couldn't do it. When I sat down to write, I felt strangely lost. I couldn't find my focus, couldn't see how the story should unfold. I'd write a sentence, then delete it, the blinking cursor a pulsing reproach. With the deadline bearing down at me, I panicked and strung together random vignettes. I felt nauseous as I hit the send button on the email to my editor.
It wasn't a surprise when she called, sounding disappointed and confused. I was usually a reliable reporter and writer. "Try it again," she said.
I did. And again I failed. The story was killed.
When my anxiety soars, I have a hard time concentrating. My mind overflows with worries, leaving scant room for information of the nondoomsday variety. For decades, psychologists have theorized that anxiety hijacks some of the brain's cognitive capacity, even in people without full-blown anxiety disorders. The idea is that there's a battle of resources and that worry gobbles up prime real estate. If your attention is focused on potential threats, you have fewer resources to devote to your goal—whether it is getting your point across in a meeting with the boss or, in my case, writing a story about a New Jersey mayor.
Research has not always borne out these theories, however. In fact, the research into anxiety's effects on cognition is mixed and inconclusive. We know that in people with anxiety disorders, planning is generally unaffected. However, they show deficits in spatial navigation and working memory (short-term memory that allows us to process and manipulate information). Working memory is what lets us follow the thread of a conversation and tally a running bar tab. It is critical for reasoning and decision making.
For those without disorders, new research is showing that situational anxiety—the kind many of us feel before a big presentation—may actually enhance working memory when the task is difficult. In a 2016 study, researchers at the NIMH had thirty people with GAD and thirty people in a control group do a working memory task called the "n-back." The task has several versions. In the 1-back, people are given a string of numbers and have to indicate if the one they are seeing is the same as or different from the number just before. In the 2-back, they need to remember the number two places before. As you can imagine, the 1-back is easy and the 3-back is quite difficult. To induce anxiety, subjects are sometimes told they might receive a shock to the wrist. At other times, participants are told that they are safe and that no shock is forthcoming.
In the study, the healthy controls did more poorly during the 1-back and 2-back when they were threatened with a shock. But during the tougher 3-back task, anxiety actually helped them do better. In the GAD patients, however, the threat of shock disrupted working memory whether the task was easy or hard. Another study by the same NIMH research group had people with GAD, social anxiety disorder, and healthy controls do the same n-back task while in an fMRI scanner. The anxious subjects had a markedly different pattern of brain activity than the nonanxious ones, which could explain the difference in performance: They had less activation of the dorsolateral prefrontal cortex. And the wonky brain activity in those subjects was similar whether they were threatened with shocks or not.
The anxiety prone, however, may not be doomed to suffer lackluster performance. They may not even have to learn to jettison the anxiety. Instead, a simple mind trick could help.
You simply tell yourself that you're excited.
It sounds absurd, but a series of studies by Alison Wood Brooks, an assistant professor at Harvard Business School, has found that when people think of their anxiety as excitement, they perform better on a range of tasks. (True, the subjects in Wood Brooks's studies weren't screened for full-blown anxiety disorders, so it is unclear how well the tactic would work for those of us whose amygdalae are already on overdrive.) Wood Brooks put young people in a variety of stressful situations. For example, some had to sing Journey's "Don't Stop Believin' " in front of a researcher. To ratchet up their anxiety, they were told that they were performing in front of a karaoke expert and would be paid based on how well they did.
In the singing study, some of the participants went right to the task. Others were told to first say "I am anxious" and to try to believe it. A third group was prompted to say "I am excited." It turns out that the participants who said "I am excited" before their performances were better at matching the pitch, tempo, and volume of the song than those in the other two groups. They also said they felt more excited than the other two groups. It wasn't that the excited group wasn't on edge: They reported that they felt as anxious as everyone else, and their heart rates were just as elevated. But simply reframing that anxiety as excitement made them sing better.
Wood Brooks got similar results when she had people give a speech and take a challenging math test. The subjects who were prompted to reappraise their anxiety as excitement scored better on the test and were judged to be more persuasive and confident speakers. In these experiments, she had some participants try to relax by stating "I am calm" before the speech task and "Try to remain calm" before the math task. But doing that didn't seem to help. Wood Brooks conjectures that it is a lot harder to transform anxiety into tranquillity than it is to convert it to excitement. With the former, you have to fight anxiety's effect on the body—the jacked-up heart rate, the butterflies in the stomach—whereas in the latter you have only to change your attitude. She calls it moving from a threat mind-set to an opportunity mind-set.
—
Thankfully, my blown front-page story was not the start of a professional downward slide. Back in New York, I redeemed myself with a string of solid articles. After another few months, the special post-9/11 group was disbanded, and I soon moved over to write about health for our then-new Personal Journal section.
My new assignment seemed both perilous and therapeutic. A lot of my anxieties revolved around illness and death. If I could somehow overcome my fear of death, or even ease it a bit, I told myself, I would not be so captive to my anxiety. I asked myself what it was about death that I feared so much. Was it the pain? The separation from those I love? The physical erasure, the nonbeing? I mulled it over, on my own and with my therapist, until I realized that I was afraid of the fear itself. When I envisioned death, I saw terror, pain, and breathlessness. I couldn't imagine a peaceful ending.
Death, I thought, would be the ultimate panic attack.
So I started spending time with people who were dying. I volunteered to write stories about aging, Alzheimer's disease, and hospice—a sort of self-imposed exposure therapy. I spent days with hospice programs in Kentucky, Washington, D.C., and California, shadowing nurses as they made home visits. I expected the patients to be bedridden, vacant, and gaunt, but many were vibrant and brimming with life. I met an elderly man with terminal leukemia who was joyfully planning a trip to visit his nephew in California. One man told me that he and his wife, both terminally ill, went to their favorite restaurant every day to eat ice cream sundaes. A nurse relayed the story of a woman dying in an inpatient hospice unit who summoned each of her family members into the room to tell them what they meant to her. Dying, it seemed, wasn't only fear and pain. I was awestruck by patients' generosity in spending even a few moments of their limited time with a nosy stranger.
Not all the stories I encountered were uplifting. In an inpatient hospice unit in California, I met a man in his forties dying of brain cancer. The nurses were tinkering with his medication in an attempt to control his searing pain. His exhausted wife by his side, the man was hoping the nurses could lessen the pain enough so he could achieve his goal of dying at home. In Lexington, Kentucky, an elderly cancer-stricken man caring for his wife with dementia sat in an afghan-strewn chair in his cozy living room. "I never thought dying would take so long," he said sadly. He wanted to hasten what I desperately feared.
I met another man, just a few years older than me, dying of ALS. His face was friendly, with the vague handsomeness of a former jock. He could talk and breathe on his own but was otherwise completely immobile, lying in a hospital bed. Photos on a dresser showed him well and smiling with friends, a can of beer in his hand. I couldn't imagine a worse way to die.
Still, seeing dying patients' regret, acceptance, and vitality gave me a way to work out some of my fears. I even wrote a story during this time entitled "Negotiating the Terms of Your Death," about how advances in pain medication and new hospice practices were giving patients more control over how and when they died. And just a few weeks before I wrote these words, I received an up-close lesson in a good death when my ninety-three-year-old grandmother passed away from kidney failure. She was lucid up until the day before she died, reminding those of us keeping vigil to eat and telling me—completely seriously—that she didn't want to take pain pills because they are "habit forming." _Hell, now's the time to try heroin if you want to, Grandma,_ I thought. She was luckier than most: She got progressively sleepier and then just slipped away.
—
Why hasn't anxiety derailed my career? I've been lucky, I think. I've never had a relapse serious enough to require me to take a leave from work. I love being a journalist. Medication helps me. For years, I took a Klonopin about thirty minutes before every one of my live TV or video appearances, part of my job as a _Journal_ writer.
I also built a support system at the office—always clueing in a few close work friends about my anxiety. Having an ally at work, someone I know I can reach out to, eases my anxiety. I don't feel trapped by my panic. I know that there is at least one person I can be authentic with, can be weak with. It is tough enough to get through a panic attack without the pressure of having to fake composure, too.
For several years, Jeff was one of my closest work friends. He was from Baton Rouge and was blunt and folksy. Newspaper reporters are not known for their fashion sense, but Jeff was in another league. He wore ripped, faded jeans and 1980s-era leather boat shoes held together by duct tape. There was a group of us at the _Journal_ then, all thirtyish, no kids, most of us single. We'd hang out after work, meeting up at Fox Hounds, a generic Irish bar with cheap beer and greasy food, to swap stories, gossip about the office, and debate the legacies of dead presidents. (Yes, we were geeks.) Even though Jeff was married with a kid and living in suburban New Jersey, he bounced around with us.
Jeff and I worked for the same section. He covered personal finance and was amazingly prolific, churning out stories at a swift pace and writing books at night. He taught me to be more efficient in my reporting. "You only need one interview to make that point," he'd say. I'd run stories by him, asking him his thoughts about this lead or that anecdote.
When I felt a panic attack coming on, I'd email Jeff: "Let's go walking." Then we'd meet in the lobby to head to Starbucks (always decaf for me) or simply to stroll around the Habitrail-like hallways of the _Journal_ 's old office complex. He would walk beside me, talking if I wanted to talk. Or we'd just wander silently, stopping if I needed water to wash down a Klonopin. He'd check in every so often. "How are you feeling?" he'd ask. "You doing okay?" It wasn't that he could relate. Jeff never seemed anxious. He was confident about his writing and didn't even seem to have a very strong sense of self-preservation. While living in California in his twenties, he had broken his neck surfing and kept right on riding the waves. But even if my anxiety was foreign to him, he never made me feel silly or absurd.
When Jeff moved back to Louisiana, I was bereft.
For years, I didn't tell my bosses about my anxiety. I knew I worked in a place with sensitive, caring people. I had seen senior editors rally around colleagues with cancer and other illnesses. One editor was very open about his OCD, and it didn't seem to stop his ascent through the company. Still, I was afraid of being judged and labeled. Of being thought less capable, of having my assignments limited. I didn't want my editors feeling like they had to protect my fragile psyche. In fact, I outed myself to my current editors only when I handed them the proposal for this book. And I could never have done that, or written this book, without the confidence of knowing that I had two decades of work experience and a solid track record.
The majority of anxious people conceal their disorders at work. Only one in four people with an anxiety disorder has told their employer, according to a 2006 survey by the Anxiety and Depression Association of America. People cited various reasons: that the disclosure would limit promotions, would be recorded in their employee file, or would be perceived as a lack of willingness to do the job.
They may have good reason to be tight-lipped. The 1990 Americans with Disabilities Act prohibits employers from discriminating against job applicants or employees with a disability, including psychiatric ones. Still, one study published in 1999 revealed that employers were seven times more likely to consider hiring someone who used a wheelchair than someone taking medication for anxiety and depression. A 1996 survey conducted by Mind, a mental health support and advocacy group in Britain, found that more than one-third of the respondents had been fired or forced to resign from a job because of their illness. Then again, these studies are about two decades old—I would like to think that we have become more enlightened since then.
I can tell how much the cultural climate has changed when I interview college students and they let me use their names, pictures, and the details of their illnesses in my stories. Many of these young people are campus mental health activists involved with advocacy groups like Active Minds and the Jed Foundation. They are driven by the desire to lessen the stigma around mental illness. And they are much braver than I am.
I will never know exactly how anxiety has affected my career. Even if I didn't struggle with it, I probably wouldn't have become a war correspondent. I haven't won a Pulitzer. I haven't been a huge risk taker in my work life. But I love what I do and have built a solid, rewarding career.
—
Anxious people often have a tough time making decisions. Not just the big ones, like should I quit this job or marry that person, but also the small, quotidian ones, like which email should I respond to first? That's because we are excellent at anticipating and visualizing bad outcomes. We also tend to interpret ambiguous information in a negative way, which psychologists call interpretation bias. On top of that, we also tend to hate uncertainty, which means we are apt to choose the safest option. If, that is, we can choose at all.
Indeed, anxious people tend to be risk averse. A number of studies have looked at the link between anxiety, decision making, and so-called risk taking behavior. Several use a psychological research tool known as the Iowa gambling task. Participants play a virtual card game where they are told they can win or lose money. Anxious players tend to make fewer risky moves.
When my husband, Sean, and I were debating where to take our honeymoon, I was editing travel stories for the _Journal_. I had the inside scoop on the hottest new hotels and destinations. Friends often asked me for vacation advice. Still, I could not decide where Sean and I should go. I spent hours on TripAdvisor, reading hundreds of hotel reviews. I bought guidebooks to France, Greece, and Italy. I quizzed nearly everyone I encountered about their favorite destinations.
We went to Ireland.
Now, I love Ireland. But we had gone there exactly one year earlier. And stayed at the same hotel, where the same Enya CD was on endless repeat in the breakfast room.
Talk about risk averse.
I don't usually have that much trouble making vacation plans. But this was my honeymoon—the trip I'd be asked about for the rest of my life. In my mind, the stakes were too high to gamble. (As if Provence would have been a gamble!)
Some studies indicate that anxious people also make less optimal decisions. In one gambling experiment, for example, highly anxious subjects lost more money than mellower ones. And when choices are clouded with uncertainty, anxious people fare even worse. It looks like the slothful prefrontal cortex activity that is implicated in anxiety disorders may be to blame for these decision-making difficulties. When scientists at the University of Pittsburgh injected an anxiety-inducing drug into rats, the rodents had more trouble with a task that required them to switch between two rules in order to obtain a reward (a tasty sugar pellet) compared to when they were given a placebo. When the anxious rats were making a difficult choice, certain neurons in the dorsomedial prefrontal cortex actually fired more slowly.
So some numbed neurons may have sent me back to Ireland.
It is no surprise that wanderlust and anxiety do not mix well. Unfortunately, I have both. I love to travel, especially in the developing world, and yet I'm terrified of malaria-carrying mosquitoes, typhoid-infused water, and dodgy hospitals. Here are just a few of the places where I've had panic attacks: on the back of a motorbike in Vietnam; in a basement tango _milonga_ in Buenos Aires; along the seaside walkway (the Malecón) in Havana; and on a massage table in Nicaragua. And on airplanes. Many, many airplanes. Anxiety is a thief that steals the present moment. So some of my headiest travel experiences—visceral, beautiful moments of strangeness—have been muted, dulled by a steady drumbeat of anxious thoughts. Still, a tenacious desire for these moments propels me on to new spots on the globe.
I did not come from a family who traveled to exotic locales. My childhood vacations mainly consisted of long car rides to southern Illinois to visit family. My sister and I fought vociferously over inches of backseat space. When our fighting got too loud or went on too long, my mother would reach back and swat the air as my sister and I ducked and weaved to elude contact. We were also big campers, heading to various state parks in Pennsylvania and Connecticut. My family did not travel lightly. Our tent was enormous, with a turquoise-and-white-striped roof, like a circus big top, and room for four sleeping bags and my sister's playpen. Our cavernous blue cooler held seemingly endless supplies—from fixings for s'mores to boxed wine for the grown-ups.
In high school, I was incredibly lucky to go on a couple of weeklong overseas school trips, one to Greece and another to France and Spain, but those were mostly about kissing my boyfriends and sneaking sips of ouzo and red wine. But just before my freshman year of college, I spent the summer in England at a study abroad program. I studied British politics, learned to drink tea with milk, and went to plays and antiapartheid rallies in London. In this program, I met kids from all over the United States, many of whom already had dog-eared passports and told me stories about castles and nightclubs in France and concerts and art in the Netherlands. I pined for my own Eurail pass.
But anxiety derailed my travel plans. In college, I was too sick to study abroad. After graduation, I optimistically planned a two-month European backpacking trip with my roommate, Lisa. But I backed out in the end. I still felt too fragile.
It wasn't until a few years after graduation, when I was between jobs, that I was able to start satisfying my wanderlust. I took a three-week trip to Ecuador with my friend Sarah. We had no real plan, just traveler's checks, my high school Spanish, and a _Lonely Planet_ guidebook stuffed into our backpacks. We crisscrossed the country in buses and planes and stayed in ten-dollar-a-night guesthouses, visiting Incan ruins near Cuenca, listening to Andean music, haggling in markets in Otavalo, and seeing the haunting paintings of Oswaldo Guayasamín in Quito. I was dazzled by the majestic mountains, the Technicolor reds and blues of the indigenous women's woolen shawls, and the glossy waist-length hair of some of the Quechua men. It was during this trip that I became infatuated with the surprise and discovery of travel, the chance meetings and serendipitous turns. In Otavalo, I wandered into the middle of a water fight between groups of laughing uniform-clad schoolchildren, bumped into a cute Canadian guy, then spent the afternoon hiking with him and his Quechua friends to a remote waterfall. Uncertainty had never been so thrilling.
From then on, I traveled as much as time and money would allow: to volcanoes in Costa Rica, beaches in Spain, and museums in Italy. Between jobs at the _Journal_ , I took a month off and went traveling through Turkey with my friend Dave, eating just-caught fish in outdoor restaurants in Istanbul, exploring the fairytale landscape of Cappadocia, and sailing around the Mediterranean in a traditional _gulet_ boat, where we slept outside on deck and dove off the bow to swim. Each day—like an apparition—a couple of young boys in a small motorboat would appear wherever we docked to sell us overpriced ice cream. I left Dave, bounced up to Berlin to visit a friend and sample the city's techno scene, then took an all-night train to Copenhagen. When I awoke, we were waterborne: Sometime in the night the train had been loaded onto a ferryboat. I walked upstairs to an outdoor deck and saw the Baltic Sea.
In my early thirties, I started traveling alone. At first it was for only a few days at a time, but even so it was transformative. Without a traveling companion, there was no buffer, no distraction from experience. I met people easily. And perhaps unexpectedly, I was sometimes less anxious on these excursions. If anxiety overwhelmed me, I didn't have to pretend I was okay, because there was no one to disappoint.
I visited an ashram in the Bahamas, one where alcohol, garlic, and onions were banned (too stimulating) and participants did four hours of yoga each day. Yogis dashed to the resort next door for contraband beer and ice cream. Revelers on party boats heckled us as we chanted in Sanskrit near the shore. "Can you believe these people come here to do yoga?" yelled a wrangler. In Buenos Aires, I took tango lessons and ate steak with young Argentines.
As intoxicating as it can be, travel can also make me feel ridiculous and ashamed. The poverty in Chiapas, garbage-strewn roadways in Nicaragua, political oppression in Cuba, begging children in Hanoi—witnessing these things makes me feel self-involved and absurd. My life is so privileged. Do I have the right to be anxious and fearful?
—
After the relapse in my late twenties, travel became more challenging. For one thing, I was doing much more of it. My boyfriend, Alan, had moved to Mexico City to take a job as a foreign correspondent, and I visited him every couple of months. Eventually I moved there for six months. To me, Mexico City in the late 1990s was fabulous. Yes, the pollution and traffic were terrible. But it was also a riot of delicious food ( _chilaquiles_ , which is basically cheese-covered Doritos, for breakfast!), welcoming people, and gobsmacking sights. I once saw a man hawking six-foot-tall crucifixes near a highway tollbooth. ( _Are those ever an impulse buy?_ I wondered.) But the reports of crime and violence made me uneasy. Several of the foreign correspondents we knew had been carjacked in taxis and then forced—at gunpoint—to take money out of ATMs.
I began to dread flying and missed more than a few flights. I would stand at the gate, panicking, as passengers boarded—sometimes with my confused and, increasingly, frustrated boyfriend beside me—unable to move. I had an overwhelming fear, an absolute superstition that _this_ flight, _this_ plane would go down.
I continued to fly. I really had no choice. I was writing about technology and often had to be in San Francisco or New York. Alan was reporting stories all over Mexico and Central America, so if I wanted to spend time with him, I had to go along. Eventually each flight got a little easier.
I'm not afraid to fly anymore. If anything, travel is an antidote to my anxiety. Anxiety shrinks my world, but travel expands it. The heightened sensations of travel, the extremes in colors and tastes, can sometimes drown out the worries and obsessions.
The most frustrating—actually heartbreaking—fallout from my anxiety is that, when I'm in the thick of it, it separates me from those I love. Anxiety is an isolation chamber where worry and fear elbow out human connection. The frenetic internal monologue of catastrophe blocks out conversation. It is as if the narrative of my life has been dubbed in a language I don't understand.
In college, during one of my breakdowns, I remember talking with my aunt Gail. "I have mitral valve prolapse," I said. "One of the valves in my heart doesn't close all the way." She looked at me strangely, her sunny smile freezing. I was confused. That is, until I realized that I had told her the exact same thing just minutes before. I had anxiety-induced amnesia. I could walk and talk but nothing held. Like booze, anxiety can cause blackouts.
It is not just a matter of forgotten conversations. I can be selfish, deaf to the needs of others. Anxiety can breed self-absorption, and it is tough to nurture relationships when you're only half there. Wracked with my own fears, what help can I be to anyone else?
I literally hide, too. I don't go out. I don't see friends. Parties, dinners, and long conversations come to an abrupt halt. There's simply no room in my head for anything besides worry. I barely have the energy to respond to texts or emails. The anxiety makes me feel so shaky, so weak, so tired, and so inept, that even that tiny effort is overwhelming. I see incoming phone calls—the names of family or friends—and watch sadly, but with a whiff of relief, as they disappear into voice mail. My world shrinks as my emotional defensive crouch becomes a physical one.
And that is with people I'm close to. It is a different kind of excruciating with acquaintances. Wearing a mask is exhausting. I feel like a fraud. I can become socially anxious, too. I'll lie in bed, replaying the conversations of the day, worrying that I've offended someone; berating myself for talking too much, talking too little, or making a stupid comment.
Even when my anxiety is at a lower volume, it is still a pushy neighbor: chatty, intrusive, and often boring as hell.
There is an upside, though. Anxiety has given me incredible moments of intimacy and love. I've been the recipient of enormous kindness and care. My college friend Susie taking me to the ER in the middle of a panic attack and making me laugh. My dear friend Leslie, walking me around the streets of the Mission in San Francisco after I fled a bar, midbeer, with a racing heart. Lovely Amy holding my hand on a bench near my office while I waited for a Klonopin to kick in. My friends' support, sensitivity, and steadfastness make me cherish them all the more.
And when anxiety is at its usual low hum, I feel like my experience with it has given me a point of connection with other people in pain, that it has made me more empathetic. That is especially true now that I'm more open about it. Among friends and colleagues, I've become the go-to girl for anxiety issues.
I've found only one study that has looked at the relationship between empathy and anxiety; Israeli researchers uncovered a link between empathy and social anxiety. However, if we look at it more broadly, a large body of research shows the upside of trauma and pain. Psychologists even have a term for this: post-traumatic growth. It refers to the potential to develop a greater appreciation for life, see new possibilities, and deepen relationships after adversity. Most often it is studied in relation to physical illnesses like cancer or to tragedies like the death of a child. But I'd argue that grappling with mental illness can lead to growth, too.
—
I rely on my girlfriends more than I do any therapist or doctor. Ianthe and Roe have been my confidantes and cheerleaders for more than a decade. We met at work. Ianthe, a dogged investigative reporter, newly hired from the _Washington Post_ , walked up to my cubicle and introduced herself. Roe, who headed up the _Journal_ 's book division, sat less than fifty feet away from me.
The three of us have had loads of fun over the years. There have been late nights dancing at East Village clubs, trips to France and Florida, country hikes—and hundreds of long dinners filled with laughter and extreme silliness. We've supported one another through cancer, the deaths of parents, job changes, breakups, and miscarriages. If I ever need to post bail, I'll call them.
They are both beautiful and brilliant. Ianthe, who grew up in New York and Colorado with four sisters, is a whirling dervish of activity and, I'm certain, could convince almost anyone to do her bidding. She can talk her way out of parking tickets and snare discounts on hotel rooms. In a hostage situation, I'd pick her to negotiate. If we're out to dinner and I find a speck floating in my glass of wine (no _way_ will I drink that!), Ianthe will simply reach over and swap glasses with me. Roe grew up in a big Italian-American family in Brooklyn. She's an epic cook whose loves are good wine, good stories, her wacky family, and her large, loyal circle of women friends. When I'm anxious, sending her texts with a litany of worries, she is there to comfort me whether it is noon or midnight.
Most research on the effects of anxiety disorders on adult relationships focuses on romantic ones. But one interesting 2013 study looked at relationships with relatives and friends, too. The results make me realize how lucky I am. People with lower quality relationships with friends and relatives, those researchers found, had higher rates of anxiety disorders. And the researchers theorized that there's a bidirectional relationship between anxiety disorders and support and intimacy in relationships: struggling relationships fuel anxiety, and anxiety stresses relationships. In another study, socially anxious women said they reveal less in their friendships.
The scientific literature on anxiety's effects on friendship in childhood and adolescence is much more robust. This makes sense, since friendships are critical to kids' social and emotional development. For anxious kids, having supportive and intimate friendships leads to reduced anxiety over time. Indeed, being part of a group (any group, not just the "popular" one), and having a close and upbeat best friendship, protects kids from feeling social anxiety.
Supportive friendships also seem to prevent anxious kids from becoming depressed adults. In a 2016 study, anxious teens who said they felt loved or part of a group were much less likely to be depressed more than a decade later. By contrast, a paucity of loving relationships and little sense of belonging and being accepted during the teen years led to depression in adulthood. Good friends also enhance treatment for anxious kids: Those with caring friends respond better to cognitive behavioral therapy.
For kids, too, there is a bidirectional relationship between anxiety and the quality of friendships. Anxious kids tend to avoid social situations. But skipping sleepovers and soccer games means they have fewer opportunities to develop social skills. The ensuing social awkwardness fuels more anxiety. And so on.
Anxious kids generally have fewer friends and feel less well liked than their peers. Kids with social anxiety, in particular, tend to have more social challenges. In experiments designed to assess social skills, they've been found to be less assertive and effective. Socially anxious girls report less acceptance and support from peers. Anxious kids more often expect to be rejected. Research has found at least some of the chill they anticipate from peers is well-founded. One study had nine-to-thirteen-year-old kids rate videotaped speeches of other children, some of whom had anxiety disorders. The raters were then asked whether they liked the kids in the videotapes and whether they thought they would make good friends. Kids with social anxiety disorder were rated the most harshly. A study from 1999 found that 75 percent of children with social phobia said they had few or no friends; half did no extracurricular activities.
Anxious kids are more likely to be bullied. In one study, a staggering 92 percent of adults with social phobia said they had been severely teased in the past. Half of the subjects with OCD and 35 percent of those with panic disorder did. Boys with social anxiety may be more vulnerable to bullying than girls, since being quiet and withdrawn goes against traditional gender roles. And in another example of a negative feedback loop, bullying can lead to increased social anxiety. Adolescents who are frequently picked on are two to three times more likely to develop an anxiety disorder, according to one 2014 study.
Anxiety has cost me at least one friend. In my early thirties, I spent a lot of time with a group of five women, all a few years older than me. They were smart and accomplished, opinionated and fun. We'd meet about once a month for potluck dinners, rotating apartments. I bonded, in particular, with a woman named Alice. She was passionate about yoga and had a ballsy way of talking about her emotions and her relationship deal breakers. I was astonished by how assertive and definite she was. Like most young women I knew, I was much more timid, even apologetic, about my desires. She was a veteran of the Landmark Forum, a self-help seminar that was an outgrowth of the 1970s "est" movement. (One of its core goals is "freedom from anxiety.") We'd have long conversations over tea about love, work, and meaning.
One weekend Alice joined me at the country house I'd rented with friends, a spare place in the Catskill Mountains, a couple of hours north of New York City. We hiked, cooked, and talked. One evening we decided to go to the tiny movie theater in a nearby town where an action movie was playing. I remember finding our seats in the already darkened theater to a booming soundtrack of gunfire and explosions.
Ten or fifteen minutes in, my heart rate kicked up, and I felt hot and slightly breathless: the telltale signs of a panic attack. I turned to Alice. "I need to walk around the block. I'm feeling anxious, like I might have a panic attack. Can you come with me?"
"You want to leave the movie right now?" she asked.
"Yes, I need to go," I said.
She did come with me, and she did walk with me. I paced around the block, Alice silent beside me, for a good half hour or so. Then I drove us back to the house. I tried to explain what a panic attack feels like and how I dealt with them.
The next morning I felt embarrassed. I apologized for aborting the movie. "Don't worry about it," Alice said, yet I felt a subtle shift, a new distance. I made an extra effort to be sunny and calm. I took a series of portraits of her next to a blooming magnolia tree, then drove us back to the city.
After that she retreated. There were no more tea dates or long talks. We still saw each other at the potlucks, but it became clear that that was as close as she wanted to get.
The truth is that some people are spooked by out-of-control anxiety. Emotional states, neuroscientists have found, are contagious, and some people don't want to catch what I have. Scientists call this "emotional contagion," based on findings that we tend to automatically mimic the expressions of others. Making a particular expression can actually induce that emotion, which means that being around an anxious person can make you feel anxious, too. In fact, it can cause levels of the stress hormone cortisol to spike.
When the anxious person is someone you love, this emotional contagion is even more pronounced. In a 2014 study, researchers in Germany and Boston had subjects perform stress-inducing tasks while they were watched via a one-way mirror or live video feed by someone of the opposite sex. In some cases, the observers were strangers; in others, the observers were the subjects' romantic partners. The tasks—giving a short speech and doing some difficult math problems—made the participants stressed and anxious; most of them saw their cortisol levels at least double. That was no surprise. But about 26 percent of the _observers_ had significant increases in cortisol, too. If they were watching a romantic partner rather than a stranger, the number jumped to 40 percent.
This might be one reason why adults with anxiety disorders are more likely to be single. With dating, the goal is usually to present your best, most confident, most alluring self, and anxiety is no aphrodisiac. Those with anxiety disorders who do marry are more likely to divorce.
I've had boyfriends who were caretakers and others who were much less supportive or indulgent. Some were clearly afraid of my fear, worried they'd be sucked into a vortex and that their lives would become as constrained and small as my own sometimes was.
When I was sixteen, I met Scott at Images, a nightclub in Brewster, New York. It was teen night, an evening for kids who were into New Wave music to flirt, dive into mosh pits, and see bands with names like Cerebral Meltdown. We got to talking, and our two groups of friends ended up at the Windmill Diner, a cheap, brightly lit twenty-four-hour spot. Scott said he was charmed by the way I ate pancakes with my fingers. I thought he was ridiculously cute.
We were an unlikely pair. Six feet tall, handsome, and dark-haired, Scott was a sports star—starter on the football team, ace pitcher in baseball—at the Catholic high school in town. He was confident and popular but an average student. I was a bit of an oddball. While I was in honors classes, ran track, and sang in an a cappella choral group, I also bought my clothes at the Salvation Army (five dollars for a grocery bag full of vintage stuff) or dressed in flannel pajama bottoms and one of my dad's suit jackets, his silk tie wrapped around my ponytail. I defined myself by the music I listened to: the Smiths, Love and Rockets, Siouxsie and the Banshees. In 1987 western Connecticut, this was not mainstream: Boston, Def Leppard, and AC/DC dominated the mixtapes of most of my schoolmates. When someone in my sociology class hissed at me, "I bet you like U2," it was not a compliment.
But it was summer, and we went to different schools, and so our disparate places in the high school pecking order didn't seem to matter. We had an idyllic few months, roaming the streets in my little Chevy with a carload of friends, singing along to music, swimming in the lake, and drinking wine coolers in assorted fields and backyards.
Then Scott left for college. I moved to Michigan, and Scott and I broke up. But by the following year, I was a freshman at Michigan, and Scott had transferred to Michigan State. We started dating again, off and on. When I got sick, Scott became the "nocturnal life raft" I described in the first chapter of this book, when my panic disorder hadn't yet been diagnosed.
Looking back, I'm astonished by his unwavering support. He was twenty years old and a full-time student at what was known as an epic party school. He had pledged a fraternity. He liked to drink, smoke pot, and hang out with his friends. I would not have pegged him as a steadfast partner in the face of mental illness.
When I got sick my senior year, Scott came through once more. What's remarkable is that by this time we weren't even dating. In fact, I had another boyfriend, although that relationship was long distance. My parents had moved to Texas, and Scott was one of the only people nearby I could count on. He was, once again, my anxiety car service, taking me to therapy appointments, doctors' visits, and the ER. I spent many weekends in his room in the beat-up apartment he shared with several of his fraternity brothers. I'd lie huddled in his bed—really just a mattress thrown on the floor—as a party swirled in the apartment beyond Scott's closed door. I'd hear girls giggling, boys boasting, and music blaring and hunch farther under the covers, feeling embarrassed and fragile.
I became physically weak. I was barely eating, and the churning anxiety zapped my energy. One episode from this time is seared into my memory. I'm in Scott's bathroom, leaning against the white-tiled wall and clutching the towel bar. I need to take a shower but I'm too wobbly to stand on my own. Tenderly, as if I'm a child, Scott undresses me and leads me under the water. Keeping a steadying grip on my elbow, he shampoos my hair, cupping a hand at my forehead so the soap doesn't run into my eyes.
I'm certain that I would not have stayed in school if it weren't for Scott. His support and care kept me from phoning my parents in Texas and demanding that they let me come home. When things got too tough in Ann Arbor, he'd whisk me back to his darkened bedroom, a cocoon where I felt safe. Scott was one of the few people with whom I could be truly authentic. No matter how scared or self-involved I was or how much of an invalid I became, he stayed. I don't remember him ever criticizing me or telling me to toughen up.
I had the immense good fortune in college to move from one understanding boyfriend to another. I met Joel during spring break of my junior year. This spring break was unusual. I still felt shaky and anxious. I did not want a repeat of the prior year's truncated and disastrous trip to Cancún, so I had a strange hybrid vacation. Several of my sorority sisters planned to travel to South Padre Island, Texas. My parents lived in San Antonio, about a four-hour drive away, so I convinced them to stay a few days in South Padre, too. That way I could hang out with my college friends during the day but retreat to the safety of my family at night or when I got too anxious.
I was on the beach when my friends and I noticed a group of guys smiling our way and generally trying to get our attention. We engaged in a volley of whispering and glances but didn't actually meet. Later that night, though, I was at a bar, one of those open-air fishing-themed spots with plastic starfish on the walls and Jell-O shots on the menu. One of the guys from the beach—tall and cute, olive-skinned with sandy brown hair arranged in an artful bedhead—walked over to me and told me his name was Joel.
He bought me a Coke. We danced to "Just Like Heaven" by the Cure. He asked for my phone number. Joel was twenty-five and an MBA student at Michigan, and we began seeing each other as soon as we got back to Ann Arbor. I fell in love with his goofiness and kindness. But Joel graduated just a few months after we met and left for a job in San Francisco. I flew to see him every few months—as often as I could pay for plane tickets with the money I made at my part-time job in a clothing store. I was still struggling with anxiety, but I remember our early relationship as light and fun, filled with dance parties with friends and meandering strolls around the Marina district.
Joel, however, recalls that anxiety reared its head as early as our third date. We were at his grad student apartment in Ann Arbor, and I started to feel panicky. I told him I needed to get some air, and we walked around the triangle-shaped block outside about ten or twenty times. "I thought it was a little weird, but okay," he told me recently.
After my December relapse, Joel bought a pager so that I could reach him anytime. (This was 1992, before cell phones were ubiquitous.) I was the only one with the number. He left the device on all night, sitting on the nightstand, so he'd wake if I needed him. I'd buzz him mid-panic attack, and he'd call and calm me down, telling me I'd be okay, that he loved me and wouldn't let anything happen to me.
Joel researched my various physical symptoms and always made sure we were close to an emergency room. One day I called him and told him my legs felt tingly and numb. He walked to a bookstore across the street from his office and began paging through a medical reference book. "Everything just kept coming up MS," he says. "That was the scariest incident, thinking that you'd have this progressive downward spiral."
It is spring break 1992, a glorious blue-sky day in San Francisco. I'm lying on Joel's bed struggling to breathe. There's a weight on my torso. Pushing my chest out to inhale seems to take formidable effort. Then I exhale in a big rush. At the time, I'm in therapy at the Anxiety Disorders Clinic, but I still think it might be something terrible. Joel has been trying to reassure me for days. "You've been able to have sex," he points out. "You couldn't do that if you were dying." But my doomsday forecasts have spawned a seed of doubt. Could it be a pulmonary embolism? Joel finds a well-regarded pulmonologist at a local hospital and gets me an emergency appointment. I lie on a cold, metal table, and a technician injects a radioactive substance into a vein in my arm.
There's no blood clot. Joel drives me to a bed and breakfast in Santa Barbara to celebrate. We drink wine and eat chocolate in bed.
Years later Joel says my anxiety sometimes made him feel helpless and scared. But it was never a drag to him, he says. "It actually drew me closer to you," he says. "I felt very protective. You were going through something really hard, and I wanted to help in any way I could."
Joel and I broke up not long after I graduated from college and moved to Washington, D.C. During my twenties, I had several boyfriends. While my anxiety was mostly under control during those years, I still felt its effects. I stayed in some relationships—like one with a controlling and belittling editor thirteen years older than me—too long. I became emotionally dependent on, and romantically entangled with, my best male friend. The relationship—marooned in that awkward gray zone between friend and boyfriend—was unfair to him and ended painfully. The friendship was destroyed. I was like a trapeze artist flinging myself from one relationship to another, sometimes keeping my grip on one guy while transitioning to another.
The thing was that I was awful at making decisions. I was petrified of making the "wrong" choice. It wasn't, I don't think, that I was afraid of being alone. I was more afraid of regret. I didn't trust myself not to change my mind about someone.
Numerous studies have shown a link between mental illness and problems in romantic relationships. While depression seems to dampen relationship quality the most, anxiety wreaks its own havoc, contributing to a glass-half-empty view of relationships. In one 2012 study of heterosexual couples in which one or both partners suffered from panic disorder or GAD, the partners with anxiety disorders judged their relationships to be of lower quality than those without disorders. This was especially true of women. Men with anxiety problems judged their relationships harshly only if their female partners also had anxiety disorders.
Some anxiety disorders seem to cause more relationship turbulence than others. In one study, men whose wives had panic disorder reported lower-quality marriages than men whose wives had other anxiety disorders. Relationship issues exacerbate anxiety, too. A 1985 study following people with agoraphobia found that those with marital problems didn't respond as well to treatment for their anxiety.
Of all the anxiety disorders, social anxiety tends to be most disruptive to relationships. Women with high levels of social anxiety say they both give to and receive from their partners less support. They say they disclose less and tend to be less satisfied in their relationships, too.
As I entered my late twenties, anxiety seemed to be more of an occupying force in my relationships. While I wasn't debilitated as I'd been in college, these relationships were more serious. They were the ones that might conceivably lead to marriage and children. The stakes were higher.
I met Alan at a nondescript restaurant on the Upper West Side during lunch with a mutual friend who was not so subtly trying to set us up. The lunch was awkward, filled with long pauses. Alan had just moved to New York from Africa, where he had been living and working as a freelance journalist for several years. He was having a tough time making the transition to New York and the seeming frivolity of life in such a peaceful, affluent place. "People here talk about going to the gym," he grumbled.
We met again, at a party a month later, and the conversation flowed more easily. A few months after that, he called and asked me out. We ended up going to an awful play and having dinner at a cheap Italian joint, now long gone, in the West Village. We laughed and talked late into the night. On our second date, we wandered around the Metropolitan Museum of Art and kissed in a hammock on the rooftop of his apartment building. A few weeks after that, he shyly asked if he could call me his girlfriend.
I fell hard for him. We bonded over reporting and writing. We read each other's stories and gave each other advice. I was wowed by his fearlessness, how he had flown to Africa with a laptop and almost no journalism experience and made his way as a freelance reporter. He told me of grim experiences: seeing bones at a church in Rwanda, seeing a mass grave of Tutsis who had been slaughtered in the country's genocide. He joked about the various parasites he'd contracted in Africa, about the worm he'd passed during a fancy dinner with diplomats. He put it in a film canister so that a doctor could identify it later. He had done things I wished I were brave enough to do.
But he wasn't cocky about it. In fact, he was often wracked by self-doubt. It was that combination of fearlessness and vulnerability that hooked me.
In New York, we threw parties, saw bands, and lounged around in Central Park. Alan taught me how to Rollerblade and rock climb, helping me pick out a bright orange harness and purple climbing shoes. But five months into our relationship, he was offered the job in Mexico City.
I told him he had to do it, but there was never any doubt that he'd go. He was miserable as an office-bound editor. He wanted to travel and cover stories. He asked me to come with him to Mexico, but at the time I was close to being made a staff reporter at the _Journal_ and felt I'd being saying goodbye to a journalism career if I left New York. We decided we'd stay together and have a long-distance relationship. After all, we still had six months before Alan had to make the move.
Within weeks of Alan accepting the new job, I had a relapse, spawned by the episode of blind spots while walking down Seventh Avenue. While Alan was throwing himself into Spanish lessons and Mexican history, I was swiftly sliding back into hypochondria. Because my doctor thought the blind spots were an ocular migraine, he had me see an ophthalmologist. The eye doctor said he thought he saw some "bulging" behind one of my eyes. (This can be a sign of a brain tumor.) He sent me to a neurologist, who did an MRI. (Was this the third—no fourth—brain MRI I'd had in my not-yet-three decades of life?) There was no tumor.
Even with the clean MRI results, I became fixated on the idea that something was wrong with my brain. I worried especially about my memory. I furtively wrote down conversations shortly after they happened, then tested myself at night to see how much I could remember. I'd wring my hands when I discovered a lapse. I tried to keep most of these worries from Alan, but I wasn't that successful. "We would be out, and you'd say 'I have a headache' or 'I feel weird, I think I have a brain tumor,' " Alan recalls. "I'd think, 'Seriously? You had one last week.' You were often imagining that you had a terminal illness."
I felt ridiculous and ashamed. Alan had seen some truly horrible things in his work. My own concerns seemed petty and small. So I did my best to hide emotionally. Between that and Alan's impending move, I felt increasingly cut off from him.
The anxiety built all summer. That August Alan and I planned a trip to Maine. We'd spend three days hiking along the Appalachian Trail, traversing three mountains more than four thousand feet high, and a few days relaxing at a rustic cabin on a lake. This would be my first real backpacking trip—carrying my gear, drinking water from streams (after adding a dose of iodine), and sleeping in a tiny tent or bunking in primitive lean-tos.
The trouble started with my tortured attempt to buy a sleeping bag for the trip. I could not do it; in my addled mind, selecting the "right" bag would magically protect me from dehydration, broken bones, homicidal bears, and other sinister scenarios. Choose the wrong bag, and I was screwed. I bought two bags and laid them out in Alan's bedroom, climbing into one and then the other over and over again. "Just pick one," Alan said, growing frustrated and confused.
My experience of that trip was like a split screen. On one side, I worried about having an asthma attack and dying. I thought about how far we were from a hospital and how long it would take help to arrive. On the other side, I marveled at a moose drinking from a pristine mountaintop lake. Alan and I made love on top of a picnic table. We laughed about the "thru-hikers" we met (people who had been hiking the trail for months) with trail names like Mousetrap and Stickman. One guy was proud that he was still wearing his original boots, now held together with duct tape. The thru-hikers dubbed Alan and me "the Weekenders." There's a photo of me from that trip: topless with khaki shorts and brown leather hiking boots, triumphant on the apex of a mountain. I look healthy and strong.
—
Several days later Alan and I are eating at a fish shack in Bar Harbor. Chattering sunburned families, red plastic baskets of lobster tails and crab claws in front of them, are all around us.
Suddenly I feel a lump in my throat. I cough. Take a swig of water. The lump is still there.
My skin feels hot. My heart beats faster.
I'm having an allergic reaction to the shellfish, I decide. My throat will close up. My throat will close up, and I will die.
"I feel like I can't breathe," I tell Alan. "I think I'm allergic to the crab. I need to get to a hospital."
He asks whether I'm sure, and when I say yes, he grabs my hand, and we run to the car. Mount Desert Island Hospital is a twenty-minute drive away.
It is getting dark. Alan is speeding along the twisting roads, glancing worriedly over at me, his arms taut on the steering wheel. I am motionless in the passenger seat. My entire focus is on moving air through the viselike grip of my constricted throat.
"Please don't let me die. Please don't let me die," I beg.
"We're almost there. You'll be okay," Alan says. He does not sound convinced.
As we pull up to the small hospital, a tiny doubt pierces the fear: _Maybe I'm having a panic attack._
The building is almost entirely dark. The few visible lights point the way to the emergency room. Alan is breathing fast, too, hopped up on adrenaline. I lean into him. "Maybe I'm just having a panic attack," I say.
My doubt grows. When I check in with a nurse, I tell her my symptoms but also that I'm prone to panic attacks. Instead of seeing a doctor right away, I pace around the waiting room. My symptoms begin to subside. Alan is quiet, shoulders slumped. He looks drained. Later he tells me that during the drive he was making plans. If I stopped breathing, he'd pull over to the side of the road and jam a hole in my trachea with one of the tools on his Leatherman, which is something like a Swiss Army knife.
My anxiety shrouds the rest of the trip. It is now an uncaged thing, ready to land on any uncertainty. On the drive home, the lump in my throat returns, and my skin feels itchy. I make Alan exit the interstate to stop at another emergency room, where I get a shot of Benadryl.
—
Back at home, I started taking Paxil, and my anxiety abated somewhat. Alan left for Mexico a few months later. For the next year and a half, we had a long-distance relationship. In some ways it was idyllic. We traveled all over Mexico. We met up for road trips to California and Nevada and Mississippi and Louisiana, fishing for crawfish off the deck of a rented house on a bayou. We visited Culebra, an island in Puerto Rico, just in time for a hurricane. We raided the grocery store for food along with the locals and huddled around a battery-powered radio in a cinder-block-walled hotel with new friends.
My anxiety waxed and waned. Alan, for the most part, tried to ignore it. He told me recently that he hadn't known what to do. "I think my instinct and the instinct of a lot of men is to solve problems, and this one didn't seem like a solvable problem. Usually, I just tried to pretend it didn't exist," he said. He did sometimes try to talk me out of my anxiety, to convince my revved-up amygdala to listen to logic. Like during the Oreo Incident.
During our vacation in Culebra, we were staying in a small wooden bungalow near the beach. I was in the kitchen eating Oreos, a treat I'd loved since childhood. I had eaten maybe two or three and reached my hand into the bag for another.
That's when I saw them.
Ants. Dozens—no, hundreds!—of ants. A mob of ants. They were swarming inside the bag, crawling on the cookies, their wiggling black bodies stark against the white filling. An intrepid few had started the trek up my hand.
I shrieked and dropped the bag. I grabbed a paper towel and spat out the cookie sludge in my mouth. But I knew it was too late. I had definitely already eaten some. Ants were now making their way down my esophagus. They were moments away from my bloodstream.
"Oh, my God, there are ants in here. I've eaten ants!" I wailed to Alan. "I need to throw up."
Alan looked inside the bag. "Okay, maybe you've eaten a couple of ants. But it doesn't seem like such a big deal. They're protein."
"No, I need to get rid of the ants. I could get sick. They could be carrying some awful disease," I said, and moved toward the bathroom.
"Look, I'll prove it to you. I'll put myself at the same risk." He reached into the bag, grabbed an ant-covered cookie, and popped it into his mouth. "Mmm, that was tasty," he said, chewing.
He swallowed and reached in and grabbed another one. "That was good protein," he said, downing the second ant-strewn Oreo. "These are really good," he said as he ate a third cookie.
I laughed. "You really are crazy."
Still, Alan's antics weren't enough to defeat my anxiety. I went to the bathroom, stuck my finger down my throat, and made myself vomit.
The time apart—me in New York, him in Mexico—was a strain. There were anguished email exchanges, flirtations with other people, and angry silences during our brief times together. Our emotional bond frayed. Finally I got permission from the _Journal_ to work from Mexico City for six months. I arrived with a six-foot-long blue duffel bag stuffed with clothes and books and moved into Alan's house in the lovely Coyoacán neighborhood, not far from the onetime home of Frida Kahlo and Diego Rivera. I was twenty-nine, and it was the first time I'd lived with a boyfriend.
I loved Mexico City. The early morning call of the tamale carts: " _Tamales, tamales_." The circus acts—acrobats, flamethrowers—performing on the streets during red lights. The riot of colors in the plaza during the Day of the Dead celebration. Even the catcalls— _gringa, gringa, rubia, rubia_ (blondie)—I heard en route to my favorite coffee spot. And always the lilt of Spanish.
I wasn't blind to the poverty and corruption. And I did notice that people with darker skin were more likely to wear the cheap blue uniforms of nannies and housekeepers, while the lighter-skinned shopped at Gucci and Zara in the tony Polanco neighborhood. Because of the pollution, I had to stop running. My asthma was kicked up by Mexico City's air, and I didn't have the money to pay for access to one of the pricey health clubs that circulated filtered air.
When Alan and I were in Mexico City, we did normal things: We rented movies, went grocery shopping, and worked in our side-by-side offices. I loved being able to pop next door to see him, still in my bathrobe, and run part of a story by him. We also kept traveling. To Panama. To Cuba. To the pyramids of Teotihuacan and the Mayan ruins of Palenque. The frenzied travel was partly anxiety-driven. I had promised the _Journal_ that I would return in January, and the specter of my departure was on my mind. Alan and I didn't talk much about what my return to New York would mean for our relationship. In hindsight, I wish I had been less focused on ticking off destinations in my _Lonely Planet_ guidebooks and rooted myself a bit more, made my own friends, and carved out more of a routine in Mexico City.
At the same time, Paxil's side effects mounted and took a toll on my relationship. My sex drive ebbed. Alan was frustrated, saying he felt rejected. I went off the medication.
When I moved back to New York, Alan and I had a vague understanding that I would stay for a few months to fulfill my commitment to the _Journal_ , then quit and move back to Mexico City. I'd freelance. We'd get engaged. But a few weeks later, during a phone call, he broke up with me. He wasn't ready for a big commitment, he said. He wanted to date other people.
Years later he told me that my anxiety was a big part of why he ended things. "I wanted an adventurous life," he said. "I worried that your issues would hold us back, that our lives would be controlled by your fears and anxieties." Because I was scared of driving on highways, Alan thought we'd be limited in where we could live or that I would be too dependent on him. He also worried that I wouldn't be able to handle the pressures of motherhood, that I'd "freak out in moments when I needed you to be in charge with a kid."
I was devastated by the breakup. My emotional whiplash quickly devolved into the rom-com version of grief. I wrote pleading letters, dialed Alan's number, and hung up. I cried to my friends. I drank too much. I kissed cute strangers. I lost weight. (The misery diet is just as effective as the anxiety diet, I discovered.)
What I didn't do was have a relapse.
In some ways, heartbreak is antithetical to anxiety. Anxiety is all about the future, about the tragedies around the corner. Grief is about the awful thing that has already happened. I sank deeply into my messy present. (Years later I cyberstalked Alan on a dating website. In the section that asks "What have you learned from past relationships?" he had written: "How to diagnose panic disorder.")
I did obsess some about the past, about all the ways I'd failed as a girlfriend. The next time, I vowed, I'd be the most loving, the most patient, the most giving girlfriend around. That vow must have been why I ignored the endless red flags about Brad.
I had met Brad several times during my relationship with Alan, but it was not until a party for a mutual friend, just a month or two after I arrived back in New York, that we had our first real conversation, filled with light teasing and easy verbal volleys. He was thirty-five, with sandy brown hair, sexy crow's-feet, and impish blue eyes. A freelance photographer and avid rock climber, he was funny and wry and smart, with a quiet confidence. But I also found him emotionally opaque. His expressions and inflections could be tough to read. Despite that (or maybe because of it), I was instantly, wildly attracted to him.
The day after the party, I emailed my friend Anne, who was Brad's roommate, to debrief about the evening. "It was so nice to see your roommate Brad again," I wrote. "He's adorable, by the way." She wrote back saying that, funnily enough, Brad had said I was adorable, too. "Actually 'lovely' was the word he used," she wrote. Later that afternoon, my phone rang at work. It was Brad, calling to ask me out.
On our first date, I was nervous. I hadn't been on a first date in more than three years, and I was still wobbly from the breakup with Alan. I drank too much and talked too much, firing off probing questions like "Do you believe in God?" We kissed good night, but Brad didn't call me again.
Over the next few months, we saw each other at parties and emailed a little. In one exchange, he reminded me that we had promised to get together over dessert. We made another date.
We started seeing each other casually, meeting up for a bike ride, an outdoor movie, or a drink. The dates were fun, but he deflected personal questions. He was stingy with compliments and gave me few clues as to how much he liked me. Each time we parted, I wondered if he'd call again.
Then September 11 happened.
Brad hopped on his bike and rode to the twin towers with his cameras immediately after the attack. His photographs from that day—of the wreckage, the firefighters, the soot-covered survivors—were featured in magazines and newspapers. Meanwhile I was writing about the aftermath for the _Journal_. We'd work all day in a frenzy and meet up at night. The tragedy around us, the shared purpose, and the disruption of any normal routine shredded any resistance. We fell into a war zone romance.
We were sitting in his bathtub when he looked at me and said: "I love your eyes." He paused. "I love you," he continued. I was elated. "I love you, too," I replied.
Still, even in those first few months, I noticed something distressing. He was nit-picking and critical. He admonished me for clanging my spoon against my cereal bowl, for laughing at my own jokes, for talking about work too much. He criticized the way I ate and the way I kissed. One night after a dinner party, I confronted him. "I know I have a lot of issues, but the way I eat my cereal isn't one of them," I began.
He apologized. "I know I have a problem."
I stayed.
But the criticisms continued. We'd be having a good time, laughing and chatting, and then he'd pull away and get quiet. "What's wrong?" I'd ask.
I used the word _basically_ too much. I kicked his shin. I spoke too loudly. Brad seemed to seethe with a quiet anger. "It must be hard to be so annoyed by so many little things," I said. The digs fueled my anxiety, which just made me clumsier, more unnatural, and I'm guessing, romantically unappealing. I'd oscillate between fury and despondency, between anger at his unreasonableness and shame at my own flaws.
Then I moved in with him.
This may sound crazy, but there was a strange logic to my actions. I had a strong suspicion that this relationship wasn't good for me and that it had to end. But I knew I couldn't quit him yet. There was too much physical attraction, and I clung to the misguided belief that if I just tried harder and was more loving, he would be less critical. Part of me couldn't believe that someone could truly be so hung up on silly and inconsequential things. It must signal something else, some core unhappiness. If I could get to the bottom of that unhappiness, he would change.
So I held out a slim hope that things would get better. But I also figured that if we moved in together, things could get much, much worse. So bad, in fact, that I would have to leave. Moving in with him, in this scenario, would actually be a huge time-saver. Instead of frittering away several more years of my life, I would sacrifice only months.
I put almost all my furniture in storage and brought nothing to Brad's apartment in Gramercy Park other than some clothes, books, and a couple of bookcases. My first week there, Brad barely spoke to me. Did he regret asking me to move in? Did he feel ambushed by my stuff? (Living together had been his idea, I reminded him.) He wouldn't tell me. Instead, he complained to his sister: My towels didn't match. My bookcases were cheap.
Over the next several months, we did have some fun. We went dancing in East Village dive bars, had friends over for dinner, and went for long, beautiful hikes in the Catskills. But Brad was icy and aloof much of the time. And without my own apartment to retreat to, I had little respite from his moods. I became increasingly nervous. After waking, my heart would race for several hours. I lost weight. I became consumed with my relationship troubles and spoke with friends about little else. My panic attacks returned with a vengeance.
I had one in the kitchen of a Catskill rental house. My heart rate shot up, my arms went numb, and my breath came in gasps. I was convinced I was dying and asked Brad to call 911. (He did. I was loaded into an ambulance and checked out at a tiny country hospital.) I had another during an ocular migraine. Brad and I had spent a long day rock climbing. On the drive home, a chunk of my vision disappeared. Yes, this had happened before, but I still panicked. Maybe this time it really was a stroke. We passed a fire station, and I asked Brad to stop so that I could wait out the symptoms within arm's reach of medical help. Two sympathetic young firefighters sat me in a metal folding chair and chatted with me until my vision returned.
The attacks became more frequent. I was a repeat visitor to the ER at NYU Hospital. It wasn't often that I actually went inside and saw a doctor; I felt safer just being on the sidewalk out front. I could frequently be found skulking around the ER entrance mid-panic attack. I'd pace up and down First Avenue, trying to breathe deeply and talk myself down from whatever medical emergency I thought I was having.
With each panic attack, Brad retreated a little further. The warm moments between us became increasingly rare, and it was only when we were with friends that I saw the funny, charming guy I had fallen for. "You hardly ever smile anymore," I said to him one morning. Brad looked at me, stone-faced, and flashed an aggressive, over-the-top grin. "Is that better?" he barked.
It is September, and I'm on the top of a mountain in New Hampshire. It is a glorious early evening. Dark shadows shift as clouds dance above the rolling green vista. My worn-in leather boots dodge the delicate white wildflowers along the rocky trail. Brad and I are on day one of a three-day hiking trip in the White Mountains. We've hiked steeply uphill all day.
I've been nervous about this trip for weeks. By now, I love backcountry backpacking—the quiet, the beauty, the physical exertion—but I'm still afraid of it, too. There's always the potential for broken bones, snakebites, and asthma attacks, all of it miles from hospitals and help. And my anxiety has been so much worse lately.
We drop our packs off at the hut where we'll stay that night and continue farther along the trail to catch more mountaintop views. I start to feel a little woozy. The rocks under my feet rear up; the undulating mountains flatten. I stop walking. "Wait," I call to Brad. "I don't feel well."
Brad stops. "Maybe you need some water," he says. He opens the top of his Nalgene bottle and hands it to me. I tell him I want to go back to the hut.
Then my dizziness turns into a full-blown panic attack. My heart gallops, and my breath shortens. _You're okay, you're okay, you're okay_ , I repeat silently to myself, like a mantra.
It's dinnertime back at the hut. Fleece-clad families sit at long wooden tables and young staffers cheerfully pass out platters of freshly baked bread. While hikers eat hungrily, the staffers sing camp songs and act out silly skits. Brad and I sit across from each other in silence. He looks exasperated. My heart thumps wildly.
We sleep in bunk beds in a room with several others. All night I huddle in a ball on my top bunk, swallowing bits of Klonopin every few hours. But this time it fails me. It doesn't calm my racing heart. Brad disappears. I don't see him for hours.
In the morning, I tell him that I just can't continue the trip to the next hut, as planned. We hike down the mountain. As I descend, the anxiety eases. By the time I reach the trailhead, I feel almost fine.
A few nights later Brad and I were sitting on the sofa in our apartment. "You lost me on top of that mountain," he said.
A few weeks later I started looking for an apartment of my own. I signed a lease. Then I told Brad I was moving out.
The days leading up to my move were both banal and surreal. We didn't fight. Nor did we talk about what was happening. Finally I asked Brad, "Do you want to process this with me at all?"
"I'm sad you're leaving," he said.
Settling into my new apartment in an old brownstone in Fort Greene, Brooklyn, I was relieved but emotionally exhausted. I went on my own version of a relationship detox. I fell asleep early on Saturday nights. I binge-watched the entire six seasons of _Sex and the City_. I painted my bedroom walls a sprightly chartreuse. I found a new therapist, whom I have seen off and on ever since, the fabulous Dr. L. I went back on Paxil. And I took stock of what I wanted in a relationship. To my usual criteria of smart, funny, and cute, I added several more must-haves: kind, emotionally available and consistent, and able to handle my anxiety.
From then on, I made it a policy to tell every man I dated—no later than the second meeting—about my anxiety. I treated it almost like having an STD.
Because the reality is that anxiety affects partners. One study followed thirty-three heterosexual couples in which the women had anxiety disorders. On the days when the women experienced high levels of anxiety, the men reported less positive relationship quality (measured by things like "partner showed concern" and "partner was dependable") and more anxiety, anger, and depression. The more the men accommodated their wives' anxiety, the angrier they were. On women's highly anxious days, they reported higher negative relationship quality (measured by, among other things, "partner was demanding" and "partner was critical").
I met Sean online, on Nerve.com. It was 2005, way before OkCupid became popular and aeons before Tinder. In the mid-2000s, Match.com and Nerve.com were the online dating behemoths. Match was more mainstream. Nerve, which was initially founded as a racy online magazine that covered sex and relationships, was where you could find musicians, film editors, and graphic designers, many of whom had a penchant for artful eyewear.
Sean and I joke that it was his hat that hooked me. Among the pictures he posted on his profile was one of him wearing a Tibetan knit hat that fanned out in an enormous black yarn Mohawk. (There was no false advertising. Another photo revealed his completely bald head.) His note to me was sweet, complimentary, and clever. But it was the slightly weird, goofy photo that compelled me to answer and make a date.
We met at a café in Nolita. He had lovely blue eyes, strong features, and a slim gym-going build. While he had the look of the hipster Brooklyn artist/professor he in fact was (black jeans, green leather jacket, black wool beanie), he was also warm, funny, and direct. He exuberantly talked up his lifelong obsession with the Beatles and chastised me for suggesting that the Rolling Stones were in the same league.
On our second date, at a wine bar in Williamsburg, I told him about my panic attacks and my college breakdowns. I did not put a rosy spin on things: I told him that my anxiety was chronic and would likely return. Sean was empathetic; he didn't seem put off at all. And he had a secret of his own to tell me that night. Although he had listed himself as "single" on his profile, he had been married before. Six years earlier his first wife had collapsed suddenly of a heart arrhythmia brought on by a long struggle with anorexia and bulimia. She died in his arms. They were both thirty-three.
At nearly every date that spring and summer—to museums, galleries, and concerts—Sean brought me roses. Actually, they were drawings and screenprints he made of roses. "For beautiful Andrea," they were inscribed. He called when he said he would. He showed up on time. He told me how much he liked me, then how much he loved me. He drove me to IKEA when I wanted bookcases, then put them together for me. When my father was diagnosed with cancer and given a grim diagnosis, he researched treatment options. He could also be refreshingly unself-conscious and silly. I knew I loved him when I saw him sitting in his underwear eating a huge bowl of grapes and guffawing to the movie _This Is Spinal Tap_. I admired his certainty, steadfastness, and directness. And it freaked me out, too.
It is fall, and Sean and I are hiking up Mount Monadnock in New Hampshire. (Yes, it seems that the pivotal moments in all my relationships happen on mountains.) We're close to the summit when I trip on a tree root and go down. As I fall, I brace myself with my left hand. My wrist bends back alarmingly when I hit the ground, and my forehead bounces off a rock. Sean reaches out to steady me as I stand up. My arm and head throb. Within minutes, my wrist and hand turn red and swell. A large bump erupts on my forehead.
Sean is calm. "Let's get you back to the car," he says.
We walk quickly down the mountain. As we descend, I start to panic. I'm not so worried about my wrist. But the bump on my head really hurts. I feel dizzy. Maybe I have a head injury. Maybe my brain is bleeding right now. I focus on my feet, dodging rocks and fallen tree branches. The car seems so far away.
The trail begins to level off. My breath comes in sharp gasps. My arms tingle. "My arms feel numb," I say. "I think something is really wrong with my head."
When we get to the car, Sean calls 911. An ambulance picks us up and takes me to a small hospital. Sean sits beside me, stroking my hair the whole way. Crutches and casts line the exam room wall. (A nurse tells us that hiking injuries on Mount Monadnock keep them in business.) My head is fine. My wrist, however, is broken. I leave with a plastic splint and instructions to see a hand specialist when I return to New York.
On the drive home, Sean stops and gets me ice cream. When we get to my apartment, he heads to a grocery store to pick up milk and other essentials, then props me up in bed, placing a pillow under my sore wrist and a bottle of Tylenol and a book within easy reach.
A year later Sean proposed to me at the Metropolitan Museum of Art, his favorite place in New York, in front of a Van Gogh painting of white roses. We married six months later.
A couple of months after our wedding, Sean and I started trying to get pregnant.
I had always yearned to have a child. I thought it would be fascinating to have a ringside seat as a little person developed. And I wanted to feel that kind of immersive, unconditional love. You could abandon any other relationship, it seemed: with friends, boyfriends, a spouse, even with siblings or parents. But not with a child. That was eternal. I was awed by the thought of it.
I didn't, however, think I would actually be able to do it. After all, pregnancy is basically a ten-month dive into uncertainty. The scary tests, the strange symptoms, and the deep unknown of first-time childbirth can rattle even women without anxiety disorders. And there was a bigger question, too: With my marked genes, would it be fair to potentially doom a child to a life of anxiety and depression?
I am now a mother. These days I often think of my genetic albatross at the playground, while goofing around with my daughter, Fiona, who is now seven. Fiona is a delight—funny, bright, and kind. She loves to draw and read ( _Pippi Longstocking_ is a favorite) and play elaborate pretend games with her friends. She can also be shy and sensitive. She's petrified of many kids' movies. Playdates have sometimes ended with her in a heaving heap because of some perceived slight. I try not to see every personality quirk through _DSM_ -colored glasses, as some sort of burgeoning psychiatric illness, but I'm not always successful. I've read the research. Studies of preschoolers have shown that young children who are clingy and don't explore their surroundings—who are behaviorally inhibited—are three times more likely to develop an anxiety disorder by adolescence than kids with other temperaments.
Anxiety is a disease of doubt. Pregnancy and new motherhood are almost defined by uncertainty and unease. I did not have an easy time of it. Almost as soon as I knew I was pregnant, my anxiety soared. I worried about everything from amnios to autism. I'd wake suddenly at three or four in the morning, my mind overflowing with catastrophe. _This is the week when neural tube defects occur,_ I'd think. _Is it happening to my baby now?_ I was obsessed with miscarriage. I'd run to the bathroom to scrutinize my underwear for blood. My heart rate was constantly elevated. My breathing was quick and shallow. I was both exhausted and jittery—as though I had pulled several all-nighters in a row but was jacked up on a pot of coffee. I lost weight when I should have been gaining.
My bottle of Klonopin was still tucked into my bag, but I couldn't take any. My psychiatrist had told me it was too dangerous, that benzodiazepines during pregnancy were linked to birth defects. So I took walks in Fort Greene Park. I tried the breathing exercises I had learned in cognitive behavioral therapy. I weighed the evidence of my worries, telling myself that most babies are healthy, that most women get through pregnancy without dying or going crazy.
It didn't work. I called my psychiatrist on his cell phone. "How am I going to get through the next nine months like this?" I wailed.
At one point my husband was so concerned, he said, "We don't have to go through with this."
And we didn't.
I was ten weeks pregnant and getting an NT scan, a detailed ultrasound. The technician, a smiling middle-aged woman, was chatty as she wielded the wand and looked at a screen. I heard the even _whoosh, whoosh, whoosh_ of the baby's heartbeat.
Then her brow furrowed, and she fell silent. She stared intently at the screen while moving the wand around.
"Is everything okay?" I asked.
"I'll have to get the doctor," she said, taking off her rubber gloves.
"Please, can you tell me? Is everything okay?" I asked again.
"I need to talk to the doctor," she insisted.
I pressed further. "Can you just tell me if it's something bad? I'm here alone. My husband is working out of state. Should I tell a friend to come meet me here? If it's bad news, I don't want to be alone."
"I'm sorry. I can't give any results. The doctor will see you shortly, I promise," she said.
It was bad. I knew it. I'd seen enough hospital shows and movies to know that this is how it goes: the silence, the look of concern, the wait for the doctor, the awful news. I sat in the waiting room and texted my husband and my friend Ianthe. "Something is wrong with the baby," I wrote.
I was ushered into a small windowless room with a doctor. "Your fetus has a cystic hygroma," the doctor said flatly. "This can mean a genetic disorder or some other defect." I began to cry hard, catching tears and snot on my sleeve. _Couldn't they have put a box of tissues in this room?_ I thought angrily.
Later that afternoon another doctor, this one softer and kinder, explained that cystic hygromas are fluid-filled cysts caused by a blockage in the lymphatic system. My baby's case was severe: Many cysts lined the neck and spine. The doctor drew me a chart. Fifty percent of fetuses with a cystic hygroma have some chromosomal abnormality. Of the other 50 percent, one-third have a major structural birth defect, such as a heart anomaly. Some pregnancies end in miscarriage or stillbirth. Babies who survive might have cerebral palsy and developmental delays. In the far right corner of the chart, in small letters, she had written 17 percent. That was our chance of having a healthy baby.
But no test she or any other doctor could order would ever tell us for sure. Even if our baby's chromosomes, organs, arms, and legs were normal, there could be some stealth syndrome. The what-ifs were endless. It was uncertainty writ large.
We terminated the pregnancy.
Weeks later I started corresponding with a woman I met on a "pregnancy loss" online message board. Her fetus had recently been diagnosed with a severe cystic hygroma. She was told that the baby would likely die before birth. Deeply religious, she decided to carry the baby to term. I followed the blog she kept about her pregnancy. She wrote about the clothes she picked out for her son's funeral, about the memorial service she was planning, even as the baby was kicking inside her. Her son lived less than an hour after delivery.
Even though I wholeheartedly wanted a child, I was relieved not to be pregnant anymore. But I felt guilty about my relief. Had my anxiety somehow caused the cystic hygroma? I wondered. Was it the Prozac? I was taking 10 milligrams daily.
Studies have indicated that about 10 percent of pregnant women in the United States receive prescriptions for SSRIs. On the advice of my psychiatrist, I had switched from Paxil to Prozac before I got pregnant. In the mid-2000s, studies had linked mothers' Paxil use during pregnancy to heart defects in their babies. At the time, many doctors considered Prozac to be the safest SSRI during pregnancy. It had been around the longest, and thousands of babies had already been exposed to it.
However, Prozac was no match for my anxiety during my own brief pregnancy. I went to see a reproductive psychiatrist, one of a growing number who specialize in treating depressed and anxious pregnant women and their vulnerable fetuses. She reassured me that Prozac was safe to take during my next pregnancy. She told me I should take Klonopin, too, if my anxiety escalated again; the risk to the baby was minimal, she said. What I shouldn't do, she said, was try to go off meds. "She merits long-term prophylaxis with an SSRI to minimize the risk of relapse including during pregnancy and lactation," the psychiatrist's report read. "Many patients require a dosage increase during pregnancy to maintain remission."
I stayed on the Prozac and hoped for the best.
Later studies emerged showing that Prozac, too, was linked to a higher risk—about double—of heart defects and skull malformations in babies exposed to the drug during the first trimester of pregnancy. There were reports of birth defects among babies whose mothers took other SSRIs as well, but more recent research seems to exonerate Zoloft and Lexapro. There is a small increased risk of neural tube defects with Celexa. Some studies have shown that babies exposed to SSRIs in utero are more likely to be born prematurely and at lower birth weights. They are also more at risk of facing a serious lung condition called pulmonary hypertension.
However, the risks of all these outcomes are very small. Most women will have unaffected babies. And studies conflict, too. One 2016 analysis involving more than 2,700 women who took SSRIs during pregnancy found that their babies were no more likely to have heart defects than women who didn't take the drugs.
After my termination, my doctor had some of the fetal cells tested to see if there was a genetic reason for the cystic hygroma. The chromosomes were normal. Although I hadn't wanted my doctor to tell me the gender, there it was, typed on the lab report: XY. A boy.
—
The road to getting pregnant again was not smooth. I was thirty-seven at the time of my D&C, a uterine surgery commonly performed after a miscarriage or to terminate a pregnancy. My doctor told me to wait until my period returned and then try again. I was exhausted, emotionally drained, and terrified of another pregnancy, but I had no time to waste. I still wanted a baby. About a month after my D&C, my period returned. It was light and short. I called my doctor, who said this was typical, that it might take a while for my body to heal and my cycle to return to normal. Another month went by. The next period was similar, barely there, this time accompanied by intense cramping. I called my doctor again. She reassured me again. I made an appointment with another gynecologist. And another. They, too, said I had to be patient. It could take several months for my body to reset.
But I wasn't reassured. I posted questions on an online pregnancy loss support group and Googled "light periods after D&C." Eventually I found my way to Ashermans.org, a site devoted to Asherman's syndrome, a condition characterized by scar tissue in the uterus. The symptoms? Light—or absent—periods and cramping. The cause? Usually a D&C or other uterine surgery. I read haunting entries from desperate women made infertile by the scarring. I posted questions, describing my periods in gory detail. Kind, helpful women wrote back, advising me on the exact tests to request to secure an accurate diagnosis. I called one of the doctors I had seen and asked for an HSG, a type of X-ray where a dye is injected into the uterus.
Sure enough, the test revealed scar tissue nearly blocking my cervix. The cause of Asherman's—uterine surgery—is, ironically, also the cure. Sean and I traveled to a specialist in suburban Boston recommended by the Ashermans.org ladies. After three surgeries and a month on estrogen pills, I was cleared to try to get pregnant again. It was early June.
By July, I had a positive pregnancy test.
I braced myself for a resurgence of anxiety, but it didn't happen. During my first trimester, I was queasy and exhausted. In my third, I was achy and had trouble sleeping. But I wasn't extraordinarily anxious. I don't know why this pregnancy was different. The bout with Asherman's, I think, overrode some of my earlier fears. I had spent months desperately afraid I wouldn't get pregnant again. I had started to research surrogacy and adoption. So this time the positive test was a relief. Part of me also wonders if my body knew on some primitive level that my first pregnancy was doomed.
As my due date approached, I became scared of birth itself. My husband and I hired a doula. Many couples employ a doula to help them have an unmedicated birth. My own sister gave birth twice at home with no drugs. My goal, however, was much more modest: I just wanted to survive the ordeal without losing my mind.
I went into labor three days after my due date. It was a warm March day, and Sean and I walked the streets of our Brooklyn neighborhood. I paused and leaned on him during contractions. The pains were close together but not particularly intense. Our doula met us at home, and the three of us drove to the hospital together. For several hours, I wandered the halls of the labor and delivery unit, climbed in and out of the shower, and at one point took my husband's hand and banged it against my forehead to distract myself from the pain.
I got an epidural, and the pain vanished. Unfortunately, this opened up space for anxiety to come roaring in. Without the pain to focus on, I worried. Was the baby okay? Was I okay? I had heard about women having strokes after delivery. Would that happen to me? My legs felt heavy and numb from the epidural. Would it leave me paralyzed? I heard a _beep, beep, beep_. An alarm rang notifying the nurses that my heart rate was markedly high. I lay motionless in the hospital bed, staring at the clock. Worrying. Worrying. My husband and my doula dozed in straight-backed chairs.
My labor stalled. The doctor gave me Pitocin to try to kick-start it. Two hours went by, then four. Nothing was happening. My doctor decided that I needed a cesarean section.
I know women have C-sections every day, but for me, the surgery was horrifying. My epidural was upped so far, it felt difficult to breathe. My arms were strapped down to padded supports on either side of me. A blue plastic sheet went up in front of me, and a team of blue-cap-and-gown-shrouded doctors and nurses milled about. There was a jarring juxtaposition between my whirring mind and my paralyzed body. I've never felt so out of control.
"I don't think I can do this," I said to my husband.
"Help me," I said to the doctors.
The anesthesiologist bent down. "We can give you a sedative," he said. "But we want to get the baby out first."
I wish I could say that I felt a rush of love or awe when I saw my daughter's wriggling, blood-streaked body emerge above the blue sheet. "It's a nine pounder!" I heard someone exclaim. But I just felt desperation. I looked to the anesthesiologist. He was pushing a syringe into my IV. I felt the balled-up muscles in my neck ease a bit. The sedative was in.
Fiona was healthy and beautiful. She was also a tough baby. For the first few months, we had feeding challenges. She wouldn't latch onto my breast. When I tried to nurse, she would ball up her hands into fists and put them in front of her face. I took to yelling "hands" to my mother, mother-in-law, and husband, a signal for them to come over and pull the baby's hands away so I could push her mouth onto me. I had rounds of painful clogged milk ducts. My daughter and I passed thrush, a yeast infection in my breasts and her mouth, back and forth. I visited a lactation consultant, who ordered me to drink raspberry leaf tea (good for milk production), stop eating dairy, and do various mouth exercises with my daughter. (Smooshing her cheeks together to make a fish face was one.)
Almost as soon as we got the feeding thing down, the crying escalated. Fiona was colicky, which is just a euphemism for what seemed like nonstop screaming. We swaddled her, shushed her, and held her while bouncing up and down on an exercise ball. Still, she cried five, six, seven hours a day. Nothing seemed to work except for Marvin Gaye's "What's Going On" on endless repeat. It was her aural pacifier.
I joined a group of new moms and met up with them and their newborns at neighborhood cafés and, sometimes, bars. Early evening at one was dubbed "Nappy Hour" because of all the diaper-clad infants and pilsner-sipping moms. The other women chatted as their babies slept, nursed, or lay passively in baby slings. It seemed as though I was always on the periphery, bouncing and swaying in a futile attempt to stop Fiona from bawling.
Since I was breastfeeding, Fiona was still getting a daily dose of Prozac. But when she was nearly three months old, we were in Florida, at my parents' house. I had run out of Prozac, and my psychiatrist had called in a prescription to a nearby Walgreens. When I got the bottle, there was an orange warning label, one I had never seen before: "Do not take this medication while breastfeeding." I stopped taking Prozac that day.
As with the emerging evidence about heart defects, scientists were finding that SSRIs had varying degrees of safety during breastfeeding. Prozac, it turns out, is found in breast milk in much higher levels compared to other drugs in its class. There have been some reports of excessive crying, irritability, and feeding problems in nursing infants whose moms were taking it. Other studies link Prozac to slow weight gain in infants. Paxil and Zoloft, which are nearly undetectable in infants' blood, are considered a safer choice.
More worrisome are the potential long-term effects on kids exposed to antidepressants in utero. The science is decidedly mixed: Some studies have found an increased risk of autism and ADHD. A 2016 study, for example, found that children born to women who took SSRIs during the second and/or third trimester of pregnancy were twice as likely to develop autism as those who weren't exposed to the drugs. Other studies have found no link between antidepressants and autism.
Another set of studies has found that exposure to SSRIs can lead to behavior problems and subtle defects in motor function and language development. In a 2016 study of preschoolers, some whose mothers had taken SSRIs during pregnancy had more behavioral issues and lower scores on an assessment of expressive language. Other studies, however, found no long-term effects. One 2015 study compared children exposed to SSRIs in utero with their unexposed siblings. When it came to certain measures of intelligence and behavior, there was no difference between them.
Some doctors say that the mixed findings should be reassuring to women who take SSRIs during pregnancy. "If there was a definite problem, it should show up consistently," says Marlene P. Freeman, associate director of the Perinatal and Reproductive Psychiatry Program at Massachusetts General Hospital.
Still, some recent research has raised new concerns. A large study published in 2016 found that adolescents whose mothers took SSRIs while pregnant with them are more than four times as likely to become depressed by age fifteen, compared to children whose mothers had psychiatric disorders but didn't take SSRIs during pregnancy. The study is one of very few to follow children beyond the age of six. And it is the first to link SSRI exposure in utero to a later risk of depression.
The results are "a bit worrisome," says Heli Malm, an obstetrician at Helsinki University Hospital and lead author of the study. She notes that the oldest children in the study are just entering the ages when mood disorders tend to arise, so the number of them with depression could increase. She also cautions that the results are preliminary.
The impetus for the study was work that researchers at Columbia University had done on rodents. Mice who were given Prozac during the first week or two of life exhibited anxious and depressed behavior when they became adults. (The first few weeks of the life of a mouse are roughly equivalent to the second and third trimesters in utero for human babies.) For example, normal mice run away when mild shocks are delivered to their feet. But the Prozac-exposed mice moved very slowly or didn't escape at all when shocked. The mice "look perfectly normal until they reach the mouse equivalent of adolescence," says Jay A. Gingrich, a psychiatry professor at Columbia University Medical Center, who led the rodent research.
The early-life exposure led to slowed firing of neurons that respond to serotonin in the prefrontal cortex. In mice, higher doses and exposure during the equivalent of the second and third trimester were linked to the most severe behavioral effects. Gingrich is exploring whether non-SSRI antidepressants lead to the same problems. Most distressing to Gingrich was that administering antidepressants to the adult mice didn't reverse the anxious or depressed behavior. "That is what keeps me awake at night," he says.
After I got off the phone with Gingrich, I walked to a quiet corner of the _Journal_ newsroom and cried. By treating my anxiety, had I sentenced my daughter to depression? I felt waves of guilt and regret. I tried to reassure myself: Fiona is not a mouse. I took a small dose—only 10 milligrams—while pregnant. (The mice were given the equivalent of 40 milligrams.) Still, wouldn't it have been more logical simply not to take antidepressants during pregnancy?
But it isn't so simple. Mothers' anxiety and depression during pregnancy have been linked to problems in babies and kids, too. And many of those are the same conditions that are associated with exposure to SSRIs in utero. Some studies have shown that depression during pregnancy increases the risk of autism. It is also linked to preterm birth and lower birth weight in babies. And high anxiety during pregnancy has been linked to ADHD symptoms in children. It can be tough to tease apart the effects of the disease and the effects of the medication.
It wouldn't be ethical to conduct a randomized-controlled clinical trial with pregnant women, choosing some to get treatment and others to go without, which means that all this research is "observational." It is impossible to control all the factors that might confound the results. It could be, for example, that women who take SSRIs during pregnancy have more serious and more chronic illnesses than women who don't take SSRIs—illnesses that are likely to persist after their babies are born. Being exposed to a parent's depression during childhood ups the risk of developing mood and anxiety disorders.
The Belgian researcher Bea Van den Bergh has been studying the long-term effects of anxiety during pregnancy since the late 1980s. She initially recruited eighty-six pregnant women and has followed them and their children ever since. None of the mothers were being treated for anxiety disorders, but some were highly anxious. In a series of studies, she and colleagues found that the children of women who were highly anxious during pregnancy were more likely to be difficult babies, with more fussiness and sleeping and eating issues. By age eight or nine, they had higher rates of anxiety, aggressive behavior, restlessness, and difficulty focusing their attention.
When the children reached their teens, the ones whose moms had been anxious during pregnancy showed an atypical pattern in their levels of the stress hormone cortisol. In girls, that was associated with higher rates of depression. When the kids were seventeen years old, mothers' high anxiety during pregnancy was linked to specific cognitive issues in both boys and girls: These offspring had a tougher time on tasks that measured "endogenous cognitive control," a way of processing information that allows you to successfully adapt your behavior to changing goals without the help of external cues.
Van den Bergh found that babies were particularly vulnerable to their mothers' anxiety during the second trimester—from about the twelfth to the twenty-second week of pregnancy. High anxiety later in pregnancy didn't seem to affect children much. Researchers at the University of California at Irvine have found that mothers' anxiety during the nineteenth week of pregnancy (yes, that specific week) might actually reduce the volume of parts of the brain related to working memory and language processing. Since the women in this research weren't being treated for psychiatric illnesses, the negative impact could be even more severe for children of women with actual anxiety disorders.
Scientists in Dresden, Germany, are following more than three hundred women and their babies to see the effect of women's anxiety disorders and depression on themselves and their children. They've found that women who had an anxiety disorder anytime during their lifetime are more likely to have babies that cry excessively. (By excessive, they mean more than three hours per day, at least three days per week and for three weeks or more.) The researchers have also found a link between mothers' history of anxiety disorders and feeding problems in their babies.
This research bolsters what is known as the fetal programming hypothesis. There's growing evidence that the uterine environment can alter the development of the fetus, especially during certain particularly sensitive time periods. This means that children of anxious moms don't just have a genetic predisposition to anxiety; anxiety may actually be transmitted to them in utero.
"Normally a child is pretty protected" during pregnancy, says Hans-Ulrich Wittchen, a coauthor of the Dresden studies. "But in the later developmental months, there are stronger environmental factors. The unborn child is very sensitive to learning."
How does the transmission occur? Researchers think that one way is that high levels of cortisol in anxious or stressed pregnant women can cross the placenta and affect the developing fetal brain. There's also evidence that anxiety can restrict blood flow to the fetus. In a fascinating study by Columbia University researchers published in 2016, stress during pregnancy was found to turn off a gene in the placenta that helps to deactivate a mother's cortisol before the stress hormone reaches the fetus. This genetic change in the placenta had effects on the fetus: The offspring with the change had lower synchronicity between their movements and heart rates, which is known as fetal coupling. Increased fetal coupling is a marker of healthy neurodevelopment.
Ideally, babies would not be exposed to either SSRIs _or_ anxiety and depression while in utero. But that can be difficult to achieve. One study found that about two-thirds of women with a history of depression who stopped their medication just before getting pregnant or early in pregnancy relapsed. Women need more choices for treatment, and doctors need to encourage women to try nondrug therapies. (The reproductive psychiatrist I saw did not mention alternatives to me.) Perhaps women could do a course of CBT while tapering their drugs before trying to become pregnant and continue therapy during their pregnancies to deal with symptoms and prevent relapse.
—
During the early months of Fiona's life, I don't think I was more anxious than any other new parent. I had quotidian worries: Was she eating enough? Was she warm enough? Too warm? Was that bottle really BPA-free? Is that a choking hazard? Should I let her gnaw on that toy that says "Made in China"? My circumstances, it seemed, had finally caught up with the natural workings of my mind. It is socially acceptable, even encouraged, for new parents to worry: The "new mom" message boards I visited were a marketplace of anxiety and reassurance.
I only had one ER visit with Fiona during her first year. Desperate to use the bathroom, I had left her asleep in the middle of our queen-size bed. A minute later I heard a thump and a cry. She had fallen onto the floor, a distance of maybe a foot. With thoughts of head injuries and brain bleeds, I scooped her up, grabbed her car seat, hustled out to a cab, still in my pajamas, and took her to the ER at Columbia University Medical Center. I had heard that they had the best pediatric neurosurgery department in the city. She was fine.
My daughter seemed to hate sleep. For the first seven months of her life, nearly every daytime nap was taken on someone's body, usually mine. I held her on my lap or wore her in a baby carrier while she dozed. I'd drape a napkin over her head while I ate but still found crumbs and the occasional blueberry in her hair. At night, I could usually get her to sleep in her crib, at least for a few hours. She would fall asleep on me, and then I would gently, gently lower her to the bed, holding my breath and willing her eyes to stay shut. Yet too often she would wake and cry as soon as her body brushed the mattress. Even after the newborn sobbing abated, Fiona seemed chronically pissed off. Until just before her first birthday, she had the air of a disgruntled old man.
Sean and I were fried. We had no family nearby to help and, with me on unpaid maternity leave, little money to hire a babysitter. We argued. If one of us stayed minutes too long in the laundry room or in the shower, we'd be welcomed back with an accusing, "Where _were_ you?"
There's a rash of new studies looking at the ill effects of sleep problems in children, such as insomnia and chronically insufficient shut-eye. Poor sleep has been linked to aggressive behavior, learning and memory problems, and obesity. It also appears to increase the risk of the later development of mental illness, including anxiety and depression: There's some evidence that sleep deprivation weakens the connection between the amygdala and the prefrontal cortex.
Like so many parents, I read the baby sleep guides and periodically tried to "sleep train" Fiona. That invariably meant hours of screaming (the baby) and knocked-back glasses of wine (me). When as a two-year-old, she wouldn't nap outside the stroller, I wheeled her back and forth in the hallway of our apartment building until she nodded off and then parked her in the bedroom.
As Fiona grew into a toddler, she became sunny, affectionate, and funny. Parenting became much less of a grind when it was accompanied by giggles, hugs, and silly impromptu dancing.
As a preschooler, Fiona was spirited and joyful, obsessed with Mary Poppins and her hot-pink scooter. She was also reserved and cautious. She hovered along the perimeter of birthday parties and music classes. At the playground, if there were more than a few children on the jungle gym, she wouldn't budge from my side. At school, she struggled when making mistakes. "I'm terrible at G's," she'd wail when practicing her letters. She took rejection hard. At her fourth birthday party, she collapsed in sobs. "Leila told me not to look at her," she cried, her mouth still ringed with chocolate frosting.
I fretted and wrung my hands. Was this evidence of an anxiety disorder in the making? The future isn't exactly rosy for anxious kids. In a 2007 study, young people ages fourteen to twenty-four who had social anxiety disorder were almost three times as likely to later develop depression than those without anxiety. Another study, published in 2004, followed children ages nine to thirteen who had been treated for an anxiety disorder. Those who still had the disorder seven years after treatment drank alcohol more frequently and were more likely to use marijuana than those whose disorders had resolved.
New research shows that serious anxiety disorders can likely be prevented if they are caught and treated when kids are still young. Children can be taught to cope so that they don't later self-medicate with drugs and alcohol or screw up plans for college and careers.
There are also new therapy programs specifically designed for healthy kids with a genetic predisposition like my daughter's. Researchers at the University of Connecticut Health Center and Johns Hopkins University School of Medicine tested an eight-week program for 136 healthy kids ages six to thirteen who each had at least one parent with an anxiety disorder. During the following year, 31 percent of kids who didn't receive the therapy developed an anxiety disorder, whereas only 5 percent of the kids who received treatment developed one.
With evidence like that, how am I going to feel if I don't do something now and my daughter falls apart when she's a teenager?
Psychology professor Ronald Rapee began treating behaviorally inhibited preschoolers more than a decade ago, with the aim of forestalling anxiety disorders. More accurately, he began treating the _parents_ of behaviorally inhibited kids. Many parents of shy, skittish children fall into the trap of being overprotective of their emotionally fragile progeny. While understandable, this just reinforces kids' burgeoning feelings of vulnerability and inadequacy, which leads to more anxiety. In a six-session program called Cool Little Kids, Rapee teaches parents to reverse that pattern by fostering "bravery." Parents are told to resist the urge to allow their kids to avoid stressful situations or rescue them when they're afraid. Moms and dads are taught to deal with their own anxieties, too, since children model the behavior they see. (Parents are the only ones seen in the program. Children aren't treated directly.)
The program started at Macquarie University, where Rapee is the founder of the school's Centre for Emotional Health. I traveled to Sydney, Australia, to meet him. The Macquarie campus, a sprawling, leafy space dotted with buildings in a cacophonous hodgepodge of architectural styles, was quiet. Most of the thirty thousand students were on their summer break. I saw only a few slightly scared-looking young people with adults in tow, perhaps prospective students.
Rapee, who is fifty-five, is soft-spoken, with little of the swagger often encountered in world-renowned scientists. His office contains a shrine to his now-teenaged daughters' childhood. A bulletin board on one wall is filled with their preschool artwork: a painting of a rainbow, a drawing of butterflies, and a portrait of their father. A note says "I love my dad."
We speak candidly about the efficacy of Cool Little Kids. There's evidence that the program does prevent some anxiety disorders, particularly in girls. One study followed 146 behaviorally inhibited preschoolers. Half the parents attended six ninety-minute sessions of the Cool Little Kids program; the other half did not. The children were assessed again eleven years later, when they were, on average, fifteen years old. Thirty-nine percent of the teenage girls whose parents had gone through Cool Little Kids had an anxiety disorder, versus 61 percent of girls in the control group. The program didn't, however, make much of a difference for boys.
Technically, Rapee's work isn't prevention. Most of the children in the Cool Little Kids program, even the three-year-olds, were already clinically anxious. "The overlap between temperament and diagnosis is all just a big messy blob," he tells me.
Talking to Rapee is sometimes disorienting. He vacillates. Parenting matters when it comes to anxiety. Parenting doesn't matter. I feel as though I am seeing scientific uncertainty—or maybe scientific rumination—up close. His latest thinking seems to boil down to this: Parenting doesn't generally make kids anxious. But if a child is already anxious, then controlling, overprotective parenting can fuel and maintain kids' anxiety.
Over the years, Rapee has become more inclined to see the controlling hand of genes. The notion scares me. My genes, my grandmother's genes, may determine my daughter's trajectory. And there may not be much I can do about it.
—
Six preschoolers sit in a circle, legs crisscrossed on colorful foam mats. It is the final meeting of the Turtle Program, an intervention for behaviorally inhibited preschoolers. A shiny gold sign exclaiming CONGRATS GRAD! hangs on the wall.
"Can anyone remind us about some of the new things we've learned in circle time?" asks Danielle Novick, one of the program's leaders.
Marie, a little girl with curly brown hair and silver sneakers, shyly raises her hand. "Being brave," she says.
"Good job," replies Novick. "Thank you." She leans over and puts a sticker on Marie's knee, a reward for speaking up. "And we learned something about our eyes. What did we learn about our eyes?" Novick continues.
"Eye contact," says a little girl with honey-blond hair and a blue skirt.
"Yes, it's good to look in someone's eyes when you're talking to them," Novick says. "They can tell that you're listening to them and that you're being friendly."
I'm watching this exchange from an adjacent room via a one-way mirror. The program is actually a study conducted by researchers at the University of Maryland on the efficacy of an eight-week treatment to prevent anxiety disorders in behaviorally inhibited preschoolers. The children in this group have all scored in the top 15 percent on a scale of behavioral inhibition. Many already have difficulties making friends, going to birthday parties, and speaking up in preschool.
In the group, the children learn social skills. They practice introducing themselves, asking another kid to play, and asking and answering questions. They learn to express their emotions and to negotiate conflict—first using puppets, which can be less stressful. The children also learn deep breathing, or what the program calls "balloon breathing," to help cope with anxiety. Ken Rubin, one of the lead investigators of the study, says that even as early as age four, behaviorally inhibited kids often have poor social skills, are being rejected by their peers, and are internalizing negative feelings about themselves. "We're trying to interrupt that whole process," says Andrea Chronis-Tuscano, the other principal investigator.
While the children are in circle time, their parents are in a room across the hall, where they are taught to ignore anxious and avoidant behavior and to praise brave behavior. The treatment is based on parent-child interaction therapy, an approach originally created for kids with behavior problems. Parents first learn child-directed interaction (CDI), a form of play where children lead. This aims to strengthen the parent-child relationship, bolster the kids' self-esteem, and combat some parents' impulse to control situations with their inhibited children.
Parents are also taught to create a fear hierarchy for their children consisting of incremental steps culminating in an ultimate goal. (Rapee's Cool Little Kids teaches this, too.) For example, if the ultimate goal is to ask another child to play, a first step might be to say hello to another child. The idea is for each step to be achievable, so that children have success and can gain confidence. The parents are coached on how to set up bravery practice (which is basically exposure therapy). They help their children to practice things like talking to a teacher or doing show-and-tell during the group. Therapists coach parents in the moment via earpieces, secret service style.
On this day, nine parents and two program leaders are preparing for the scavenger hunt that will be today's bravery practice. Each family is assigned an animal. Group leader Christina Danko passes out a piece of paper with pictures of six animals; the goal is to find all the critters shown. To do that, the children will need to approach each of the other families to ask the name of their animals so that they can check them off. For these kids, the task is going to be difficult. It will be the first time that all the parents and kids have been together, and each child will be exposed to ten new adults.
The parents—with help from Danko—decide on goals for their children. One mother says that she thinks her son will be able to say "Hi," and then "Monkey" when asked which animal he has. But Danko doesn't think the child is quite ready to ask other families a question, so Mom will make the inquiries. Kids who aren't ready to respond to questions verbally are allowed to point to the pictures of their animals instead.
The parents file across the hall and into the children's room, where they tell their kids the goals and role-play interactions. Then Danko calls for the hunt to begin. The noise volume in the room rises. Soon kids are covered in stickers: 1ST RATE, COOL, TOP NOTCH, they say. Marie has one in her hair. Another little boy has one on his forehead.
The din is joyful.
Then, crying.
One boy has tears running down his face. He's hiding behind his mother, clinging to her leg, "Mommyyy. I want to leaavvee!" he yells. His mother looks panicked, as if she'd love nothing more than to escape, too. Danko stands beside her, coaching her. "Tell him to stand next to you," Danko says. "Stand next to me," the mom says to her son. When the boy does as he's told, Danko reminds the mom to praise him for it.
After a snack of mini donuts, the wailing little boy calms down. Danko congratulates the parents for hanging in there. By not leaving, they've communicated to their son that they won't back down and that he can survive uncomfortable situations.
Ultimately, the Maryland study will include 150 kids. Half will be enrolled in the Turtle Program and half, the control group, will do Rapee's less-intensive Cool Little Kids. The study is gathering physiological data on the children, like heart rate variability. And researchers are observing parents and kids together to assess such aspects of parenting as overcontrol, warmth versus negativity, and fostering independence. The kids will be observed at school, too. The study hopes to discern which kids benefit most from the program and whether a parent's anxiety, parenting style, or the child's own physiology affect how much the kids improve.
The researchers take pains to emphasize that they are not trying to change these kids' personalities—to turn shy and introverted children into extroverts. "Impairment is really the key," says Chronis-Tuscano. "We know how important social relationships are to people's happiness and success in life, and we don't want their inhibition to hold them back from doing anything." In an earlier small pilot study, the Turtle Program reduced anxiety symptoms in behaviorally inhibited kids. Before the treatment, nearly three-quarters of the kids met criteria for social anxiety disorder. Afterward less than a third did.
Marie's parents, Nancy and Brandon, say they knew they needed to get help for their daughter after a birthday party for another child. Marie, who was three at the time, was excited for the party and looking forward to seeing her friends in her playgroup. But during the celebration Marie spent the entire time clinging to her mother's leg. "She loves other kids. But she just freezes and gets very scared. The fear and anxiety were really holding her back and preventing her from being herself and enjoying her life," Nancy says.
This behavior was typical. At home, Marie sang and danced and chattered nonstop, but around other people she was painfully shy, almost silent. Once when Nancy had a friend over who Marie had met before, Marie hid under the dining room table and cried. Nancy and Brandon were worried about the future, too. Both describe themselves as socially anxious. Nancy had been diagnosed with social anxiety disorder in her thirties; she had a tough time mingling at parties and says her anxiety limited her friendships. Medication and therapy helped tremendously. "I didn't want Marie to struggle with it for decades like we did," Nancy says.
On Nancy and Brandon's fear hierarchy, the top spot—their main goal for Marie—was to attend a birthday party and play with the other children. Nancy and Brandon broke that goal down into small steps: making eye contact with a new child, saying hello, saying her name. At their weekly excursion to the farmer's market, Marie's parents told her if she waved to three other kids, they'd buy her a Popsicle. "She started waving to everyone," Nancy says.
Nancy and Brandon changed their own behavior, too. They used to apologize for Marie's silence or answer for her. They'd pull her out of situations where she was uncomfortable. They let Marie quit a ballet class when she had trouble separating from them at drop-off. Now they push her to be brave and have stopped using the word _shy_ in her presence. Recently, she has taken to calling herself Brave Marie. The program has made a real difference, the couple says. Indeed, Marie made a triumphant appearance at a birthday party just the week before. Now four, Marie clung to Nancy at the party at first, but soon she was doing crafts with the other kids and playing with the birthday girl. Although she didn't engage with kids she didn't know, Nancy and Brandon say this is huge progress.
Back in the Turtle Program the graduation ceremony begins. Novick calls each child forward to receive a diploma. CERTIFICATE FOR BEING BRAVE, it reads. One little boy skips across the room and beams as he shows his mom his diploma. Then he turns to me—an adult he doesn't know—and waits for me to congratulate him, too.
—
These days I'm much less worried about my daughter. In the last couple of years, she's become markedly more confident. She's still sensitive to shame and rejection, but she's more likely to stand up for herself. At her kindergarten graduation performance, she even stepped in and delivered the lines of another little girl overcome by stage fright. And when her class decided to sing "Happiness" from _You're a Good Man, Charlie Brown_ at the first-grade talent show, she volunteered to be Charlie Brown.
In a funny twist, it has become clear to me that my husband, Sean, is sometimes the more anxious parent. He's the one who panics when Fiona has a fever and admonishes her to be careful on the playground. If there's anything that worries me, it's Fiona's outsize fear of many kids' movies. Is it the equivalent of my childhood clown phobia—an omen of greater anxiety to come? Since prevention programs now exist for a range of mental health issues (not just anxiety disorders, but depression and psychosis, too), and since we know that mental illness is at least partly genetic, am I being neglectful by not enrolling Fiona in an intervention while she's still young?
While I was in Sydney, I tried to get some free advice. I told Rapee about my daughter's fears—that she's not only petrified of movie monsters and villains but also hates it when anyone in a movie is nasty or mean. We got through only a few minutes of _The_ _Wizard of Oz_ , I told him. She made me turn it off at the appearance of Miss Gulch, the nasty woman who snatches Toto and later transforms into the Wicked Witch.
I told Rapee that I wanted to take my daughter to see _Paddington_ , a movie about the talking bear that loves marmalade, so I showed her the trailer. It was frenetic. Paddington floods the bathroom and whooshes down a staircase in a bathtub. "I'm not seeing that movie," Fiona said. "It's too scary." I asked Rapee whether I should push her to see it. If the _Paddington_ avoidance was part of a bigger picture, I could work on it, he said. "Will it scar her?" I asked. The only downside, he said, was that she might have nightmares afterward.
So a couple of weeks after I returned to Brooklyn, during a frigid Presidents' Week when Fiona didn't have school, I took her to our local theater, a beat-up old place where the screens don't seem much bigger than some TVs. When I told her where we were headed, Fiona said she didn't want to go. "We can leave if it's too scary," I promised.
I could feel Fiona bracing for fear from the movie's first scenes. By the time an earthquake leveled Paddington's home in "darkest Peru" and killed his uncle, she had left her seat and scrambled onto my lap. When the villain, an icy Nicole Kidman, captured Paddington and threw him into a black van with TAXIDERMIST on the side, Fiona began to sob uncontrollably. "We can go," I said, and moved to get up. "No," she wailed, tears and snot running down her face.
We stayed. But Paddington's escape was drawn out and perilous. He nearly fell into a fiery pit. He was almost shot. Fiona's sobbing escalated, then abated. I asked her again whether she wanted to leave. An emphatic no. "Paddington will be okay," I whispered to her. And he was.
When the lights went up, I heard another mother say, "That poor kid got so scared." I felt awful and embarrassed, like I was a terrible parent. I told Fiona how proud I was of her.
That night and the next day Fiona talked incessantly about the movie. Not the scary parts but the parts she liked. Paddington making marmalade. And especially about the villain's eventual comeuppance: The taxidermist played by Kidman is arrested and sentenced to community service at a petting zoo, where a monkey she had planned on stuffing gets his revenge. He pushes a button, and hay and manure fall on Kidman's head. Fiona tells that part of the story over and over.
But when my husband asks her if she liked the movie, Fiona shakes her head. "It was too scary."
I'm still not sure what, if anything, I accomplished. As with everything else in parenting, I'm winging it.
After more than twenty-five years of living with anxiety disorders, I know better than to hope for a cure. I have easy years and tough years. When things are rough and anxiety threatens to derail my life and keep me from my family and work, I reach for medication (now Lexapro and my ever faithful Klonopin). I see my longtime psychologist. I try new forms of therapy.
Even when things are going smoothly, I'm careful. I arrange my life so I can sleep eight hours a night (sometimes nine). I rarely drink. I do yoga and take walks in the park.
I had always worried that when something truly terrible did happen (and if you live long enough, it always does), I wouldn't be able to handle it, that it would paralyze me. But that hasn't happened.
Ten years ago my father called to tell me he wasn't feeling well. He was achy and tired. Maybe he had the flu, he said. My mother was away visiting my sister, and my father often falls into a slight funk when he's alone, so I wasn't worried. A few weeks later, though, my mother called to say that my dad was in the hospital with kidney failure. I flew to Florida, where my parents had moved years earlier.
After a few days of tests, we learned that Dad had multiple myeloma, a virulent and incurable cancer of the blood.
He was put in the ICU and immediately began an intense regimen of chemotherapy. The hospital also tried an experimental course of continuous dialysis. It was terrible and surreal to see him so pale and supine in that hospital bed. At fifty-seven, he had been biking and Rollerblading just weeks before.
Back in New York, I put on my reporter's hat and researched his condition and its treatments for hours each day. While at work one evening, I stumbled upon one study that gave the life expectancy for patients with multiple myeloma that presents with kidney failure: three months. I broke down and called Sean. He drove to pick me up and held me while I cried.
After that I pulled myself together. I pushed my father to get a second opinion at the University of Arkansas for Medical Sciences in Little Rock. Data I found showed that their aggressive approach—which then involved two stem cell transplants—seemed to yield the longest survival rates.
We have no idea whether moving my father's treatment to Little Rock made a difference. But after many grueling months of treatment and one nearly fatal bout of sepsis, he has been in remission ever since.
I had my own cancer scare four years ago after I noticed that a mole on my cheek looked a little funny. What had been a flat brown spot was now raised and tinged with red. I went to my dermatologist, who said it was nothing, but I couldn't shake the feeling that something was off. I obsessively checked it in the mirror. I went back to the dermatologist. Still fine, she said. Still not reassured, I decided to see a more senior partner in the practice. She biopsied it and, a few days later, called me. "It's melanoma," she said, with urgency in her voice. "It has to be removed now."
Thankfully, the cancer seemed to be contained. Still, I got a second opinion. And a third. And a fourth. The problem was that the doctors didn't agree on a course of treatment. A few thought I could get away with cutting out just the spot. Others recommended a more aggressive approach that would involve removing a larger patch of skin. I decided to be cautious and then developed a huge crush on the plastic surgeon who dug a two-inch hole in my face.
The cancer dramas were overwhelming and nerve-wracking, but they didn't crush me. Real peril, I have found, galvanizes me. I make decisions and get stuff done. It's fear—not danger—that shuts me down.
—
I take some solace in the fact that anxiety may dissipate as we get older. Indeed, the rates of anxiety disorders dip as people enter their fifties. Is it wisdom or the growing awareness of our mortality that causes us to chill out? "Anxiety disorders have a tendency to burn out. You just can't stay anxious your whole life," says Harvard's Ron Kessler.
But after all my reporting and all my interviews with scientists, one major question still nagged at me: Why do the rates of anxiety disorders seem to be rising among young people? The numbers are particularly troubling for college students. Between 2008 and 2016, the number of college students diagnosed with or treated for anxiety problems jumped from 10 to 17 percent. Are we facing some generational mental health apocalypse?
I went back to the site of my own college breakdowns—the University of Michigan—to try to find out. I arrived in Ann Arbor in late April, in the middle of finals, which seemed a fitting time to be asking questions about anxiety. The libraries and cafés were filled with students hunched over laptops and scribbling in notebooks.
I met with student mental health advocates in the local Starbucks. Grant Rivas and Shelby Steverson are nineteen-year-old first-year students. Anna Chen is twenty-three and a graduating senior. All three are articulate, passionate, and slightly formal, rebuffing my offers to buy them coffee.
I asked them why they thought their generation seemed so prone to anxiety. They felt, they said, a relentless pressure to succeed academically. Their middle and high school years had been filled with talk of the recession, they told me, and a bachelor's degree is no longer any guarantee of a job, so they and many of their friends were gunning for graduate school and competitive internships. Every class, every test, every paper is high stakes. Rivas, who was wearing a yellow T-shirt that said MAIZE RAGE, said he was planning to apply for a spot in the undergraduate public policy program. "You've got to be really on top of your game from day one," he said. "If you get a B plus instead of the A minus, that little GPA difference can matter." He said a friend applying to the undergrad business program was so stressed out about an economics grade that he landed in the hospital with a panic attack. He could think of at least a dozen friends who were on psychotropic medications.
Steverson, who grappled with anxiety, depression, and ADHD, started feeling the pressure in middle school in Crystal Lake, Illinois, when students were first put on academic tracks. If you weren't in the top level in middle school, you wouldn't qualify for honors classes in high school, which meant that you wouldn't be prepared for Advanced Placement tests. And competitive colleges want to see AP classes. "If you want to get into these top schools, all of a sudden your résumé for college is gone," Steverson said. "So in sixth grade, kids were freaking out."
The students said social media has only amplified the stress. They knew that Facebook and Instagram were highlights reels—the party photos and boasting only a sliver of real life. But when they're feeling lonely or down, "it can be easy to compare the bad day you just had to everyone's smiling pictures," said Chen, the president of Michigan's chapter of Active Minds, the national student mental health advocacy group.
"You know how you can edit your education on Facebook, and it shows up in people's news feed? And people will like or comment on it and congratulate you?" Chen asked the group.
"You're going to so-and-so university," chimed in Steverson.
"Or you're going to intern at Microsoft," said Chen.
"And you get one hundred likes on it," said Steverson.
"And you feel really good about yourself," finished Chen.
Unless, of course, you're the one staying home and scooping ice cream for the summer.
Rivas argued that the culture of social media self-promotion has infected real-life interactions. "There's a very big push to seem like you have it all together," he said. Studies looking at the relationship between the use of social media and psychological well-being are mixed, but some do show a link to anxiety and depression. And certain types of behavior—like passively scrolling through Facebook news feeds without posting status updates—appear more likely to lead to feelings of loneliness.
The Michigan these students describe is a Darwinian pressure cooker, with kids obsessed with grades and routinely pulling all-nighters. This is not how I remember it. But the school is a lot harder to get into—and a lot more expensive—than when I went there. When I was a student in 1990, in-state tuition at Michigan was $3,502 a year. Now it's $16,218 for juniors and seniors. Even taking into account inflation, tuition has jumped nearly two and a half times. Adding room and board and books pushes the in-state cost to about $30,000 a year. The out-of-state cost is more than double that. In the United States, the average college senior who has taken out student loans will graduate with about $29,000 in debt, a figure that has jumped more than 50 percent in a decade.
"I see a lot more stress and anxiety and striving for perfectionism," said Todd Sevig, a psychologist and the director of Michigan's Counseling and Psychological Services, known as CAPS. Because of all the pressures in middle school and high school, "they are pretty fried when they get here. Sometimes I think students feel like they can't fail."
I met with Sevig and Christine Asidao, CAPS's associate director of community engagement and outreach education. CAPS provides individual and group therapy to Michigan students. Since arriving in Ann Arbor, I had heard several students grumble about wait times to see a therapist and about the pressure to end treatment before they're ready, but they universally had good things to say about Sevig, noting his commitment and approachability. Soft-spoken, gray-bearded, and bespectacled, Sevig has been working at CAPS since 1989, the year I had my first breakdown.
I posed the same question to Sevig and Asidao that I had to the students: Why are young adults now so much more anxious?
"When I was here, getting a B wasn't the end of the world," I told them.
"But it is now," said Asidao.
Besides the increased pressure to get good grades, Sevig and Asidao said students also might be more anxious because their parents didn't allow them to fail or flounder earlier: Some young adults face their first real defeats only after getting to college. But they also believe that much of the apparent rise in anxiety issues is an illusion. Reduced stigma around mental health issues is leading to an increase in help-seeking behavior, they said, and the success of their own outreach is causing more students to ask for assistance, too.
Starting in about 2008, CAPS dramatically ramped up its prevention programs. A year earlier, Seung-Hui Cho, a senior at Virginia Tech with a history of mental health problems, had shot and killed thirty-two people and wounded seventeen others. Then in February 2008, a graduate student at the University of Illinois killed five people and injured twenty-one in a lecture hall at Northern Illinois University. He, too, had previously been treated for psychological issues. All of a sudden, the mental health of college students and the responsibilities of universities were heavily covered by the media.
CAPS became a robust and highly visible presence on campus. It now does dozens of "tabling" events at university gatherings and festivals; staff members talk to students and hand out pamphlets about anxiety, depression, and stress. It jazzed up its website, adding quick screening questionnaires for GAD, depression, PTSD, and other psychiatric illnesses, and a series of videos of students talking about their own mental health issues. It created a YouTube channel and Facebook and Instagram accounts, and launched a Stressbusters app with inspirational quotes and relaxation exercises. It hosts a biannual Play Day, with balloon animals, chair massages, and Legos, to encourage students to take breaks and relax.
CAPS staffers are also trying to boost resilience among students, teaching them that it is okay to mess up, that obstacles will come up and they can learn how to cope with them. To that end, CAPS launched the "Wellness Zone" in 2011—a darkened room with three massage chairs, a light therapy machine, and meditation cushions. Between 3,000 and 4,000 students use the zone each year.
Around campus, I noticed small wooden plaques hanging from trees. DO SOMETHING: STOP STUDENT SUICIDE, they read. Underneath students wrote uplifting or imploring messages. "I lost someone to suicide. I've wanted to commit suicide. They both suck. Please don't," one pleaded. This was a CAPS effort, too.
When I was a student, I didn't know anyone who had visited CAPS. I didn't even know it existed. "When you were here, we primarily stayed in our offices and did a lot of individual therapy, along with the occasional workshop with RAs or student groups," said Sevig. Back then CAPS had one training program and one psychiatrist who came in for only a few hours a week. Now it has eight training programs and three psychiatrists working full-time. The increase in staff is a necessity: During the fall of 2015, CAPS faced an unprecedented 40 percent increase in the number of students visiting over the previous year. Between 2009 and 2016, demand for CAPS services increased by 36 percent.
"Previous generations would never touch the door of a therapist, that was the worst thing in the world," says Sevig. "That has really changed, and that's a beautiful thing."
CAPS sees many students who have already been treated for mental health problems in middle school or high school. By 2009, about 22 percent of students arriving on campus had had some previous counseling. Some students have had IEPs, or independent education plans, and received various types of services, so they feel comfortable asking for similar help in college. Indeed, like many other colleges, Michigan has seen soaring numbers of students formally requesting academic accommodations—like extra time to take tests, or permission to take exams in a smaller, separate room—because of psychiatric illnesses. Of course, not all students who seek help at CAPS have a psychiatric diagnosis. Plenty of students come in looking for support after an event like a fight with a boyfriend or girlfriend. But since 2008, anxiety has been the number-one issue for students visiting CAPS.
To accommodate larger numbers of students, CAPS does more group therapy. During the school year, they run thirty groups on topics from social anxiety to eating disorders, and for specific communities like women of color and LGBT students. CAPS has also added after-hours phone counseling. Students can call at three a.m. if they need to talk to someone. In tandem with these changes, the number of student advocacy groups devoted to mental health has skyrocketed over the last year at Michigan, from two to ten. The last few student government presidents have made mental health a center of their platforms, too.
I wish I could say that Michigan is typical, but in fact it has more mental health resources than many other colleges around the country. Almost 30 percent of schools don't provide psychiatric services to students, only referrals to outside practitioners.
—
The student mental health advocates I met say there is still stigma in some corners of campus, especially in the Greek system, among certain groups of international students, and in some communities of color. But most said they felt incredibly supported by friends, family, and the larger university community. Indeed, in a 2015 survey, 60 percent of young adults said seeing a mental health professional is a sign of strength; only 35 percent of adults older than twenty-five did.
I admit that I am nervous for these young people. I wonder what will happen when they leave this cocoon and enter the working world. Will their openness about their mental illnesses limit their career prospects?
I asked Cheyenne Stone, a freckled, smiley twenty-two-year-old senior who is heading to graduate school at Michigan. She is the executive director of the Wolverine Support Network, a student organization that runs peer support groups. (Students talk about everything from social anxiety to failing a test.) She's dealt with depression, OCD, and substance abuse and has written blog posts about her experiences.
"Mental health is a huge part of who I am. I would need an employer who understands that," Stone said. "I think if there is an employer who has a problem with the facts of my advocacy work, I don't want to work there anyway."
Anna Learis, an eighteen-year-old freshman, is equally unapologetic. She told me that when she decided to speak publicly about her panic attacks, her mother tried to dissuade her. "She's like, 'One day your possible employers are going to Google your name, and they're going to see that and then they're not going to want to hire you,' " Learis said. "I was like, 'Mom, the whole point of it is to address the stigma of mental health so people don't do that.' "
Learis, who says she's been anxious since she was about five years old, performed at Michigan's yearly _Mental Health Monologues_ , a show that features about a dozen students talking about mental health. She spoke about how her anxiety affects her boyfriend, whom she summons when she has panic attacks and who took her to the psychiatric ER a few months ago. When Learis has an attack, she scratches her arms until they bleed. "My skin feels like it's crawling. I don't notice I'm scratching until afterward when I see my hand bleeding," she says. On her wrists, jagged purple scars peek out from the long sleeves of her black-and-white-striped dress.
Learis, an engineering major, has an academic scholarship, which means she has to maintain a 3.0 grade point average. The stress fuels her anxiety. "If I don't do well on a test, I could fail a class. I'll lose the scholarship. We'll have to find the money to pay for it. I'll have to transfer schools. All about one test." She's trying to get approval to take tests in a smaller, quieter room. One of her friends who had a broken arm got to take a test in the smaller room. (The seats were bigger.) Learis doesn't see why her anxiety should be treated any differently.
I can't help but wonder—enviously, if I'm honest about it—what my college years would have been like if I had known about CAPS, if I had gone to the Wolverine Support Network meetings, if I had been able to participate in the _Mental Health Monologues_. These young people are energetic, passionate, and fearless. They, along with the adult leaders who support them, have transformed their campus into a place where mental health is a priority and mental illness isn't shameful. I have no doubt that in the years ahead, they'll revolutionize our workplaces, too.
—
Since my own college days, I've done two more rounds of CBT. I pursued the last one a couple of years ago, after spending months dealing with a strange tingling on the left side of my body. The tingling ran from my thigh to my knee, from my shoulder to my wrist, and sometimes from my cheek to my forehead. I worried about strokes and rare cancers. I visited a neurologist and had MRIs of my brain and my neck. I spent far too much time with Google.
It wasn't the first time I'd had weird neurological symptoms, but my new psychiatrist, Dr. S, gave me two new diagnoses: conversion disorder and somatic symptom disorder. Conversion disorder is characterized by medically unexplained neurological symptoms, coupled with "significant distress or impairment," according to the _DSM_. (Freud would have called it hysteria.) It often occurs alongside panic disorder and depression. Somatic symptom disorder involves distressing physical symptoms and significant worry about them. People with somatic symptom disorder "appraise their bodily symptoms as unduly threatening, harmful or troublesome and often think the worst about their health," says the _DSM_.
Medically unexplained symptoms are strikingly common. One study of primary care patients in Germany found that mystery symptoms made up two-thirds of all symptoms. For most people, however, the reassuring words of a doctor or a negative test result are enough to ease their minds.
The goal of CBT this time was not to make the weird symptoms go away but to teach me to live with them, to see them as benign and ignore them. I wrote down my irrational fears: that I was having a stroke, that I had ALS. Then I wrote down the evidence that these thoughts were likely false. (All my test results had come back normal.) I was given relaxation exercises and encouraged to meditate. (A confession, Dr. S: I didn't meditate.) I compiled lists of things that made me happy—reading to my daughter, calling a friend—and picked one to do when the symptoms surged.
The CBT worked. After several months, I was less worried. And while I still get a tingly leg or arm every once in a while, the symptoms are largely gone.
When people ask me which therapy they should choose for anxiety, I always recommend CBT. But I've also dipped in and out of psychodynamic therapy, a school that views anxiety as originating from relationship experiences. I did a stint in my twenties, and I've seen my most recent therapist, Dr. L, who practices a mix of psychodynamic therapy and CBT, off and on since my early thirties. We've talked about how, as a child, I yearned for more rules and guidance. About how I struggled to be comfortable with anger, both my own and others'. She's helped me navigate relationships with friends and family.
Psychodynamic therapy may sound like self-indulgent navel-gazing, but there is some evidence that it is beneficial for anxiety disorders. A 2014 meta-analysis found that after a course of psychodynamic therapy almost half of patients had their anxiety disorders go into remission. And it has had a monumental impact on me. I've gotten better at noticing my feelings and figuring out where they come from. I've gotten to know my emotional minefields and become braver and more authentic in relationships. Psychodynamic therapy has helped me grow up. And when anxiety hits, I feel less sideswiped. I have an emotional home base.
—
Grounding myself in the present moment also helps to keep anxiety at bay. Even dusting or scrubbing the toilets can quiet my worrying. (Yes, I am becoming my mother.)
Baking is one of my favorite soothing activities. The tactile pleasure of kneading flour into butter. The focus, but also slight mindlessness, of following a recipe. The wonderful alchemy of transforming a collection of ingredients into a pie or cake. And of course the accolades from family and friends. The closest I've ever felt to being a celebrity was when I rode the New York City subway with a still-steaming blueberry pie on my lap, my hands in oven mitts. "Can I have a piece?" passengers shamelessly asked.
Healthy habits—getting enough sleep, eating well, reducing stress, exercising regularly—aren't especially novel, and they are decidedly unglamorous. But they are critical to keeping my anxiety in check. The leeway for neglect is very slim.
Insomnia and other sleep problems are common in people with anxiety disorders. Sleeping fewer hours than normal is associated with anxiety in teenagers. Going to sleep late, not getting enough sleep, and being drowsy during the day is linked to anxiety in kids. Depressed or anxious people who sleep too much (ten hours or more) or too little (six hours or less) are at greater risk of having more chronic illnesses.
Some studies have found that difficulty sleeping is a precursor to a bout of anxiety or depression. There's evidence that sleep problems increase the risk of developing PTSD after trauma. Poor sleep may also weaken the effects of CBT: Research indicates that good sleep is critical for consolidating memories in extinction learning.
Various theories explain the relationship between sleep and anxiety. Scientists have discovered that when people without psychiatric disorders are deprived of sleep, their amygdala activity in response to negative stimuli increases and the connections between the amygdala and the medial prefrontal cortex are weakened. Since an anxious person already has a revved-up amygdala, it could be that sleep problems turn up the volume even further.
So I go to bed early enough to make sure I get my eight hours. But that doesn't mean I stay asleep. I'm prone to waking up—and staying up—at two a.m. or three a.m., dark, solitary times that are ripe for anxiety. Without the tethers of the day's routines, my mind hopscotches: I must remember to call my niece to wish her a happy birthday. How will I possibly get all my work done before my next deadline? Am I spending enough time with my daughter? My friend Amy never responded to my email. Have I done something to upset her? Should I cook fish or chicken for dinner tomorrow? How will we pay for college? Is the tightness in my belly cancer?
My husband and daughter are still and asleep. I skulk around the apartment, from bed to sofa to bathroom.
Exercise seems the easier fix, though it took me a while to figure out what I enjoyed and how to fit it into my life. I'm not keen on running or lifting weights. I love yoga but I rarely have time to schlep to a studio for a ninety-minute—or even an hour-long—class. Then I found online yoga. Now I do anywhere from fifteen minutes to a half hour in the morning before my daughter wakes. I feel stronger. And I've noticed that, since starting it, my Klonopin use has taken a nosedive. I don't think it's a coincidence.
Cardio is important for me, too, and not just because it's good for my body. A lot of my anxiety has involved worries about my heart. So I take the stairs and use a seven-minute workout app on my phone. They are short bursts of exposure therapy. Indeed, this interoceptive exposure, or exposure to feared bodily sensations, is a core element of CBT for panic disorder. In scientific studies, exercise is modestly effective at reducing anxiety symptoms. It is best at reducing so-called anxiety sensitivity, or the fear of the bodily sensations caused by anxiety. There are many theories about why exercise helps. Some scientists have pointed to exercise's ability to boost brain-derived neurotrophic factor (BDNF), a protein important for maintaining mood that is sometimes reduced in people with anxiety disorders. Regular aerobic exercise also lowers activity in the HPA axis.
It's even better if I can get that exercise in a park. Spending time in nature can reduce stress and even improve cognition. It may also calm anxiety. Researchers at Stanford and the University of San Francisco had people take a fifty-minute walk. One group walked in a grassy park; the other along a busy street. After the stroll, the people who spent time in the park had decreased anxiety compared to those who walked along the street.
One meta-analysis found that rates of anxiety disorders were 21 percent higher in urban areas than in rural ones.
I'm not ready to move to the country yet. I'm also convinced that there is no one best way to deal with anxiety. Everyone finds his or her own salves. A neighbor with GAD finds solace in music and meditation apps. For Cheyenne Stone, it is sleeping eight hours a night and surrounding herself with supportive friends. For Anna Learis, it is spending thirty minutes doing her makeup in the morning, a ritual she finds calming.
Since my anxiety often seems to manifest itself in weird physical symptoms, I've needed to find some way to discern when I need an MRI versus a dose of Klonopin. I've been down the rabbit hole of specialists and expensive tests before. I need a guide to interpret my noisy body. My primary care physician, Dr. G, does this. She's warm, thoughtful, and supersmart. She doesn't dismiss my concerns out of hand or use my anxiety as a knee-jerk scapegoat, but she's not an alarmist either. And she doesn't kick the can by immediately sending me to a specialist, leaving the problem for someone else to figure out. Most important, I trust her. She helps me manage my hypochondria. She asks me specifically what my worst fear is about a particular symptom. Then she'll tell me why she's ruled that out.
A few months ago I had a persistent burning feeling in my lungs. It lasted for weeks. Dr. G first had me use my asthma inhaler. When that didn't help, she had me try Klonopin for several days to see if reducing my anxiety level would lessen the symptom. Only when that didn't work did she send me to a pulmonologist. His assessment? Probably a postviral syndrome that would go away within a few weeks. And it did.
Another time I called her with a frantic question. "I think I have a leptomeningeal carcinomatosis," I said in a rush. "I'm dizzy sometimes. I have that tingling on the left side of my body."
"That is a very rare cancer," she said. "Where did you hear about it?"
I blushed and stammered. "I was looking at People.com and read that this actress Valerie Harper has it. I looked up the symptoms, and I have a bunch of them."
"You had a normal neurological exam the last time I saw you," she said. "We would have seen some abnormality if you had this type of cancer."
This kind of hand-holding takes time. And it isn't cheap. Dr. G doesn't take insurance. I pay out of pocket and then hope my insurance company will reimburse me. Unfortunately, this quality of care is not available to many.
As I've conducted the research for this book, I've been mulling a question. If I could wish my anxiety away, would I?
I certainly don't see my anxiety as a gift. And I don't buy the platitude that everything happens for a reason. When my anxiety is at its worst, it's deeply painful, erasing love and life. Even when it's more moderate, anxiety is a huge energy and time suck.
Still, I've come to realize that the question is unanswerable. When I try to envision my life without all the experiences anxiety has given me—as well as the ones it has taken away—I don't recognize myself. At this point, anxiety and I are too tightly bound. Take my struggles with anxiety away and I'm someone else.
Anxiety has been good to me, too. Without it, I might have listened to the first doctor who told me that the spot on my cheek was nothing.
Anxiety is a great bullshit detector. Reams of studies have looked at the mind-body connection. In anxious people, that link seems amplified. When my marriage feels off-kilter, when I'm avoiding some necessary confrontation or saying yes to too many superfluous obligations, I feel it in my hopped-up amygdala. Weirdly, anxiety makes me live a more authentic life. And a more empathic one. Anxiety has made me ask for help, made me vulnerable, and thereby deepened my friendships.
A background hum of uneasiness has motivated me to work harder, travel farther, speak more honestly, and curiously, take more risks than I might have otherwise. People who have a brush with death often talk of how it has given them a sense of what really matters. An omnipresent fear of disaster, a constant bracing for catastrophe can do that, too. Time takes on more urgency.
Anxiety means I'm simply not mellow enough to take things for granted. And that has made my life all the richer.
# 1. THE ANTICIPATION OF PAIN
estimated number of people: Ronald C. Kessler et al., "Twelve-Month and Lifetime Prevalence and Lifetime Morbid Risk of Anxiety and Mood Disorders in the United States," _International Journal of Methods in Psychiatric Research_ 21, no. 3 (2012): 169–84.
about 40 million American adults: "Facts and Statistics," Anxiety and Depression Association of America, https://www.adaa.org/about-adaa/press-room/facts-statistics.
anxiety disorders cost the United States: Paul E. Greenberg et al., "The Economic Burden of Anxiety Disorders in the 1990s," _Journal of Clinical Psychiatry_ 60, no. 7 (1999): 427–35.
According to a spring 2016 survey: American College Health Association National College Health Assessment, _Spring 2016 Reference Group Executive Summary_ (American College Health Association, 2016).
up from about 10 percent: American College Health Association National College Health Assessment, _Fall 2008 Reference Group Executive Summary_ (American College Health Association, 2008).
Depression may get most of the headlines: In 2015 the National Institutes of Health spent $156 million for research on anxiety disorders and $390 million on depression. _Estimates of Funding for Various Research, Condition, and Disease Categories_ , National Institutes of Health, https://report.nih.gov/categorical_spending.aspx.
In people with a history: Ronald C. Kessler, "The Global Burden of Anxiety and Mood Disorders: Putting ESEMeD Findings into Perspective," _Journal of Clinical Psychiatry_ 68, suppl. 2 (2007): 10–19.
doesn't often lead to suicidal acts: Matthew K. Nock et al., "Mental Disorders, Comorbidity and Suicidal Behavior: Results from the National Comorbidity Survey Replication," _Molecular Psychiatry_ 15, no. 8 (2010): 868–76.
Someone who develops an anxiety disorder: Ronald C. Kessler, Harvard Medical School, interview by author.
"the dizziness of freedom": Søren Kierkegaard, _The Concept of Anxiety_ (Princeton, NJ: Princeton University Press, 1980), 61.
varies by culture: American Psychiatric Association, _Diagnostic and Statistical Manual of Mental Disorders,_ 5th ed. (Washington, DC: American Psychiatric Publishing, 2013), 216. Cited hereinafter as _DSM_ -5.
studies show that, in Japan: Ronald C. Kessler et al., "The Global Burden of Mental Disorders: An Update from the WHO World Mental Health (WMH) Surveys," _Epidemiologia e psichiatria sociale_ 18, no. 1 (2009): 23–33.
Andreas of Charystos: Allan V. Horwitz, _Anxiety: A Short History_ (Baltimore: Johns Hopkins University Press, 2013), 27.
pantophobia: I can't read the word _pantophobia_ without thinking of the scene in _A Charlie Brown Christmas_ when Charlie Brown consults Lucy's "Psychiatric Help, 5 cents" booth. Trying to get to the bottom of his despair, Lucy asks him about a litany of phobias, including fears of crossing bridges (gephyrophobia) and of the ocean (thalassophobia). "Do you think you have pantophobia?" she finally asks. "What's pantophobia?" says Charlie Brown. "The fear of everything," Lucy says. "That's it!" Charlie Brown yells, sending Lucy somersaulting back across the snow.
In the Classical period: Andrea Tone, _The Age of Anxiety: A History of America's Turbulent Affair with Tranquilizers_ (New York: Basic Books, 2009), 6–7.
"It was as if a light of relief": Quoted in Horwitz, _Anxiety_ , 37.
emerging concept of nervous disorders: Ibid., 48–49.
In 1869, George Miller Beard: Ibid., 64–66.
The Greek physician Hippocrates: Cecilia Tasca et al., "Women and Hysteria in the History of Mental Health," _Clinical Practice and Epidemiology in Mental Health_ 8 (2012): 110–19.
"irritable heart syndrome": Andrea Tone, "Listening to the Past: History, Psychiatry and Anxiety," _Canadian Journal of Psychiatry_ 50, no. 7 (2005): 373–80.
a groundbreaking paper: Sigmund Freud, _Collected Papers_ (London: Hogarth Press, 1953), 1:76–106.
he abandoned this theory: Horwitz, _Anxiety_ , 85–91.
When that response is initiated: Harvard Medical School has done a nice write-up of the stress response and the HPA axis. "Understanding the Stress Response," Harvard Medical School, http://www.health.harvard.edu/staying-healthy/understanding-the-stress-response.
In his experiments, LeDoux: Two major papers detailing LeDoux's 1980s lesion work are Joseph E. LeDoux et al., "Subcortical Efferent Projections of the Medial Geniculate Nucleus Mediate Emotional Responses Conditioned to Acoustic Stimuli," _Journal of Neuroscience_ 4, no. 3 (1983): 683–98; and Jiro Iwata et al., "Intrinsic Neurons in the Amygdaloid Field Projected to by the Medial Geniculate Body Mediate Emotional Responses Conditioned to Acoustic Stimuli," _Brain Research_ 383 (1986): 195–214.
one of two routes: Joseph LeDoux, _The Emotional Brain: The Mysterious Underpinnings of Emotional Life_ (New York: Simon & Schuster, 1996). Also see LeDoux's most recent book, _Anxious: Using the Brain to Understand and Treat Fear and Anxiety_ (New York: Viking, 2015).
The part of the cow that most: Ibid., 11.
Studies have found that the amygdala: Shmuel Lissek et al., "Classic Fear Conditioning in the Anxiety Disorders: A Meta-Analysis," _Behaviour Research and Therapy_ 43, no. 11 (2005): 1391–424.
In many studies, those with anxiety disorders: Here's a good summary of the attention bias literature: Yair Bar-Haim et al., "Threat-Related Attentional Bias in Anxious and Nonanxious Individuals: A Meta-Analytic Study," _Psychological Bulletin_ 133, no. 1 (2007): 1–24.
"intolerance of uncertainty": Dan W. Grupe and Jack B. Nitschke, "Uncertainty and Anticipations in Anxiety: An Integrated Neurobiological and Psychological Perspective," _Nature Reviews Neuroscience_ 14 (2013): 488–501.
Researchers at the University of California: Alan Simmons et al., "Intolerance of Uncertainty Correlates with Insula Activation During Affective Ambiguity," _Neuroscience Letters_ 430, no. 2 (2008): 92–97.
In Davis's lab: Michael Davis et al., "Phasic vs Sustained Fear in Rats and Humans: Role of the Extended Amygdala in Fear vs Anxiety," _Neuropsychopharmacology_ 35, no. 1 (2010): 105–35.
In the 1990s, Christian Grillon: Christian Grillon, "Models and Mechanisms of Anxiety: Evidence from Startle Studies," _Psychopharmacology_ 199, no. 3 (2008): 421–37.
In one critical experiment: Christian Grillon and Michael Davis, "Fear-Potentiated Startle Conditioning in Humans: Explicit and Contextual Cue Conditioning Following Paired Versus Unpaired Training," _Pschophysiology_ 34 (1997): 451–58.
Using the new equipment: Salvatore Torrisi et al., "Resting State Connectivity of the Bed Nucleus of the Stria Terminalis at Ultra-High Field," _Human Brain Mapping_ 36 (2015): 4076–88.
As researchers Dan Grupe: Dan W. Grupe and Jack B. Nitschke, "Uncertainty and Anticipations in Anxiety."
# 2. SCARY CLOWNS AND THE END OF DAYS
more likely to develop a wide range of disorders: Renee Goodwin et al., "Panic Attack as a Risk Factor for Severe Psychopathology," _American Journal of Psychiatry_ 161, no. 12 (2004): 2207–14.
four out of thirteen possible: _DSM_ -5, 208.
Children who experience fearful spells: Eva Asselmann et al., "Associations of Fearful Spells and Panic Attacks with Incident Anxiety, Depressive and Substance Use Disorders: A 10-Year Prospective Longitudinal Community Study of Adolescents and Young Adults," _Journal of Psychiatric Research_ 55 (2014): 8–14.
_Sesame Street_ segment on YouTube: " _Sesame Street_ : A Clown's Face," https://www.youtube.com/watch?v=Vs5VYOnpMrw.
These are all typical: For an excellent chart detailing normal fears in childhood and adolescence, see Katja Beesdo et al., "Anxiety and Anxiety Disorders in Children and Adolescents: Developmental Issues and Implications for DSM-V," _Psychiatric Clinics_ 32, no. 3 (2009): 483–524.
Specific phobia is one of the earliest: Ronald C. Kessler et al., "Age of Onset of Mental Disorders: A Review of Recent Literature," _Current Opinion in Psychiatry_ 20, no. 4 (2007): 359–64.
phobia of buttons: Lissette M. Saavedra and Wendy K. Silverman, "Case Study: Disgust and a Specific Phobia of Buttons," _Journal of the American Academy of Child and Adolescent Psychiatry_ 41, no. 11 (2002): 1376–79.
The most common involve animals: National Alliance on Mental Illness, _Specific Phobias_ , fact sheet.
these fears developed over millennia: Randolph M. Nesse and George C. Williams, _Why We Get Sick: The New Science of Darwinian Medicine_ (New York: Vintage, 1994), 210.
A 2010 study of about fifteen hundred: Julia Trumpf et al., "Specific Phobia Predicts Psychopathology in Young Women," _Social Psychiatry and Psychiatric Epidemiology_ 45, no. 12 (2010): 1161–66.
the prediction set forth: John R. Gribbin and Stephen H. Plagemann, _The Jupiter Effect_ (New York: Walker & Co., 1974).
early maltreatment can alter the HPA axis: Carlo Faravelli et al., "Childhood Stressful Events, HPA Axis and Anxiety Disorders," _World Journal of Psychiatry_ 2 _,_ no. 1 (2012): 13–25.
When researchers at the University of Wisconsin: Ryan J. Herringa et al., "Childhood Maltreatment Is Associated with Altered Fear Circuitry and Increased Internalizing Symptoms by Late Adolescence," _Proceedings of the National Academy of Sciences_ 110, no. 47 (2013): 19119–24.
physical illness and economic adversity: Jennifer Greif Green et al., "Childhood Adversities and Adult Psychopathology in the National Comorbidity Survey Replication (NCS-R) 1: Associations with First Onset of DSM-IV Disorders," _Archives of General Psychiatry_ 67, no. 2 (2010): 113.
A study that surveyed nearly seven hundred: Nicholas B. Allen et al., "Prenatal and Perinatal Influences on Risk for Psychopathology in Childhood and Adolescence," _Development and Psychopathology_ 10 (1998): 513–29.
a history of asthma: Michelle G. Craske et al., "Paths to Panic Disorder/Agoraphobia: An Exploratory Analysis from Age 3 to 21 in an Unselected Birth Cohort," _Journal of the American Academy of Child and Adolescent Psychiatry_ 40, no. 5 (2001): 556–63.
adults with asthma, emphysema, and bronchitis: See, for example, R. D. Goodwin et al., "A 10-Year Prospective Study of Respiratory Disease and Depression and Anxiety in Adulthood," _Annals of Allergy, Asthma and Immunology_ 113, no. 5 (2014): 565–70.
A 2008 study showed that those: Renee D. Goodwin et al., "Childhood Respiratory Disease and the Risk of Anxiety Disorder and Major Depression in Adulthood," _Archives of Pediatrics and Adolescent Medicine_ 162, no. 8 (2008): 774–80.
There's also some evidence: Jordan W. Smoller et al., "The Human Ortholog of Acid-Sensing Ion Channel Gene ASIC1a Is Associated with Panic Disorder and Amygdala Structure and Function," _Biological Psychiatry_ 76, no. 11 (2014): 902–10.
In the UCLA and New Zealand study: Craske et al., "Paths to Panic Disorder/Agoraphobia."
Researchers in Australia wanted to see: Jennifer L. Hudson and Ronald M. Rapee, "Parent-Child Interactions and Anxiety Disorders: An Observational Study," _Behaviour Research and Therapy_ 39 (2001): 1411–27.
In a big 2007 review: Bryce D. McLeod et al., "Examining the Association Between Parenting and Childhood Anxiety: A Meta-Analysis," _Clinical Psychology Review_ 27 (2007): 155–72.
In a small study using this paradigm: Jennifer Lau et al., "Fear Conditioning in Adolescents with Anxiety Disorders: Results from a Novel Experimental Paradigm," _Journal of the American Academy of Child and Adolescent Psychiatry_ 47, no. 1 (2008): 94–102.
Another larger study published in 2013: Jennifer C. Britton et al., "Response to Learned Threat: An fMRI Study in Adolescent and Adult Anxiety," _American Journal of Psychiatry_ 170, no. 10 (2013): 1195–1204.
# 3. MY GRANDMOTHER'S MADNESS
genes are responsible for 30 to 40 percent: John M. Hettema et al., "A Review and Meta-Analysis of the Genetic Epidemiology of Anxiety Disorders," _American Journal of Psychiatry_ 158, no. 10 (2001): 1568–78. In twin studies, scientists compared the similarities of a trait (which could also be an illness such as anxiety disorders) in pairs of identical twins to those of fraternal twins. Since both kinds of twins grow up in similar environments, the greater similarity in the trait among identical twins can be largely attributed to genes. Jordan Smoller's _The Other Side of Normal_ (New York: HarperCollins, 2012) has a nice explanation of twin studies on page 63.
For schizophrenia, Gladys's diagnosis: Ming T. Tsuang et al., "Genes, Environment and Schizophrenia," _British Journal of Psychiatry_ 40, Suppl. (April 2001): s18–s24.
Having a first-degree relative: Jordan W. Smoller et al., "The Genetics of Anxiety Disorders," in _Primer on Anxiety Disorders: Translational Perspectives on Diagnosis and Treatment_ , ed. Kerry J. Ressler et al. (Oxford: Oxford University Press, 2015), 61.
In a 2013 study, genetic: Cross-Disorder Group of the Psychiatric Genomics Consortium, "Genetic Relationship Between Five Psychiatric Disorders Estimated from Genome-Wide SNPs," _Nature Genetics_ 45, no. 9 (2013): 984–94.
insulin coma therapy: There's a terrific description of ICT by Max Fink, the former head of an ICT unit at a New York mental hospital, on the website for the documentary _A Brilliant Madness_. The film tells the story of the mathematician John Nash, who was treated with ICT for schizophrenia: http://www.pbs.org/wgbh/amex/nash/filmmore/ps_ict.html. Also see Edward Shorter and David Healy, _Shock Therapy: A History of Electroconvulsive Treatment in Mental Illness_ (New Brunswick, NJ: Rutgers University Press, 2007).
In Mendota's 1955 annual report: Mendota State Hospital, _Report to State Board of Public Welfare_ , March 23, 1955.
divided into "quiet" and "disturbed": Mendota State Hospital, _Report to State Board of Public Welfare_ , June 14, 1961.
a movement to provide more freedom: Mendota State Hospital, _Report to the State Board of Public Welfare_ , May 14, 1958, and May 27, 1959.
Antipsychotic drugs were instant hits: Mendota State Hospital, _Report to the State Board of Public Welfare_ , May 23, 1956.
staff members were complaining: Mendota State Hospital, _Report to State Board of Public Welfare_ , May 25, 1960.
Electroconvulsive therapy was first employed: Edward Shorter, _A History of Psychiatry_ (Hoboken, NJ: John Wiley & Sons, 1997), 218–24.
During the 1960s, a movement arose: In 1963, President John F. Kennedy signed the Community Mental Health Act, legislation that aimed to build a network of community mental health centers. The goal was for people to receive treatment at home; many patients would no longer have to spend years in crowded psychiatric institutions, some of which were rife with abuse and neglect. But only half the community centers were built and most were not fully funded. See "Kennedy's Vision for Mental Health Never Realized," Associated Press, October 20, 2013.
The vast majority: "Mental Health Reporting," fact sheet, University of Washington School of Social Work, http://depts.washington.edu/mhreport/facts_violence.php.
One of the most extensively researched is the SLC6A4 gene: For a nice, clear write-up of the serotonin transporter story, see Smoller, _Other Side of Normal_ , 68–70.
Women are about twice as likely: Carmen P. McLean et al., "Gender Differences in Anxiety Disorders: Prevalence, Course of Illness, Comorbidity and Burden of Illness," _Journal of Psychiatric Research_ 45, no. 8 (2011): 1027–35.
girls "catch" fear more easily: Michelle G. Craske, _Origins of Phobias and Anxiety Disorders: Why More Women Than Men?_ (Oxford: Elsevier, 2003), 176–203.
In one study, mothers presented two toys: Friederike C. Gerull and Ronald M. Rapee, "Mother Knows Best: Effects of Maternal Modelling on the Acquisition of Fear and Avoidance Behaviour in Toddlers," _Behaviour Research and Therapy_ 40, no. 3 (2002): 279–87.
In a University of California, Berkeley study: Patricia K. Kerig et al., "Marital Quality and Gender Differences in Parent-Child Interaction," _Developmental Psychology_ 29, no. 6 (1993): 931–39.
Morrongiello had a hunch: Barbara A. Morrongiello and Tess Dawber, "Mothers' Responses to Sons and Daughters Engaging in Injury-Risk Behaviors on a Playground: Implications for Sex Differences in Injury Rates," _Journal of Experimental Child Psychology_ 76 (2000): 89–103.
Morrongiello and her colleague: Barbara A. Morrongiello and Theresa Dawber, "Parental Influences on Toddlers' Injury-Risk Behaviors: Are Sons and Daughters Socialized Differently?" _Journal of Applied Developmental Psychology_ 20, no. 2 (1999): 227–51.
girls tended to see it as riskier than boys: Barbara A. Morrongiello and Heather Rennie, "Why Do Boys Engage in More Risk Taking Than Girls? The Role of Attributions, Beliefs, and Risk Appraisals," _Journal of Pediatric Psychology_ 23, no. 1 (1998): 33–43.
When girls engage in risky behaviors: Barbara A. Morrongiello et al., "Understanding Gender Differences in Children's Risk Taking and Injury: A Comparison of Mothers' and Fathers' Reactions to Sons and Daughters Misbehaving in Ways That Lead to Injury," _Journal of Applied Developmental Psychology_ 31 (2010): 322–29.
By late elementary school, girls: Craske, _Origins of Phobias and Anxiety Disorders_ , 185.
Surprisingly, men's _physiological_reactions: Ibid., 194–95.
In one study, thirty-four women: Mohamed A. Zeidan et al., "Estradiol Modulates Medial Prefrontal Cortex and Amygdala Activity During Fear Extinction in Women and Female Rats," _Biological Psychiatry_ 70, no. 10 (2011): 920–27.
Men generally encounter more traumatic events: Naomi Breslau et al., "Trauma Exposure and Posttraumatic Stress Disorder: A Study of Youths in Urban America," _Journal of Urban Health: Bulletin of the New York Academy of Medicine_ 81, no. 4 (2004): 530–44.
more likely to be the victims: Craske, _Origins of Phobias and Anxiety Disorders_ , 179–80.
Studies by Kagan and others: K. A. Degnan and N. A. Fox, "Behavioral Inhibition and Anxiety Disorders: Multiple Levels of a Resilience Process," _Development and Psychopathology_ 19 (2007): 729–46, referred to in Lauren M. McGrath et al., "Bringing a Developmental Perspective to Anxiety Genetics," _Development and Psychopathology_ 24, no. 4 (2012): 1179–93.
Twin studies have found: Jordan W. Smoller et al., "Genetics of Anxiety Disorders: The Complex Road from DSM to DNA," _Depression and Anxiety_ 26 (2009): 965–75.
Kagan started his temperament work: Kagan details his studies in the following books, among others: Jerome Kagan, _Galen's Prophecy: Temperament in Human Nature_ (New York: Basic Books, 1994); and Jerome Kagan and Nancy Snidman, _The Long Shadow of Temperament_ (Cambridge, MA: Belknap Press of Harvard University Press, 2004). Also see Robin Marantz Henig, "Understanding the Anxious Mind," _New York Times_ , September 29, 2009.
only those BI kids whose mothers were overcontrolling: Erin Lewis-Morrarty et al., "Maternal Over-Control Moderates the Association Between Early Childhood Behavioral Inhibition and Adolescent Social Anxiety Symptoms," _Journal of Abnormal Child Psychology_ 40, no. 8 (2012): 1363–73.
BI kids who are put in day care: Nathan Fox, interview by author.
who have an attention bias to threat: Koraly Pérez-Edgar et al., "Attention Biases to Threat Link Behavioral Inhibition to Social Withdrawal over Time in Very Young Children, _Journal of Abnormal Child Psychology_ 39, no. 6 (2011): 885–95; and Koraly Pérez-Edgar et al., "Attention Biases to Threat and Behavioral Inhibition in Early Childhood Shape Adolescent Social Withdrawal," _Emotion_ 10, no. 3 (2010): 349–57.
Kids with BI who are adept at attention shifting: Lauren K. White et al., "Behavioral Inhibition and Anxiety: The Moderating Roles of Inhibitory Control and Attention Shifting," _Journal of Abnormal Child Psychology_ 39, no. 5 (2011): 735–47.
# 4. FROM CBT TO KARAOKE
This was called cognitive reappraisal: David H. Barlow and Michelle G. Craske, _Mastery of Your Anxiety and Panic_ (New York: Oxford University Press, 2007).
About half of anxiety disorder patients: Amanda G. Loerinc et al., "Response Rates for CBT for Anxiety Disorders: Need for Standardized Criteria," _Clinical Psychology Review_ 42 (2015): 72–82.
a meta-analysis of twenty-seven studies: The effect size was .73. Effect size is a statistical definition that allows scientists to compare the results of many different studies. In general, an effect size of .2 is considered small, .5 is medium, and .8 or greater is large. In the studies included in the meta-analysis, the placebo conditions involved contact with therapists and education about anxiety—things that alone can help patients and skew research results—but excluded other treatment that scientists thought could be effective. See Stefan G. Hofmann and Jasper A. J. Smits, "Cognitive-Behavioral Therapy for Adult Anxiety Disorders: A Meta-analysis of Randomized Placebo-Controlled Trials," _Journal of Clinical Psychiatry_ 69, no. 4 (2008): 621–32.
CBT actually shrank: K.N.T. Månsson et al., "Neuroplasticity in Response to Cognitive Behavior Therapy for Social Anxiety Disorder," _Translational Psychiatry_ 6 (2016): e727.
have a colorful history: Edward Shorter, _A History of Psychiatry_ (Hoboken, NJ: John Wiley & Sons, 1997), 119–36.
John Watson, an American psychologist: Edward Shorter, _A Historical Dictionary of Psychiatry_ (Oxford: Oxford University Press, 2005), 57, 102–3.
Freud claimed: Ibid., 113.
In 1971, psychiatrist Manuel Zane: Kate Stone Lombardi, "Phobia Clinic, 1st in U.S., Offers Road to Recovery for 25 Years," _New York Times_ , November 24, 1996.
psychiatrist Arthur Hardy: "Arthur B. Hardy, 78, Psychiatrist Who Treated a Fear of Going Out," _New York Times_ , October 31, 1991.
These iconoclasts: Dr. Martin Seif, interview with the author.
People with panic disorder wait: Philip S. Wang et al., "Failure and Delay in Initial Treatment Contact After First Onset of Mental Disorders in the National Comorbidity Survey Replication," _Archives of General Psychiatry_ 62 (2005): 603–13.
This is particularly true of African Americans: See, for example, Joshua Breslau et al., "Lifetime Risk and Persistence of Psychiatric Disorders Across Ethnic Groups in the United States," _Psychological Medicine_ 35, no. 3 (2005): 317–27, and Joseph A. Himle et al., "Anxiety Disorders Among African Americans, Blacks of Caribbean Descent, and Non-Hispanic Whites in the United States," _Journal of Anxiety Disorders_ 23, no. 5 (2009): 578–90.
One study followed sixty-three panic disorder patients: T. A. Brown and D. H. Barlow, "Long-term Outcome in Cognitive-Behavioral Treatment of Panic Disorder: Clinical Predictors and Alternative Strategies for Assessment," _Journal of Consulting and Clinical Psychology_ 63, no. 5 (1995): 754–65.
exposure therapy appointments in the morning: Alicia E. Meuret et al., "Timing Matters: Endogenous Cortisol Mediates Benefits from Early-Day Psychotherapy," _Psychoneuroendocrinology_ 74 (2016): 197–202.
had a greater reduction in anxiety: B. Kleim et al., "Sleep Enhances Exposure Therapy," _Psychological Medicine_ 44 (2014): 1511–19.
In a 2016 study of patients: Henny A. Westra et al., "Integrating Motivational Interviewing with Cognitive-Behavioral Therapy for Severe Generalized Anxiety Disorder: An Allegiance-Controlled Randomized Clinical Trial," _Journal of Consulting and Clinical Psychology_ 84, no. 9 (2016): 768–82.
the Unified Protocol: David H. Barlow and Katherine Ann Kennedy, "New Approaches to Diagnosis and Treatment in Anxiety and Related Emotional Disorders: A Focus on Temperament," _Canadian Psychology_ 57, no. 1 (2016): 8–20.
asking patients to vividly imagine: Tomislav D. Zbozinek et al., "The Effect of Positive Mood Induction on Reducing Reinstatement Fear: Relevance for Long Term Outcomes of Exposure Therapy," _Behaviour Research and Therapy_ 71 (2015): 65–75.
success in modifying exposure therapy: Michelle G. Craske et al., "Maximizing Exposure Therapy: An Inhibitory Learning Approach," _Behaviour Research and Therapy_ 58 (2014): 10–23.
in ACT you're taught to accept: Steven C. Hayes, _Get Out of Your Mind & Into Your Life_ (Oakland, CA: New Harbinger, 2005).
twelve sessions of ACT or CBT: Joanna J. Arch et al., "Randomized Clinical Trial of Cognitive Behavioral Therapy Versus Acceptance and Commitment Therapy for Mixed Anxiety Disorders," _Journal of Consulting and Clinical Psychology_ 80, no. 5 (2012): 750–65.
Another 2012 paper: Kate B. Wolitzky-Taylor et al., "Moderators and Non-Specific Predictors of Treatment Outcome for Anxiety Disorders: A Comparison of Cognitive Behavioral Therapy to Acceptance and Commitment Therapy," _Journal of Consulting and Clinical Psychology_ 80, no. 5 (2012): 786–99.
In a meta-analysis of thirty-nine studies: In patients with anxiety disorders, the treatment had a large effect size of .97. See Stefan G. Hofmann, "The Effect of Mindfulness-Based Therapy on Anxiety and Depression: A Meta-Analytic Review," _Journal of Consulting and Clinical Psychology_ 78, no. 2 (2010): 169–83.
There's even a book: James Jacobson, _How to Meditate with Your Dog_ (Kihei, HI: Maui Media, 2010).
There's emerging research that acupuncture: See, for example, Nick Errington-Evans, "Randomised Controlled Trial on the Use of Acupuncture in Adults with Chronic, Non-Responding Anxiety Symptoms," _Acupuncture in Medicine_ 33, no. 2 (2015): 98–102; Hyojeong Bae et al., "Efficacy of Acupuncture in Reducing Preoperative Anxiety: A Meta-Analysis," _Evidence-Based Complementary and Alternative Medicine_ (2014); and Karen Pilkington et al., "Acupuncture for Anxiety and Anxiety Disorders: A Systematic Literature Review," _Acupuncture in Medicine_ 25 (2007): 1–10.
In one admittedly tiny study: Frederick J. Heide and T. D. Borkovec, "Relaxation-Induced Anxiety: Mechanisms and Theoretical Implications," _Behaviour Research and Therapy_ 22, no. 1 (1984): 1–12.
Another small study of college students: G. R. Norton et al., "Characteristics of Subjects Experiencing Relaxation and Relaxation-Induced Anxiety," _Journal of Behavior Therapy and Experimental Psychiatry_ 16, no. 3 (1985): 211–16.
A 2016 meta-analysis: Stefan Hofmann et al., "Effect of Hatha Yoga on Anxiety: A Meta-Analysis," _Journal of Evidence-Based Medicine_ 9, no. 3 (2016): 116–24.
In a small study with GAD patients: In the control treatment, half the time the probe replaced a threatening word; half the time it replaced a neutral word. So there was no attention training. See Nader Amir et al., "Attention Modification Program in Individuals with Generalized Anxiety Disorder," _Journal of Abnormal Psychology_ 118, no. 1 (2009): 28–33.
A study with social phobia patients: Nader Amir et al., "Attention Training in Individuals with Generalized Social Phobia: A Randomized Controlled Trial," _Journal of Consulting and Clinical Psychology_ 77, no. 5 (2009): 961–73.
some evidence shows: T. Shechner et al., "Attention Bias Modification Treatment Augmenting Effects on Cognitive Behavioral Therapy in Children with Anxiety: Randomized Controlled Trial," _Journal of the American Academy of Child and Adolescent Psychiatry_ 53, no. 1 (2014): 61–71.
In a 2015 meta-analysis, ABM: The effect size was .42. See Marian Linetzsky et al., "Quantitative Evaluation of the Clinical Efficacy of Attention Bias Modification Treatment for Anxiety Disorders," _Depression and Anxiety_ 32, no. 6 (2015): 383–91.
In a 2015 study, Zilverstand: Anna Zilverstand et al., "fMRI Neurofeedback Facilitates Anxiety Regulation in Females with Spider Phobia," _Frontiers in Behavioral Neuroscience_ (June 8, 2015).
In another study, researchers at Yale: D. Scheinost et al., "Orbitofrontal Cortex Neurofeedback Produces Lasting Changes in Contamination Anxiety and Resting-State Connectivity," _Translational Psychiatry_ 3, no. 4 (2013): e250.
# 5. MAY CAUSE DIZZINESS
In a 1998 study of panic disorder: Robert B. Pohl et al., "Sertraline in the Treatment of Panic Disorder: A Double-Blind Multicenter Trial," _American Journal of Psychiatry_ 155, no. 9 (1998): 1189–95.
In a 2004 study looking at escitalopram: Jonathan R. T. Davidson et al., "Escitalopram in the Treatment of Generalized Anxiety Disorder: Double-Blind, Placebo Controlled, Flexible-Dose Study," _Depression and Anxiety_ 19 (2004): 234–40.
Studies that reveal that: Annelieke M. Roest et al., "Reporting Bias in Clinical Trials Investigating the Efficacy of Second-Generation Antidepressants in the Treatment of Anxiety Disorders: A Report of 2 Meta-Analyses," _JAMA Psychiatry_ 72, no. 5 (2015): 500–10.
He is a coauthor of a review paper: S. Borges et al., "Review of Maintenance Trials for Major Depressive Disorder: A 25-Year Perspective from the US Food and Drug Administration," _Journal of Clinical Psychiatry_ 75, no. 3 (2014): 205–14.
In clinical trials by Pfizer: "Zoloft," Pfizer, October 2016, http://labeling.pfizer.com/ShowLabeling.aspx?id=517#page=1.
At least a third of people: Eduard Maron and David Nutt, "Biological Predictors of Pharmacological Therapy in Anxiety Disorders," _Dialogues in Clinical Neuroscience_ 17, no. 3 (2015): 305–17.
In one study, fourteen people: Jack B. Nitschke et al., "Anticipatory Activation in the Amygdala and Anterior Cingulate in Generalized Anxiety Disorder and Prediction of Treatment Response," _American Journal of Psychiatry_ 166, no. 3 (2009): 302–10.
In another study, researchers in Oxford: Andrea Reinecke et al., "Predicting Rapid Response to Cognitive-Behavioural Treatment for Panic Disorder: The Role of Hippocampus, Insula, and Dorsolateral Prefrontal Cortex," _Behaviour Research and Therapy_ 62 (2014): 120–28. For a nice summary of the state of biomarker research for anxiety disorders, see Maron and Nutt, "Biological Predictors of Pharmacological Therapy."
Klonopin can cause: "Klonopin Tablets," Genentech, 2013, www.gene.com/download/pdf/klnopin_prescribing.pdf.
Entire workbook programs: Michael W. Otto et al., _Stopping Anxiety Medication: Panic Control Therapy for Benzodiazepine Discontinuation_ (Psychological Corp., 2000).
The number of American adults: Marcus A. Bachhuber et al., "Increasing Benzodiazepine Prescriptions and Overdose Mortality in the United States, 1996–2013," _American Journal of Public Health_ 106, no. 4 (2016): 686–88.
And most people on benzos: M. J. Garvey and G. D. Tollefson, "Prevalence of Misuse of Prescribed Benzodiazepines in Patients with Primary Anxiety Disorder or Major Depression," _American Journal of Psychiatry_ 143, no. 12 (1986): 1601–3.
One study published in the journal _BMJ_ : Sophie Billioti de Gage et al., "Benzodiazepine Use and Risk of Alzheimer's Disease: Case-Control Study," _BMJ_ 349 (2014).
I'm reassured by a more recent study: Shelly L. Gray et al., "Benzodiazepine Use and Risk of Incident Dementia or Cognitive Decline: Prospective Population Based Study," _BMJ_ 352 (2016).
A range of pharmacological treatments: Andrea Tone, _The Age of Anxiety: A History of America's Turbulent Affair with Tranquilizers_ (New York: Basic Books, 2009) _,_ 21–24.
Miltown was developed by Frank Berger: Ibid., 35.
In 1949, Berger took a job: Ibid., 43.
After a few studies in humans: Ibid., 48–52.
a full third of all prescriptions: Ibid., xvi.
a Hollywood sensation: Ibid., 55–63.
The team doctors: Ibid., 114.
One ad published: Ibid., 75–76.
At Hoffmann–LaRoche: Ibid., 120–30.
it became the bestselling: Ibid., 137.
Klein and Fink published a paper: Donald F. Klein and Max Fink, "Psychiatric Reaction Patterns to Imipramine," _American Journal of Psychiatry_ 119, no. 5 (1962): 432–38.
"The chief characteristic of these disorders": _Diagnostic and Statistical Manual of Mental Disorders_ (American Psychiatric Association Mental Hospital Service, 1952), 31–34.
_DSM_-II, published in 1968: _Diagnostic and Statistical Manual of Mental Disorders_ , 2nd ed. (American Psychiatric Association, 1968).
he wanted the new edition: Hannah S. Decker, _The Making of DSM-III: A Diagnostic Manual's Conquest of American Psychiatry_ (Oxford: Oxford University Press, 2013).
Psychoanalysts pushed back: Ibid., 278.
One study compared two groups: Tone, _Age of Anxiety_ , 90.
Despite the runaway success: Ibid., 153.
A 1968 study, for example: Ibid., 179.
A Valium ad published in 1970: Reprinted in ibid., 157.
former first lady Betty Ford: Donnie Radcliffe, "Betty Ford Dies at 93: Former First Lady Founded Iconic Clinic," _Washington Post_ , July 8, 2011.
Senator Edward Kennedy convened: Tone, _Age of Anxiety_ , 204–5.
began recommending the SSRIs: American Psychiatric Association, "Practice Guideline for the Treatment of Patients with Panic Disorder," _American Journal of Psychiatry_ 155 (1998).
GlaxoSmithKline won FDA approval: Tone, _Age of Anxiety_ , 217–18.
One TV spot featured a businessman: Paxil social anxiety ad, https://www.youtube.com/watch?v=rR8rBEFulw4.
In 2009, GlaxoSmithKline said: Greg Miller, "Is Pharma Running Out of Brainy Ideas?" _Science_ 329 (2010): 502–4. A good summary of the recent retreat by pharmaceutical companies can be found at Steven E. Hyman, "Revolution Stalled," _Science Translational Medicine_ 4, no. 155 (2012): 155cm11.
Pexacerfont: Vladimir Coric et al., "Multicenter, Randomized, Double-Blind, Active Comparator and Placebo-Controlled Trial of a Corticotropin-Releasing Factor Receptor-1 Antagonist in Generalized Anxiety Disorder," _Depression and Anxiety_ 27 (2010): 417–25.
Verucerfont: "Neurocrine Announces Top-Line Results of Corticotropin Releasing Factor Antagonist GSK561679 for Treatment of Major Depressive Disorder," press release, Nuerocrine Biosciences, September 14, 2010, http://phx.corporate-ir.net/phoenix.zhtml?c=68817&p=irol-newsArticle&highlight=&ID=1471129.
Some scientists think that: George F. Koob and Eric P. Zorilla, "Update on Corticotropin-Releasing Factor Pharmacotherapy for Psychiatric Disorders: A Revisionist View," _Neuropsychopharmacology Reviews_ 37 (2012): 308–9.
launched a program dubbed "Fast-Fail": "FAST: Fast-Fail Trials," fact sheet, National Institute of Mental Health, http://www.nimh.nih.gov/research-priorities/research-initiatives/fast-fast-fail-trials.shtml.
In a pivotal study, Davis: William A. Falls et al., "Extinction of Fear-Potentiated Startle: Blockade by Infusion of an NMDA Antagonist into the Amygdala," _Journal of Neuroscience_ 12, no. 3 (1992): 854–63.
In 2002, Davis, Ressler, and colleagues: "Facilitation of Conditioned Fear Extinction by Systemic Administration or Intra-Amygdala Infusions of D-Cycloserine as Assessed with Fear-Potentiated Startle in Rats," _Journal of Neuroscience_ 22, no. 6 (2002): 2343–51.
Davis and Ressler then teamed up: Kerry J. Ressler et al., "Cognitive Enhancers as Adjuncts to Psychotherapy: Use of D-Cycloserine in Phobic Individuals to Facilitate Extinction of Fear," _Archives of General Psychiatry_ 61, no. 11 (2004): 1136–44.
In one trial, DCS failed: Eric A. Storch et al., "D-cycloserine Does Not Enhance Exposure-Response Prevention Therapy in Obsessive-Compulsive Disorder," _International Clinical Psychopharmacology_ 22, no. 4 (2007): 230–37.
DCS sped up improvement: Stefan G. Hofmann et al., "D-cycloserine as an Augmentation Strategy with Cognitive-Behavioral Therapy for Social Anxiety Disorder," _American Journal of Psychiatry_ 170, no. 7 (2013): 751–58.
One study of veterans: Brett T. Litz et al., "A Randomized Placebo-Controlled Trial of D-cycloserine and Exposure Therapy for Posttraumatic Stress Disorder," _Journal of Psychiatric Research_ 46 (2012): 1184–90.
Hofmann, who had done the trials: Stefan G. Hofmann, interview by author; and S. G. Hofmann, "D-cycloserine for Treating Anxiety Disorders: Making Good Exposures Better and Bad Exposures Worse," _Depression and Anxiety_ 31 (2014): 175–77.
people have taken MDMA: For an in-depth survey of compounds being studied in anxiety disorders, see Boadie W. Dunlop et al., "Pharmacological Mechanisms of Modulating Fear and Extinction," in _Primer on Anxiety Disorders: Translational Perspectives on Diagnosis and Treatment_ , ed. Kerry J. Ressler et al. (New York: Oxford University Press, 2015), 367–431.
# 6. COLD CALLS, AIRPLANES, AND INDECISION
A 2005 study by Australian researchers: Geoff Waghorn et al., "Disability, Employment and Work Performance Among People with ICD-10 Anxiety Disorders," _Australian and New Zealand Journal of Psychiatry_ 39 (2005): 55–66.
While both anxiety disorders and depression: Inger Plaisier et al., "Depressive and Anxiety Disorders On-the-Job: The Importance of Job Characteristics for Good Work Functioning in Persons with Depressive and Anxiety Disorders," _Psychiatry Research_ 200 (2012): 382–88.
Of the more than ten million Americans: _Annual Statistical Report on the Social Security Disability Insurance Program_ , 2015, Social Security Administration, 2015, table 6, http://www.socialsecurity.gov/policy/docs/statcomps/di_asr/2015/sect01b.html#table6.
Indeed, people with panic disorder: Martin M. Antony et al., "Dimensions of Perfectionism Across the Anxiety Disorders," _Behaviour Research and Therapy_ 36 (1998): 1143–54.
Research shows, however, that anxiety: Joachim Stöber and Jutta Joormann, "Worry, Procrastination, and Perfectionism: Differentiating Amount of Worry, Pathological Worry, Anxiety and Depression," _Cognitive Therapy and Research_ 25, no. 1 (2001): 49–60.
A review of more than two hundred: Piers Steel, "The Nature of Procrastination: A Meta-Analytic and Theoretical Review of Quintessential Self-Regulatory Failure," _Psychological Bulletin_ 133, no. 1 (2007): 65–94.
More than a century ago, in 1908: In Yerkes and Dodson's famous experiment, mice presented with two boxes, one black and one white, were taught to go only into the white box. The researchers did this by giving the mice shocks each time they began to enter the black box. When the task was difficult, the mice learned best when the shocks given were medium strength. When the shocks were weaker or stronger, the mice learned more slowly and made more errors. Only when the task was really easy did the mice continue to perform better as the shocks increased in strength. The researchers made the task harder by decreasing the amount of light shining on the boxes, making it tougher for the mice to tell the difference between the colors. See Robert M. Yerkes and John D. Dodson, "The Relation of Strength of Stimulus to Rapidity of Habit-Formation," _Journal of Comparative Neurology and Psychology_ 18, no. 5 (1908): 459–82.
a range of studies in people: S. J. Lupien et al., "The Effects of Stress and Stress Hormones on Human Cognition: Implications for the Field of Brain and Cognition," _Brain and Cognition_ 65, no. 3 (2007): 209–37.
A study of beginning nursing students: L. McEwan and D. Goldenberg, "Achievement Motivation, Anxiety and Academic Success in the First Year Master of Nursing Students," _Nurse Education Today_ 19, no. 5 (1999): 419–30.
Canadian researchers, for example: Alexander M. Penney et al., "Intelligence and Emotional Disorders: Is the Worrying and Ruminating Mind a More Intelligent Mind?" _Personality and Individual Differences_ 74 (2015): 90–93.
A small 2012 study: Jeremy D. Coplan et al., "The Relationship Between Intelligence and Anxiety: An Association with Subcortical White Matter Metabolism," _Frontiers in Evolutionary Neuroscience_ 3, no. 8 (2012): 1–7.
Ein-Dor and his colleague Orgad Tal: Tsachi Ein-Dor and Orgad Tal, "Scared Saviors: Evidence That People High in Attachment Anxiety Are More Effective in Alerting Others to Threat," _European Journal of Social Psycholog_ y 42, no. 6 (2012): 667–71.
For decades, psychologists have theorized: Michael W. Eysenck et al., "Anxiety and Cognitive Performance: Attentional Control Theory," _Emotion_ 7, no. 2 (2007): 336–53. Also see also Oliver J. Robinson et al., "The Impact of Anxiety upon Cognition: Perspectives from Human Threat of Shock Studies," _Frontiers in Human Neuroscience_ 7 (2013).
The idea is that: Michael W. Eysenck, "Anxiety, Learning, and Memory: A Reconceptualization," _Journal of Research in Personality_ 13, no. 4 (1979): 363–85.
In a 2016 study, researchers at the NIMH: Katherin E. Vytal et al., "Induced-Anxiety Differentially Disrupts Working Memory in Generalized Anxiety Disorder," _BMC Psychiatry_ 16 (2016): 1–9.
Another study by the same NIMH: Nicholas L. Balderston et al., "Anxiety Patients Show Reduced Working Memory Related DLPFC Activation During Safety and Threat," _Depression and Anxiety_ (2016): 1–12.
It sounds absurd, but a series of studies: Alison Wood Brooks, "Get Excited: Reappraising Pre-Performance Anxiety as Excitement," _Journal of Experimental Psychology: General_ 143, no. 3 (2014): 1144–58.
Only one in four people: "Workplace Stress and Anxiety Disorders Survey," Anxiety and Depression Association of America, http://www.adaa.org/workplace-stress-anxiety-disorders-survey.
Still, one study published in 1999: D. A. Koser et al., "Comparison of a Physical and Mental Disability in Employee Selection: An Experimental Examination of Direct and Moderated Effects," _North American Journal of Psychology_ 1 (1999): 213–22, referenced in Kay Wheat et al., "Mental Illness in the Workplace: Conceal or Reveal?" _Journal of the Royal Society of Medicine_ 103, no. 3 (2010): 83–86.
A 1996 survey: Jim Read and Sue Baker, "Not Just Sticks and Stones: A Survey of the Stigma, Taboos and Discrimination Experienced by People with Mental Health Problems," _Mind_ (1996).
Anxious people often have a tough time: C. Giorgetta et al., "Reduced Risk-Taking Behavior as a Trait Feature of Anxiety," _Emotion_ 12, no. 6 (2012): 1373–83. And for an overview, see Catherine A. Hartley and Elizabeth A. Phelps, "Anxiety and Decision-Making," _Biological Psychiatry_ 72, no. 2 (2012).
In one gambling experiment: Andrei C. Miu et al., "Anxiety Impairs Decision-Making: Psychophysiological Evidence from an Iowa Gambling Task," _Biological Psychology_ 77 (2008): 353–58.
When scientists at the University of Pittsburgh: Junchol Park et al., "Anxiety Evokes Hypofrontality and Disrupts Rule-Relevant Encoding by Dorsomedial Prefrontal Cortex Neurons," _Journal of Neuroscience_ 36, no. 11 (2016): 3322–35.
# 7. THE ISOLATION CHAMBER
I've found only one study: Y. Tibi-Elhanany and S. G. Shamay-Tsoory, "Social Cognition in Social Anxiety: First Evidence for Increased Empathic Abilities," _Israel Journal of Psychiatry_ 48, no. 2 (2011): 98–106.
However, if we look at it more broadly: For a good primer on post-traumatic growth, see Posttraumatic Growth Research Group, Department of Psychology, University of North Carolina at Charlotte, <https://ptgi.uncc.edu>.
But one interesting 2013 study: Jacob A. Priest, "Anxiety Disorders and the Quality of Relationships with Friends, Relatives, and Romantic Partners," _Journal of Clinical Psychology_ 69, no. 1 (2013): 78–88.
In another study, socially anxious women: S. Cuming and R. M. Rapee, "Social Anxiety and Self-Protective Communication Style in Close Relationships," _Behaviour Research and Therapy_ 48, no. 2 (2010): 87–96.
For anxious kids, having supportive: Julie Newman Kingery et al., "Peer Experiences of Anxious and Socially Withdrawn Youth: An Integrative Review of the Developmental and Clinical Literature," _Clinical Child and Family Psychological Review_ 13 (2010): 91–128.
being part of a group: A. M. La Greca and H. M. Harrison, "Adolescent Peer Relations, Friendships, and Romantic Relationships: Do They Predict Social Anxiety and Depression?" _Journal of Clinical and Child Adolescent Psychology_ 34, no. 1 (2005): 49–61.
In a 2016 study, anxious teens: N. C. Jacobson and M. G. Newman, "Perceptions of Close and Group Relationships Mediate the Relationship Between Anxiety and Depression over a Decade Later," _Depression and Anxiety_ 33, no. 1 (2016): 66–74.
Good friends also enhance treatment: J. R. Baker and J. L. Hudson, "Friendship Quality Predicts Treatment Outcome in Children with Anxiety Disorders," _Behaviour Research and Therapy_ 51, no. 1 (2013): 31–36.
Anxious kids generally: Julie Newman Kingery et al., "Peer Experiences."
Research has found at least: Timothy L. Verduin and Philip C. Kendall, "Peer Perceptions and Liking of Children with Anxiety Disorders," _Journal of Abnormal Child Psychology_ 36, no. 4 (2008): 459–69.
A study from 1999: D. C. Beidel et al., "Psychopathology of Childhood Social Phobia," _Journal of American Academy of Child and Adolescent Psychiatry_ 38, no. 6 (1999): 643–50.
Anxious kids are more likely to be bullied: A. M. Crawford and K. Manassis, "Anxiety, Social Skills, Friendship Quality, and Peer Victimization: An Integrated Model," _Journal of Anxiety Disorders_ 25, no. 7 (2011): 924–31.
In one study, a staggering 92 percent: Randi E. McCabe et al., "Preliminary Examination of the Relationship Between Anxiety Disorders in Adults and Self-Reported History of Teasing or Bullying Experiences," _Cognitive Behaviour Therapy_ 32, no. 4 (2003): 187–93.
Boys with social anxiety: Kingery, "Peer Experiences."
And in another example of a negative feedback: R. R. Landoll et al., "Cyber Victimization by Peers: Prospective Associations with Adolescent Social Anxiety and Depressive Symptoms," _Journal of Adolescence_ 42 (2015): 77–86.
Adolescents who are frequently picked on: Lexine A. Stapinski et al., "Peer Victimization During Adolescence and Risk for Anxiety Disorders in Adulthood: A Prospective Cohort Study," _Depression and Anxiety_ 31, no. 7 (2014): 575–82.
Emotional states, neuroscientists have found: Elaine Hatfield et al., "Emotional Contagion," _Current Directions in Psychological Science_ 2, no. 3 (1993): 96–100.
In a 2014 study, researchers in Germany: Veronika Engert et al., "Cortisol Increase in Empathic Stress Is Modulated by Emotional Closeness and Observation Modality," _Psychoneuroendocrinology_ 45 (2014): 192–201.
This might be one reason why adults: Priest, "Anxiety Disorders and the Quality of Relationships."
partners with anxiety disorders judged: Piotr Pankiewicz et al., "Anxiety Disorders in Intimate Partners and the Quality of Their Relationship," _Journal of Affective Disorders_ 140 (2012): 176–80.
men whose wives had panic disorder: Jane D. McLeod, "Anxiety Disorders and Marital Quality," _Journal of Abnormal Psychology_ 103, no. 4 (1994): 767–76.
A 1985 study: W. Monteiro et al., "Marital Adjustment and Treatment Outcome in Agoraphobia," _British Journal of Psychiatry_ 146 (1985): 383–90.
Women with high levels of social anxiety: E. Porter and D. L. Chambless, "Shying Away from a Good Thing: Social Anxiety in Romantic Relationships," _Journal of Clinical Psychology_ 70, no. 6 (2014): 546–61.
followed thirty-three heterosexual couples: Talia I. Zaider et al., "Anxiety Disorders and Intimate Relationships: A Study of Daily Processes in Couples," _Journal of Abnormal Psychology_ 119, no. 1 (2010): 163–73.
# 8. WORRIES ABOUT MY DAUGHTER
About 10 percent of pregnant women: William O. Cooper et al., "Increasing Use of Antidepressants in Pregnancy," _American Journal of Obstetrics & Gynecology_ 196, no. 6 (2007).
In the mid-2000s, studies had linked: See, for example, G. M. Thormahlen, "Paroxetine Use During Pregnancy: Is It Safe?," _Annals of Pharmacotherapy_ 40, no. 10 (2006): 1834–37; and B. Bar-Oz et al., "Paroxetine and Congenital Malformations: Meta-Analysis and Consideration of Potential Confounding Factors," _Clinical Therapeutics_ 29, no. 5 (2007): 918–26.
linked to a higher risk—about double: Jennifer Reefhuis et al., "Specific SSRIs and Birth Defects: Bayesian Analysis to Interpret New Data in the Context of Previous Reports," _BMJ_ 351 (2015).
more likely to be born prematurely: Rita Suri et al., "Effects of Antenatal Depression and Antidepressant Treatment on Gestational Age at Birth and Risk of Preterm Birth," _American Journal of Psychiatry_ 164, no. 8 (2007): 1206–13; and T. F. Oberlander et al., "Neonatal Outcomes After Prenatal Exposure to Selective Serotonin Reuptake Inhibitor Antidepressants and Maternal Depression Using Population-Based Linked Health Data," _Archives of General Psychiatry_ 63, no. 8 (2006): 898–906.
serious lung condition: Sophie Grigoriadis et al., "Prenatal Exposure to Antidepressants and Persistent Pulmonary Hypertension of the Newborn: Systematic Review and Meta-Analysis," _BMJ_ 348 (2014).
no more likely to have heart defects: Irene Petersen et al., "Selective Serotonin Reuptake Inhibitors and Congenital Heart Anomalies: Comparative Cohort Studies of Women Treated Before and During Pregnancy and Their Children," _Journal of Clinical Psychiatry_ 77, no. 1 (2016): e36–e42.
is found in breast milk: Tiffany Field, "Breastfeeding and Antidepressants," _Infant Behavior and Development_ 31, no. 3 (2008): 481–87; and Jan Oystein Berle and Olav Spigset, "Antidepressant Use During Breastfeeding," _Current Women's Health Review_ 7 (2011): 28–34.
link Prozac to slow weight gain: C. D. Chambers et al., "Weight Gain in Infants Breastfed by Mothers Who Take Fluoxetine," _Pediatrics_ 104, no. 5 (1999).
increased risk of autism and ADHD: C. C. Clements et al., "Prenatal Antidepressant Exposure Is Associated with Risk for Attention-Deficit Hyperactivity Disorder but Not Autism Spectrum Disorder in a Large Health System," _Molecular Psychiatry_ 20, no. 6 (2015): 727–34.
twice as likely to develop autism: T. Boukhris et al., "Antidepressant Use During Pregnancy and the Risk of Autism Spectrum Disorder in Children," _JAMA Pediatrics_ 170, no. 2 (2016): 117–24.
no link between antidepressants and autism: Merete Juul Sørensen et al., "Antidepressant Exposure in Pregnancy and Risk of Autism Spectrum Disorders," _Clinical Epidemiology_ 5 (2013): 449–59.
more behavioral issues: Katrina C. Johnson et al., "Preschool Outcomes Following Prenatal Serotonin Reuptake Inhibitor Exposure: Differences in Language and Behavior, but Not Cognitive Function," _Journal of Clinical Psychiatry_ 77, no. 2 (2016): e176–e182.
no long-term effects: See for example, Rita Suri et al., "Acute and Long-Term Behavioral Outcome of Infants and Children Exposed in Utero to Either Maternal Depression or Antidepressants: A Review of the Literature," _Journal of Clinical Psychiatry_ 75, no. 10 (2014): e1142–e1152.
no difference between them: Irena Nulman et al., "Neurodevelopment of Children Prenatally Exposed to Selective Reuptake Inhibitor Antidepressants: Toronto Sibling Study," _Journal of Clinical Psychiatry_ 76, no. 7 (2015): e842–e847.
to become depressed by age fifteen: Heli Malm et al., "Gestational Exposure to Selective Serotonin Reuptake Inhibitors and Offspring Psychiatric Disorders: A National Register-Based Study," _Journal of the American Academy of Child and Adolescent Psychiatry_ 55, no. 5 (2016): 359–66.
Being exposed to a parent's depression: Myrna M. Weissman et al., "Offspring of Depressed Parents: 20 Years Later," _American Journal of Psychiatry_ 163 (2006): 1001–08.
higher rates of anxiety, aggressive behavior: Bea R. Van den Bergh and Alfons Marcoen, "High Antenatal Maternal Anxiety Is Related to ADHD Symptoms, Externalizing Problems, and Anxiety in 8- and 9-Year-Olds," _Child Development_ 75, no. 4 (2004): 1085–97.
levels of the stress hormone cortisol: Bea R. H. Van den Bergh et al., "Antenatal Maternal Anxiety Is Related to HPA-Axis Dysregulation and Self-Reported Depressive Symptoms in Adolescence: A Prospective Study on the Fetal Origins of Depressed Mood," _Neuropsychopharmacology_ 33, no. 3 (2008): 536–45.
tougher time on tasks: Maarten Mennes et al., "Long-Term Cognitive Sequelae of Antenatal Maternal Anxiety: Involvement of the Orbitofrontal Cortex," _Neuroscience and Biobehavioral Review_ 30 (2006): 1078–86; and Maarten Mennes et al., "Developmental Brain Alternations in 17 Year Old Boys Are Related to Antenatal Maternal Anxiety," _Clinical Neurophysiology_ 120 (2009): 1116–22.
reduce the volume of parts of the brain: Claudia Buss et al., "High Pregnancy Anxiety During Mid-Gestation Is Associated with Decreased Gray Matter Density in 6–9 Year-Old Children," _Psychoneuroendocrinology_ 35, no. 1 (2010): 141–53.
babies that cry excessively: Johanna Petzoldt et al., "Maternal Anxiety Disorders Predict Excessive Infant Crying: A Prospective Longitudinal Study," _Archives of Disease in Childhood_ 99, no. 9 (2014): 800–806.
feeding problems in their babies: J. Petzoldt et al., "Maternal Anxiety Versus Depressive Disorders: Specific Relations to Infants' Crying, Feeding and Sleeping Problems," _Child: Care, Health and Development_ 42, no. 2 (2015): 231–45.
transmitted to them in utero: Bea R. H. Van den Bergh et al., "Antenatal Maternal Anxiety and Stress and the Neurobehavioural Development of the Fetus and Child: Links and Possible Mechanisms. A Review," _Neuroscience and Biobehavioral Reviews_ 29 (2005): 237–58.
can cross the placenta: Michael T. Kinsella and Catherine Monk, "Impact of Maternal Stress, Depression and Anxiety on Fetal Neurobehavioral Development," _Clinical Obstetrics and Gynecology_ 52, no. 3 (2009): 425–40.
stress during pregnancy: Catherine Monk et al., "Distress During Pregnancy: Epigenetic Regulation of Placenta Glucocorticoid-Related Genes and Fetal Neurobehavior," _American Journal of Psychiatry_ 173, no. 7 (2016): 705–13.
just before getting pregnant: L. S. Cohen et al., "Relapse of Major Depression During Pregnancy in Women Who Maintain or Discontinue Antidepressant Treatment," _Journal of the American Medical Association_ 295, no. 5 (2006): 499–507.
almost three times as likely: Katja Beesdo et al., "Incidence of Social Anxiety Disorder and the Consistent Risk for Secondary Depression in the First Three Decades of Life," _Archives of General Psychiatry_ 64, no. 8 (2007): 903–12.
drank alcohol more frequently: Philip C. Kendall et al., "Child Anxiety Treatment: Outcomes in Adolescence and Impact on Substance Use and Depression at 7.4 Year Follow-Up," _Journal of Consulting and Clinical Psychology_ 72, no. 2 (2004): 276–87.
developed an anxiety disorder: Golda S. Ginsburg et al., "Preventing Onset of Anxiety Disorders in Offspring of Anxious Parents: A Randomized Controlled Trial of a Family-Based Intervention," _American Journal of Psychiatry_ 172, no. 12 (2015): 1207–14.
Thirty-nine percent of the teenage girls: Ronald M. Rapee, "The Preventative Effects of a Brief, Early Intervention for Preschool-Aged Children at Risk for Internalizing: Follow-Up into Middle Adolescence," _Journal of Child Psychology and Psychiatry_ 54, no. 7 (2013): 780–88.
met criteria for social anxiety disorder: Andrea Chronis-Tuscano et al., "Preliminary Evaluation of a Multimodal Early Intervention Program for Behaviorally Inhibited Preschoolers," _Journal of Consulting and Clinical Psychology_ 83, no. 3 (2015): 534–40.
# 9. STAYING GROUNDED
number of college students diagnosed with: American College Health Association National College Health Assessment, _Spring 2016 Reference Group Executive Summary_ (American College Health Association, 2016); and American College Health Association National College Health Assessment, _Fall 2008 Reference Group Executive Summary_ (American College Health Association, 2008).
a link to anxiety and depression: See, for example, H. C. Woods and H. Scott, "#Sleepyteens: Social Media Use in Adolescence Is Associated with Poor Sleep Quality, Anxiety, Depression and Low Self-Esteem," _Journal of Adolescence_ 51 (2016): 41–49.
feelings of loneliness: Moira Burke et al., "Social Network Activity and Social Well-Being," _CHI '10 Proceedings of the SIGCHI Conference on Human Factors in Computing Systems_ (2010): 1909–12.
tuition at Michigan: "Cost of Attendance," Office of Financial Aid, University of Michigan, https://finaid.umich.edu/cost-of-attendance/.
about $29,000 in debt: _Student Debt and the Class of 2014,_ Institute for College Access and Success, October 2015, http://ticas.org/sites/default/files/pub_files/classof2014.pdf.
had had some previous counseling: _College Student Mental Health Survey,_ Phase III, Counseling and Psychological Services, https://caps.umich.edu/files/caps/CSMHSfinal.pdf.
don't provide psychiatric services: _Annual Survey 2015_ , Association for University and College Counseling Center Directors. http://www.aucccd.org/assets/documents/aucccd%202015%20monograph%20-%20public%20version.pdf.
a sign of strength: "A Survey About Mental Health and Suicide in the United States," by Harris Poll on behalf of the Anxiety and Depression Association of America, the American Foundation for Suicide Prevention and the National Action Alliance for Suicide Prevention, 2015, https://www.adaa.org/sites/default/files/College-Aged_Adults_Survey_Summary-1.14.16.pdf.
Conversion disorder is characterized: _DSM_ -5, 318–21.
somatic symptom disorder: Ibid., 311–15.
mystery symptoms made up two-thirds: Natalie Steinbrecher et al., "The Prevalence of Medically Unexplained Symptoms in Primary Care," _Psychosomatics_ 52, no. 3 (2011): 263–71.
evidence that it is beneficial: John R. Keefe et al., "A Meta-Analytic Review of Psychodynamic Therapies for Anxiety Disorders," _Clinical Psychology Review_ 34, no. 4 (2014): 309–23.
associated with anxiety in teenagers: M. Sarchiapone et al., "Hours of Sleep in Adolescents and Its Association with Anxiety, Emotional Concerns, and Suicidal Ideation," _Sleep Medicine_ 15, no. 2 (2014): 248–54.
is linked to anxiety in kids: F. E. Fletcher et al., "The Association Between Anxiety Symptoms and Sleep in School-Aged Children: A Combined Insight from the Children's Sleep Habits Questionnaire and Actigraphy," _Behavioral Sleep Medicine_ (2016): 1–16.
greater risk of having more chronic illnesses: Josine G. van Mill et al., "Sleep Duration, but Not Insomnia, Predicts the 2-Year Course of Depressive and Anxiety Disorders," _Journal of Clinical Psychiatry_ 75, no. 2 (2014): 119–26.
difficulty sleeping is a precursor: M. L. Jackson et al., "Sleep Difficulties and the Development of Depression and Anxiety: A Longitudinal Study of Young Australian Women," _Archives of Women's Mental Health_ 17, no. 3 (2014): 189–98.
increase the risk of developing PTSD: Rebecca C. Cox and Bunmi O. Olatunji, "A Systematic Review of Sleep Disturbance in Anxiety and Related Disorders," _Journal of Anxiety Disorders_ 37 (2016): 104–29.
good sleep is critical for consolidating memories: A. K. Zalta et al., "Sleep Quality Predicts Treatment Outcome in CBT for Social Anxiety Disorder," _Depression and Anxiety_ 30, no. 11 (2013): 1114–20.
their amygdala activity in response to negative: Cox and Oltunji, "A Systematic Review of Sleep Disturbance in Anxiety and Related Disorders."
exercise is modestly effective: K. Jayakody et al., "Exercise for Anxiety Disorders: Systematic Review," _British Journal of Sports Medicine_ 48, no. 3 (2014): 187–96.
boost brain-derived neurotrophic factor: Lindsey B. DeBoer et al., "Exploring Exercise as an Avenue for the Treatment of Anxiety Disorders," _Expert Review of Neurotherapuetics_ 12, no. 8 (2012): 1011–22.
lowers activity in the HPA axis: Elizabeth Anderson and Geetha Shivakumar, "Effects of Exercise and Physical Activity on Anxiety," _Frontiers in Psychiatry_ 4 (2013).
time in nature can reduce stress: David G. Pearson and Tony Craig, "The Great Outdoors? Exploring the Mental Health Benefits of Natural Environments," _Frontiers in Psychology_ 5 (2014).
time in the park had decreased anxiety: Gregory N. Bratman et al., "The Benefits of Nature Experience: Improved Affect and Cognition," _Landscape and Urban Planning_ 138 (2015): 41–50.
21 percent higher in urban areas: J. Peen et al., "The Current Status of Urban-Rural Differences in Psychiatric Disorders," _Acta Psychiatrica Scandinavica_ 121 (2010): 84–93.
_On Edge_ was a team endeavor. I could never have written it without the encouragement, support, and guidance of so many friends, family members, and colleagues. My agent, Gary Morris at the David Black Agency, believed in the book when it was only a few hurried paragraphs sent to him in an email. Through the years it took me to report and write it, Gary has been a fierce advocate, a stalwart sounding board, and a true mensch.
I had the good fortune to land at Crown Publishing, where the brilliant Molly Stern helms an outfit filled with the best in the business. My editor, the incredibly gifted and sharp-eyed Rachel Klayman, smoothed out my language, untangled my logic, and always pushed me to make this book better. Sarah Breivogel and Alaina Waagner got the word out about _On Edge_ with creativity, tenacity, and passion. Claire Potter brought tremendous hard work and enthusiasm to the project. Jon Darga made things run smoothly and good-naturedly answered my many questions. Thanks also to Lance Fitzgerald, Robert Siek, Courtney Snyder, and everyone else on the _On Edge_ team.
At the _Wall Street Journal_ , editors Mike Miller and Emily Nelson have allowed me to pursue the most fun, most rewarding hybrid beat of psychology, health, and travel and gave me crucial time off to work on this book. Adam Thompson's deft editing makes me look good. Thanks to Elizabeth Bernstein, Elizabeth Holmes, and Sumathi Reddy for commenting on drafts of the manuscript. They, along with Rachel Bachman, Ellen Byron, Ray Smith, and the entire Personal Journal crew, made it a joy to go to work every day. Former editors John Blanton and Hilary Stout were early supporters of _On Edge_ and taught me so much about writing and editing and always did so with incredible generosity, humor, and grace. Thanks also to Dick Tofel, who first hired me at the _Journal_ , and Jim Pensiero, who sent me on my way to becoming a reporter. Rebecca Blumenstein, Cynthia Crossen, Kathy Deveny, Laurie Hays, Dan Hertzberg, Dennis Kneale, and Paul Steiger were important early mentors. Wendy Bounds, Sam Walker, and Jeff Zaslow helped me when I was first contemplating the proposal for this book.
Anxiety researchers and clinicians are among the most generous and patient people around. Danny Pine has steered me to the best research, introduced me to important contacts, and saved me from making several mistakes. I am lucky to count him as a mentor and friend. Jordan Smoller is not only a remarkable scientist, but a wonderful writer as well: He read an early draft of the manuscript and provided important feedback.
Thank you also to Anne Marie Albano, Christine Asidao, Yair Bar-Haim, David Barlow, Katja Beesdo-Baum, Andrea Chronis-Tuscano, Michelle Craske, Christina Danko, Michael Davis, Nathan Fox, Jay Gingrich, Christian Grillon, Michelle Hampson, Steven Hayes, Stefan Hofmann, Jerry Kagan, Ned Kalin, Ron Kessler, Don Klein, Joe LeDoux, Heli Malm, Carmen McLean, Francis McMahon, Barbara Morrongiello, Danielle Novick, Ron Rapee, Kerry Ressler, Jeff Rossman, Ken Rubin, Todd Sevig, Robert Temple, Bea Van den Bergh, Greg Van Rybroek, Ulli Wittchen, and Anna Zilverstand.
I'm also very grateful to the late Alies Muskin and her staff at the Anxiety and Depression Association of America.
I'm in awe of the passion, commitment, and openness of the college mental health advocates I've met. Thank you for sharing your stories with me, supporting each other, and fighting for mental health every day. Thanks to Sara Abelson, Alison Malmon, Pam McKeta, and everyone at Active Minds. Also to Victor Schwartz and the crew at the Jed Foundation. A big shout-out to Anna Chen, Anna Learis, Grant Rivas, Shelby Steverson, and Cheyenne Stone at Michigan. Go Blue!
Receiving a Rosalynn Carter Fellowship for Mental Health Journalism allowed me to really launch this project. Our initial meeting in Atlanta was the first time I spoke about my anxiety in a professional public setting. Thank you to Mrs. Carter, Rebecca Palpant Shimkets, and the Carter Center staff, mentors, and fellows for the work you do supporting journalism and combating stigma.
So many friends have encouraged and supported me along the way. Roe D'Angelo and Ianthe Dugan read my drafts, steadied my nerves, and were the very best cheerleaders. A huge thank you also to Amy Bennett, Sabina Broadhead, Mike Cronin, Elisabeth Eaves, Chelsea Emery, Francis Freisinger, Susie Hassan, Gabrielle Kahn, Ron Lieber, Anna Loengard, Jeff Opdyke, Annie Murphy Paul, Josh Prager, Richard Robb, David Roche, Joel Smernoff, David Stone, Johannes and Karin Weidenmueller, Rubina Yeh, Leslie Wright, and Alan Zarembo. The members of the Invisible Institute are a continual source of wisdom and inspiration.
I wrote most of this book at the Ditmas Workspace in Ditmas Park, Brooklyn, where Ben Smith and Liena Zagare created a wonderful home for neighborhood writers and the indefatigable Gina, Tom, and Erica Anderson now nurture a growing creative community. Thanks to my fellow quiet room denizens Gabe Heller, David Rogers, and Adam Sternbergh for the camaraderie and conversation. We're lucky to have the Milk & Honey café a short walk away where Max and the baristas have kept me fueled with decaf.
Thank you to the therapists and doctors—especially Dr. G and Dr. L—who have helped keep me healthy.
Most of all, I thank my family. My parents, Anita and Gary Petersen, have put me back together more times than I can recall. My immensely talented sister, Dana Petersen Murphy, talked to me about her own anxiety, and she and her husband, Sean Murphy, fed and housed me during my Wisconsin reporting trips. My aunt Susan Koeferl provided crucial details about my grandmother's illness and was so open about a very painful period in her life. My cousin Renee Jahnke secured our grandmother's records from Mendota. Beverly and Bob Gallagher are the most generous, loving in-laws. Ditto to my fabulous sisters-in-law and their husbands: Jennifer and Sean Briody and Rose and Patrick Gallagher. The Bisel clan in Salem and elsewhere has been this book's unofficial marketing team. Denise Paul has taken such good care of Fiona since she was a baby and gives me the peace of mind I need to work.
If this book had an MVP, it would be my husband, Sean Gallagher. He talked me through setbacks, kept the music playing, made me pizza, and tore up his own schedule so I had the time to report and write. And he gave me Fiona. My heart, my joy. I missed out on a lot of adventures during the years I've been working on this book. But, yes, Mama can go play now.
# ABOUT THE AUTHOR
Andrea Petersen is a contributing writer at the _Wall Street Journal,_ where she reports on psychology, health, and neuroscience. She is the recipient of a Rosalynn Carter Fellowship for Mental Health Journalism. She lives in Brooklyn, New York, with her husband and daughter.
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1. Cover
2. Title Page
3. Copyright
4. Contents
5. Dedication
6. Author's Note
7. Prologue
8. Chapter 1: The Anticipation of Pain: Defining Anxiety
9. Chapter 2: Scary Clowns and the End of Days: Anxiety in Childhood
10. Chapter 3: My Grandmother's Madness: The Genetics of Anxiety
11. Chapter 4: From CBT to Karaoke: Nondrug Therapies for Anxiety
12. Chapter 5: May Cause Dizziness: Medications for Anxiety
13. Chapter 6: Cold Calls, Airplanes, and Indecision: Anxiety at Work and on the Road
14. Chapter 7: The Isolation Chamber: Anxiety in Love and Friendship
15. Chapter 8: Worries About My Daughter: The Education of an Anxious Parent
16. Chapter 9: Staying Grounded: Learning to Live with Anxiety
17. Notes
18. Acknowledgments
19. About the Author
1. Cover
2. Cover
3. Title Page
4. Contents
5. Start
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The Northwest Ohio Athletic League, which has a long tradition of wrestling excellence, has added a new wrinkle to its format this season.
The NWOAL will host nine quads, each hosted by a different school.
The quads will bring four teams to one site at a particular night, with each team wrestling twice at a particular site. The format has two dual matches taking place on side-by-side mats at the same time.
In some ways [the new format] is good, and in some ways it s bad, Liberty Center coach Mitch Aring said. The advantages are that it saves points [dates] on the schedule, and it gives you a chance to see other teams, even if you don t wrestle against them.
The biggest disadvantage is that, if you have a rivalry with another team, it s not as big because there s another match going on at the mat next to you, and also the match may not take place at home.
With just two of the nine quads having been completed at this point, Wauseon coach Mike Ritter said NWOAL coaches are taking a wait and see attitude with the format.
When you have a lot of teams at one site, it s good for the kids because they get more competition, Ritter said. It also doesn t take as long, so that s fan-friendly.
We ve only had one, and it seemed to work pretty well, so we ll see if that continues.
No matter what format is used, the expectation is that the league will be both deep and strong again this year.
Liberty Center has emerged as a consensus favorite, with Wauseon, Delta and Montpelier the main challengers along with Bryan and Archbold.
The main reason the Tigers have become the favorite is the depth and quality of returnees.
We ve set our expectations very high, Aring said. We re setting a goal of advancing to state, because if you reach that goal, other goals such as league, sectional and district titles fall into place.
The Tigers have both negative and positive motivation at this early point in the season. The negative comes from last year s district meet, during which only two of those nine qualifiers advanced to state.
A lot of our guys have a sour taste in their mouth from not qualifying [for state] last year, Aring admitted.
It has made our practice room very intense this year.
The positive came last week, when LC beat Wauseon in its first quad match-up.
The final score of 36-31 was deceptive since theTigers forfeited four weight classes. Liberty Center won eight of the 10 matches that took place.
Hopefully that gave our guys a lot of confidence, Aring said. When we get some guys back in the lower weights [that we forfeited], we feel that will give us a chance to really do something.
But Wauseon still has a nice team from top to bottom. They will be a force to be reckoned with.
The Indians also have a good combination of depth and talent, with senior state qualifier Michael Perez (119) joined by district qualifiers Brandon Volkman (145), Carson Frey (135) and Marc Schuette (160).
We ve got some expectations, because we have a group of experienced kids back, Ritter said. We re hoping that the hard work these kids put in during the off-season pays off during the year.
Defending league champ Delta took a graduation hit as five state qualifiers were lost. The young Panther lineup will be led by senior Jonny Tolson, who finished eighth in Division III at 112.
A team to watch is Montpelier, which returns five district qualifiers. Senior Nick Kreischer (119/125) will be joined by 17 other letter winners, including fellow district wrestlers Korbin Castillo (130), D.J. Ferguson (103), Kyle McCarty (171) and Matt Wells (215), all juniors.
Archbold also lost seven wrestlers from last year s lineup but returns seniors Chad Rufenacht at 152, a returning state qualifier, and Jared Leininger at 160, who advanced to the district meet last year.
Bryan finished second in the NWOAL last year despite not having a single league champ, and the Golden Bears expect to use depth to compete for another title.
A total of 17 letter winners are back, led by district qualifiers Shayne Combs (135/140) and Donny Ramos (112), both seniors, and junior Dylan Zedaker (135/140).
Patrick Henry may not have big numbers, but the wrestlers the Patriots do have are definitely talented. The leaders include sophomore Xavier Dye (160), who qualified for the state meet last year, while junior Alex Lopez (145) finished seventh at 112 two years ago.
Swanton is led by senior Austin Reiner (171), a two-time district qualifier, while Evergreen features a pair of district qualifiers in Brandon Bettinger, a sophomore at 112, and Jeff Smith, a senior at 130.
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Cobweb
Need Something To Do Sunday?
Believe it or not, the holiday season is in full swing. Remember that day when you ate a bunch of food and watched football with a slew of people allegedly related to you? That was Thanksgiving. And now it's pre-Christmas crazed holiday shopping time.
If you're behind on your holiday shopping, scared to go to the mall, or simply want to look at some pretty cool stuff, head to Paisley Roberts today. The home of creative cards and gifts is having its annual open house from 11 a.m.-3 p.m.
You can cruise the collection of greeting cards, personalized stationary, pens that write for years, and a slew of other awesomely random gifts. The gift-wrap pros will make your purchase look perfect under the tree, and you can grab a snack or beverage while locating that ideal stocking stuffer. |
Nintendo today announced two new $150 Pokemon X/Y 2DS bundles that will arrive at Target and Toys R Us locations across the United States starting on December 6.
Target will offer the Pokemon X 2DS bundle with a pre-installed copy of the game and a red system. Meanwhile, Toys R Us will stock a blue Pokemon Y 2DS bundle featuring a pre-installed copy of the role-playing game.
The Nintendo 2DS retails for $130, while Pokemon X/Y sells for $40, meaning shoppers are saving $20 by purchasing the bundle. Nintendo sold more than 4 million copies of Pokemon X/Y within 48 hours of the game's release in October, and 2 million combined copies have been sold to date in North America.
Nintendo originally launched the Nintendo 2DS on October 12 alongside Pokemon X/Y. The system plays all Nintendo 3DS games (but not in 3D) and is backwards compatible with Nintendo DS titles.
Shoppers in the United States have a variety of options for Nintendo portables this holiday season. In addition to the new Pokemon X/Y bundle, Nintendo is offering 3DS bundles for Luigi's Mansion: Dark Moon, The Legend of Zelda: A Link Between Worlds, and Mario & Luigi: Dream Team.
For more on Pokemon X/Y, check out GameSpot's review. |
The Lufthansa Airport Bus Service
Lufthansa Airport Buses
Enjoy comfort with the usual Lufthansa quality. For no matter which airline you are flying with, you can travel comfortably to and from the airport with the Lufthansa Airport Bus or the shuttle services operated by our cooperation partners.
Thanks to appropriate frequencies and minimal transfer times, the airport bus is a convenient way to catch your flight. Please note that for the airport bus route Bahrain – Dammam there are different rules relating to booking, check-in and baggage as well as different facilities on the bus. You will find detailed information about this on the route information page.
You will benefit from a service that is aligned precisely to the flight connections at our Frankfurt Airport hub. What is more, the Lufthansa Airport Bus covers the routes Porto – Vigo and Bahrain – Dammam. Thanks to appropriate frequencies and minimal transfer times, you can catch your flights with ease. Passengers who are not catching an onward flight with Lufthansa or who are booked on a flight with another airline can, of course, also purchase tickets for Lufthansa Airport Bus connections.
Please see the Lufthansa timetable for information on the arrival and departure times of the Lufthansa airport buses.
Booking
You can book tickets for the Lufthansa Airport Bus in exactly the same way as you would book a Lufthansa flight directly online at LH.com. To do this, simply enter Frankfurt as your departure airport and Kaiserslautern Central Station (Hbf. KLT), Saarbrucken (SDB) or Strasbourg (XER) as your destination airport. Alternatively, you can also book the Lufthansa Airport Bus through a Lufthansa agency.
Please note that, as for a flight, you need a ticket in advance for the Airport Bus. Unfortunately you cannot buy a ticket from the bus driver.
For the Lufthansa Airport Bus Bahrain – Dammam route, different rules apply to booking. Please read more about these on the route information page.
Check-in and Baggage
Travel on the airport bus from Kaiserslautern to Frankfurt Airport
Lufthansa airport bus passengers arriving at Frankfurt Airport can – like all other passengers – use the baggage check-in options that are available to them in Departure Hall A. Passengers who are only travelling with carry-on baggage can proceed directly to their departure gate.
After landing in Frankfurt passengers collect their baggage and pass through Customs. Please note that it is not possible for baggage to be transported automatically to Kaiserslautern because of customs regulations.
As usual collect your baggage after landing and after clearing customs take it with you to the Lufthansa Airport Bus
Important information about the airport bus routes from Kaiserslautern, Saarbrucken or Strasbourg to Frankfurt Airport
html_list
Always allow at least 60 minutes between flight and bus.
For capacity reasons baggage allowance is limited to two pieces per passenger.
The check-in deadline for the Lufthansa Airport Bus is 15 minutes before departure. If you are not at the bus stop by this time, your seat may be given to another passenger.
Passengers must travel as originally booked and then travel and complete their trip as per this reservation.
For almost all routes you can print out your boarding pass for the Lufthansa airport bus and your connecting flight from as early as 23 hours before departure on your own PC or have it issued as a mobile boarding pass.
For the journey to Kaiserslautern, Saarbrucken or Strasbourg you can get your boarding pass for the Lufthansa Airport Bus from any Lufthansa check-in machine at Frankfurt Airport or directly from the bus driver. Unfortunately, no through-check-in is possible, as it would be for two consecutive flights. You can sit wherever you wish on the bus.
To enable smooth processing at the bus stop, please check in for the bus immediately upon arrival at Frankfurt Airport.
The Lufthansa Airport Bus fleet consists solely of four-star category, First Class coaches. Comfortable seats, air conditioning and a toilet, as well as reading lamps, anti-glare blinds and footrests are standard. Wi-Fi is also available to you.
Airport Shuttle Services
Individual and comfortable – the Lufthansa airport shuttles on the routes from Heidelberg to Frankfurt Airport and from Munich city centre to Munich Airport as well as the airport shuttle on the route from Regensburg to Munich Airport.
Related topics
The Lufthansa Guide Service
International passengers can use the individual Lufthansa Guide Service at Frankfurt and Munich airports. The guides help passengers find their way around the airport and the service is available in many languages. |
There are continuing commercial requirements for apparatus adapted to receive and store products emanating from various types of machines. These needs are particularly prevalent in the manufacture and handling of electrical devices which are produced on automatic fabricating machines. Numerous examples of racking and magazining devices have been developed to receive various electrical devices. In U.S. Pat. No. 3,520,048 issued July 14, 1970 to W. F. Esseluhn et al. there is shown apparatus for feeding racks of partially assembled discrete electrical components, e.g., diodes in and out of automatic assembly machines. An automatic magazining apparatus is shown in U.S. Pat. No. 2,846,832 issued Aug. 12, 1958 to E. W. Larsen et al. wherein electrical devices such as wire spring relay parts are fed from an automatic assembly machine into receiving slots formed in a series of magazines which are successively moved in a load position. The magazines are rotated into a receiving position and then indexed to present each slot to receive an electrical device.
In recent years electrical devices, such as dual in-line packages known as DIP's, have been fabricated and secured to lead frames consisting of a pair of spaced metallic strips having inwardly extending groups of spaced leads. Examples of such fabricating techniques are shown in U.S. Pat. No. 4,054,238 issued Oct. 18, 1977 to H. E. Lloyd et al. and in U.S. Pat. No. 4,003,125 issued Jan. 18, 1977 to C. W. Wallick. In co-pending application Ser. No. 072,394, filed on even date herewith in the names of J. R. Meal and D. K. Sandmore, there is shown a method and apparatus for assembling rolled metallized film capacitors onto leads depending from a continuous metallic carrier strip. This co-pending application also discloses facilities for boxing and encapsulating the capacitors. |
Breaking news for everyone's consumption
FDA Releases Inspection Form 483 for SanGar Plant
Another day brings more bad news for still-closed SanGar Fresh Cut Produce. This time it was the release of the FDA Form 483 report containing observations of the federal food safety inspectors who were in the San Antonio produce distribution plant from Oct. 14 to 26.
It came out after FDA said its own test results were positive for the Listeria bacteria that has been linked to the deaths of elderly Texans.
SanGar was closed by order of the Texas Department of State Health Services on Oct. 20 under a state law that gives it the power to act when there is an imminent threat to human life.
SanGar will not be able to reopen until after a Nov. 17 Texas administrative hearing. In the meantime, it cannot process food and must manage the recall of all the product shipped from the San Antonio facility since January.
Both Texas and FDA have found the deadly Listeria bacteria on SanGar’s chopped celery and from multiple locations inside the plant.
Texas is investigating a 10-case cluster of Listeria cases that have included five deaths. Seven of those illnesses and at least four deaths were linked to SanGar fresh-cut salary.
SanGar officials say they want to reopen and are working with Texas officials and the FDA toward that goal. Carrie Williams, state health department spokesman, says multiple negative test results on food and environmental surfaces will be required before SanGar can reopen.
From the Form 483 observations listed below, the Texas produce company clearly has its work to do:
Observation 1: Failure to protect against contamination of food and food contact surfaces with microorganisms.
Observation 2: Failure to conduct cleaning and sanitizing operations for utensils and equipment in a manner that protects against contamination of food, food-contact surfaces, and food-packaging materials.
Observation 3: Employees did not wash hands thoroughly in an adequate hand-washing facility at any time their hands may have become soiled or contaminated.
Observation 4: Personnel with adverse health conditions are not instructed to report to their supervisors.
Observation 5: Failure to clean food-contact surfaces and utensils as frequently as necessary and to protect against contamination of food.
Observation 6: Failure to take apart equipment as necessary for thorough cleaning.
Observation 7: Failure to take effective measures to protect finished food from contamination by raw materials and refuse.
Observation 8: Failure to store raw materials in a manner that protects against contamination.
Observation 9: The design, construction, and use of equipment and utensils fail to preclude the adulteration of food with contaminants.
Observation 10: Failure to maintain equipment, containers, and utensils used to store food in a manner that protects against contamination.
Observation 11: Lack of adequate drainage of areas that may contribute to contamination of food by seepage, food-borne filth, and providing a breeding place for pests.
Observation 12: Failure to hold foods that can support the rapid growth of undesirable microorganisms at a temperature that prevents the food from becoming adulterated.
Observation 13: The plant is not constructed in such a manner as to allow floors and walls to be adequately cleaned and kept clean and kept in good repair.
Observation 14: Plumbing constitutes a source of contamination to food, water supplies, equipment, and utensils. |
Montreal – A Jewish man wearing a yarmulke was assaulted this week by a taxi driver in Montreal.
The taxi driver was blocking the door to an underground garage at a condo building Sunday in the Saint-Laurent borough of Montreal. When the driver of a car honked to signal that he should move away from the door, the taxi driver apparently noted the other driver’s kippah and shouted, “I won’t move for any fucking Jews!” He also threatened to kill the other driver.
The victim then attempted to photograph the taxi number in order to file a complaint, at which point the driver exited his car and punched the Jewish man repeatedly and shouted antisemitic slurs until a parking supervisor intervened, B’nai Brith Canada said in a statement. The victim’s phone also was smashed. The victim required attention at a local hospital.
A woman who intervened was reportedly struck by the taxi driver. |
Q:
Angular - Can't see how to hide this API Key
I have the following code in my angular app declaration - an API key for Facebook (to implement Share button):
.run(function($FB){
$FB.init('9xxxxxxxxxxxx94');
})
So i know the general answer to this - 'API keys should be kept on the server side', however I don't see how i actually implement this.
The share call-method is made on the front end, so even if my server kept the API key and sent it, surely it's still visible on the front end, else how would the share button work?
So my question, how do I hide that Facebook API Key?
Thanks.
A:
Requesting the key
The first thing that happens is that the client will request a key. This will only happen on certain pages like the sign up and log in pages. The idea here is that we want to make sure that only users browsing with a known client (in this case the official website or core client as it’s called) are allowed to take actions like creating or authenticating a user.
So when the client app requests the login page the server generates a unique token based on information sent in the request. The information used is always something the server knows, something the client knows, and something both know. So for example the server can generate a unique key based on User agent + current time + secret key. The server generates a hash based on this information and then stores a cookie containing only the hash on the client machine.
Setting permissions
At this point our key really isn’t a key anymore. It has been transformed into an access token. The server should then take this access token and store it for later retrieval. You can put the key in a database but since data of this type needs to be retrieved often I would suggest using a key-value store like Redis to cut down on database reads/writes and boost performance.
When you store the token you should also store a separate piece of data to indicate what permissions are associated with the token. In this case our token is acting only as a way to register and authenticate users so we store it next to a value that indicates who the token belongs to (the app’s web UI) and what permissions it has (limited to create and authenticate users). We treat it just like we would any other API client that way we can capture stats and control how it is used.
Authorizing a request
When the client then makes the POST request to create a new user or log in the server will check to see if the client sent an identifying cookie along with the request. If not, we reject the request. If it does send the cookie, the server should once again generate the hash using the values used previously (these values are either already known or sent with the request anyway so we’re not really taxing the server much) compare it to the cookie being sent to us, and if the values match allow the request to proceed.
Sources - Securing API Keys
OR
Simply send a request to your Server and let him handle your request with the hidden API-key and just return the result of your request to your front-end.
|
# This file was generated in the Smart Agent repo and copied here, DO NOT EDIT HERE.
collectd/redis:
Config:
- default: ''
doc: Path to a python binary that should be used to execute the Python code. If
not set, a built-in runtime will be used. Can include arguments to the binary
as well.
elementKind: ''
required: false
type: string
yamlName: pythonBinary
- default: null
doc: ''
elementKind: ''
required: true
type: string
yamlName: host
- default: null
doc: ''
elementKind: ''
required: true
type: integer
yamlName: port
- default: ''
doc: 'The name for the node is a canonical identifier which is used as plugin
instance. It is limited to 64 characters in length. (**default**: "{host}:{port}")'
elementKind: ''
required: false
type: string
yamlName: name
- default: ''
doc: Password to use for authentication.
elementKind: ''
required: false
type: string
yamlName: auth
- default: null
doc: Specify a pattern of keys to lists for which to send their length as a metric.
See below for more details.
elementKind: object
elementStruct:
doc: ListLength defines a database index and key pattern for sending list lengths
fields:
- default: null
doc: The database index.
elementKind: ''
required: true
type: uint16
yamlName: databaseIndex
- default: null
doc: Can be a globbed pattern (only * is supported), in which case all keys
matching that glob will be processed. The pattern should be placed in single
quotes ('). Ex. `'mylist*'`
elementKind: ''
required: true
type: string
yamlName: keyPattern
name: ListLength
package: pkg/monitors/collectd/redis
required: false
type: list
yamlName: sendListLengths
- default: 'false'
doc: If `true`, verbose logging from the plugin will be enabled.
elementKind: ''
required: false
type: bool
yamlName: verbose
sendListLengths:
- default: null
doc: The database index.
elementKind: ''
required: true
type: integer
yamlName: databaseIndex
- default: null
doc: Can be a globbed pattern (only * is supported), in which case all keys matching
that glob will be processed. The pattern should be placed in single quotes
('). Ex. `'mylist*'`
elementKind: ''
required: true
type: string
yamlName: keyPattern
|
Introduction
============
Gastrointestinal stromal tumours (GISTs) comprise 1 to 3% of all gastrointestinal malignancies. They are typically defined as tumours whose behaviour is driven by mutations in the *KIT* gene or *PDGFRA* gene, and may or may not stain positively for *KIT* gene \[[@B1]\]. Due to the presence of tyrosine kinase receptors within the tumour tissue, GIST is thought to originate from gastrointestinal pacemaker cells, the interstitial cells of Cajal (ICC). Sometimes tumours with the same morphological and immunohistochemical characteristics as GISTs are detected outside the alimentary canal, hence they are called extragastrointestinal stromal tumours (EGISTs). The biological behaviour of these tumours is uncertain and the malignancy rates are difficult to predict \[[@B2]\]. Here we present an unusual case of EGIST that presented with multiple gooseberry-like nodules involving the whole abdominal cavity, the omentum, peritoneum and small bowel mesentery, which makes a radical resection difficult.
Case presentation
=================
A 65-year-old Sudanese man, who was previously well, presented with vague central abdominal pain. The pain was increasing gradually. It was constant, associated with progressive abdominal distension for the past 6 months and mild loss of weight despite good appetite. A physical examination revealed distended abdomen with multiple firm nodules in his abdomen. Liver and spleen were not palpable. The results of haematological tests were within normal range; an ultrasound of his abdomen revealed multiple nodules of varying sizes in the peritoneal cavity. A computed tomography scan of his abdomen showed numerous nodules of different sizes, 1 to 3cm in diameter each, filling the peritoneal cavity and the surrounding bowel loops with intense peripheral enhancement (Figures [1](#F1){ref-type="fig"}, [2](#F2){ref-type="fig"} and [3](#F3){ref-type="fig"}). Ultrasound-guided biopsy was not conclusive. Gastroscopy and colonoscopy showed normal stomach and colon. Exploration revealed multiple firm gooseberry-like nodules of different sizes ranging between 1 and 5cm in diameter (Figures [4](#F4){ref-type="fig"}, [5](#F5){ref-type="fig"}, [6](#F6){ref-type="fig"} and [7](#F7){ref-type="fig"}), involving the greater omentum, peritoneal cavity and the mesentery, but liver texture was normal. The main bulk of the tumour was excised together with the greater omentum and part of the mesentery, however, residual tumour remained stuck to the small bowel and great vessels. The postoperative period was uneventful, and he was discharged 5 days later. Histopathology reported presence of sheets of cellular tumour composed of spindle cells infiltrating smooth muscle fibres, with positive CD117 stain. Hence the diagnosis of GIST was made. The patient was then referred to an oncologist and received imatinib but with little improvement in his symptoms.
{#F1}
{#F2}
{#F3}
{#F4}
{#F5}
{#F6}
{#F7}
Discussion
==========
GISTs are uncommon tumours of the gastrointestinal tract (GIT). They originate from ICC in the stomach, but they can appear anywhere along the GIT. GISTs rarely occur outside the alimentary canal; hence, those that do are called EGISTs. The behaviour of GISTs ranges from benign to cancerous. Bülbül Doğusoy studied 1160 cases of GISTs. He reported a male-to-female ratio of 1.22 and a mean age of 56.75 years. He found the stomach to be the most common location (45.0%), followed by the small intestine (32.0%), omentum-peritoneum (12.6%), large intestine (9.3%), and oesophagus (1.1%) \[[@B3]\]. Miettinen *et al.* analysed 95 patients with GISTs designated as omental masses in 49 males and 46 females, with a median age of 60 (range: 27 to 88) years. This tumour was found as a single mass in 51 patients, and as multiple masses in 39 patients. He added that omental GISTs unattached to the alimentary canal often resemble gastric GISTs and multiple omental GISTs often resemble small intestinal GISTs suggesting that they may be metastatic \[[@B4]\]. Reith *et al.* reported that the majority of EGISTs are large, that is \<10cm in diameter, when first detected, whereas small (and presumably early) EGISTs are rarely encountered because they seldom produce symptoms. Two of their four cases were smaller than 5cm and detected during unrelated workup \[[@B5]\]. Genetically, EGISTs express CD117 (c-kit receptor; 100%), CD34 (50%), neuron-specific enolase (44%), smooth muscle actin (26%), desmin (4%), and S-100 protein (4%) \[[@B5]\]. The clinical, pathological and prognostic features of GISTs are widely known, whereas data about EGISTs are very few and the incidence, histogenesis and histological predictors of outcome are not yet defined \[[@B6]\]. Many studies have been done to identify the origin of EGIST, Miettinen and Lasota reported that omental and mesenteric EGISTs are derived from stomach and small intestine respectively, representing tumours that, for some reason, have detached from their gastrointestinal original site during their development \[[@B7]\]. However, Reith *et al.* reported that extragastrointestinal soft tissue stromal tumours are histologically and immunophenotypically similar to their gastrointestinal counterpart, but EGISTs have an aggressive course more akin to small intestinal than gastric stromal tumours \[[@B5]\]. There are many questions about the association between GIST and EGIST. AbdullGaffar showed that the association between non-incidental GISTs and extra-GIT tumours is difficult to determine in the majority of cases. This association is most probably a coincidental finding. AbdullGaffar reported a case series of possible association of GISTs with extra-GIT tumours in female patients and, like other studies, AbdullGaffar suggested that patients, especially women, with GISTs should be investigated and followed up for the possibility of coexisting GIT and extra-GIT neoplasms \[[@B8]\].
Regarding the prognosis in relation to the site of origin, a study of more than 1000 cases of GIST subdivided into five locations (oesophagus, stomach, small and large bowels, versus peritoneum, mesentery, and omentum) found that the tumour site had an independent prognostic factor. Oesophageal tumours had the most favourable prognosis, whereas peritoneal tumours had the lowest survival rate \[[@B9]\]. This seems to be due to the early diagnosis of oesophageal GISTs related to the early appearance of symptoms. By contrast, in the other sites, especially the abdominal cavity, patients had slow onset of disease and symptoms remained vague until the tumour became large in size.
Despite significant advances in new chemotherapeutic drugs, radical surgery remains the only method for long-term survival. Although further data are required to evaluate its use in the adjuvant and neoadjuvant settings, imatinib mesylate currently provides the most effective treatment option in the management of advanced cases \[[@B10]\]. In our case complete surgical tumour resection remains a dilemma because it was extremely difficult to remove the whole nodules and the only option that remained was imatinib.
Conclusions
===========
Our case was rare case of EGIST in a man who presented with vague abdominal pain and progressive abdominal distension. Exploration revealed multiple gooseberry-like nodules of different sizes that involved the whole abdominal cavity. Radical excision was not possible. On histopathology the tumour was CD117 positive. The patient underwent debulking surgery and received imatinib with little improvement in his symptoms.
Consent
=======
Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.
Abbreviations
=============
EGIST: Extragastrointestinal stromal tumour; GIST: Gastrointestinal stromal tumour; GIT: Gastrointestinal tract; ICC: Interstitial cells of Cajal.
Competing interests
===================
The authors declare that they have no competing interests.
Authors' contributions
======================
AA and HH admitted the patient and requested the relative investigations. AM, EEA, NA, and MA performed the surgery and the postoperative follow up. AE processed the histopathology and its report. NA wrote the manuscript. MI participated in its design and coordination and helped to draft the manuscript and reviewed the paper for English editing. All authors read and approved the final manuscript.
Acknowledgement
===============
We would like to thank the Head of Medical Records for her help.
|
List of rural localities under jurisdiction of Moscow
This is a list of rural localities under the jurisdiction of Moscow. Moscow (, ; ) is the capital and most populous city of Russia, with 13.2 million residents within the city limits, 17 million within the urban area and 20 million within the metropolitan area. Moscow is one of Russia's federal cities, granting it a status of both an inhabited locality and a constituent federal subject.
Novomoskovsky Administrative Okrug
Rural localities in Novomoskovsky Administrative Okrug:
1st Rabochiy Poselok
Kartmazovo, Moscow
Vatutinki
Troitsky Administrative Okrug
Rural localities in Dobrinsky District:
LMS
See also
Lists of rural localities in Russia
References
*
Moscow |
Q:
Minimum of $f_n(x)= \sum\limits_{i=0}^{n} (-1)^{i} |x+i|$
How does one systematically find the minimum of
$$f(x)= \sum_{i=0}^{n} (-1)^{i} |x+i|$$
where $x \in \mathbf{R}$? Experimentation on Wolfram Alpha shows a specific pattern, but I'm thinking about using bounding arguments. If $f(x)= \sum_{i=0}^{n} |x+i|$, then repeated uses of the triangle inequality works, but I can't seem to use the triangle inequality to bound $\sum_{i=0}^{n}(-1)^{i} |x+i|$.
A:
Let $n=2m-1$ be odd. The simple function
$$\phi(x):=|x|-|x+1|=\left\{\eqalign{&\ \quad1\qquad\quad(x\leq-1) \cr &-2x-1\quad(-1\leq x\leq0)\cr&\quad-1\qquad\ \ (x\geq0)\cr}\right.$$
is $\equiv1$ for $x\leq-1$, then has a ramp of slope $-2$ in the interval $[{-1},0]$, and is $\equiv-1$ for all $x\geq0$.
Since
$$f_{2m-1}(x)=\sum_{j=0}^{m-1} \phi(x+2j)$$
the function $f_{2m-1}$ is a sum of $m$ copies of $\phi$ translated to the left by amounts $2j\geq0$ $(0\leq j\leq m-1)$. It therefore has $m$ such descending ramps, the leftmost beginning at $-1-2(m-1)=-(2m-1)$. It follows that $f_{2m-1}$ is monotonically decreasing and takes its minimum $-m$ in all points $x\geq0$.
Now
$$f_{2m}(x)=f_{2m-1}(x)+|x+2m|\ .$$
Here the term $|x+2m|$ is decreasing with slope $-1$ for $x\leq-2m$ and increasing with slope $1$ for $x\geq2m$. In the interval $[{-2m},0]$ this steady increase of $x\mapsto |x+2m|$ interferes with the cascade of ramps of $f_{2m-1}$, resulting in a horizontal zigzag of period $2$ and amplitude $1$. At $x=0$ we are at the lower end of the last ramp, and from then on $f_{2m}$ will definitely increase with slope $1$. The minimum of $f_{2m}$ can therefore be found by computing $f_{2m}(0)$, and is found to be
$$f_{2m}(0)=f_{2m-1}(0)+|0+2m|=-m+2m=m\ .$$
|
Synchrony and covariation of firing rates in the primary visual cortex during contour grouping.
The visual system imposes structure onto incoming information, by grouping image elements of a single object together, and by segregating them from elements that belong to other objects and the background. One influential theory holds that the code for grouping and segmentation is carried by the synchrony of neuronal discharges on a millisecond time scale. We tested this theory by recording neuronal activity in the primary visual cortex (area V1) of monkeys engaged in a contour-grouping task. We found that synchrony was unrelated to contour grouping. The firing rates of V1 neurons are also correlated across trials. We demonstrate that this rate covariation is mainly determined by fluctuations in visual attention. Moreover, we show that rate covariation depends on perceptual grouping, as it is strongest between neurons that respond to features of the same object. |
406 N.W.2d 674 (1987)
BOARD OF COUNTY COMMISSIONERS, McLEAN COUNTY, North Dakota, Plaintiff and Appellee,
v.
PETERSON EXCAVATING, INC., Defendant and Appellant.
Civ. No. 11274.
Supreme Court of North Dakota.
May 28, 1987.
*675 Merle A. Torkelson, State's Atty., Washburn, for plaintiff and appellee.
Gary H. Lee, of Bosard, McCutcheon & Rau, Minot, for defendant and appellant.
VANDE WALLE, Justice.
Peterson Excavating, Inc. (Peterson), has appealed from a judgment in favor of the Board of County Commissioners, McLean County (the County), for damages for repairing a paved highway injured by Peterson. We affirm.
The County paved County Highway 15 between Garrison and Lake Sakakawea in 1966. The County repaired the highway when needed and performed routine maintenance consisting of yearly sealing of "alligatored" areas and surface cracks.
In 1981, a marina construction project was begun at Fort Stevenson State Park, which required that gravel be hauled to the site over County Highway 15 in 1983. On March 1, 1983, the State imposed weight restrictions on North Dakota Highway 37, which intersects County Highway 15, and the County placed a Class II weight-restriction sign on the right side of County Highway 15. The State Highway Commissioner removed the weight restriction on Highway 37 on May 24, 1983. The County, however, did not remove the weight restriction or the sign from County Highway 15 until July because of abnormally wet conditions.
Peterson began hauling gravel over County Highway 15 on May 24, 1983, and completed its hauling on June 7, 1983. On May 24 and 25 Peterson hauled 143 loads that were each about 16,000 pounds over Class II restrictions. On May 25 Peterson reduced its loads at the request of the County highway superintendent, who informed Peterson that Class II restrictions were still in place. The next 163 loads hauled on May 25 and 26 were each about 6,000 pounds over Class II restrictions. Peterson thereafter hauled 890 loads that were each 1,000 to 2,000 pounds over Class II restrictions.
The County repaired County Highway 15 in the summer of 1983 at a cost of $12,734.90 and sued Peterson for damages in that amount. The trial court found Peterson 85 percent responsible for the damage to the road and judgment was entered against Peterson for $10,824.67, plus costs and disbursements.
Peterson has raised the following issues on appeal:
"1. Whether the Trial Court erred, as a matter of law, in determining that a party could be held liable to a County for damages done to a County highway if the party held liable was, at all relevant times, in compliance with State load restrictions, and there existed no valid County load restrictions.
"2. Whether the Trial Court's findings that the Defendant's activity proximately caused the damages to Plaintiff's roads, was clearly erroneous.
"3. Whether the Trial Court's findings that Defendant's activity proximately caused 85 percent of the damages to Plaintiff's roads, when there existed in the record no evidence to support such a finding is clearly erroneous."
The County did not impose Class II weight restrictions by enacting a resolution as required by § 39-12-03, N.D.C.C. Peterson was in compliance with the State's weight restrictions and asserts that because there was no resolution enacted there was no valid county restriction, and there can be no claim against it for damage to the highway. Under the circumstances of this case, we deem the lack of a resolution to be irrelevant.
Relying on § 1-01-06, N.D.C.C.,[1] § 1-02-01, N.D.C.C.,[2] and In re White, 69 N.D. 61, *676 284 N.W. 357, 358 (1939) ["if a particular statute is so designed that it covers the entire field to which it relates, it does so to the exclusion of the common law"], Peterson asserts that in enacting Ch. 39-12, N.D.C.C., "the legislature has set up a comprehensive plan relating to the setting of load limits for State and local highways," constituting an exclusive remedy precluding liability in a negligence action. We disagree.
Chapter 39-12, N.D.C.C., provides for the imposition of size, width, height, and weight restrictions on vehicles operated on public highways; special permits for vehicles of excessive size or weight; $10 and $20 fees for violations; and charges determined by the number of pounds by which a vehicle exceeds weight restrictions, with such charges appropriated for use by the State Highway Department. The chapter does not deal with compensation for damage to highways. As we observed in State ex rel. Hjelle v. A Motor Vehicle Described As a 1973 Brockway Tractor, Etc., 299 N.W.2d 557, 563 (N.D.1980), "[t]he charge under § 39-12-17, NDCC, is for extraordinary use of the highway, not for actual damage, and there is no burden on the state to prove actual damage." Thus, since Ch. 39-12 deals with extraordinary use of a highway and not with damage to a highway, the chapter does not preclude an action to recover damages for negligence in damaging a highway, at least where, as here, no statutory recovery has been attempted. To hold as Peterson urges would lead to the conclusion that one could knowingly destroy a county highway with a heavy vehicle and the county would have no recourse. We construe statutes to avoid absurd results. County of Stutsman v. State Historical Society, 371 N.W.2d 321 (N.D.1985).
In the early case of The Town of Troy v. The Cheshire R.R. Co., 23 N.H. 83, 98-99 (1851), the court said:
"If the bridge, erected by the town, and which they are bound to maintain, ... is destroyed, either wantonly or negligently, by others, the town may, upon what we think are unquestionable principles of common law and common justice, commence their suit against the wrong-doer, and recover all such damages as they have sustained by his wrongful act, ...
"These principles are of course equally applicable to any injury done to a highway, as to a bridge."
See also, Town of Newport v. Brewer, 566 S.W.2d 873 (Tenn.1978); Commonwealth v. Pine Coal Co., 414 S.W.2d 134 (Ky.App. 1967); Lincoln County v. Bruesch, 197 Or. 571, 254 P.2d 690 (1953); State v. F.W. Fitch Co., 236 Iowa. 208, 17 N.W.2d 380, 382 (1945) ["This common-law remedy is not necessarily superseded by statutes providing penalties or new remedies."]; 40 Am.Jur.2d Highways, Streets, and Bridges § 605 (1968); 40 C.J.S. Highways § 228 (1944).
On May 25, 1983, the County highway superintendent told Gerald Klimpel, the vice-president of Peterson, that Class II weight restrictions were still in effect. Klimpel then telephoned James Peterson, president of Peterson, who asked, "Are they really damaging the road?" and Klimpel said, "Yeah, there's gotta be three or four broken spots." Peterson then reduced the size of its loads and continued hauling. It is apparent from the foregoing testimony that Peterson knew that it was damaging the highway but continued to haul heavy loads, although of reduced size. This was an unreasonable use of the highway, subjecting Peterson to liability for damage caused thereby. We agree with the court in Town of Newport v. Brewer, supra, 566 S.W.2d at 876:
"The knowing subjection of a public street, highway or bridge to a use or load that it cannot accommodate and for which it was not designed by one who is *677 aware that such use is inflicting substantial damage thereto, must, in our opinion, be regarded as an unreasonable and, therefore, negligent use for which the user may be held liable."
We note that the Legislature has also provided, in § 24-12-01, N.D.C.C., that "[n]o person shall willfully ... break, or otherwise injure or destroy any public highway,... without first securing permission from the person or governing body having jurisdiction and control thereof."
The trial court found that Peterson's "heavily loaded trucks were the major and primary, although not the exclusive, cause of the road damage"; that "the condition of the road was adequate for normal vehicular use within the restricted load limits"; and that "other vehicular traffic proximately caused some damage to the road." Peterson asserts that the trial court's finding that it proximately caused damage to the road is clearly erroneous.
There was testimony that there was some preexisting deterioration of the highway, but that it was in "good," "normal," or "average" condition. While Peterson was not the only user of the highway, there was testimony that its loads were the heaviest. A civil engineer who was qualified as an expert testified that in his opinion it was "more probable than not that the excess weight" of Peterson's trucks caused the damage to the road. We conclude that the trial court's finding that Peterson damaged the road is not clearly erroneous.
The trial court found Peterson "85 percent responsible for the deterioration and damage to the road." Peterson asserts that that finding is clearly erroneous. The evidence supports the trial court's findings that Peterson's trucks were the "major and primary" cause of the damage and that other traffic caused "some" damage. In the unique circumstances presented in this case, where the County has suffered an apparently indivisible injury, the "major and primary" cause of which was Peterson's trucks, but "some" of which was caused by others unknown to an unknown extent, a precise apportionment of Peterson's responsibility is difficult at best. Our review of the record has not left us with a definite and firm conviction that a mistake has been made. Consequently, the trial court's finding is not clearly erroneous.
The County has asserted that the trial court should have found Peterson responsible for 100 percent of the damages and that it should be awarded $12,734.90. The County did not cross-appeal and may not seek a more favorable result on appeal than it received in the trial court. Burlington Northern R.R. Co. v. Scheid, 398 N.W.2d 114 (N.D.1986).
The judgment is affirmed.
ERICKSTAD, C.J., and GIERKE, MESCHKE and LEVINE, JJ., concur.
NOTES
[1] "1-01-06. Code excludes common law.In this state there is no common law in any case where the law is declared by the code."
[2] "1-02-01. Rule of construction of code.The rule of the common law that statutes in derogation thereof are to be construed strictly has no application to this code. The code establishes the law of this state respecting the subjects to which it relates, and its provisions and all proceedings under it are to be construed liberally, with a view to effecting its objects and to promoting justice."
|
Sawrey, Kim
This research examines ultrasonic vocalization (USV) emission by infant prairie voles (Microtus ochrogaster). Rodent pups of many species emit USVs (Anderson, 1954), commonly in response to stressors such as isolation and hypothermic conditions (Alli... |
Specifications table {#s0005}
====================
Subject areaBiologyMore specific subject areaRice cultivationType of dataTable, excel filesHow data was acquirediTRAQ labeling (Applied Biosystems)SCX chromatography and AKTA Purifier system (GE Healthcare)Q-Exactive MS (Thermo Finnigan) and Easy nLC (Proxeon Biosystems, now Thermo Fisher Scientific)MASCOT engine (Matrix Science, London, UK; version 2.2)Rice sequence database (uniprot\_*Oryza_sativa*.fasta, released in February 2013, 144512 sequences)Data formatRaw and analyzedExperimental factorsPanicles that headed on the same day were chosen and tagged, and the flowering date of each spikelet on the tagged panicles was recorded. Fifteen tagged panicles were sampled at 7 days and 14 days after anthesis. Superior spikelets (SS) and inferior spikelets (IS) were collected, in addition, three irrigation patterns were set from c, i.e. shallow water irrigation (water status was controlled at 0 kPa), light wetting-drying irrigation (water status was controlled at −20 kPa), and heavy wetting-drying irrigation (water status was controlled at −40 kPa).Experimental featuresIsobaric tags for relative and absolute quantification (iTRAQ)Data source locationSuzhou, ChinaData accessibilityThe mass spectrometry proteomics data have been deposited to the Proteome Xchange Consortium (<http://www.proteomexchange.org/>) via the PRIDE partner repository with the dataset identifier PXD001046.Other datasets are directly provided with this article.
Value of the data {#s0010}
=================
•The data including the raw data of protein and peptide identification and quantization can be reused by other scientists investigating hybrid rice under various conditions.•The bioinformatics data can provides insight into the biological function of the successfully identified proteins.
1. Experimental design, materials and methods {#s0015}
=============================================
Panicles that headed on the same day were chosen and tagged, and the flowering date of each spikelet on the tagged panicles was recorded. Fifteen tagged panicles were sampled at 7 days and 14 days after anthesis. Superior spikelets (SS) and inferior spikelets (IS) were collected, in addition, three irrigation patterns were set from c, i.e. shallow water irrigation (water status was controlled at 0 kPa), light wetting-drying irrigation (water status was controlled at −20 kPa), and heavy wetting-drying irrigation (water status was controlled at −40 kPa).
1.1. Rice cultivation {#s0020}
---------------------
Field experiments were carried out in an experimental farm of Taihu Area Institute of Agricultural Sciences, Su Zhou, Jiangsu province, China in 2011, with large-panicle hybrid Japonica rice Yongyou 8 (according to the test for an average of 181 grains with 26.3 g weight per panicle) as the material. Seedlings were sown on 20th May and transplanted on 25th June at a hill spacing of 0.3 m×0.15 m with 1 seedling per hill. The soil of the field was paddy soil that contained 2.42% organic matter and 158.4, 8.4 and 127.0 mg kg^−1^ available N--P--K respectively. Field management was in accordance with the conventional technique for high-yield cultivation, N fertilizer (225 kg/hm2), basal-tiller N fertilizer to ear-grain N fertilizer (6:4), the basal to ear-grain N was 2:1, and ear-grain N fertilizer was used when the last fourth or fifth leaves came out. P fertilizer was converted into P~2~O~5~ (70 kg/hm2) as the basal fertilizer and K fertilizer was converted into K~2~O (150 kg/hm^2^) according to the ratio of basal-tiller N fertilizer to ear-grain N fertilizer (5:5).
1.2. Collection of superior and inferior spikelets {#s0025}
--------------------------------------------------
Panicles that headed on the same day were chosen and tagged, and the flowering date of each spikelet on the tagged panicles was recorded. Two hundred panicles that headed on a same day were tagged. The flowering date and position of each spikelet on the tagged panicles were recorded. Fifteen tagged panicles were sampled at 7 days and 14 days after anthesis (DAA, the day was accounted from the first day after flowering). Superior spikelets (SS) and inferior spikelets (IS) were collected according to the previous report [@bib2], then were frozen in liquid N~2~ and then stored at −70 °C for protein extraction.
1.3. Water stress treatment {#s0030}
---------------------------
Three irrigation patterns were set from c, i.e. shallow water irrigation (water status was controlled at 0 kPa), light wetting-drying irrigation (water status was controlled at −20 kPa), and heavy wetting-drying irrigation (water status was controlled at −40 kPa). The test base was covered by weather shed. The water status was determined at 7:00--8:00 and 16:00--17:00 every day by a portable digital measuring instrument for soil water potential and temperature (TRS-II, Zhejiang Tuopu Equipment Co., Ltd.). Shallow water irrigation was performed when the water status was lower than the set value.
1.4. Protein extraction and digestion {#s0035}
-------------------------------------
Frozen rice tissue was finely powdered in liquid nitrogen, and precipitated for 1 h with 25 ml TCA/acetone (1:9, containing 65 mM DTT) at −20 °C. The homogenate was centrifuged and the pellets were air-dried, dissolved in 30 μL STD buffer (4% SDS, 150 mM Tris--HCl, pH 8.0), incubated with boiling water for 5 min, cooled to room temperature, and diluted with 200 μL of UA buffer (8 M urea, 150 mM Tris--HCl, pH 8.0). The homogenate was centrifuged, the supernatants were collected and the protein content was determined by a BCA protein assay reagent ([Table 1](#s0065){ref-type="sec"}).
The retained protein was washed with 200 μL of UA buffer, centrifuged, and added with 100 μL of UA buffer containing 0.05 M iodoacetamide. The mix was incubated for 20 min in dark and then centrifuged under the above conditions. The filter was then washed three times with 100 μL of UA buffer, 100 μL of DS buffer (50 mM triethylammonium bicarbonate, pH 8.5) was added. Then the solution was centrifuged for 10 min in the same condition. This step was repeated twice. Finally, 40 μL of DS buffer containing 3 μg trypsin (Promega) was added to each filter. The samples were incubated overnight at 37 °C, and the resulting peptides were collected by centrifugation. The peptide content was estimated by UV density at 280 nm.
1.5. iTRAQ reagent labeling and liquid chromatography (LC) {#s0040}
----------------------------------------------------------
iTRAQ labeling was performed according to the manufacturer׳s instructions (Applied Biosystems). Briefly, the peptide mixtures were reconstituted with 30 μL of iTRAQ dissolution buffer. The label method of every sample (45 μg) using iTRAQ Reagent-8plex Multiplex Kit (AB SCIEX) is shown in [Table 1](#t0005){ref-type="table"}, and every sample was labeled twice. The aliquots of iTRAQ were combined with peptide mixtures from 5 different samples, respectively, and incubated at room temperature for 1 h. REF was a mixture containing same-amount proteins of the five samples.
Prior to LC-MS/MS analysis, the peptides were purified to eliminate excess labeling reagent by SCX chromatography using an AKTA Purifier system (GE Healthcare). A 10 μL solution from each peptide fraction was injected for nanoLC-MS/MS analysis using a Q-Exactive MS (Thermo Finnigan) equipped with Easy nLC (Proxeon Biosystems, now Thermo Fisher Scientific). The peptide mixture (5 μg) was loaded onto a C18-reversed phase column packed in-house with RP-C18 resin (5 μm) in buffer A (0.1% formic acid) and separated with a linear gradient of buffer B (0.1% formic acid in 80% acetonitrile) at a flow rate of 250 nL/min controlled by IntelliFlow technology over 140 min.
1.6. Electrospray Ionization (ESI) tandem MS (MS/MS) analysis by Q exactive {#s0045}
---------------------------------------------------------------------------
MS data were acquired using a data-dependent top10 method dynamically choosing the most abundant precursor ions from the survey scan (300--1800 m/z) for the HCD fragmentation. The target value was determined based on predictive Automatic Gain Control (pAGC). The dynamic exclusion duration was 60 s. Survey scans were acquired at a resolution of 70,000 at m/z 200, and resolution for the HCD spectra was set to 17,500 at m/z 200. The normalized collision energy was 30 eV, and the underfill ratio, which specifies the minimum percentage of the target value likely to be reached at maximum fill time, was defined as 0.1%. The instrument was run with peptide recognition mode enabled ([Supplementary table 2](#s0065){ref-type="sec"}).
1.7. Sequence database searching and data analysis {#s0050}
--------------------------------------------------
MS/MS spectra were searched using MASCOT engine (Matrix Science, London, UK; version 2.2) against a rice sequence database (uniprot_Oryza_sativa.fasta, released in February 2013, 144512 sequences). The MASCOT search results were further processed using ProteomicsTools (version 3.05). Assembling protein identifications were qualitatively analyzed by Proteome Discoverer1.4 software. All data were reported based on 99% confidence for protein identification as determined by false discovery rate (FDR) ≤1%. Isobaric Labeling Multiple File Distiller and Identified Protein iTRAQ Statistic Builder were used to calculate the ratios of protein, in which Sample REF was used as the reference, based on the weighted average of the intensities of report ions in each identified peptide ([See Supplementary table 1](#s0065){ref-type="sec"}). The final ratios were then normalized with the median average protein ratio, assuming that most proteins remained unchanged in abundance. Only the protein identification that was inferred from the unique peptide identification in two independent experiments was considered. Statistical analysis was conducted using a one-way ANOVA. P-values≤0.05 by Tukey׳s test were considered significant. Among the statistically significant proteins detected by the ANOVA test (p\<0.05), proteins abundances that changed less than 1.5-fold or 1.2-fold were discarded ([See Supplementary table 4](#s0065){ref-type="sec"}).
1.8. Bioinformatics analysis of the differentially abundant proteins {#s0055}
--------------------------------------------------------------------
Sequence data of the selected the differentially abundant proteins were retrieved from UniProtKB database (Release 2013_07) in batches in FASTA format. The retrieved sequences were locally searched against Swiss-Prot database (plant) using the NCBI BLAST+ client software (ncbi-blast-2.2.28±win32.exe) to find homolog sequences from which the functional annotation was transferred to the studied sequences. In this study, the top 10 blast hits with E-value less than 1e−3 for each query sequence were retrieved and loaded into Blast2GO (Version 2.6.6) for Gene Ontology (GO) mapping and annotation. The sequences without BLAST hits and the un-annotated ones were then selected to go through InterProScan against EBI databases to retrieve the functional annotations. The GO project described the roles of proteins in three domains: biological process, molecular function and cellular component. Following annotation and annotation augmentation, enzyme codes were sequentially mapped to annotated sequences and metabolic pathways in Kyoto Encyclopedia of Genes and Genomes (KEGG, <http://www.genome.jp/kegg/>) [@bib3] ([Supplementary table 3](#s0065){ref-type="sec"}).
Supplementary materials {#s0065}
=======================
Supplementary data
Supplementary data
Supplementary data
Supplementary data
Supplementary data associated with this article can be found in the online version at [doi:10.1016/j.dib.2014.08.001](http://dx.doi.org/10.1016/j.dib.2014.08.001){#ir0015}.
######
Protein contents of inferior spikelets 8 DAA under 0 kPa (IS8DAA, A), superior spikeletes on 8 DAA (B, SS8DAA) under 0 kPa, and inferior spikelets on 15 DAA under 0 kPa (C, IS15DSS), −20 kPa (D) or −40 kPa (E).
Sample A B C D E
------------------------- ------ ------ ------ ------ ------
Protein content (μg/μL) 7.86 8.12 8.25 7.24 7.40
|
import React from 'react';
import PropTypes from 'prop-types';
import { connect } from '../utils/griddleConnect';
import compose from 'recompose/compose';
import mapProps from 'recompose/mapProps';
import getContext from 'recompose/getContext';
import { classNamesForComponentSelector, stylesForComponentSelector } from '../selectors/dataSelectors';
const EnhancedPaginationContainer = OriginalComponent => compose(
getContext({
components: PropTypes.object,
}),
connect(
(state, props) => ({
className: classNamesForComponentSelector(state, 'Pagination'),
style: stylesForComponentSelector(state, 'Pagination'),
})
),
mapProps((props) => {
const { components, ...otherProps } = props;
return {
Next: components.NextButton,
Previous: components.PreviousButton,
PageDropdown: components.PageDropdown,
...otherProps
};
})
)((props) => <OriginalComponent {...props} />);
export default EnhancedPaginationContainer;
|
Q:
Multidimensional Fourier series
On $\mathbb{T}$, we have approximation series $\{f_n\}$ of $f\in L^p,p\in[1,\infty)$ in the form of $f_n(x)=\sum_{|k|\le n}a_{n,k}e^{ikx}$, converging to $f$ in $L^p$. (for example, we can consider convolution with Fejer kernel)
Can we do something similar for $\mathbb{T}^n$ as well?
A:
Summability is no problem, for example if $K_n(t)$ is the Fejer kernel then $K_n(s)K_n(t)$ is an approximate identity on $\Bbb T^2$. Now, convergence for multiple Fourier series is a serious problem...
|
Diagnostic utility of the WISC-III developmental index as a predictor of learning disabilities.
Wechsler's Deterioration Index (WDI) was developed as an indicator of cognitive impairment in adults but has been applied to children, because neuropsychological deficits have often been hypothesized to account for learning difficulties during the development period. Renamed the Wechsler Developmental Index, this measure has been used to discriminate among groups of children with and without learning disabilities. The present study replicated those findings with the Wechsler Intelligence Scale for Children-Third Edition, but also applied more appropriate diagnostic efficiency statistics to analyze the actual diagnostic utility of the WDI. These analyses revealed that the WDI performed at chance levels when distinguishing 611 students diagnosed with learning disabilities from those diagnosed with emotional disabled (n = 80) or mental retardation (n = 33), as well as from 2,200 simulated random nondisabled cases. It was concluded that mean group differences were not adequate and that ipsative indicators must be definitively validated in experimental environments before they can be applied in practice. |
Maryland Pastel Society artist opportunities
PSA ACTIVITIES
Workshops and Classes
The Pastel Society of America hosts a variety of workshops and classes taught by award-winning artists instruct throughout the year. The school instructors are noted for their one-on-one rapport with students at all levels. To view the schedule for classes and workshops, please visit their webpage for details. |
/*
* (C) Copyright 2009
* Vipin Kumar, ST Micoelectronics, [email protected].
*
* See file CREDITS for list of people who contributed to this
* project.
*
* This program is free software; you can redistribute it and/or
* modify it under the terms of the GNU General Public License as
* published by the Free Software Foundation; either version 2 of
* the License, or (at your option) any later version.
*
* This program is distributed in the hope that it will be useful,
* but WITHOUT ANY WARRANTY; without even the implied warranty of
* MERCHANTABILITY or FITNESS FOR A PARTICULAR PURPOSE. See the
* GNU General Public License for more details.
*
* You should have received a copy of the GNU General Public License
* along with this program; if not, write to the Free Software
* Foundation, Inc., 59 Temple Place, Suite 330, Boston,
* MA 02111-1307 USA
*/
#ifndef __SPR_UDC_H
#define __SPR_UDC_H
/*
* Defines for USBD
*
* The udc_ahb controller has three AHB slaves:
*
* 1. THe UDC registers
* 2. The plug detect
* 3. The RX/TX FIFO
*/
#define MAX_ENDPOINTS 16
struct udc_endp_regs {
u32 endp_cntl;
u32 endp_status;
u32 endp_bsorfn;
u32 endp_maxpacksize;
u32 reserved_1;
u32 endp_desc_point;
u32 reserved_2;
u32 write_done;
};
/* Endpoint Control Register definitions */
#define ENDP_CNTL_STALL 0x00000001
#define ENDP_CNTL_FLUSH 0x00000002
#define ENDP_CNTL_SNOOP 0x00000004
#define ENDP_CNTL_POLL 0x00000008
#define ENDP_CNTL_CONTROL 0x00000000
#define ENDP_CNTL_ISO 0x00000010
#define ENDP_CNTL_BULK 0x00000020
#define ENDP_CNTL_INT 0x00000030
#define ENDP_CNTL_NAK 0x00000040
#define ENDP_CNTL_SNAK 0x00000080
#define ENDP_CNTL_CNAK 0x00000100
#define ENDP_CNTL_RRDY 0x00000200
/* Endpoint Satus Register definitions */
#define ENDP_STATUS_PIDMSK 0x0000000f
#define ENDP_STATUS_OUTMSK 0x00000030
#define ENDP_STATUS_OUT_NONE 0x00000000
#define ENDP_STATUS_OUT_DATA 0x00000010
#define ENDP_STATUS_OUT_SETUP 0x00000020
#define ENDP_STATUS_IN 0x00000040
#define ENDP_STATUS_BUFFNAV 0x00000080
#define ENDP_STATUS_FATERR 0x00000100
#define ENDP_STATUS_HOSTBUSERR 0x00000200
#define ENDP_STATUS_TDC 0x00000400
#define ENDP_STATUS_RXPKTMSK 0x003ff800
struct udc_regs {
struct udc_endp_regs in_regs[MAX_ENDPOINTS];
struct udc_endp_regs out_regs[MAX_ENDPOINTS];
u32 dev_conf;
u32 dev_cntl;
u32 dev_stat;
u32 dev_int;
u32 dev_int_mask;
u32 endp_int;
u32 endp_int_mask;
u32 reserved_3[0x39];
u32 reserved_4; /* offset 0x500 */
u32 udc_endp_reg[MAX_ENDPOINTS];
};
/* Device Configuration Register definitions */
#define DEV_CONF_HS_SPEED 0x00000000
#define DEV_CONF_LS_SPEED 0x00000002
#define DEV_CONF_FS_SPEED 0x00000003
#define DEV_CONF_REMWAKEUP 0x00000004
#define DEV_CONF_SELFPOW 0x00000008
#define DEV_CONF_SYNCFRAME 0x00000010
#define DEV_CONF_PHYINT_8 0x00000020
#define DEV_CONF_PHYINT_16 0x00000000
#define DEV_CONF_UTMI_BIDIR 0x00000040
#define DEV_CONF_STATUS_STALL 0x00000080
/* Device Control Register definitions */
#define DEV_CNTL_RESUME 0x00000001
#define DEV_CNTL_TFFLUSH 0x00000002
#define DEV_CNTL_RXDMAEN 0x00000004
#define DEV_CNTL_TXDMAEN 0x00000008
#define DEV_CNTL_DESCRUPD 0x00000010
#define DEV_CNTL_BIGEND 0x00000020
#define DEV_CNTL_BUFFILL 0x00000040
#define DEV_CNTL_TSHLDEN 0x00000080
#define DEV_CNTL_BURSTEN 0x00000100
#define DEV_CNTL_DMAMODE 0x00000200
#define DEV_CNTL_SOFTDISCONNECT 0x00000400
#define DEV_CNTL_SCALEDOWN 0x00000800
#define DEV_CNTL_BURSTLENU 0x00010000
#define DEV_CNTL_BURSTLENMSK 0x00ff0000
#define DEV_CNTL_TSHLDLENU 0x01000000
#define DEV_CNTL_TSHLDLENMSK 0xff000000
/* Device Status Register definitions */
#define DEV_STAT_CFG 0x0000000f
#define DEV_STAT_INTF 0x000000f0
#define DEV_STAT_ALT 0x00000f00
#define DEV_STAT_SUSP 0x00001000
#define DEV_STAT_ENUM 0x00006000
#define DEV_STAT_ENUM_SPEED_HS 0x00000000
#define DEV_STAT_ENUM_SPEED_FS 0x00002000
#define DEV_STAT_ENUM_SPEED_LS 0x00004000
#define DEV_STAT_RXFIFO_EMPTY 0x00008000
#define DEV_STAT_PHY_ERR 0x00010000
#define DEV_STAT_TS 0xf0000000
/* Device Interrupt Register definitions */
#define DEV_INT_MSK 0x0000007f
#define DEV_INT_SETCFG 0x00000001
#define DEV_INT_SETINTF 0x00000002
#define DEV_INT_INACTIVE 0x00000004
#define DEV_INT_USBRESET 0x00000008
#define DEV_INT_SUSPUSB 0x00000010
#define DEV_INT_SOF 0x00000020
#define DEV_INT_ENUM 0x00000040
/* Endpoint Interrupt Register definitions */
#define ENDP0_INT_CTRLIN 0x00000001
#define ENDP1_INT_BULKIN 0x00000002
#define ENDP_INT_NONISOIN_MSK 0x0000AAAA
#define ENDP2_INT_BULKIN 0x00000004
#define ENDP0_INT_CTRLOUT 0x00010000
#define ENDP1_INT_BULKOUT 0x00020000
#define ENDP2_INT_BULKOUT 0x00040000
#define ENDP_INT_NONISOOUT_MSK 0x55540000
/* Endpoint Register definitions */
#define ENDP_EPDIR_OUT 0x00000000
#define ENDP_EPDIR_IN 0x00000010
#define ENDP_EPTYPE_CNTL 0x0
#define ENDP_EPTYPE_ISO 0x1
#define ENDP_EPTYPE_BULK 0x2
#define ENDP_EPTYPE_INT 0x3
/*
* Defines for Plug Detect
*/
struct plug_regs {
u32 plug_state;
u32 plug_pending;
};
/* Plug State Register definitions */
#define PLUG_STATUS_EN 0x1
#define PLUG_STATUS_ATTACHED 0x2
#define PLUG_STATUS_PHY_RESET 0x4
#define PLUG_STATUS_PHY_MODE 0x8
/*
* Defines for UDC FIFO (Slave Mode)
*/
struct udcfifo_regs {
u32 *fifo_p;
};
/*
* USBTTY definitions
*/
#define EP0_MAX_PACKET_SIZE 64
#define UDC_INT_ENDPOINT 1
#define UDC_INT_PACKET_SIZE 64
#define UDC_OUT_ENDPOINT 2
#define UDC_BULK_PACKET_SIZE 64
#define UDC_IN_ENDPOINT 3
#define UDC_OUT_PACKET_SIZE 64
#define UDC_IN_PACKET_SIZE 64
/*
* UDC endpoint definitions
*/
#define UDC_EP0 0
#define UDC_EP1 1
#define UDC_EP2 2
#define UDC_EP3 3
/*
* Function declarations
*/
void udc_irq(void);
void udc_set_nak(int epid);
void udc_unset_nak(int epid);
int udc_endpoint_write(struct usb_endpoint_instance *endpoint);
int udc_init(void);
void udc_enable(struct usb_device_instance *device);
void udc_disable(void);
void udc_connect(void);
void udc_disconnect(void);
void udc_startup_events(struct usb_device_instance *device);
void udc_setup_ep(struct usb_device_instance *device, unsigned int ep,
struct usb_endpoint_instance *endpoint);
#endif /* __SPR_UDC_H */
|
<div align="center">
<img src="https://cloud.githubusercontent.com/assets/399657/23590290/ede73772-01aa-11e7-8915-181ef21027bc.png" />
<div>a plugin for <a href="https://github.com/spencermountain/wtf_wikipedia/">wtf_wikipedia</a></div>
<!-- npm version -->
<a href="https://npmjs.org/package/wtf-plugin-html">
<img src="https://img.shields.io/npm/v/wtf-plugin-html.svg?style=flat-square" />
</a>
<!-- file size -->
<a href="https://unpkg.com/wtf-plugin-html/builds/wtf-plugin-html.min.js">
<img src="https://badge-size.herokuapp.com/spencermountain/wtf-plugin-html/master/builds/wtf-plugin-html.min.js" />
</a>
<hr/>
</div>
<div align="center">
<code>npm install wtf-plugin-html</code>
</div>
Output all, or part of a wikipedia article in HTML.
```js
const wtf = require('wtf_wikipedia')
wtf.extend(require('wtf-plugin-html'))
let doc = wtf('hello [[world]]')
doc.html()
// 'hello <a href="./world">world</a>'
```
work-in-progress
MIT
|
Utopia's Ladies Clutch With Face Trims will put a playful spin on your attires. It feels effortless to wear and has been thoughtfully crafted to make the most of its space. Wear yours over a black attire at the weekend. |
Q:
Drawing a diagram of a three-cycle
How to draw this kind of circle on LaTeX?
A:
For a true circular shape, use arcs instead of the to path.
\documentclass[tikz,border=2pt]{standalone}
\begin{document}
\begin{tikzpicture}[->,scale=.7]
\node (i) at (90:1cm) {$i$};
\node (j) at (-30:1cm) {$j$};
\node (k) at (210:1cm) {$k$};
\draw (70:1cm) arc (70:-10:1cm);
\draw (-50:1cm) arc (-50:-130:1cm);
\draw (190:1cm) arc (190:110:1cm);
\end{tikzpicture}
\end{document}
A more compact form using \foreach can be like this (with the same result as above):
\documentclass[tikz, border=2pt]{standalone}
\begin{document}
\begin{tikzpicture}[->,scale=.7]
\foreach \a/\t in {90/i,-30/j,210/k}{
\node (\t) at (\a:1cm) {$\t$};
\draw (\a-20:1cm) arc (\a-20:\a-100:1cm);
}
\end{tikzpicture}
\end{document}
Edit: (in response to the OP's comment)
The arrows.meta library offers you the possibility to draw (almost) any arrow tip you may think of. To have the same look as that Metapost arrow tip, you can pass the following option to your environment:
-{Stealth[inset=0pt,length=4.5pt,angle'=35, round, bend]}
after loading the arrows.meta and bending libraries, of course.
\documentclass[tikz, border=2pt]{standalone}
\usetikzlibrary{arrows.meta, bending}
\begin{document}
\begin{tikzpicture}[-{Stealth[inset=0pt,length=4.5pt,angle'=35,round,bend]}, scale=.7]
\foreach \a/\t in {90/i,-30/j,210/k}{
\node (\t) at (\a:1cm) {$\t$};
\draw (\a-20:1cm) arc (\a-20:\a-100:1cm);
}
\end{tikzpicture}
\end{document}
Here is now how this looks:
A:
Just for variety, you could also draw something like this using smartdiagram. The default produces rather more colourful diagrams with rather oversized nodes and undersized contents, for your purposes:
\smartdiagram[circular diagram:clockwise]{%
$i$,$j$,$k$
}
However, the sizing can be quite easily dealt with:
\smartdiagramset{module minimum width=0, module minimum height=0, text width=1em, font=\large}
as can the overly colourful appearance:
\smartdiagramset{uniform color list=gray!20 for 3 items, arrow color=gray, uniform arrow color=true}
Simply use circular diagram, omitting the clockwise, for the anti-clockwise direction:
Complete code:
\documentclass{article}
\usepackage{smartdiagram}
\begin{document}
\smartdiagram[circular diagram:clockwise]{%
$i$,$j$,$k$
}
\bigskip
\smartdiagramset{module minimum width=0, module minimum height=0, text width=1em, font=\large}
\smartdiagram[circular diagram:clockwise]{%
$i$,$j$,$k$
}
\bigskip
\smartdiagramset{uniform color list=gray!20 for 3 items, arrow color=gray, uniform arrow color=true}
\smartdiagram[circular diagram:clockwise]{%
$i$,$j$,$k$
}
\bigskip
\smartdiagram[circular diagram]{%
$i$,$j$,$k$
}
\end{document}
A:
Here is a solution for LuaLatex using luamplib to make inline graphics. The mplibcode environment creates an hbox, which I have centered on the baseline using $\vcenter{...}$.
\documentclass{article}
\usepackage{luamplib}
\usepackage{unicode-math}
\setmainfont{TeX Gyre Schola}
\setmathfont{TeX Gyre Schola Math}
\begin{document}
\mplibcodeinherit{enable}
A circle going anti-clockwise $\vcenter{
\begin{mplibcode}
path C; C = fullcircle scaled 32 rotated 90;
beginfig(0);
numeric a, b;
for i=0 upto 2:
a := 8/3 i;
b := 8/3 (i+1);
drawarrow subpath (a,b) of C
cutbefore fullcircle scaled 16 shifted point a of C
cutafter fullcircle scaled 16 shifted point b of C;
label(textext("$" & char (105+i) & "$"), point a of C);
endfor
endfig;
\end{mplibcode}}$ or clockwise $\vcenter{
\begin{mplibcode}
beginfig(0);
numeric a, b;
for i=0 upto 2:
a := 8/3 i;
b := 8/3 (i+1);
drawarrow subpath (b,a) of C
cutbefore fullcircle scaled 16 shifted point b of C
cutafter fullcircle scaled 16 shifted point a of C;
label(textext("$" & char (105+i) & "$"), point a of C);
endfor
endfig;
\end{mplibcode}}$ as you prefer.
\end{document}
Notes
The units are PostScript points 72 pt = 1in, 28.35 pt = 1cm.
The predefined fullcircle path runs anticlockwise starting from "3 o'clock", so I rotated it here by 90° to make it start at the top.
I've set \mplibcodeinherit{enable} so that the definition of path C can be reused in the second figure
There are 8 points in a fullcircle, so the three points I needed were points 0, 8/3 and 16/3 of C. Note that point 24/3 of C == point 8 of C == point 0 of C.
subpath (a,b) of C returns the subsection of path from point a to point b, which I've shortened using the (slightly cumbersome) cutbefore and cutafter facilities.
You can reverse a subpath by swapping the order of the arguments.
textext() is a luamplib extension that allows you to build up the correct dynamic string. Note that I've assumed that my font has the lower case alphabet in the standard ASCII positions.
For more on Metapost see: http://www.tug.org/metapost.html
For more on luamplib see: https://www.ctan.org/tex-archive/macros/luatex/generic/luamplib
|
Consultation
– Consultation Coming soon –
Casa Ceramica, will be looking to offer a dedicated and private consultation service to our customers. This service will include; dedicated site visits, specialist design advice & other exclusive services. |
Q:
Windows Phone link from Tile error
I have a list of theaters and I created a secondary tile from my application to navigate directly to specific theater. I pass the id of the theater in query string :
I load the theaters from a WCF service in the file "MainViewModel.cs"
In my home page, I have a list of theaters and I can navigate to a details page.
But when I want to navigate from the tile, I have an error...
The Tile :
ShellTile.Create(new Uri("/TheaterDetails.xaml?selectedItem=" + theater.idTheater, UriKind.Relative), tile, false);
My TheaterDetails page :
public partial class TheaterDetails : PhoneApplicationPage
{
theater theater = new theater();
public TheaterDetails()
{
InitializeComponent();
}
protected override void OnNavigatedTo(NavigationEventArgs e)
{
if (!App.ViewModel.IsDataLoaded)
{
App.ViewModel.LoadData();
}
if (DataContext == null)
{
string selectedIndex = "";
if (NavigationContext.QueryString.TryGetValue("selectedItem", out selectedIndex))
{
int index = int.Parse(selectedIndex);
theater = (from t in App.ViewModel.Theaters
where t.idTheater == index
select t).SingleOrDefault();
DataContext = theater;
....
....
....
The error :
https://dl.dropboxusercontent.com/u/9197067/error.png
Like if the data were not loaded...
Do you have an idea where the problem come from ?
The solution could be easy but I am a beginner... Maybe it's because I load the data asynchronously and the application doesn't wait until it's done...
Thanks
EDIT :
My LoadData() method :
public void LoadData()
{
client.GetTheatersCompleted += new EventHandler<ServiceReference1.GetTheatersCompletedEventArgs>(client_GetTheatersCompleted);
client.GetTheatersAsync();
// Other get methods...
this.IsDataLoaded = true;
}
private void client_GetTheatersCompleted(object sender, ServiceReference1.GetTheatersCompletedEventArgs e)
{
Theaters = e.Result;
}
A:
So the solution that I found, thanks to Servy in this post : Using async/await with void method
I managed to use async/await to load the data.
I replaced my LoadData() method by :
public static Task<ObservableCollection<theater>> WhenGetTheaters(ServiceClient client)
{
var tcs = new TaskCompletionSource<ObservableCollection<theater>>();
EventHandler<ServiceReference1.GetTheatersCompletedEventArgs> handler = null;
handler = (obj, args) =>
{
tcs.SetResult(args.Result);
client.GetTheatersCompleted -= handler;
};
client.GetTheatersCompleted += handler;
client.GetTheatersAsync();
return tcs.Task;
}
public async Task LoadData()
{
var theatersTask = WhenGetTheaters(client);
Theaters = await theatersTask;
IsDataLoaded = true;
}
And in my page :
protected override async void OnNavigatedTo(NavigationEventArgs e)
{
if (!App.ViewModel.IsDataLoaded)
{
await App.ViewModel.LoadData();
}
|
Sports Briefs (July 11, 2013)Little Lizards football camp DARDANELLE — Keenan Field will host the annual Little Lizards football camp from 9 a.m. to noon Monday through Wednesday. Cost of the camp is $40. For more information, call coach Josh Price at (479) 477-0606. Church league softball signups Registration is underway for the fall season of church league softball to all area churches. Entry fee is $425 due July 31. Games will be played on Monday and Thursday nights. F...
Sports Briefs (July 7, 2013)Sixth annual Sand Lizard golf tournament July 27 DARDANELLE — The sixth annual Sand Lizard Golf Tournament will begin at 8 a.m. on July 27 at the Lion’s Den Golf Course. Cost for a two-person team is $120 and includes lunch. Prizes will be awarded for longest drive, closest to the pin as well as door prizes. Cogswell Motors will sponsor a $25,000 hole-in-one contest. For more information, call Teresa Smallwood at (479) 477-2226 or Lion’s Den G...
Little league players shine light on futureThere are as many reasons to play baseball as there are players that play the game. From T-ball, softball to baseball, players of all age groups come together on the diamond each summer for a whole host of reasons. There are players in the Arkansas River Valley who play baseball with little recognition or accolades, aside from that given by the family members in the stand. They are future high school players, future church league softball play...
Sports Briefs (June 27, 2013)Russellville Ski Area Trail dedication The city of Russellville invites the public to the dedication of the Russellville Ski Area Trail at 10 a.m. on Tuesday. The trail is located at 3694 Pleasant View Road in the competition water ski area on Pleasant View Park. The trail was funded by the parks portion of the one-cent sales tax. Dover youth football deadline is Saturday DOVER — Registration for participation in Dover Youth Football for the 2...
Sports Briefs (June 23, 2013)Outdoors, recreation meeting Tuesday The city of Russellville invites its citizens and other interested persons to a public meeting at 5:30 p.m. Tuesday at the Hughes Community Center, 1000 East Parkway. The purpose of the meeting is to identify potential outdoor park and recreation needs and priorities for 2014. Following the identification process, city officials will select those priorities to be submitted to the Arkansas Department of Park...
Youth leagues try to rein in ’bad news parents’ BUFFALO GROVE, Ill. (AP) — No parent here has rushed onto a playing field to jump a referee who made an unpopular call. No adult has gotten angry and slugged or pushed a coach or a young player, as has happened elsewhere. Nor have there been any of those embarrassing sideline brawls you sometimes see posted on online video sites. At least nobody’s admitting to it. Still, parent behavior in this quiet suburb north of Chicago has been questionab...
Arkansas Tech football camp teaches focusIt’s odd how athletic my son is becoming as he grows older. It’s odd because I wonder where he gets it. It’s no secret — I was never any good at sports. I was a lousy football player, even though I enjoyed being a part of the team. Going even further back, I was no good at little league baseball. The last time I played catch (until very recently), I missed a ball thrown from my father and caught it with my face instead of my glove. My son, Gre...
Tech’s youth football camp comes to a closeThone Stadium at Buerkle Field felt the weight of a different proportioned athlete than usual during the Arkansas Tech University Youth Football Camp that began Monday and came to a close today. Tech’s yard lines were covered with pint-sized football players, ages 6-12, from across the Arkansas River Valley between 8 a.m. to noon for each day of the camp, which according to Wonder Boys graduate assistant coach Reggie Fish was a refreshing chan...
Hector hosts Wicked Wildcat peewee campHECTOR — Wicked Wildcat peewee basketball camp took place Monday through Thursday inside the Multi-Purpose Building on the Hector school campus. Next year’s students in grades 3-5 and grades 6-7 participated in separate morning camps. They learned fundamentals of both offense and defense and competed in several events including obstacle course, free throw contest, hot shot, and 1 on 1 tournament. Campers also competed for a hustle award every ...
Spring Lake hosts annual children's fishing derbyThe 25th annual Spring Lake Fishing Derby hostd 87 youngers 4-10 years of age on June 8. This popular event is sponsored by the Yell County Wildlife Federation (YCWF), Arkansas Game and Fish Commission (AGFC) and U.S. Forest Service along with four dozen local co-sponsor donors that help fund the event. The children caught 211 pounds of channel catfish stocked by the AGFC in a netted cove at the west side of the lake on the Ozark National Fore...
Sports Briefs (June 9, 2013)Pirates basketball camp this week The Dover Pirates will host a boys basketball camp from 8:30-11:30 a.m. on Wednesday through Friday at the Dover High School Gym. The entry fee of $45 will include a T-shirt. Awards will be given in each division for various contests. Student athletic trainer workshop on July 22-23 CLARKSVILLE — University of the Ozarks head athletic trainer Chad Floyd will conduct a student athletic trainer workshop July 22-2...
Little leaguer overcomes challenges to play ballNot every little league player one day goes pro. Not every child is born with the same athletic abilities. For some, playing the game isn’t about winning or losing. Some play for the love of the game or the chance to experience something new. Sergio Gonzalez, 8, isn’t the typical baseball player. With hands that are missing fingers and have some digits fused together, activities such as holding a baseball or bat become difficult. “I told him t...
Prosecutors seek maximum for guilty youth coach TEXARKANA, Ark. (AP) — Federal prosecutors are seeking the maximum sentence for a former Texarkana-area youth baseball coach who pleaded guilty to molesting young players. Prosecutors are limited in the sentence they can pursue for 60-year-old Walter Richard Roberts because he pleaded guilty to alleged offenses that occurred in 1992. The Texarkana Gazette reported the maximum sentence for Roberts would be 10 years. The law has since been updat...
Russellville conducting free physicalsFree physicals for Russellville School District athletic and spirit groups will be given today and Wednesday. Male athletes need to report to the Russellville Junior High cafeteria at 6 p.m. today. Female athletes need to report to the Russellville Junior High School cafeteria at 6 p.m. Wednesday. All students need to enter the junior high on the west side under the covered walkway. Physical forms should be picked up from coaches at the middle...
ATU volleyball offers summer skill campsThe Arkansas Tech volleyball program and head coach Kristy Bayer will conduct a series of summer camps at Tucker Coliseum, with the first camp on May 29-30 at Tucker Coliseum. Camp information and online registration is available at www.arkansastechvolleyballcamps.com. The first camp will be the Lil’ Suns Camp from 6-8 p.m. on May 29-30. The evening sessions are open to grades 1-5, and are designed to help beginning volleyball players learn ba...
Sports Briefs (May 16, 2013)Pottsville peewee football sign-ups Saturday at City Hall POTTSVILLE — Peewee football and flag football registration for those in grades K-6 will take place from 9 a.m. to noon Saturday at Pottsville City Hall. Warrior athletics banquet Saturday LAMAR — The Lamar Warrior Booster Club will host the fifth annual athletic awards banquet at 5:30 p.m. May 18 in the Lamar Elementary Cafeteria. This year’s honorary speaker will be Robert Mummey, ass...
Predators win Van Buren tournament, 2nd in ConwayThe Predators 14-year-old baseball team won the Battle of the Bats tournament in Van Buren and finished second in a recent tournament in Conway. In pool play in Van Buren, the Predators beat the River Valley Rage 3-1, lost to the Maumelle Bulldogs 6-1 and went into bracket play as the third seed. The Predators needed just four innings to beat the River Valley Rage 15-0 in the semifinals. Layton Bicanovsky got things going in the top of the fir...
Mighty Ducks win Twin City ShootoutSHREVEPORT, La. — The Mighty Ducks had a close match in the championship game of the USSSA Twin City Shootout Super NIT against the Keller Crush-Royal, but was still able to edge their opponent 7-6 to secure the title. The Crush led 3-0 early on, but the Ducks answered with four runs in the bottom of the second inning. Jackson Shrivner entered in the second and shut the Crush down. Arkansas held on for the eventual 7-6 victory. “There were a l... |
# This file is part of the sos project: https://github.com/sosreport/sos
#
# This copyrighted material is made available to anyone wishing to use,
# modify, copy, or redistribute it subject to the terms and conditions of
# version 2 of the GNU General Public License.
#
# See the LICENSE file in the source distribution for further information.
import unittest
from sos.utilities import ImporterHelper
class ImporterHelperTests(unittest.TestCase):
def test_runs(self):
h = ImporterHelper(unittest)
modules = h.get_modules()
self.assertTrue('main' in modules)
if __name__ == "__main__":
unittest.main()
# vim: set et ts=4 sw=4 :
|
I was never linked by blogs that took part in Blogroll Amnesty Day". I never asked to be. And I really don't care that much about the "big boys of blogging" not linking to me. But the fact is, blog with lots of incoming links show up higher in Google searches. Putting together this blog is my small effort toward helping make sure the perspective of the de-linked can be heard.
About "Blogroll Amnesty Day"
In Brief
Every incoming link, even to your own diary on a community blog, benefits the owner of the blog. Much the way people started rethinking whether they wanted to shop at WalMart, it's worth considering where you want to "spend" your links.
There's a list of prominent people--officeholders, candidates and others, who have posted diaries at Kos here. At some point, we need to start looking at that list to see who among those people we would like to start contacting, and, in a calm, intelligent manner, expressing our desire that they engage in some "netroots outreach" on sites that are run in a more "democratic" manner. |
NOTE: If you have problems downloading Art Design Colors, please do not use download managers and after 30 minutes your download ticket will be expired, you will have to reload this page to download again this wallpaper. |
Errors in preparation and administration of parenteral drugs in neonatology: evaluation and corrective actions.
The medication iatrogenic risk is quite unevaluated in neonatology Objective: Assessment of errors that occurred during the preparation and administration of injectable medicines in a neonatal unit in order to implement corrective actions to reduce the occurrence of these errors. A prospective, observational study was performed in a neonatal unit over a period of one month. The practice of preparing and administering injectable medications were identified through a standardized data collection form. These practices were compared with summaries of the characteristics of each product (RCP) and the bibliography. One hundred preparations were observed of 13 different drugs. 85 errors during preparations and administration steps were detected. These errors were divided into preparation errors in 59% of cases such as changing the dilution protocol (32%), the use of bad solvent (11%) and administration errors in 41% of cases as errors timing of administration (18%) or omission of administration (9%). This study showed a high rate of errors during stages of preparation and administration of injectable drugs. In order to optimize the care of newborns and reduce the risk of medication errors, corrective actions have been implemented through the establishment of a quality assurance system which consisted of the development of injectable drugs preparation procedures, the introduction of a labeling system and staff training. |
Download App
Apparitions : Arts / research based ‘AR’ experience – ‘bringing back the bygone’. If you would like the free iPhone App please send us your email and we will send you a link as soon as its available.
iPhone public release date : 01.09.18
Name(required)
Email(required)
The artwork is totally free – you will be able to download the ‘Apparitions’ app and collect your special trigger postcards from a Borough Wines in Robertson St, Hastings tourist information & the library – we will have a map and links to all the places here soon.There are three experiences and these can be accessed by anyone with a mobile phone who has downloaded the bespoke free ‘AR’ application ‘Apparitions’. Initially we are releasing this on the App Store for Apple devices ( iPads & iPhones ) until we have raised a little extra funding for the build and release of the same app for Android phones.
If you are interested in trying this for yourself, please drop me a line here.
Each experience requires headphones to access the soundscape attached to it, time travelling from the launch of the bygone site to its demise. Some of these are being created by me by binaural specialists in Liverpool Kinocho (www.kinocho.com). Kinocho have become known for their hi-fidelity sonic reproductions of sound spaces, creating authentic and realistic spatial listening experiences that are easily accessed by the public. The company is noted for its binauralisation process, in which their own blend of psycho-acoustic processing creates convincing 3D spaces with realistic kinetic audio.
Augmented Reality (AR) is a live direct or indirect view of a physical, real-world environment whose elements are “augmented” by computer-generated sensory input such as sound, video, graphics or GPS data and displayed whilst looking at the screen via the camera in most smart phones – android and iPhone.
Apparitions will be future-proofed and expandable, eventually working across both major phone platforms, initially be populate by 2 sites – The Memorial Clocktower, St Leonards pier ( both demolished). The chosen bygone architecture will digitally re-appear as 3D models with binaural soundscapes, triggered when the user is standing with a camera phone in range of the original site with the special app installed from archival footage from museums collections.
Updates :
11.11.17 1st phase beta testing iPhone / iPad
01.04.18 – ACE funding achieved
03.06.18 – 3D models in development using Sketchup
21.06.18 – first binaural soundscape version delivered
18.07.19 – two drafts of soundscapes and 3 D models in SketchUp optimised for mobile phone |
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International development : political and social realities of development : recognition and response : selections from addresses, papers and roundtables [of] the 13th World Conference of the Society for International Development held in San José, Costa Rica, February 22-25, 1973 |
[Herovici's picropolychromium. Application to the identification of type I and III collagens].
A staining technique differentiating two colorimetric types of connective fibers had been proposed by Herovici previously to the identification of collagen types. This technique has been applied to skin, lung and liver specimens and the results have been compared with immunotyping and literature data on collagen types I, III and IV. The conclusions are focused on the ability of the technique to identify at a first approach collagen types I and III, which are known to be of crucial importance in mechanical tissular properties. |
Labels
Thursday, February 6, 2014
Mob Wives Ep 410 "Life Sentences"
Tonight's episode began with Alicia getting ready to go to Eddie's sentencing. She's been waiting forever for him to be sentenced and the day has finally arrived find out how much time he will get. Next Renee and Natalie finally meet up to talk about the things that went on in Vegas and why Renee didn't go to her Halloween party last week. When they first sit down, Renee tells Natalie that with everything that happened between them in Vegas that its probably not a good idea for her to be a part of her Mob Candy line anymore. Natalie agrees. When Natalie asks Renee why she didn't show up to her Halloween party, she says that she didn't want to walk into the lion's den feeling like she was being set up. Renee agrees that she didn't feel like their apologies towards each other in Vegas were sincere. Renee tells her that she would like to try to be friends with Natalie. Natalie still feels hurt by what happened in Vegas and that she was disloyal to Alicia. Renee says that she only owes her loyalty to the people who she wants to be loyal to and that's it. Renee takes off because Natalie still isn't accepting her apology.
Over at Ang's house, she gets a call from Alicia about how Eddie's sentencing went. Alicia tells her that the judge accepted his plea deal and he will be home in a year and a half. Ang says that's great news and now all Alicia has to do is wait for her to be sentenced.
Drita is on the phone with Lee and she fills him in on how her rap song is going. She feels like she's a Brady Bunch because she's a softy now ever since Lee came home and she has nothing to rap about. She then tells him that she's organizing a lunch for all the girls so that they can all get their issues out.
When the girls meet up for lunch that Drita set up Ang and Alicia tell Drita that Renee is not coming. Renee called Ang and told her that she couldn't make. They are all upset that Renee didn't show up. Alicia wants to talk to Renee not about Renee.
Later Drita meets up with Renee to find out why she didn't show up at the lunch with everyone. Renee tells her that since the meet up with Natalie didn't go well she didn't want to sit across from her and Alicia. Drita thinks Renee hates them both. Renee says that she doesn't care enough about them to hate them. Drita says that she wants to do dinner at her house with everyone and insists that Renee come. Renee says she will.
As Drita is making dinner for the girls, she's really hoping that this time Renee shows up. When everyone gets to Drita's, no one has heard from Renee so they're not sure if she's gonna show up or not. Meanwhile, Renee's on her way to Drita's and even though she's not looking forward to seeing everyone she's gonna show up anyways. The dinner gets cut off to next week's episode. Don't miss next week's all new episode of Mob Wives Thursday at 9 PM.only on VH1. |
Breer: Pats missing Hernandez on Sunday “a virtual certainty”
Pregame work for NE-DEN—Patriots TE Aaron Hernandez is a virtual certainty to miss the Bronco game, I’m told, but could be back for Wk 6.
New England is still loaded without Hernandez, as evidenced by their 52 points and 580 yards of offense against Buffalo. Rob Gronkowski still looms as a devastating TE, and Denver has had their problems covering that position. But Gronk also missed practice yesterday due to a hip injury.
However you cut it, the Patriots being without Hernandez is a boon to Denver's chances on Sunday. |
Title
Authors
Document Type
Article
Journal/Book Title/Conference
Ecology
Volume
90
Publisher
Ecological Society of America
Publication Date
2009
First Page
1708
Abstract
Desert ecosystems have long served as model systems in the study of ecological concepts (e.g., competition, resource pulses, top-down/bottom-up dynamics). However, the inherent variability of resource availability in deserts, and hence consumer dynamics, can also make them challenging ecosystems to understand. Study of a Chihuahuan desert ecosystem near Portal, Arizona, USA, began in 1977. At this site, 24 experimental plots were established in 1977 and divided among controls and experimental manipulations. Experimental manipulations over the years include removal of all or some rodent species, all or some ants, seed additions, and various alterations of the annual plant community. While some of these manipulations were discontinued early on, others (i.e., ant and rodent manipulations) have been maintained throughout the study. Monitoring of the composition and abundances of ants, plants, and rodents has occurred continuously on all 24 plots. From 1977 to 2002, individual-level data on rodents (i.e., species, sex, size, reproductive condition) were collected monthly for each plot. From 1983 to 2002, the species-level abundances of plants were sampled on permanent quadrats. From 1977 to 2002, the species-level abundance of ant colonies was recorded for each plot, and from 1988 to 2002 additional information on ant abundances were recorded. Finally, from 1980 to 2002 we recorded precipitation at the study site. These data have been used in a variety of publications documenting the effects of the experimental manipulations as well as the response of populations and communities to longterm changes in climate and habitat. Sampling is ongoing and this database will be periodically updated. |
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Posted - 07/28/2010 : 11:51:26 I'm not sure if this is at the right spot or not...but I'm looking for a pool manager for a head to head style hockey pool. Does this one do that? And if not is there another one out there other than Yahoo...can't use Yahoo as it's a work pool and we can't access Yahoo....but we can access Pickup
2 L A T E S T R E P L I E S (Newest First)
Beans15
Posted - 07/29/2012 : 18:01:02 ESPN also does head to head.
Daniel Alfredsson is the MVP of the universe. All hail the Ottawa Senators!!!!!
Guest4031
Posted - 07/29/2012 : 15:05:17 Yahoo is the only one that I know of either |
Protein kinase C-mediated phospholipase D activity is increased by linolenic acid supplementation in NG 108-15 cells.
Phospholipase D activation was studied in NG 108-15 cells after manipulation of the phospholipid fatty acid composition. Cultivation of cells in media containing different polyunsaturated fatty acids induced extensive and specific changes in the phospholipid fatty acid composition. General for all phospholipids was an increase in polyunsaturated fatty acids at the expense of monounsaturated fatty acids. To examine phospholipase D activation, cells were stimulated with phorbol esters in the presence of ethanol and the formation of phosphatidylethanol was analyzed. In cells cultured with linolenic acid, a significantly higher amount of phosphatidylethanol was formed compared to control cells. On the other hand, supplementation with linoleic, arachidonic or docosahexaenoic acids did not induce any changes in phospholipase D activity. The effect was not due to free fatty acids in the cell culture medium and thus probably induced by fatty acids incorporated into membrane phospholipids or fatty acid metabolites. The results indicate a specific effect of linolenic acid and/or its metabolites on protein kinase C-mediated phospholipase D activity. |
NASA Engineer Thinks Drones Will Save the Earth. Here’s How
A company known as BioCarbon Engineering has developed a way to use drone technology as a solution to the relentless devastation of the Earth’s forests. The company, founded by ex-NASA engineer Lauren Fletcher, plans to combat deforestation by using drones to replant trees far more efficiently than current methods allow.
Deforestation is an issue that continues to devastate one of Earth’s most vital resources and threaten the balance of climate all over the world. In the Amazon alone, 232,000 square miles of dense rainforest (1/5 of the Amazon’s entire area) have been destroyed in the last 40 years to serve resource-hungry industries. Worldwide, over 6.5 billion trees die victims of deforestation each year.
Current methods to replenish what’s been lost, including hand planting and spreading seeds by helicopter, are expensive and too inefficient to keep up with the decline of the global tree population. Drones, however, streamline the reforestation process, making it faster, cheaper and with higher success rates. With two operators, each handling up to 6 drones, Fletcher thinks it’s possible to plant up to 100,000 trees per day at just 15% of the cost of current methods. Watch him tell the story of his project below:
How does it work?
First, the drones are sent out to create a 3D map of the area to be reforested. Then, the maps are analyzed to plan a seeding pattern according to the area’s terrain. Irene Fedorenko, co-founder of BioCarbon Engineering, explains how this trumps current methods:
“We can modify what to plant, and where, so you have the highest chance of survival. If you do aerial spreading—you just spread seeds wherever—maybe they hit a rock, maybe they hit a swamp, and they’re not going to survive. But we can basically control for that.”
Next, the drones head back out and fire seed pods at a speed that allows for ground penetration. Each drone carries a mix of seed pods, and shoots the correct ones into the correct places on its flight path with pinpoint precision. And seeing as multiple drones can be operated by one person, labor is freed up to monitor and care for the seedlings after planting.
Fletcher, who spent 20 years at NASA, is pledging to plant 1 billion trees per year using the technology.
The company will begin its work this month, when they team up with the Worldwide International Foundation to tackle deforestation in Myanmar. WIF have been leading planting efforts in the South-East Asian country, where they’ve already hand-planted 750 hectares of mangrove trees. With drones, they’ll be able to plant another 1 million trees over 250 acres in a fraction of the time.
Following efforts in Myanmar, the team is hoping to take their drone technology to South Africa and the Amazon rainforest, to help combat the unbridled destruction of precious and ancient ecosystems.
Visit BioCarbon Engineering’s website to find out more about the project. |
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Interview with Howard Tullman, President and CEO of Tribeca Flashpoint Media Arts Academy
Howard Tullman, co-founder of Tribeca Flashpoint Media Arts Academy, founder of over a dozen high-tech companies, adjunct professor at the Kellogg Graduate School of Management at Northwestern University, and member of both Governor Quinn and Mayor Emanuel’s technology and innovation councils, will share with Chicago Council on Science and Technology members some of the tools, trends and technologies that will transform businesses in the coming year this Thursday, Sept. 20.
We visited Tullman at Tribeca Flashpoint, and he shared with us some of his wisdom on a variety of subjects in advance of the program. Following is an edited transcript.
Q: Last week, you made the case that the ongoing Chicago Public Schools teachers strike would help education entrepreneurs (Inc., “Why the Chicago Teachers' Strike Will Help Education Entrepreneurs,” The Perspiration Principles, Sept. 14, 2012), noting that children attending charter schools were all still in class, and that this presented a “unique opportunity to demonstrate that more and more effective out-of-class and self-directed (or computer-enhanced) learning opportunities are available to students of all ages.”
If a demand shift occurs, how do you see a system as large as Chicago’s adapting to changing needs or wants of parents and students?
A: I had 300 Chicago Public School teachers here for a conference recently. Solitary learning will take place at home, outside of a classroom. Inside the class, students will work in groups, problem solve together. Teachers will circulate around. Students can work at their own rate of progress.
The great thing is teachers can develop a video in 15 minutes, put it up at essentially no cost, and its available 24/7; it’s an aid that didn’t exist before, and frees up the teacher. There are a series of aides that exist that never existed before. Harvard, other schools are posting free content with really great professors. A kid can go online, see a really great teacher, and understand something in a different way. It’s changing the way things are taught. [Massive open online courses, or MOOCs, let colleges reach vast audiences free or at relatively low cost, and have been offered to date at over a dozen prestigious organizations].
Chicago schools have to figure out how to move from the current model: it cannot be ‘I talk, you listen.’ It’s not the same learning, its differentiated learning. A significant portion of principals and teachers, time has passed them by. It’s the same in business, companies are dominated by IT departments who say, ‘leave your smartphones at the door.’ The kids know and understand the technology and we teach them not to use it. It’s very scary.
Q: You once said there were three things that separated entrepreneurial winners from losers: starting with what you have, avoiding perfection, and failing fast. ( Inc., “Great Entrepreneurs Do These 3 Things,” The Perspiration Principles, Aug. 29, 21012). Which of these three things do you see most often violated?
A: People don’t fail fast. Not small companies, but big companies. They aren’t faced with existential dilemmas. There is a department or division of a project, and they are just avoiding blame; ‘fess up. But they are indifferent. It’s the whole school of disruptive innovation, when the big company sees the train coming down the track—they are doing things that are just good enough, waiting until everything is perfect.
You need to launch; don’t try to guess. Go with the LVP, or least viable product. Get the market to tell you what they will like. Nobody has that much wisdom.
Q: What is your biggest learning experience?
A: At the school, it’s been that all the technology is not as valuable to employers as the people skills are.
Collaboration, teamwork, a great work ethic and passion is what matters most.
Q: Any other thoughts?
A: The most frightening trend regarding technology and education is the personalization of everything. It’s great for marketers, and it seems nice when you log on somewhere and it knows your preferences. But education is discovery. When you walk into a bookstore, and you stumble onto a book about dinosaurs or whatever that you never would have found, it’s nice. But the more personal information you provide, the more the system feeds back what you already know—you never get outside of the box. Your search is no longer objective. It’s a very different world now. When you used to look something up at a library, you knew the sources were researched, and validated. Now, you don’t know the source. A five- or six- year old doesn’t know that he or she can’t trust that what they find is not objective. |
Friday, July 1, 2011
Behold, or look? (John 1)
While the introductory statements in John 1:1-13 serve as ambiguously bold claims about Christ Jesus by John the evangelist and author, let us take a moment and reflect further on the importance of the pivot point in this chapter as a whole: vv. 29-34. For the purpose of this interpretative work I will not be using the adjective “look” as is presented in the NIV. Instead, I will look at the first person singular aorist imperative (Biblos, 2011) “behold” as is found in numerous translations (cf. ESV, NASB, KJV). Behold is a:
1. First person: spoken by John the Baptist
2. Singular: speaking only about Jesus
3. Aorist(verb tense): “said to be ‘simple occurrence’ or ‘summary occurrence’, without regard for the amount of time taken to accomplish the action (NT Greek, n.d.).
4. Imperative(verb mood): “The imperative mood is a command or instruction given to the hearer, charging the hearer to carry out or perform a certain action” (NT Greek, n.d.).
Who? What? When? Where? Why? These are still the best questions to ask because they reveal all sides of every story. John uses seemingly non-technical language, but it is masterfully used in a technically brilliant manner. The understanding of the text takes on new dimension when seeing it with the word “behold” rather than “look.” To look at something could infer (in modern understanding) to look, and then to look away. This action could be a glance, or a stare, but none-the-less, it does not always imply a sustained action. Behold on the other hand draws the reader to understand that which is to beholden. While behold may be an adjective with some antiquated feeling, it serves to better-convey the Baptist's mood when the Christ was drawing near. Let us take a peek into the etymological Greek foundations of behold.
The Greek language is very specific compared to the English language. The Bible in English (now) and Greek (then) is akin to viewing the earth’s surface from two vantage points: English is like seeing the topography from 30,000’ while Greek is like seeing the topography from 3,000’. You still get the same general picture from the former, but there is so much more depth the closer you look with the latter.
Both the Baptist and the evangelist are stressing a serious point: the Christ, whom God beheld as the One to save man from the sin that consumed him, was to be beheld by man as the Redeemer from all sin. The crux of this entire passage (chapter one) builds from the introduction of Jesus as the Everlasting Word – there from the start – and finally appearing as promised by God; as announced by John the Baptist.
From this point, when Jesus’ earthly body, as seen by all human eyes in the flesh, is testified to by the Baptist, He begins to call His disciples. We see what little it takes for them to follow but what immense steps they must take once they do. The same is true of us today. We do not follow cleverly crafted words on a page, we follow the fulfillment of God’s Chosen Servant; words that were powerful enough to create everything into existence. |
Effect of influenza epidemics on Australian mortality.
The effect of influenza epidemics on all major causes of death has been examined. The results showed an increase in total mortality, and a fall in life expectancy, during epidemic years. Using the 1974 epidemic as an example, an increase in mortality was found in all age groups, with the greatest percentage in increases occurring in the very young and the very old. For all ages combined, the greatest percentage increases in mortality were for respiratory diseases, while the greatest absolute increases in mortality were for cardiovascular diseases, especially ischaemic heart disease. A thrombotic mechanism is suggested to explain the increase in mortality from cardiovascular diseases. |
Autocatalysis-driven clock reaction II: kinetics of the pentathionate-periodate reaction.
The pentathionate-periodate reaction has been investigated by spectrophotometrically monitoring the total amount of iodine evolved in the presence of phosphoric acid/dihydrogen phosphate buffer at 468 nm. The majority of the main characteristics of the title system is very reminiscent of that found recently in the pentathionate-iodate reaction, a system that led us to classify generally the clock reactions. Along with the pentathionate-iodate reaction the title system is proposed to belong to the autocatalysis-driven clock reactions as well. The kinetic model of the pentathionate-iodate system published recently was implemented by the necessary reactions of periodate to compose a 24-step kinetic model in which the mechanisms of the pentathionate-iodine, pentathionate-iodate, bisulfite-periodate, bisulfite-iodate, iodide-periodate, and the well-known Dushman reactions are combined. A thorough analysis revealed that the direct pentathionate-periodate reaction plays a role only to produce iodide ion via a finite sequence of reactions, and once its concentration reaches a certain level, the reaction is almost exclusively governed by the pentathionate-iodine, the iodide-periodate, and the Dushman reactions. As expected strong catalytic effect of the buffer composition is also found that can readily be explained by its well-known catalytic influence on the Dushman reaction. |
Q:
When should an Erlang function return ok?
I often see Erlang functions return ok, or {ok, <some value>}, or {error, <some problem>}.
Suppose my function returns an integer N. Should my function return just N, or {ok, N}?
Or suppose my function includes the call io:function("Yada yada"). Should it return ok or nothing at all?
Or suppose I'm making a record or fun. Should I return {ok, R} or (ok, F}?
Thanks,
LRP
A:
It's a matter of style, but making reasonable choices goes a long way toward making your code more readable and maintainable. Here are some thoughts based on my own preferences and what I see in the standard library:
If the function can return with both a success and a recoverable failure case, you may want the success case to look like {ok, _} or ok. Good examples are: orddict:find/2 and application:start/1. We do this so both cases can be easily pattern matched when making the call.
If the function has only a success case with a meaningful result, then just return the result as there is no need to add additional information. In fact if you were to wrap the result in a tuple, then you can't easily chain calls together e.g. foo(bar(N)) may not work if bar/1 returns {ok, _}. Good examples are: lists:nth/2 and math:cos/1.
If the function has only a success case without a meaningful result, the common idiom is to return ok or true as opposed to whatever the last returned value in the function happened to be. Good examples are: ets:delete/1 and io:format/1.
A:
Suppose my function returns an integer N. Should my function return just N, or {ok, N}?
If there is no possibility of error at all, or any error indicates a programming error, N. If there may be a good reason to fail, return {ok, N} (and {error, Reason} in case of failure).
Should it return ok or nothing at all?
In Erlang, you can't return nothing at all. If you don't have a meaningful return value, ok will do fine.
|
Lightning News
Lightning Recall D Mike Vernace From Norfolk
The Tampa Bay Lightning have recalled defenseman Mike Vernace from the Norfolk Admirals of the American Hockey League today, vice president and general manager Steve Yzerman announced.
Vernace, 6-foot, 216 pounds, has played in eight games with Tampa Bay this season, averaging 8:33 in ice time per game. He last appeared for the Lightning on November 20 against the Buffalo Sabres, logging 4:41 of ice time and landing two hits. He made his debut with Tampa Bay on October 9 against Atlanta and played a season-high 16:33 in ice time October 16 at Florida. He has played in 20 career NHL games with the Lightning and Colorado Avalanche.
A native of Toronto, Ontario, Vernace has skated in 45 games with the Admirals this season, recording six goals and 20 points. He ranks second among team defensemen for goals and power-play goals and is also first for points.
Vernace was signed by the Lightning as a free agent on July 29, 2010. He was originally drafted by the San Jose Sharks in the seventh round, 201st overall, of the 2004 NHL Entry Draft. |
Savannah Vinsant
Savannah Vinsant (born June 25, 1993) is an American trampoline gymnast. She competed at the first Summer Youth Olympic Games. Vinsant also represented the United States at the 2012 Summer Olympics. She became the first ever U.S. trampoline athlete to qualify for the finals. Savannah finished sixth place during the trampoline finals. She was the youngest female trampoline competitor at the games.
Early life
Vinsant's parents are Neil and Ramonda Vinsant. Savannah Vinsant began gymnastics in 2000. She had always lived in cities that had trampoline gyms. However, when her family moved, in 2005, to Newton that changed. Her family drove her a constant back-and-forth trips to practices in Orange and Lafayette, La. until it became too much. It seemed as though at this point Vinsant's trampoline career would likely end, just shortly after it had started. "We didn't think she was going to bounce again," said her father. Savannah made it quite clear that she was not going to take giving up the sport quietly. "I hate y'all. I hate y'all for making me quit," Ramonda recalled Savannah telling her during one heated argument. The parents, who had taken courses in judging and coaching, began training Savannah on their own. They trained her on a 7-by-14-foot competition trampoline (a rectangular trampoline with a different bed than regular outdoor trampolines) – in their backyard. Soon roughly 40 children began coming to Savannah's house and joined her with her practices. Her parents then offered to build a gym in their front yard.
In 2007, Vinsant filled out an application to attend the U.S. Olympic Training Center without her parents' permission. She called her mother from Newton High School and told her she was sick and her parents would need to get her now. Her mother took her home from school, where the then 14-year-old Savannah received a call from the Olympic Training Center saying she was a few years too young to attend. Vinsant lived in Newton from the time she was 10 until one month before her 16th birthday, when she left home to train for the Olympics.
The gym now is the headquarters for more than 200 aspiring trampolinists.
Journey to the Olympics
London qualification
On November 21, 2011 in Birmingham, England, Vinsant finished tenth at the 2011 World Trampoline and Tumbling Championships with a score of 98.445. With her performance, she advanced to the women's individual trampoline final and secured a spot for the U.S. team at the next summer's 2012 Olympic Games in London.
Although Vinsant's scores qualified the United States for an Olympic spot, she still had to compete in a series of qualification competitions to earn her place to represent the United States at the Olympics. Savannah won all three of the qualification competitions securing her spot easily. "I'm speechless – I have no words for it", was her reaction upon being named to the Olympic team, "I'm filled with joy and I'm at peace that it's over. I had a big group of girls out there with me this year who were awesome, and they definitely kept me on my toes all year. I'm honored to be representing Team USA."
London 2012
Vinsant competed on August 4, 2012 at the London Olympics. She was the youngest competitor of the female field. In the compulsory round, she scored a 46.400 for her routine that included a half in Rudy out and would be standing in 11th place. However, Vinsant's second routine, her optional routine, would score a 54.955, which moved her to seventh place in the prelims with a total score of 101.355. This would grant her one of the eight places in the finals competition on the same day. Vinsant became the first U.S. trampolinist to qualify to the finals at an Olympic Games. "I wanted to make finals, but overall I just wanted to do 20 skills," she said. "Making it to finals in seventh, I was shocked actually– I thought that was a pretty high standard for me to reach."
During the finals portion of the competition, Vinsant's routine featured a Triffus tuck, half Rudi tuck, full in Rudi out straight, double back pike, Rudi out pike, half in half out pike, full Brani pike, half half tuck, half out pike and full full pike. She scored a 54.965 and finished sixth.
Vinsant said of her overall performance in London, "I was very pleased with all of my performances today. This gives me a lot of confidence. I was the youngest competitor here and making finals really hit the pace for me. I will work to get my difficulty, time of flight and execution better so that I can be up in the medals at the next Olympics."
Accomplishments
Business
In 2015, Savannah Vinsant Thompson launched Hangtime TNT Gymnastics, LLC., a trampoline and tumbling gymnastics club and cheerleading academy. In 2017, Coach Savannah's team had their first national champion and regional champions. All 2017 Hangtime TNT athletes became a State Champion in one of the three trampoline and tumbling events at the State Championships held in Lafayette, LA. Savannah is also very proud of her recreational program as it has grown and became very successful. She is able to give children something they will never forget at Hangtime TNT. Hangtime TNT is more than a gym, it is an experience children will remember forever. Savannah's dream was to own her own gym and become a positive role model for the youth.
School
2014 SLCC Associate of General Studies Degree
2007 Student of the Year
Class of 2010 Valedictorian
Trampoline
National results
2018 USA Gymnastics Trampoline Championships, Greensboro, North Carolina - 1st- TR
2013 U.S. T&T Championships, Kansas City, Mo. - 4th-TR
2013 U.S. Elite Challenge, Frisco, Texas - 1st-TR; 2nd-SY
2012 USA Gymnastics Trampoline Championships, San Jose, Calif. – 1st-TR
2012 Stars & Stripes Cup, Cleveland, Ohio – 1st-TR
2012 Elite Challenge, Tulsa, Okla. – 1st-TR; 2nd-SY
2011 U.S. Elite Championships, San Antonio, Texas – 1st-TR
2011 U.S. Elite Challenge, Fort Worth, Texas – 1st-SY; 6th-TR
2011 Winter Classic, Houston, Texas – 8th-TR
2010 Visa Championships, Hartford, Conn. – 6th-TR
2010 U.S. Elite Challenge, Virginia Beach, Va. – 3rd-TR
2010 Fairland Classic, Laurel, Md. – 1st-TR
2009 Final Selection Event, Las Vegas, Nev. – 1st-TR, SY (15–16) (Jr. Div.)
2009 Visa Championships, Dallas, Texas – 2nd-TR; 6th-SY (Jr. Div.)
2009 U.S. Elite Challenge, Ft. Smith, Ark. – 1st-TR; 2nd-SY (Jr. Div.)
2009 Winter Classic, Birmingham, Ala. – 3rd-TR; 6th-SY (Jr. Div.)
2008 Stars and Stripes Cup, Colorado Springs, Colo. – 2nd-SY; 5th-TR (Jr. Div.)
2008 Visa Championships, Houston, Texas – 1st-TR; 2nd-SY (Jr. Div.)
2008 U.S. Elite Challenge, Mobile, Ala. – 1st-TR, SY (Jr. Div.)
International results
2013 Aalsmeer Flower Cup, Aalsmeer, Netherlands - 2nd-TR
2012 Olympic Games, London, England – 6th-TR
2012 Taiyuan World Cup, Taiyuan, China – 3rd-TR
2012 Kellogg's Pacific Rim Championships, Everett, Wash. – 2nd-SY; 3rd-Team; 8th-TR
2011 World Championships, Birmingham, England – 4th-TR (Team); 7th-TR
2011 Loule Cup, Loule, Portugal. – 8th-TR
2011 Salzgitter World Cup, Salzgitter, Germany – 5th-SY; 8th-TR
2011 Canada Cup, Alberta, Canada – 5th-TR, SY
2011 Flower Cup, Aalsmeer, Netherlands – 1st-TR
2010 Pan American Cup, Guadalajara, Mexico –
2010 World Championships, Metz, France –
2010 Youth Olympic Games, Singapore – 5th-TR
2009 World Championships, St. Petersburg, Russia – 1st-TR (15–16)
2009 Canada Cup, Okotoks, Alberta, Canada – 1st-SY; 2nd-TR (Jr. Div.)
2007 World Age Group Competition, Quebec City, Quebec, Canada – 2nd-TR (13–14) (Jr. Div.)
2005 International Age Group Competition, Eindhoven, Netherlands – 1st-TR; 5th-DM, SY (11–12) (Jr. Div.)
References
Category:American female trampolinists
Category:1993 births
Category:Living people
Category:Olympic gymnasts of the United States
Category:Gymnasts at the 2012 Summer Olympics
Category:Gymnasts at the 2010 Summer Youth Olympics |
the one i went to a few months back also did this and they refused to waive the fee for software i didn't ask for, i told them ok i'll just purchase one online at a different store. there is a reason why BB's sales have decreased yearly and to a point where they were rumored to be heading towards bankruptcy protection.
there is really no change, they have been doing this for so many years. A few years ago everyone did stories and exposed this scam however after this BB head office sort of relinquished its power letting the GM have the overall final say on decisions made in the store. Ive had several runins with these GMs and they will gladly tell you to call head office and that they will tell you the same thing that its ultimately the store GMs decision. I guess this is there way to continue the scam while letting corporate get away with it, but we all know who really pushes these incentives in the end.
Same inquired about a Laptop and told me that OS is not set up on computer and they wanted to charge me... The employee thinks I am so stupid. I just told him I dont want the computer to piss him off lol
i thought BestBuy and FS got in trouble for this a years back and they said they'd stop this fraud. i thought i even saw news articles on the matter....?
Futureshop is worse for this because their sales people make huge commissions on the setup fees, it's one of their biggest commission items and they make a killing on boxing day by doing this scam.
Yep I remember that. It was crazy on RFD that boxing day. So many people where furious. It made it to the Toronto Star even. Didn't know they are still doing this. This should be illegal or you should put the 'setup fee' in your advertising at the very least.
My jaw dropped reading this thread. I have never purchased a laptop before, and I build my own desktops. Like, I don't even get how this works. So you go to buy a box with a laptop, but it's already been opened? wtflol
My jaw dropped reading this thread. I have never purchased a laptop before, and I build my own desktops. Like, I don't even get how this works. So you go to buy a box with a laptop, but it's already been opened? wtflol
LOL pretty much, you would be surprised the amount of saps who actually pay $150 for someone to startup your computer enter your name and burn a copy of the backup discs which can be obtained for free online. (oh! and they also help you install your copy of MS Office, cause apparently its super hard to do so LOL) They do this to be "customer centric" so that customers dont have to wait and computers are pre-done so that customers who pay the extra $150 can leave immediately after they pay for it.
I used to work returns and the amount of angry customers who come back (usually the unsuspecting mom/dad/grandmother/gradfather) asking for a refund on services they did not even want. Some did not even know they were charged the $150, these guys are real crooks they prey on the elderly and the uninformed.
LOL pretty much, you would be surprised the amount of saps who actually pay $150 for someone to startup your computer enter your name and burn a copy of the backup discs which can be obtained for free online. (oh! and they also help you install your copy of MS Office, cause apparently its super hard to do so LOL) They do this to be "customer centric" so that customers dont have to wait and computers are pre-done so that customers who pay the extra $150 can leave immediately after they pay for it.
I used to work returns and the amount of angry customers who come back (usually the unsuspecting mom/dad/grandmother/gradfather) asking for a refund on services they did not even want. Some did not even know they were charged the $150, these guys are real crooks they prey on the elderly and the uninformed.
The same case happened to me a few years ago, the line at laptop/TV cashier was moving very very slow. 2 sales people( both of them quite young, probably still in college), they insisted I need that $60 back up disc. I said no twice. they lowered to $40. no again. one of them ignored my words, just added to my invoice. I could see the screen , and pointed out. She then changed to $25. I used very firm tongue to confirm just need the laptop. right now, I will say , it's not my 1st boxing day here, pls do right before I use F***G word to you. that game wasted me about 15 min, at that time I knew why the line was so slow.
I will report this to some regulation agency if happen again.
weeks ago, I filed a compliant about cellphone hardware upgrade fee to CCTS http://www.ccts-cprst.ca/ , my cell C/O called me days ago and waived for me.
Everyone could have done this to stop those legit " robberies" . |
Metal-binding domains and the metal selectivity of the vanadium(IV)-binding protein VBP-129 in blood plasma.
Ascidians are well known to accumulate extremely high levels of vanadium in their blood cells. Several key proteins related to vanadium accumulation and physiological function have been isolated from vanadium-rich ascidians. Of these, vanadium(IV)-binding protein-129 (VBP-129) is a unique protein that has been identified from the blood plasma of an ascidian Ascidia sydneiensis samea, but its metal binding domains are not known. In this study, several deletion and point mutants of VBP-129 were generated, and their metal binding abilities were assessed by immobilized metal ion affinity chromatography (IMAC) and electron spin resonance spectroscopy (ESR). The internal partial protein, VBP-Int41, did not bind to V(IV), but the two constructs, VBP-N52 and VBP-Int55, added with additional 11 or 14 neighboring amino acids bound to V(IV). Mutations for cysteine-47 and lysine-50 in VBP-Int55 diminished V(IV)-binding in VBP-Int55, suggesting that these amino acid residues play important roles in binding V(IV). ESR titration analysis revealed that VBP-129, VBP-N52 and VBP-Int55 could bind to 6, 3 and 2 V(IV) ions, respectively. ESR spectrum analysis indicated a N(2)O(2) coordination geometry, which is similar to vanabins. The cysteines may contribute to the maintenance of the three-dimensional structure that is necessary for binding V(IV) ions. VBP-129 did not have a V(V)-reductase activity, as expected from its tissue localization in blood plasma. This study provided the evidences that VBP-129 possesses V(IV)-binding domains that make a similar coordination to V(IV) as those by vanabins but VBP-129 acts solely as a V(IV)-chaperon in blood plasma. |
function texMath(state, silent) {
let startMathPos = state.pos;
if (state.src.charCodeAt(startMathPos) !== 0x24 /* $ */) {
return false;
}
// Parse tex math according to http://pandoc.org/README.html#math
let endMarker = '$';
startMathPos += 1;
const afterStartMarker = state.src.charCodeAt(startMathPos);
if (afterStartMarker === 0x24 /* $ */) {
endMarker = '$$';
startMathPos += 1;
if (state.src.charCodeAt(startMathPos) === 0x24 /* $ */) {
// 3 markers are too much
return false;
}
} else if (
// Skip if opening $ is succeeded by a space character
afterStartMarker === 0x20 /* space */
|| afterStartMarker === 0x09 /* \t */
|| afterStartMarker === 0x0a /* \n */
) {
return false;
}
const endMarkerPos = state.src.indexOf(endMarker, startMathPos);
if (endMarkerPos === -1) {
return false;
}
if (state.src.charCodeAt(endMarkerPos - 1) === 0x5C /* \ */) {
return false;
}
const nextPos = endMarkerPos + endMarker.length;
if (endMarker.length === 1) {
// Skip if $ is preceded by a space character
const beforeEndMarker = state.src.charCodeAt(endMarkerPos - 1);
if (beforeEndMarker === 0x20 /* space */
|| beforeEndMarker === 0x09 /* \t */
|| beforeEndMarker === 0x0a /* \n */) {
return false;
}
// Skip if closing $ is succeeded by a digit (eg $5 $10 ...)
const suffix = state.src.charCodeAt(nextPos);
if (suffix >= 0x30 && suffix < 0x3A) {
return false;
}
}
if (!silent) {
const token = state.push(endMarker.length === 1 ? 'inline_math' : 'display_math', '', 0);
token.content = state.src.slice(startMathPos, endMarkerPos);
}
state.pos = nextPos;
return true;
}
export default (md) => {
md.inline.ruler.push('texMath', texMath);
};
|
1480239313 Good. Light to moderate wear to covers/corners. Trade paperback binding. Tiny stain to edge of pages. First few pages dirty. Support Last Word Books & Press and independent booksellers.
Stock Description, May Not Reflect Item
Jesse Skylock Holmes thinks he's a pretty good detective. He should be since his father, Detective Douglas Holmes, who works for the Mason Police Department, trained him to observe the smallest details from the time he wore diapers. So when there's an unveiling of a statue of the town founder, Zachariah Mason, and his head is cut off, Jesse is on the case. He gets help from his two best friends, Austin MacGreggor and Poe Jones. They have competition searching for the head by two popular girls in school, Daytona Drew and Laura Ricci. Who finds the head first? Who becomes the hero/heroines of the town? In their search, the boys discover something shocking: a hundred year old body. The body is hiding two secrets. One, that the town founder, Zachariah murdered him, and two, he is hiding a clue on him, a clue that can lead to a buried treasure. Can the boys find this clue and follow it? Will they discover this hidden treasure that people have been searching for for over one hundred years Join Jesse, Austin, and Poe on their adventure as they unravel a mystery and use their scientific skills and gadgets to solve it. |
Those scenes had some cute details to them—Lombardozzi’s blunt, funny advice played well against the ashen Matt Czuchry, who has done award-worthy work all season as the embattled Cary. But they also felt like tiring stall tactics in a plot that had long ago run out of thread. Cary wasn’t going to prison. If he were—if showrunners Robert and Michelle King had decided to explore that plot—he’d have been there already. The palpable relief I felt at Cary’s liberation at the end of the episode was more to do with finally being free of the storyline. Especially after the antics Kalinda had to pull to get him off.
Kalinda breaks the law all the time to get things done, but she’s a skilled investigator who knows how to cover her ass, and her infractions are usually committed with the safe knowledge that no one’s going to call her on it. Not so much here, where she manipulates court evidence to make it seem like the cop on Cary’s case (John Ventimiglia) ignored evidence that might have dropped the charges against him. The episode did not treat this as an easy decision, or a justifiable one: Kalinda’s horror when her ploy succeeds, and the cop’s loud protests, suggest this issue will not go away anytime soon.
But despite Kalinda’s bond with Cary—and Archie Panjabi and Matt Czuchry’s fine work together over the years—it felt like a bridge too far to have her make such a tremendously stupid move to save him from two years in jail. To have Kalinda, such a self-possessed character, potentially sacrifice her freedom to save a man she’s romantically interested in, even one as sympathetic as Cary, rang hollow—and the slapstick way it occurred, with the technologically incompetent Diane somehow pulling the falsified data off her computer and introducing it into evidence before Kalinda could stop her, didn’t help.
But Cary’s exoneration still played beautifully. Czuchry nailed his palpable relief, and the show didn't edge away from the element of irony that’s been present all season—Alicia, the firm, and the judicial system itself in the end, scrambling to save an entitled white man who might go to jail for associating with a black drug trafficker. This week, we see a zoomed-in shot of Cary’s checking account (more than $250,000 in the bank, good job buddy!) and hear the presiding judge apologize for his ordeal at the hands of over-eager prosecutors. We’re on his side, no doubt, but the show’s self-awareness of Cary’s privilege was one of the brightest, best-handled notes of the episode.
Alicia’s debate camp served mostly as welcome relief from the tension of Cary’s looming sentencing, although it had some comedic details that were too weirdly goofy (like Chris Elliott’s baffling appearance as a stoned professor standing in for her opponent). Alicia’s campaign stories always consist of the same arc, which we saw again here—she’s detached and disinterested because of other storylines happening around her, but finally leaps into the political fray with glee and shows surprising acumen. |
Q:
High ground combat modifier and how it applies to fly and spider climb
I'm confused when it comes to the high ground combat modifier and fly or spider climb effects. Its clear that any ranged attack does not gain a high ground bonus. But just what exactly gives you high ground? A couple inches or feet?
At what height would you need to be in order to gain high ground while flying? One of my players often hovers or moves just above the ground. Is this sufficient for the bonus?
If you were on a wall using spider climb, could/would you gain it?
Since charge can be used while flying, if you charged down to an enemy do you gain it?
When you are larger than an opponent would you gain it, for example a large creature attacking a medium?
A:
The Advantage is for Higher Ground, not just Height
The advantages conferred in combat by high ground are not just awarded for being above your opponent. In order to have "higher ground," you have to have a position where your opponent must fight gravity to advance.
A flying character, regardless of whether they're two inches or two feet off the ground, does not have a high ground advantage because their opponent does not need to move uphill in order to attack into their space - unless they're directly above their target, in which case they're still not at an advantage because vertical reach is easier than horizontal reach.
The same goes for a climbing creature. Unless the climbing creature is attacking from a slope, where their opponent would have to cross uphill terrain in order to reach them, they do not receive any bonus.
As for how much height would be needed assuming it was ground, that's subject to DM's discretion. I would personally say that you need at least a foot of difference (a 20% grade over 5 feet) - a single stair-step is enough to grant the bonus, but anything less than that isn't.
Large creatures - while they don't get a Higher Ground bonus just for being tall - could use their longer legs to advance over larger gaps in elevation, requiring more elevation for someone to have the high ground on them. (a 20% grade is a 20% grade, but 5-feet of it might no longer be enough) There's noting in RAW to back that up, though, so it would really be up to the DM.
|
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The Greek crisis is not going away in a hurry. Even if the various parliaments and law makers across the Eurozone ratify the latest agreement between the Euro Group and Greece, it will be sometime, maybe a few weeks, maybe a month, maybe longer, before… |
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Brilliant game! For those of you wondering what the heck micro time trial is, there's a spring facing the right at the beginning of the game, with a small board that shows a score. When you jump on it, it sends you to a pace with yellow squiggles which you must collect in the right order. If you fall, you have to start all over again. But don't worry, it's not a very long course :) Good luck!
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For all those that got over the 500,000 in challenge mode but didn't get the badge, do this: DO NOT exit through the door. Let the countdown timer reach zero. I got 800k on my first go in the challenge mode then exited through the door with time to spare, but it didn't give me the badge. Second go around, I got 700k and I was struggling to get to the door when I ran out of time, then it gave me the badge.
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For the people commenting saying "OMG GLITCH, IF YOU PRESS THE 0 IT GOES WHITE!!!" Let me let you in on a little secret.
This is actually intentional, Brad has all the numbers linked to different parts of the game to he can get to them fast. He just forgot to take them out for this public demo. If you press "9" You'll go to the secret squiggle hills, "8" : The Science room, and "1" will lead you back to the start. all the other numbers are linked to locations in the game that were not released for public testing.
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so i made it all the way through, even on the return to squigglyville screen. beat medium badge and got credit but still wont give me the easy badge for completion. any ideas why?
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There are 331 squiggles. To enter the secret Squiggle Hill you have to roll, NOT slide, on the inclined platform near the "That way" sign, then wall-run and wall-jump to reach the platform with a door. Open the door and you will find the secret Squiggle Hill! + so everybody can see ;)
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I love this game so much, but what made the original fancy pants so fun was being able to gain super speed and keep on running. Sort of like sonic the hedgehog games. In this one we are forced to go slow and hunt down the squiggles instead of just blasting through them with the fun fun speed that we had in the first one.
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The game combines elements of classic platformers from days of old;sonic style speed, super mario 64 exploration and playground-like levels, and a playful atmosphere (don't touch any keys for a minute or so). One of the best platformers out there, in any format.
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If you aren't getting the medium badge, don't exit the challenge level. If you do, your score won't be counted. Just let the time run out. Too bad that only a few people will see this...
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This is fantastic, although the acrobatic tricks are kind of hard to grasp. Jumping feels severely delayed at times. A counter that states the max amount of squiggles that you can get in one playthrough would be much appreciated. Still, I've always enjoyed the smooth animation and playful nature of these games. Anyway, 5/5.
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Great game! the music fits well into the feel of the game (at least in the start). artwork is, like always, mind-blowing. 5/5. and i dont think that im lying if i say that this was where the whole kongregate community was waiting for.
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to the left of the challenge door, i jumped up on that purple tube and ran toward the wall, then the camera stopped panning. its frozen there, but my character still runs freely in the world.
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I love Fancy Pants. Great game so far! I found a glitch, though. In the first screen with water, I dove in and came up under the oil slide (on the left). I popped up out of the water and got stuck in the slide/wall in a permanent "falling" animation.
Hey, do you like games? So do we — that’s what makes Kongregate the best source of free games online. We have thousands upon thousands of free online games, from both one-man indies and large studios, rated and filtered so you can play the best of the best. Read more » |
---
abstract: 'The dynamics of a decohering two-level system driven by a suitable control Hamiltonian is studied. The control procedure is implemented as a sequence of radiofrequency pulses that repetitively flip the state of the system, a technique that can be termed quantum “bang-bang” control after its classical analog. Decoherence introduced by the system’s interaction with a quantum environment is shown to be washed out completely in the limit of continuous flipping and greatly suppressed provided the interval between the pulses is made comparable to the correlation time of the environment. The model suggests a strategy to fight against decoherence that complements existing quantum error-correction techniques.'
address: |
d’Arbeloff Laboratory for Information Systems and Technology,\
Department of Mechanical Engineering, Massachusetts Institute of Technology,\
Cambridge, Massachusetts 02139
author:
- 'Lorenza Viola[^1] and Seth Lloyd[^2]'
title: |
Dynamical suppression of decoherence\
in two-state quantum systems
---
Introduction
============
The design of strategies able to protect the evolution of a quantum system against the irreversible corruption due to environmental noise represents a challenging conceptual issue. In particular, since maintaining quantum coherence is a crucial requirement for exploiting the novel possibilities opened up by quantum parallelism, practical implementations of quantum computation and communication proposals require methods to effectively resist the action of quantum decoherence and dissipation [@review; @unruh; @palma]. Roughly speaking, two classes of procedures are available to overcome the decoherence problem: either passive stabilization or active manipulation of the quantum state. The first kind of solutions, recently formalized as [*Error-Avoiding Codes*]{} [@rasetti], relies on the existence of a subspace of states that, owing to special symmetry properties, are dynamically decoupled from the environment. The second approach, pionereed in [@shor] and closer in spirit to quantum control theory [@butko; @seth1], embraces today a variety of sophisticated schemes known as [*Error-Correcting Codes*]{} [@steane; @calderbank; @laflamme; @bennett; @gottesman; @cirac; @divincenzo; @schumacher; @vaidman; @luming; @slotine]. Basically, loss of information is corrected by monitoring the system and conditionally carrying on suitable feedback operations.
In this work we investigate a third strategy for reducing noise and decoherence. This strategy, which can be termed quantum “bang-bang” control after its classical analog [@bang], works by averaging out the unwanted effects of the environmental interaction through the application of suitable open-loop control techniques on the system. The basic idea is that open-system properties, specifically decoherence, may be modified if a time-varying control field acts on the dynamics of the system over time scales that are comparable to the memory time of the environment. In particular, we work out an exact model for a two-state quantum system ([*qubit*]{}) coupled to a thermal bath of harmonic oscillators, where decoherence is dynamically suppressed through repeated effective time-reversal operations on the combined system $+$ bath. Although the phenomenon is mathematically reminiscent of the quantum Zeno effect [@zeno], the essential physical idea comes from refocusing techniques in nuclear magnetic resonance spectroscopy (NMR) [@slichter]. Since the discovery of spin echoes in 1950 [@hahn], clever pulse methods have been developed in NMR to eliminate much of the dephasing arising from variations in the local magnetic field acting on each spin. Because the latter effect can be thought in terms of an interaction with some classical environment, it is not obvious [*a priori*]{} whether similar techniques work in the presence of a quantum mechanical environment and purely nonclassical effects like entanglement. Our result answers this question in the affirmative, and points out the role of the reservoir correlation time as a further parameter to be engineered in the struggle for preserving quantum coherence.
The plan of the paper is the following. In Section II, a general model of a two-state system interacting with a thermal environment is reviewed and its decoherence properties in the absence of control recalled. In Section III, the evolution under the action of a sequence of perturbative kicks is analyzed. Complete quenching of decoherence is established as a limiting situation. In Section IV, the conditions for an effective decoherence reduction are clarified with reference to a variety of possible environmental configurations and the method is compared to different quantum error-correction techniques. We close by discussing possibilities for future work.
Single-qubit dephasing mechanism
================================
Our goal is to investigate how decoherence properties of an open quantum system may be modified through the application of an external controllable interaction. Decoherence is a process whereby quantum systems lose their ability to exhibit coherent behavior such as interference [@gellmann; @zurek; @griffiths; @omnes]. We start by introducing a model that allows investigation of the problem in its simplest nontrivial configuration. The physical system we are interested in is a single two-state quantum system, representing the elementary memory cell of quantum information (qubit). Although not strictly necessary, it will be convenient to think of the physical qubit as realized by a spin-$1/2$ system, which will provide us with direct reference to the well established language of Nuclear Magnetic Resonance [@slichter] and the rapidly growing field of NMR quantum computation [@nmr; @nmr1]. Decoherence arises due to the coupling to a quantized environment, here schematized as a continuum of harmonic modes. We assume that the dynamics of the overall qubit $+$ bath is ruled by the following Hamiltonian: $$H_0 = H_S + H_B +H_{SB} = \hbar \omega_0 \, {\sigma_z \over 2} +
\sum_k \, \hbar \omega_k b_k^\dagger b_k +
\sum_k \, \hbar \sigma_z (g_k b_k^\dagger + g_k^\ast b_k) \;,
\label{hamiltonian}$$ where the first and second contribution $H_S$ and $H_B$ describe, respectively, the free evolution of the qubit and the environment, and the third term $H_{SB}$ describes a bilinear interaction between the two. $\sigma_z$ is the standard diagonal Pauli matrix, with qubit basis states denoted as $|i \rangle$, $i=0,1$, while $b_k^\dagger,b_k$ are bosonic operators for the $k^{\text{\small th}}$ field mode, characterized by a generally complex coupling parameter $g_k$. In the Schrödinger picture, the state of the combined system $(S+B)$ is represented by a density operator $\rho_{tot}(t)$ and the reduced qubit dynamics is thereupon recovered from a partial trace over the environment degrees of freedom: $$\rho_S(t)=\sum_{i,j=0,1} \, \rho_{ij}(t) \,|i \rangle \langle j| =
\mbox{Tr}_B \{ \rho_{tot}(t) \} \;.
\label{trace}$$ Hamiltonian (\[hamiltonian\]), which corresponds to a special case of the so-called spin-boson problem [@leggett], has been used by many authors to model decoherence in quantum computers [@unruh; @palma; @rasetti]. In particular, we adhere closely to the notations of [@palma]. The basic fact about the dynamics induced by (\[hamiltonian\]) is that, since $[\sigma_z, H_0]=0$, the interaction with the environment has the two memory states $|0\rangle, |1\rangle$ as eigenstates. In other words, the model describes a purely decohering mechanism, where no energy exchange between qubit and bath is present. In NMR terminology, this implies that no $T_1$-type of decay takes place [@slichter]. Equivalently, in terms of errors, only phase errors are introduced. However, neglecting the effects associated to quantum dissipation is justified, in a sense, by two related reasons: energy exchange processes not only produces amplitude errors which need to be corrected even in the classical computation, but they typically involve time scales much longer than decoherence mechanisms. In addition, being exactly soluble, the model (\[hamiltonian\]) has the advantage of allowing a clear picture of the decoherence properties in the absence of control. To this end, since spin populations are not affected by the environment, the relevant quantity is the qubit coherence $\rho_{01}(t)$ (of course, $\rho_{10}(t)=\rho_{01}^\ast(t)$).
It will be convenient to move to the interaction picture associated to the free dynamics $(H_S+H_B)$, corresponding to the transformed state vector $$\tilde{\rho}_{tot}(t)=\mbox{e}^{i (H_S+H_B)t/\hbar} \, \rho_{tot}(t) \,
\mbox{e}^{-i (H_S+H_B)t/\hbar}
\label{interaction}$$ and to the effective Hamiltonian $$\tilde{H}(t)=\tilde{H}_{SB}(t)= \hbar\sigma_z \sum_k \,
\Big( g_k b_k^\dagger \mbox{e}^{i \omega_k t} +
g_k^\ast b_k \mbox{e}^{-i \omega_k t} \Big) \;.
\label{effective}$$ Time evolution is determined by the time-ordered unitary operator $$\tilde{U}_{tot}(t_0,t)=T\exp\bigg\{ -{i \over \hbar} \int_{t_0}^t
ds \, \tilde{H}(s) \bigg\} \;,
\label{timeprod}$$ which can be evaluated exactly and can be written, up to a global $c$-number phase factor, in the following form: $$\tilde{U}_{tot}(t_0,t)= \exp\bigg\{ {\sigma_z \over 2}
\sum_k \Big( b_k^\dagger \mbox{e}^{i \omega_k t_0} \xi_k(t-t_0) -
b_k \mbox{e}^{-i \omega_k t_0} \xi_k^\ast(t-t_0) \Big) \bigg\} \;,
\label{timeop1}$$ where the following complex function has been introduced: $$\xi_k(\Delta t) = {2 g_k \over \omega_k} \,
\Big( 1- \mbox{e}^{i \omega_k \Delta t} \Big) \;.
\label{csi}$$ Note that the separate dependence of (\[timeop1\]) on both initial time $t_0$ and evolution interval $(t-t_0)$ is consistent with the time-reversal property $\tilde{U}_{tot}(t,t_0)\tilde{U}_{tot}(t_0,t)=\openone$. A nice discussion on the entanglement generated by $\tilde{U}_{tot}(t_0,t)$ between qubit and field states is given in [@palma]. We are interested in calculating $$\tilde{\rho}_{01}(t)=\langle 0|\, \mbox{Tr}_B \{ \,
\tilde{U}_{tot}(t_0,t) \tilde{\rho}_{tot}(t_0) \tilde{U}_{tot}^\dagger(t_0,t)
\, \} \, |1 \rangle \;.
\label{rho01}$$ This can be done without approximations under two standard assumptions:
$(i)\;$ qubit and environment are initially uncorrelated, i.e. $$\rho_{tot}(t_0)= \rho_S(t_0) \otimes \rho_B(t_0) \;;
\label{factorized}$$ $(ii)$ the environment is initially in thermal equilibrium at temperature $T$, i.e. $$\rho_B(t_0)= \prod_k \, \rho_{B,k}(T) = \prod_k \,
\Big( 1- \mbox{e}^{\beta \hbar \omega_k} \Big) \,
\mbox{e}^{-\beta \hbar \omega_k b_k^\dagger b_k } \;.
\label{thermal}$$ In Eq. (\[thermal\]), $\beta= 1/k_B\, T$, being $k_B$ the Boltzmann constant. For simplicity, we choose henceforth units such that $\hbar =k_B =1$. Conditions (\[factorized\])-(\[thermal\]) are easily translated to interaction picture and, inserting (\[timeop1\]) into (\[rho01\]), the problem is reduced to a single-mode trace: $$\tilde{\rho}_{01}(t) = \tilde{\rho}_{01}(t_0) \cdot \prod_k \,
\mbox{Tr}_k \Big\{\, \rho_{B,k}(T)
\, {\cal D} ( \mbox{e}^{i \omega_k t_0} \xi_k(t-t_0) ) \, \Big\}
= \tilde{\rho}_{01}(t_0) \cdot \mbox{e}^{ - \Gamma_0(t_0,t) }
\;, \label{singletrace}$$ where, in the first equality, the harmonic displacement operator ${\cal D}(\xi_k)$ is given by $${\cal D}(\xi_k) = \mbox{e}^{\, b_k^\dagger \xi_k - b_k \xi_k^\ast} \;,
\label{displace}$$ and the second equality defines the time-dependent function $\Gamma_0(t_0,t)$. The final step is to recognize that, for each mode, the quantity in curly brackets in (\[singletrace\]) is nothing but the symmetric order generating function for a thermal harmonic oscillator [@hillery]. Thus, the explicit expression for $\Gamma_0(t_0,t)$ is $$\Gamma_0(t_0,t)=\Gamma_0(t-t_0) = \sum_k \, { |\xi_k(t-t_0)|^2 \over 2}
\coth \bigg({\omega_k \over 2T} \bigg) \;.
% & = & \sum_k 4|g_k|^2 \coth\bigg({\omega_k \over 2T} \bigg)
%{1-\cos \omega_k(t-t_0) \over \omega_k^2} \;.
\label{gamma0}$$ Being $\Gamma_0$ a real function, it correponds to pure damping in (\[singletrace\]). Accordingly, this function characterizes completely the dynamics of the decoherence process destroying the qubit phase information. Of course, the complete evolution in the original Schrödinger picture includes oscillation at the natural frequency $\omega_0$, $$\rho_{01}(t)=\mbox{e}^{i \omega_0 (t-t_0) - \Gamma_0(t-t_0)} \,
\rho_{01}(t_0) \;,
\label{lab}$$ while, using (\[timeop1\]), one can check that $\rho_{ii}(t)=\rho_{ii}(t_0)$, $i=0,1$.
Deeper insight into the time dependence of the decoherence process is gained if the continuum limit is made explicit in (\[gamma0\]). By substituting $|\xi_k(t-t_0)|^2$ through (\[csi\]), we get $$\Gamma_0 (t-t_0) = \int_0^\infty d\omega \,
\bigg[ \sum_k \delta(\omega-\omega_k) |g_k|^2 \bigg]\,
4 \coth\bigg( {\omega \over 2T} \bigg)
{1-\cos \omega(t-t_0) \over \omega^2} \;.
\label{spectral}$$ The quantity in square brackets is known as the spectral density $I(\omega)$ of the bath. It turns out that, once the initial state is specified, complete information about the effect of the environment is encapsulated in this single function. As a general feature, the spectral density is characterized by a certain ultraviolet cut-off frequency $\omega_c$ such that $I(\omega) \rightarrow 0$ for $\omega > \omega_c$. Although the specific value of $\omega_c$ depends on a natural cut-off frequency varying from system to system, the existence of a finite $\omega_c$ is always demanded on physical grounds. Indeed, assuming that the environment does not have a high frequency cut-off means, generally, that energy can be dissipated instantaneously [@paz]. If, for instance, decoherence arises from the coupling to a phonon field, the natural cut-off frequency can be identified with the Debye frequency. In general, $\tau_c \sim \omega_c^{-1}$ sets the fastest time scale (or the memory time) of the environment. When a specific choice will be useful, we will assume a spectral density with the following functional form: $$I(\omega) = {\alpha \over 4} \, \omega^n \, \mbox{e}^{-\omega/\omega_c}
\;, \label{density}$$ the parameter $\alpha > 0$ measuring (in suitable units) the strength of the system-bath coupling and the index $n>0$ classifying different environment behaviors [@palma; @leggett; @paz].
In addition to $\tau_c$, another time scale $\tau_{\beta} \sim T^{-1}$, associated with the temperature of the bath, is expected to play a major role in the evolution of the qubit coherence. This is manifest if Eq. (\[spectral\]) is written in the equivalent form $$\Gamma_0 (t-t_0) = 4\, \int_0^\infty d\omega \, I(\omega)\,
\Big( 2\, \overline{n}(\omega,T) +1 \Big)\,
{1-\cos \omega(t-t_0) \over \omega^2} \;,
\label{spectral2}$$ where $\overline{n}(\omega,T)=\exp(-\omega/2T)
\mbox{cosech}(\omega/2T)$ is the average number of field excitations at temperature $T$. In this way, effects due to the thermal noise are formally separated from the ones due to purely vacuum fluctuations. Because of the different frequency composition, the two kinds of fluctuations dominate on different time scales, the relative importance of vacuum to thermal contributions being determined by $\tau_{\beta}$. This multiplicity of time scales is one of the factors that makes the decoherence process quite complicated. It should be important to keep in mind that there is [*no*]{} generic decohering behavior, and in particular that the qubit dynamics depends crucially on both temperature and the details of the spectral function $I(\omega)$. We will comment further on this point later.
Pulsed evolution of quantum coherence
=====================================
Let us now define a procedure aimed at modifying the decoherence properties discussed so far. We choose to implement it as a suitable perturbation acting on some observables $\{ {\cal O}_i\}$ of system $S$. This is obtained by adding to (\[hamiltonian\]) a time-dependent term $\sum_i \, \gamma_i(t) {\cal O}_i$, where the input functions $\{\gamma_i(t)\}$ are assumed to be programmable at will, e.g. a given schedule of time-varying magnetic fields in the case of a spin-qubit. In control terminology, this realizes a so-called open-loop configuration [@seth1]. Closed-loop (or feedback) configurations have been also proposed in recent years to manipulate decoherence in some quantum optical systems [@milburn]. There are many possible choices for the control Hamiltonian. Leaving aside the problem of controllability of the system (\[hamiltonian\]) at the abstract level, we make here a pragmatic choice, partly suggested by semiclassical considerations.
Suppose that the perturbation we add is able to induce spin-flip transitions. By inspection of the spin-bath interaction Hamiltonian $H_{SB}$, opposite contributions arise when the spin belongs to the down or up eigenstate. Since a relative minus sign will be present during time evolution, the effect of the $H_{SB}$ coupling will eventually average out provided the spin is flipped rapidly enough. There are two reasons why a mechanism of this kind is expected to be possible. First, as we already mentioned, similar methods are routinely used in NMR experiments to get rid of the effects of some unwanted interactions [@slichter]. For instance, in the so-called spin-flip narrowing, line broadening resulting from magnetic dipolar coupling is reduced by repetitively flipping the spins among distinct energy configurations. The major difference here is that the undesired decohering coupling is contributed by the infinitely-many quantized degrees of freedom of the heat bath. The second reason is related to the finite response time $\tau_c$ of the environment itself. In general, if perturbations act on the system more rapidly than this fastest time scale present in the bath, we expect that memory effects would be relevant, and that this non-Markovian dynamics would eventually lead to modified decoherence properties.
Having anticipated the intuitive idea, we start by writing the total Hamiltonian as $$H(t)=H_0 + H_{rf}(\omega_0,t) \;,
\label{ham2}$$ where $H_{rf}(\omega_0,t)$ represents a monochromatic alternating magnetic field applied at resonance. At this level, the problem can be related to variants of the complete spin-boson model, none of them is exactly solvable [@leggett]. The main simplification we introduce is to substitute the continuous-mode operation, where the actions of the bath and the controlling field are necessarily simultaneous, with a pulsed-mode operation analogous to classical “bang-bang” control. Then, under the working assumption that the typical decoherence time of the system and the duration of pulses define two widely different time scales, we solve the problem by putting
$(i)\;$ $H_{SB}=0$ within each pulse;
$(ii)$ $H_{rf}=0$ between successive pulses.
As usual, we invoke the rotating wave approximation and only look at the co-rotating component of the rf-field. The radiofrequency perturbation is assumed of the following form: $$H_{rf}(\omega_0,t)= \sum_{n=1}^{n_P}\, V^{(n)}(t) \Big[
\cos \Big( \omega_0(t-t^{(n)}_P)\Big) \sigma_x +
\sin \Big( \omega_0(t-t^{(n)}_P)\Big) \sigma_y \Big] \;,
\label{rf}$$ with $t^{(n)}_P = t_0 + n \Delta t$, $n=1,\ldots,n_P$, and $$V^{(n)}(t) = \left\{ \begin{array}{lc}
V \hspace{3mm} & t^{(n)}_P \leq t \leq t^{(n)}_P + \tau_P \;, \\
0 \hspace{3mm} & \text{elsewhere} \;.
\end{array} \right.
\label{V}$$ Eqs. (\[rf\])-(\[V\]) schematize a sequence of $n_P$ identical pulses, each of duration $\tau_P$, applied at instants $t=t^{(n)}_P$. The separation $\Delta t$ between pulses is assumed to be an input of the model. The amplitude of the field is equal to $V$ during each pulse and will be further specified below together with $\tau_P$. In order to depict the evolution associated to a given pulse sequence, it is convenient to think the latter as formed by successive elementary cycles of spin-flips, a complete cycle being able to return the spin back to the starting configuration. We begin by analyzing the time evolution during the first spin cycle.
[**A. The elementary spin-flip cycle**]{}
As in Sec. II, we exploit the interaction representation (\[interaction\]). Some instructive steps of an alternative derivation based on Heisenberg formalism are sketched in the Appendix. The interaction picture transformed Hamiltonian is now $$\tilde{H}(t)=\tilde{H}_{SB}(t) + \tilde{H}_{rf}(t) \;,
\label{effective2}$$ where $\tilde{H}_{SB}(t)$ is given in (\[effective\]), and $\tilde{H}_{rf}(t)$ is evaluated by using (\[rf\]) and the properties of Pauli matrices. We get $$\tilde{H}_{rf}(t)= \sum_{n=1}^{n_P} \, V^{(n)}(t) \,
\mbox{e}^{i \omega_0 {\sigma_z \over 2} t^{(n)}_P } \sigma_x
\mbox{e}^{-i \omega_0 {\sigma_z \over 2} t^{(n)}_P } \;.
\label{rftilde}$$ According to (\[rftilde\]), the time dependence due to the rotating field is completely removed within each pulse. In fact, the interaction representation (\[interaction\]) on spin variables is identical, at resonance, with the description in the rotating frame associated to (\[rf\]) [@slichter]. The counter-rotating term that is omitted within RWA is seen to be negligible at resonance. For the first spin cycle, $n_P=2$ and we have the following sequence: evolution under $\tilde{H}_{SB}(t)$ during $t_0 \leq t \leq t^{(1)}_P$; pulse $P_1$ at time $t^{(1)}_P$; evolution under $\tilde{H}_{SB}(t)$ during $t_P^{(1)}+\tau_P \leq t \leq t^{(2)}_P$; pulse $P_2$ at time $t^{(2)}_P$. After a total time $t_1=t_0 + 2 \Delta t+ 2 \tau_P$, the first cycle is complete. In terms of evolution operators, we have: $$\tilde{U}_P(t_0,t_1)= \tilde{U}_{P_2} \tilde{U}_{P_1} \,\Big[
\tilde{U}_{P_1}^{-1} \tilde{U}_{tot}(t^{(1)}_P + \tau_P, t^{(2)}_P)
\tilde{U}_{P_1} \Big] \Big[ \tilde{U}_{tot}(t_0,t^{(1)}_P) \Big ] \;.
\label{timeop2}$$ We can read the evolutions in the absence of rf-field directly from (\[timeop1\]), for instance $$\tilde{U}_{tot}(t_P^{(1)}+\tau_P,t^{(2)}_P)= \exp\bigg\{ {\sigma_z \over 2}
\sum_k \Big( b_k^\dagger \mbox{e}^{i \omega_k (t_0+\Delta t+ \tau_P)}
\xi_k(\Delta t) - b_k \mbox{e}^{-i \omega_k (t_0+\Delta t + \tau_P)}
\xi_k^\ast(\Delta t) \Big) \bigg\} \;.
%\label{timeop1}$$ Concerning the evolution operator associated to the generic $j^{\text{\small th}}$ pulse, this is found by exponentiating (\[rftilde\]) ($n=j$): $$\tilde{U}_{P_j}=\exp\Big\{ -i \,V \tau_P \,
\mbox{e}^{i \omega_0 {\sigma_z \over 2} t^{(j)}_P } \sigma_x
\mbox{e}^{-i \omega_0 {\sigma_z \over 2} t^{(j)}_P } \Big\} =
\mbox{e}^{i \omega_0 {\sigma_z \over 2} t^{(j)}_P }
\mbox{e}^{-i V \tau_P \sigma_x}
\mbox{e}^{-i \omega_0 {\sigma_z \over 2} t^{(j)}_P } \;.
\label{timep}$$ In order to proceed, we have to say more about pulses. We require $$\{ \tilde{U}_{P_1}, \sigma_z \} =0 \;, \hspace{3cm}
[ \tilde{U}_{P_2} \tilde{U}_{P_1}, \sigma_z] =0 \;,
\label{pulses}$$ $\{\,,\,\}$ and $[\,,\,]$ denoting anticommutator and commutator respectively. These conditions imply, as expected from the intuitive explanation, that $P_1,P_2$ are $\pi$-pulses, satisfying $2\,V\tau_P= \pm \, \pi$. To simplify things, we imagine that $\tilde{H}_{rf}(t)$ is large enough to produce (almost) instantaneous spin-flips. Accordingly, $\tau_P \rightarrow 0$ henceforth and we have to deal with ideal “kicks” of infinite power. Putting things together, we find $$\tilde{U}_{P_2}\tilde{U}_{P_1} = - \, \mbox{e}^{i \omega_0 {\sigma_z \over 2}
(t_1-t_0) } \;,$$ $$\tilde{U}_{P_1}^{-1} \tilde{U}_{tot}(t^{(1)}_P, t^{(2)}_P)
\tilde{U}_{P_1} =
\exp\bigg\{ - {\sigma_z \over 2}
\sum_k \Big( b_k^\dagger \mbox{e}^{i \omega_k (t_0+\Delta t)}
\xi_k(\Delta t) - b_k \mbox{e}^{-i \omega_k (t_0+\Delta t)}
\xi_k^\ast(\Delta t) \Big) \bigg\} \;,
\label{transformed}$$ and we are therefore ready to write down the final result for the cycle evolution operator: $$\tilde{U}_P(t_0,t_1) =
\exp\bigg\{ i \omega_0 \, {\sigma_z \over 2} (t_1-t_0) +
{\sigma_z \over 2}
\sum_k \Big( b_k^\dagger \mbox{e}^{i \omega_k t_0}
\eta_k(\Delta t) - b_k \mbox{e}^{-i \omega_k t_0}
\eta_k^\ast(\Delta t) \Big) \bigg\} \;,
\label{pulsed}$$ where, as before, $c$-number phase factors have been omitted and $$\eta_k(\Delta t) =\xi_k (\Delta t)
\Big(\mbox{e}^{i \omega_k \Delta t} -1 \Big) =
- {2 g_k \over \omega_k} \Big( 1-\mbox{e}^{i \omega_k \Delta t} \Big)^2 \;.
\label{eta}$$ It is interesting to compare the evolution described by (\[pulsed\]) with the one in the absence of pulses. By recalling (\[timeop1\]), evaluated at time $t_1=t_0 + 2 \Delta t$, we report two differencies: a phase factor proportional to $\sigma_z$ and the duration of the cycle; a combination $\eta_k(\Delta t) \propto (\xi_k(\Delta t))^2$ in place of $\xi_k (2 \Delta t)$. The first difference corresponds to the fact that, due to the pulses, the oscillation at the natural frequency $\omega_0$ is lost once the evolution is transferred back to Schrödinger picture (see (\[lab\])). The second difference, as it will be seen in a moment, is the signal that decoherence properties are modified.
[**B. Decoherence properties after a pulse sequence**]{}
The next step is to generalize the description to an arbitrary number $N$ of elementary spin-flip cycles, the $n^{\text{\small th}}$ cycle ending at time $$t_n=t_0 + 2 n \Delta t \;, \hspace{3cm}n=1,\ldots,N\;,
\label{endtime}$$ and the number of $\pi$-pulses involved in the sequence being $n_P=2N$. This is straight forward since Eq. (\[pulsed\]) enables us to write down the evolution operator for the $n^{\text{\small th}}$ cycle: $$\tilde{U}_P(t_{n-1},t_n) =
\exp\bigg\{ i \omega_0 \, {\sigma_z \over 2} 2\Delta t +
{\sigma_z \over 2}
\sum_k \Big( b_k^\dagger \mbox{e}^{i \omega_k t_{n-1}}
\eta_k(\Delta t) - b_k \mbox{e}^{-i \omega_k t_{n-1}}
\eta_k^\ast(\Delta t) \Big) \bigg\} \;.
\label{pulsedn}$$ The time development corresponding to $N$ cycles is then governed by the time-ordered finite product $$\tilde{U}_P^{(N)}(t_0,\ldots,t_N) = \tilde{U}_P({t_{N-1},t_N}) \ldots
\tilde{U}_P(t_1,t_2)
\tilde{U}_P(t_0,t_1)
\;. \label{finitep}$$ Note that, at variance with conventional spin-flip narrowing [@slichter], $\tilde{U}^{(N)}_P \neq (\tilde{U}_P)^N$, the dependence on intermediate times $\{t_j\}$ in the sequence being introduced by the environment dynamics. A closed formula for $\tilde{U}^{(N)}_P(\{t_j\})$ can still be found quickly since, by neglecting state-independent global phase factors that are irrelevant to density matrix propagation, we are allowed to treat the factors in (\[finitep\]) as commuting operators. We get $$\tilde{U}_P^{(N)}(t_0,\Delta t) =
\exp\bigg\{ i \omega_0 \, {\sigma_z \over 2} 2N \Delta t +
{\sigma_z \over 2}
\sum_k \Big( b_k^\dagger \mbox{e}^{i \omega_k t_0}
\eta_k(N,\Delta t) - b_k \mbox{e}^{-i \omega_k t_0}
\eta_k^\ast(N,\Delta t) \Big) \bigg\} \;,
\label{sequence}$$ where $$\eta_k(N,\Delta t) = \eta_k(\Delta t)\sum_{n=1}^N \,
\mbox{e}^{2i(n-1)\omega_k \Delta t}\;,
\label{etak}$$ and definition (\[endtime\]) has been exploited. Of course, the results of Sec. IIIA are recovered for $N=1$. A more interesting check can be done by relating the evolution (\[sequence\]) to the corresponding propagator in the absence of pulses. The trick is to switch back the minus sign in the definition (\[eta\]) of $\eta_k(\Delta t)$, that has been recognized as the key dynamical effect due to the pulsing procedure. Since $\xi_k(\Delta t )(\mbox{e}^{i \omega_k \Delta t} +1)= \xi_k(2 \Delta t)$, we are left with $$\xi_k(2\Delta t )\sum_{n=1}^N \mbox{e}^{2i (n-1)\omega_k \Delta t}
= \, \xi_k(2 N\Delta t) = \xi_k(t_N-t_0)$$ in place of (\[etak\]). Therefore, this procedure gives $$\tilde{U}_{tot}(t_0,t_N) =
\exp\bigg\{ {\sigma_z \over 2}
\sum_k \Big( b_k^\dagger \mbox{e}^{i \omega_k t_0}
\xi_k(t_N-t_0) - b_k \mbox{e}^{-i \omega_k t_0}
\xi_k^\ast(t_N-t_0) \Big) \bigg\} \;,$$ which does agree with the direct evaluation based on (\[timeprod\]). It may be worth some times to let the connection with unperturbed evolution be explicit, which is done by writing $$\eta_k(N,\Delta t)=\xi_k(2 N \Delta t) - 2 \,\xi_k (\Delta t) \sum_{n=1}^N
\mbox{e}^{2i (n-1)\omega_k \Delta t} \;,
\label{eta2}$$ where the contribution due to the pulse sequence shows up in the form of a typical interference factor.
The decoherence properties corresponding to the pulsed qubit $+$ bath evolution (\[sequence\]) are derived through the steps outlined in Sec. II for the unperturbed case. Incidentally, we still expect that spin populations are unchanged after a sequence of $N$ complete spin cycles, while qubit coherence at final time $t_N=t_0 + 2N \Delta t$ is given by $$\tilde{\rho}_{01}(t_N)=\langle 0|\, \mbox{Tr}_B \{ \,
\tilde{U}_P^{(N)}(t_0,\Delta t) \tilde{\rho}_{tot}(t_0)
\tilde{U}_P^{(N)\,\dagger} (t_0,\Delta t) \, \} \, |1 \rangle \;.
\label{rho01p}$$ The result is $$\tilde{\rho}_{01}(t_N)=\mbox{e}^{-i \omega_0 (t_N-t_0) -
\Gamma_P(N,\Delta t)} \, \tilde{\rho}_{01}(t_0) \;,
\label{lab2}$$ where $$\Gamma_P(N, \Delta t) = \sum_k \, { |\eta_k(N,\Delta t)|^2 \over 2} \,
\coth\bigg( {\omega_k \over 2T} \bigg) \;.
\label{gammap}$$ Comparing with (\[gamma0\]), the mathematical prescription for decoherence in the presence of pulses looks very simple: just use $\eta_k(N,\Delta t)$ instead of $\xi_k(t_N-t_0)$ for each mode of the bath. However, the final effect leading to (\[gammap\]) is not easy to figure out and it is useful to compare first the decoherence due to a single mode with frequency $\omega$ with and without pulses respectively. Apart from identical time-independent factors, we have to consider $$|\eta(N,\omega\Delta t)|^2 = 4 \, (1-\cos \omega\Delta t)^2 \, \Big[
N+ \sum_{n=0}^{N-1} \, 2 n \cos\Big( 2(N-n) \omega \Delta t\Big) \Big] \;,
\label{uno}$$ vs. $$|\xi (N,\omega \Delta t)|^2 = 2 \,(1- \cos 2N \omega \Delta t ) =
2 \,(1-\cos \omega (t_N-t_0)) \;,
\label{due}$$ where (\[csi\]) and (\[etak\]) have been used and an identical proportionality factor is understood. The unperturbed contribution $|\xi|^2$ simply oscillates between values $0,4$ with a period $(\pi/N)$. The function $|\eta|^2$, instead, is strongly oscillating for increasing $N$, developing $2(N-1)$ local minima and a sharply-peaked absolute maximum at $\omega \Delta t=\pi$. Constructive interference is highest at the maximum, leading to a value $|\eta|^2_{\text{\small Max}}=16\,N^2$ that can be very large, while destructive interference strongly damps the function for $\omega \Delta t
< \pi/2$, which is a zero for both $|\eta|^2$ and $|\xi|^2$ for any $N$. One can show that $$|\eta(N, \omega \Delta t) |^2 \, \leq \, |\xi(N, \omega \Delta t) |^2
\hspace{2cm}\text{on }[0, {\pi / 2} ] \text{ for any } N\;.
\label{diff}$$ Back to decoherence properties, condition (\[diff\]) means that, for a mode at frequency $\omega$, a finite region $\omega \Delta t \leq \pi/2$ exists, where the contribution to decoherence is [*smaller*]{} in the presence of pulses. Since the “correcting region” is entered for small $\Delta t$ values, this effect takes place in the regime of rapid flipping we expected. Since, moreover, smaller $\Delta t$ values require longer pulse sequences in order to evolve the system over the same interval, it is useful to consider an interesting limiting case.
[**C. The limit of continuous flipping and suppression of decoherence**]{}
Let us study an idealized situation represented by the following mathematical limit: $$\left\{ \begin{array}{c}
\Delta t \rightarrow 0 \;, \\
N \rightarrow \infty \;, \\
2N\Delta t = t_N-t_0 \;.
\end{array} \right.
\label{limit}$$ It is convenient to rewrite the decoherence function (\[gammap\]) by exploiting (\[eta2\]) to separate formally the unperturbed and the interference contributions. Thus $$\Gamma_P(N,\Delta t)=\sum_k \, {|\xi_k(2N \Delta t)|^2 \over 2} \,
\coth\bigg( {\omega_k \over 2T}\bigg) \,\Big| 1-f_k(N,\Delta t) \Big|^2\;,
\label{gammap2}$$ where $$f_k(N,\Delta t)= 2\, {\xi_k(\Delta t) \over \xi_k(2N\Delta t)}
\sum_{n=1}^N \,\mbox{e}^{2i (n-1)\omega_k \Delta t }\;.
\label{fk}$$ In this way, $\Gamma_0(t_N-t_0)$ is recovered by putting $f_k=0$ for each mode, see (\[gamma0\]). We evaluate the asymptotic limit of $f_k(N, \Delta t)$ as follows: $$\begin{aligned}
\lim_{\Delta t \rightarrow 0} f_k(N, \Delta t) & = &
{ \mbox{e}^{-i\omega_k t_0} \over 1-\mbox{e}^{i \omega_k(t_N-t_0)} }
\lim_{\Delta t \rightarrow 0}
{ (1-\mbox{e}^{i \omega_k \Delta t}) \over \Delta t }
\sum_{n=1}^N \, 2 \Delta t \, \mbox{e}^{i \omega_k t_{n-1} } \nonumber \\
& = &
{ \mbox{e}^{-i\omega_k t_0} \over 1-\mbox{e}^{i \omega_k(t_N-t_0)} }
\lim_{\Delta t \rightarrow 0}
{ (1-\mbox{e}^{i \omega_k \Delta t}) \over \Delta t }
\int_{t_0}^{t_N} ds\, \mbox{e}^{i \omega_k s} \nonumber \\
& = &
\lim_{\Delta t \rightarrow 0}
\bigg[ {\sin \omega_k \Delta t \over \omega_k \Delta t} + i \,
{1- \cos \omega_k \Delta t \over \omega_k \Delta t} \bigg] =\, 1 \;.
\label{limit2}\end{aligned}$$ If this result holds for an arbitrary field mode, then the implications for the decoherence properties are transparent: $$\lim_{\Delta t \rightarrow 0} \Gamma_P(N, \Delta t) =0\;,
\label{suppress}$$ i.e. in the limit of continuous flipping, decoherence is completely and exactly eliminated for any temperature and any spectral density function.
Obviously, there is no hope that a continuous limit of this kind would be ever attained in practice. However, situation (\[limit\]) should be approached if $\Delta t$ is made small compared to the fastest characteristic time present in the dynamics of the system. From the considerations of Sec. II, the environment correlation time $\tau_c$ certainly provides a lower bound since there is no spectral content of the environmental noise at frequency higher than $\omega_c$. Hence, we expect that a sufficient condition in order to meet (\[limit\]) is $$\omega_c \, \Delta t \lesssim 1 \;.
\label{condition}$$ The question on whether we can do better than this may be not completely obvious, since time scales different from $\tau_c$ are also involved in the decoherence process. In what follows, we try to understand this point both by presenting a physical explanation for the decoherence suppression and by analyzing some specific situations.
[**D. Physical interpretation**]{}
People familiar with quantum Zeno effect [@zeno] may have found some similarities with the behavior we are discussing. In particular, the basic mathematical modification associated with pulses is a function $|\eta_k|^2$, which is O$(\omega_k^4 \Delta t^4)$ for short time intervals, compared to $|\xi_k|^2=\mbox{O}(\omega_k^2 \Delta t^2)$. Moreover, (\[limit\]) is formally the same continuous limit involved in many quantum Zeno related proposals, notably the one by Cook [@cook]. In both cases, a preexisting dynamics - the qubit $+$ bath evolution here, a stimulated two-level transition in Cook’s scheme - is modified through a pulsing procedure. Pulses respectively represent spin-flip interactions, short enough that the action of the bath is made negligible, or measurement pulses, long enough that the coupling to the external environment (the measuring apparatus) is made appreciable. A dynamical inhibition phenomenon occurs when pulses become sufficiently frequent. One can say that two opposite configurations are realized for decoherence: with continuous measurements, the interaction with the bath is always “on” and internal dynamics becomes frozen; in the limit of continuous flipping, it is the two-level controlled dynamics that dominates, and the interaction with the bath tends to be always “off”, as indicated by (\[suppress\]). However, the analogy stops from a more physical point of view.
A more interesting interpretation of the decoherence suppression (\[suppress\]) can be obtained by connecting it to effects already observed in magnetic resonance experiments, like spin-echoes, solid-echoes, or spin-flip narrowing [@slichter]. All of these are basically time-reversal experiments. In order to capture the basic physical mechanism of our model, let us go back to the elementaty spin-cycle (Sec. IIIA) and look more carefully at the evolution operator (\[timeop2\]). This is made of two pieces: a free evolution during the first $\Delta t$, followed by an evolution governed by (\[transformed\]) during the second interval $\Delta t$. It is this transformed operator that [*simulates*]{} the effect of a time-reversal. In fact, backward propagation during the second part of the cycle would correspond to $$\tilde{U}_{tot}(t_0+\Delta t, t_0)= \exp\bigg\{ - {\sigma_z \over 2}
\sum_k \Big( b_k^\dagger \mbox{e}^{i \omega_k t_0}
\xi_k(\Delta t) - b_k \mbox{e}^{-i \omega_k t_0}
\xi_k^\ast(\Delta t) \Big) \bigg\} \;,
\label{back}$$ By comparison with (\[transformed\]), forward propagation in the presence of rf-kicks only differs for an additional term $\mbox{e}^{i \omega_k \Delta t}$ affecting each mode. This phase factor, due to the dynamics of the bath oscillators, is ultimately responsible for the decoherence properties in the pulsed evolution of the system. If not for this phase difference between (\[transformed\]) and (\[back\]), we would have $\eta_k(\Delta t)=0$ and no decoherence. Instead, reversal is approximate since the bath restarts at time $t_0+\Delta t$ after the first pulse with a dephased initial condition (see also Appendix). However, if $\mbox{e}^{i \omega_k \Delta t} \approx 1$ for each mode, then the couple of kicks produces an exact time-reversal and, by iteration, we arrive at (\[suppress\]). Equivalently, if the bath Hamiltonian can be considered as a constant, then the total Hamiltonian (\[hamiltonian\]) acquires a minus sign and the system retraces the previous evolution. The validity of this condition depends on the time scale we are considering. For a single mode of frequency $\omega$, the time needed to produce appreciable dephasing is $\tau \approx \omega^{-1}$, so we expect decoherence correction for $\tau/\Delta t \gtrsim 1$. This is in agreement with both the interpretation of (\[diff\]) and the semiclassical NMR argument [@slichter], where motional effects are predicted for $\tau$ comparable to the mean time spent in a given spin configuration (here $\Delta t$). For the whole environment, the correlation time $\tau_c$ is the minimum time scale over which the dynamics is approximately unchanged, and the same reasoning leads to a physical explanation of the rapid flipping condition (\[condition\]).
As a final remark, we point out that the mechanism accomplishing time-reversal in our model is purely [*macroscopic*]{} in the sense that no reference is made to the dynamical state of the system. This is different from the familiar case of the Maxwell demon, that effectively reverses a dynamical evolution by operating over some microscopic variables (like velocities) at a given instant. Rather, the reversal is obtained by changing the sign of the system Hamiltonian through the action of suitable external fields (control). A different kind of demon, the so-called Loschmidt demon, has been introduced by some authors to account for this behavior [@pines]. In this terminology, the spin-flip procedure realizes in principle a Loschmidt demon for a decohering qubit.
Analysis and examples
=====================
In this section we try to give some semiquantitative picture of the decoherence mechanisms discussed so far. We focus our attention on a representative class of reservoirs, corresponding to so-called Ohmic environments. The appropriate spectral density is given by (\[density\]) with $n=1$. The time dependence of the decoherence is summarized by the following expression: $$\Gamma(t)=\alpha \, \int_0^\infty d\omega \,
\mbox{e}^{-\omega/\omega_c} \Big( 2\,\overline{n}(\omega,T) + 1 \Big) \,
{ 1- \cos \omega t \over \omega} \,
\Big| 1-f(\omega,N,\Delta t) \Big|^2\;,
\label{ohmic}$$ where we assume $t_0=0$. Eq. (\[ohmic\]) reproduces the unperturbed behavior of Sec. II when $f=0$, in which case $\Gamma(t) = \Gamma_0(t)$, Eq. (\[gamma0\]). In the presence of $N$ spin-flip cycles, Eq. (\[ohmic\]) is found from the continuous limit of $\Gamma_P(N,\Delta t)$ in (\[gammap\]), with $f(\omega,N,\Delta t)$ given by (\[fk\]). According to Sect. III, in this case we are interested at decoherence after a complete pulse sequence, i.e. $t=t_N=2N \Delta t$. For a fixed strength $\alpha$ of the system-reservoir coupling, the properties of the environment enter (\[ohmic\]) with two parameters, $\omega_c \sim \tau_c^{-1}$, $T \sim \tau_{\beta}^{-1}$.
Let us first analyze decoherence in the absence of any correction, $f=0$. Qualitatively different behaviors arise depending on the relationship between the cut-off frequency $\omega_c$ and the thermal frequency $\omega_{\beta}=T$. Typically, two extreme situations are considered.
$(i)\;$ $\omega_c \ll \omega_{\beta}$: high-temperature limit or [*classical*]{} environment:
Decoherence dynamics is relatively easy to describe in this regime since, due to the exponential dependence on the cut-off, $\omega_c$ is actually the only characteristic frequency accessible to the system. The environment looks classical in the sense that its quantized structure cannot be appreciated compared to the thermal quantum $\omega_{\beta}$. Accordingly, thermal fluctuations always dominate over vacuum ones and, after a short transient O$(\tau_{\beta})$ where decoherence is almost ineffective, dynamics becomes very fast and coherence is lost completely after a time comparable to $\tau_c$. In general, one expects that in this limit equivalent results are obtained by assuming a heat bath of classical harmonic oscillators. A mixed quantum-classical derivation for a two-state open system is given for instance in [@grigo].
$(ii)$ $\omega_c \gg \omega_{\beta}$: low-temperature limit or [*quantum*]{} environment:
In this limit a more complex interplay between thermal and vacuum effects arises. Thermal fluctuations are only effective for $t > \tau_{\beta}$ and, due to the exponential suppression of $\overline{n}(\omega,T)$, they are almost totally contributed by low frequency modes $\omega \lesssim \omega_{\beta}$. The effects of vacuum fluctuations dominate on an intermediate region $\tau_c < t < \tau_{\beta}$, a nonvanishing contribution remaining, however, at longer time scales $t > \tau_{\beta}$. The frequency composition of the fluctuations is now less clear: while modes below the thermal threshold are still responsible for the long-time dynamics $t > \tau_{\beta}$, frequencies in the range up to $\omega_c$ mostly contribute for $t < \tau_{\beta}$ but are also present beyond $\tau_{\beta}$. As a consequence, even at thermal time scales $t > \tau_{\beta} \gg \tau_c$, high frequency modes contribute appreciably to the decoherence process and characteristic times O$(\tau_c)$ are still relevant in the underlying dynamics.
Typical decoherence curves $\mbox{e}^{-\Gamma(t)}$ for the Ohmic environment are found by numerical integration of (\[ohmic\]) and are shown in Fig. 1 for two choices corresponding to high- and low-temperature limit, $\omega_c/T=10^{-2}$ and $\omega_c/T=10^2$ respectively. The partial contributions due to thermal and vacuum fluctuations are indicated separately where possible. In the low-temperature case, a quiet ($t<\tau_c$), a quantum ($\tau_c < t < \tau_{\beta}$) and a thermal ($t > \tau_{\beta}$) regime are easily identified in the process, as indicated above and discussed in more detail by many authors [@unruh; @palma; @leggett]. In both configurations, the qubit coherence decays exponentially fast once the thermal regime is well established, $$\mbox{e}^{-\Gamma(t)} \approx \mbox{e}^{-t/t_{th}} \;,
\label{tth}$$ for a suitable time constant $t_{th}$. In models where the decoherence rate is constant in time, Eq. (\[tth\]) is usually assumed as the definition of a typical decoherence time, $t_{dec}=t_{th}$. In our case, since the whole behavior of $\Gamma(t)$ is required for a complete knowledge of the decoherence dynamics, the definition of a characteristic time for loss of unitarity is less clear. Oversimplifying things, the situation can be summarized as follows: for both the high- and the low-temperature regimes, a characteristic time exists, indicating the departure of coherence from unity. This time is determined by the shortest between the two time scales $\tau_c, \tau_\beta$. Once this transient is over, the duration of the actual decoherence process is at least comparable to $\tau_c$ in the classical environment, and to $\tau_\beta$ in the quantum one. If this information is used as an estimate for a characteristic decoherence time, we are lead to $t_{dec}\approx \mbox{O}(\tau_c/\alpha)$ for the high-temperature limit and $t_{dec}\approx \mbox{O}(\tau_\beta/\alpha)$ for the low-temperature limit respectively. For identical values of $\alpha$ and $\omega_c$, decoherence occurs extremely faster in the former case, as expected on intuitive grounds.
We now come back to examine how decoherence is improved in the presence of spin-flip cycles. With the interference contribution $f$ restored in (\[ohmic\]), we have calculated numerically the decoherence values obtained when a fixed time interval $t$ is divided in an increasing number of cycles of duration $2 \Delta t$, i.e. $$\Delta t = {t \over 2N}\;, \hspace{2cm}N=1,2,\ldots,N_{\text{max}}\;.$$ The behavior of $\mbox{e}^{-\Gamma(t)}$ as a function of the pulse frequency $1/\Delta t$ has been studied, and the procedure repeated for different representative times. The results for the high- and low-temperature reservoirs considered above are shown in Figs. 2, 3 respectively. The unperturbed values of decoherence at the appropriate times can be read from Fig. 1. We see that, as predicted by (\[suppress\]), decoherence-correction starts as soon as the region $\tau_c/\Delta t \gtrsim 1$ is entered. For times short enough that $\omega_c \,t < 2N$, this may by even accomplished with a single cycle. In general, once this condition is fulfilled, no further reduction of $\Delta t$ is demanded to evolve the system in a decoherence-free way. However, a warning also emerges from Fig. 3: if flipping is not frequent enough, not only does the correction effect disappear, but decoherence can be actually made worse compared to the one in the absence of pulses. The explanation of this behavior is rooted into the interference mechanism that builds up the correction factor (\[eta\]): in a sense, decoherence can be subtracted almost completely from the frequency range $\omega \Delta t \lesssim 1$ only at the expense of enhancing the decoherence contributions from modes outside that region. This intrinsic feature of the model is also relevant to understand why, despite of the differences existing between the high- and low-temperature decoherence properties, the same condition $\omega_c \Delta t \lesssim 1$ is required to prevent both thermal and vacuum noises. In fact, this condition comes quite natural for a classical environment, but one might at first wonder why a weaker condition $\omega_{\beta} \Delta t \lesssim 1$ would not suffice for the quantum case, even if the frequencies $\omega \lesssim \omega_{\beta}$ contain the fraction that mostly contributes at times of the order of $t_{dec}$. The reason for this failure is the presence of vacuum fluctuations. By satisfying condition $\omega_{\beta} \Delta t \lesssim 1$, we do get rid of thermal dephasing, but we do not correct completely vacuum noise until $\omega_c \Delta t \lesssim 1$. Precisely, we are missing modes of intermediate frequency $\omega_{\beta} \lesssim \omega \lesssim \omega_c$ that, although of minor importance at long times, may introduce amplified decoherence contributions if not properly corrected.
We conclude with a few comments on the relevance of our procedure for quantum information processing. While the idealized character of the model prevents us from a quantitative discussion of implementation criteria, we can compare with the principles underlying current quantum error-correction proposals. Essentially, these are schemes to encode redundantly information in such a way that it can be restored also when errors due to external sources have occurred. The syndrome-identification and the error-correction stages may be regarded as a feedback configuration: suitable measurement protocols are required both in conventional schemes [@shor; @steane; @calderbank; @laflamme; @bennett; @gottesman; @cirac; @divincenzo; @schumacher] and in alternate techniques based on the quantum Zeno effect [@vaidman; @luming], while conditional logic is exploited in the coherence-preserving routines proposed in [@slotine]. In any case, error-correction methods have the effect of reducing the error rate per unit time and, in order to be effective, they must be repeated at time intervals $\Delta t$ shorter than the typical decoherence time of the system, i.e. $t_{dec}/\Delta t
\gtrsim 1$. In comparison to quantum error correction schemes, our procedure exhibits two fundamental differences: no ancillary bits are required to store the information; no measurements are performed. In principle, these could be advantageous features, since encoding would be more efficient and, by avoiding measurements, no slow-down of the computational speed would be introduced. In addition, rather than reducing the error rate, this method would suppress completely the error source provided the appropriate condition $\tau_c /\Delta t \gtrsim 1$ is fulfilled. From a more practical perspective, it is the accessibility of this rapid flipping limit, demanding fast and short pulses, $\tau_c /\Delta t \gtrsim 1$ and $\tau_P /\Delta t \ll 1$, that determines the viability of the procedure itself. If such requirements can be satisfied, our method might be valuable in configurations where $t_{dec}$ tends to be shorter than $\tau_c$ [@nota2] or, even in case $t_{dec}$ is longer compared to $\tau_c$, for systems where tipping the state is easier than exploiting conventional error-correction protocols. While the existence of an interaction able to implement a NOT gate by inverting the state is demanded for any two-level system relevant to quantum computation, both the present technological capabilities for applying $\pi$-pulses and the relevant environmental cut-off frequencies depend considerably on the specific physical system and the mechanism responsible for decoherence. Some important time scales for various prospective qubits can be found in [@review].
Conclusions
===========
Our work demonstrates the possibility to modify the evolution of a quantum open system through the application of an external controllable interaction. A prototype situation involving a two-level system coupled to a quantized reservoir in thermal equilibrium has been worked out in detail and dynamical suppression of quantum decoherence has been evidenced. From the perspective of quantum information, the analysis suggests a different direction compared to conventional quantum error-correction techniques, based on the idea of forcing the system into a dynamics that disturbs the decoherence process. Our present study for a specific example brings up, among other issues, the question of whether similar decoherence correction mechanisms would be operating under more general conditions, including either different open system dynamics, or different control configurations, or both. In particular, an interesting possibility could emerge from examining decoherence properties within a fully quantum mechanical description where the control degrees of freedom are explicitly included and the system is driven by a quantum controller as recently proposed in [@seth1].
One of us (L. V.) is grateful to Carlo Presilla for enlightening discussions and a critical reading of the manuscript. This work was supported by ONR, by AFOSR, and by DARPA/ARO under the Quantum Information and Computation initiative (QUIC) and the NMR Quantum Computing initiative (NMRQC).
Heisenberg representation
=========================
Compared to the interaction picture, the Heisenberg representation has two advantages: first, it does not require preliminary transformations on the state vector; second, it gives to a certain extent a more intuitive description of the spin motion. In this Appendix, we outline the evolution of the qubit coherence, by restricting ourselves to the first elementary spin-flip cycle. In the Heisenberg picture, the relevant information is contained in $$\sigma_+(t) = {1 \over 2} \Big( \sigma_x(t) + i\, \sigma_y(t) \Big) \;,
\label{a1}$$ since, by averaging over the quantum state, $\langle \sigma_+(t) \rangle =
\rho_{01}(t)$. As in Sec. III, we evaluate the qubit dynamics under the separate action of the spin-bath Hamiltonian $H_{SB}$ and the radiofrequency perturbation $H_{rf}$. The description of a $\pi$-pulse turns out to be extremely simple in the Heisenberg representation. Nothing happens to the bath operators $b_k,b^\dagger_k$ in the limit of instantaneous pulses, while spin dynamics is governed by the equations $$\dot{\sigma}_\alpha = -i\,\Big[\sigma_\alpha, \Big(
H_S+H_{rf}(\omega_0,t) \Big) \Big]\;, \hspace{2cm}\alpha=x,y,z\;,
\label{a2}$$ with $H_{rf}(\omega_0,t)$ given in (\[rf\]). By denoting with $t_P^{-\,(+)}$ the instants immediately before (after) a pulse respectively, a very simple result is found: $$\left\{ \begin{array}{lcl}
\sigma_z(t^+_P) & = & -\, \sigma_z(t^-_P)\;, \\
\sigma_+(t_P^+) & = & (\sigma_+(t_P^-))^\dagger\;.
\end{array} \right.
\label{a3}$$ The action on $\sigma_z$ corresponds, in particular, to the pictorial spin-flip effect operated by a $\pi$-pulse. Now denote as $G_{tot}(t_i,t_j)$ the operator evolving coherence from $t_i$ to $t_j$ in the absence of rf-pulses, i.e. $$\sigma_+(t_j)= G_{tot}(t_i,t_j)\, \sigma_+(t_i) \;.
\label{a4}$$ Then, using relation (\[a3\]) for $\sigma_+$ twice, we find the following representation for the coherence evolution during the first complete cycle: $$\sigma_+(t_0 + 2 \Delta t) = G_{tot}(t_0,t_0+\Delta t) \, \sigma_+(t_0) \,
G_{tot}^\dagger (t_0+ \Delta t, t_0+ 2 \Delta t) \;,
\label{a5}$$ to be compared with $$\sigma_+(t_0 + 2 \Delta t) = G_{tot}(t_0+\Delta t, t_0+ 2\Delta t)
\,G_{tot}(t_0, t_0+ \Delta t)\, \sigma_+(t_0)
\label{a6}$$ in the absence of pulses. Even before knowing the explicit form of $G_{tot}$, we see from (\[a5\])-(\[a6\]) that the presence of a time-reversed evolution during the second interval $\Delta t$ of the cycle is already enucleated at this stage.
In order to evaluate the propagator $G_{tot}$, the Heisenberg equations for the coupled spin $+$ bath motion have to be solved. From Hamiltonian (\[hamiltonian\]) we get $$\left\{ \begin{array}{lcl}
\dot{b}_k & = & -i \omega_k b_k -i g_k \sigma_z \;, \\
\dot{b}_k^\dagger & = & +i \omega_k b^\dagger_k +i g_k^\ast \sigma_z \;, \\
\dot{\sigma}_+& = & i \omega_0 \sigma_+ + 2i \sum_k \,
(g_k b_k^\dagger + g_k^\ast b_k)\, \sigma_+ \;, \\
\dot{\sigma}_z & = & 0 \;.
\end{array} \right.
\label{a7}$$ Since instantaneous pulses introduce discontinuous changes in operators, the propagators $G_{tot}(t_0,t_0+\Delta t)$, $G_{tot}(t_0+\Delta t,t_0+2 \Delta t)$ have to be considered separately, by solving (\[a7\]) with initial conditions at $t=t_0$, $t=t_P^+=t_0 +
\Delta t$ respectively.
$(i)\;\; t_0 \mapsto t_0 +\Delta t$:
Since $\sigma_z(t)=\sigma_z(t_0)$, the equations for the bath variables are completely solved by $$b_k(t) = \mbox{e}^{-i \omega_k(t-t_0)} b_k(t_0)- \sigma_z(t_0)
{g_k \over \omega_k} \Big( 1-\mbox{e}^{-i \omega_k (t-t_0)} \Big)\;,
\label{a8}$$ and $b_k^\dagger(t)=(b_k(t))^\dagger$. These solutions should be inserted in the expression for $\sigma_+(t)$: $$\sigma_+(t)=\mbox{T}\exp\bigg\{ i \int_{t_0}^t \, ds\,
\Big[ \omega_0 + 2(g_k b^\dagger_k(s) + g_k^\ast b_k(s) ) \Big] \bigg \}
\,\sigma_+ (t_0) \;. \label{a9}$$ The time-ordered exponential can be evaluated exactly and the following result is found for the first propagator: $$\begin{aligned}
G_{tot}(t_0,t_0+\Delta t) & = &
\exp\bigg\{ i \omega_0 \Delta t + 4i {|g_k|^2 \over \omega_k}
\Big(\Delta t - {\sin \omega_k \Delta t \over \omega_k} \Big)
(\openone -\sigma_z(t_0)) \bigg\} \nonumber \\
& \cdot & \exp\bigg\{ - \sum_k \Big( b_k^\dagger (t_0) \xi_k(\Delta t) -
b_k (t_0) \xi_k^\ast(\Delta t) \Big) \bigg\} \;,
\label{a10}\end{aligned}$$ where the same notation for $\xi_k(\Delta t)$ has been used, Eq. (\[csi\]).
$(ii)\; t_0 + \Delta t \mapsto t_0 +2 \Delta t$:
By exploiting (\[a10\]), we can immediately write down the expression for the propagator $G_{tot}^\dagger(t_0+\Delta t,t_0+2 \Delta t)$ in terms of the new initial condition at $t=t^+_P$: $$\begin{aligned}
G_{tot}^\dagger(t_0+\Delta t,t_0+2\Delta t) & = &
\exp\bigg\{ - i \omega_0 \Delta t - 4i {|g_k|^2 \over \omega_k}
\Big(\Delta t - {\sin \omega_k \Delta t \over \omega_k} \Big)
(\openone -\sigma_z(t_P^+)) \bigg\} \nonumber \\
& \cdot & \exp\bigg\{ + \sum_k \Big( b_k^\dagger (t_P^+) \xi_k(\Delta t) -
b_k (t_P^+) \xi_k^\ast(\Delta t) \Big) \bigg\} \;.
\label{a11}\end{aligned}$$ Now everything can be evaluated with respect to the initial time of the cycle. We exploit (\[a3\]) for $\sigma_z(t^+_P)$ and, since $b_k(t_P^+)=b_k(t_P^-)=
b_k(t_0+ \Delta t)$, bath operators evolve as $$b_k(t_0+\Delta t) = \mbox{e}^{-i \omega_k \Delta t} b_k(t_0)- \sigma_z(t_0)
{g_k \over \omega_k} \Big( 1-\mbox{e}^{-i \omega_k \Delta t} \Big)\;,
\label{a12}$$ and Hermitian conjugate. As we discussed in the text, the presence in (\[a12\]) of an initial condition dephased by $\mbox{e}^{\pm i \omega_k
\Delta t}$ for each environmental mode is the ultimate source of decoherence. We arrive at the following expression for the cycle evolution: $$\begin{aligned}
\sigma_+(t_0+2 \Delta t) & = &
\exp\bigg\{ i \varphi_1(\Delta t) (\openone -\sigma_z(t_0)) + \sum_k
\Big( b_k^\dagger (t_0) \eta_k(\Delta t) -
b_k (t_0) \eta_k^\ast(\Delta t) \Big)
+ i \varphi_2 (\Delta t) \bigg\} \nonumber \\
& \cdot & \sigma_+(t_0)
\exp\bigg\{ i \sigma_z(t_0) \varphi_2 (\Delta t) -
i \varphi_1(\Delta t) (\openone + \sigma_z(t_0)) \bigg\} \;,
\label{a13}\end{aligned}$$ where $$\begin{aligned}
\varphi_1(\Delta t) & = &
4 \sum_k {|g_k|^2 \over \omega_k}
\Big(\Delta t - {\sin \omega_k \Delta t \over \omega_k} \Big) \;,
\nonumber \\
\varphi_2(\Delta t) & = &
8 \sum_k {|g_k|^2 \over \omega_k^2} \sin \omega_k \Delta t
\, (1 - \cos \omega_k \Delta t) \;.
\label{a14}\end{aligned}$$ The final step is to calculate the coherence evolution as $$\rho_{01}(t_0+2\Delta t) = \langle \sigma_+(t_0+2\Delta t)\rangle =
\sum_{j=0,1} \langle j |\, \mbox{Tr}_B \{ \, (\rho_B \otimes \rho_S) \,
\sigma_+(t_0+2 \Delta t) \,\}\, | j \rangle \;.
\label{a15}$$ By inserting (\[a13\])-(\[a14\]), phase factors drop out and we find $$\rho_{01}(t_0+2\Delta t)= \rho_{01}(t_0) \,
\mbox{e}^{- \Gamma_P (N=1, \Delta t)} \;,
\label{a16}$$ in agreement with the result found from Eqs. (\[lab2\])-(\[gammap\]) in the Schrödinger representation. The procedure can be generalized to arbitrary $N$ and the complete expression $\Gamma_P(N,\Delta t)$ is thereby recovered.
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This may happen in the high-temperature and/or strong-coupling limit, or for different classes of environment not considered here. See \[3\] for supra-Ohmic qubit decoherence.
[^1]: Electronic address: [email protected]
[^2]: Electronic address: [email protected]
|
Vinyl Slider Windows
Use these Vinyl Slider Windows in your Hawaii Home!
This simple style of vinyl slider window is good for locations in your Hawaii home that require less ventilation. The Single vinyl slider window typically comes in an aluminum frame, but the Double and Triple versions are recommended in vinyl. The three panes of the Triple Slider Window make it a very cost-effective choice when you need to fill a large window space without sacrificing on looks. Built-in limiting devices help keep the vinyl window secure, and the glass panels can be lifted out for easy cleaning.
Be sure to come by our Hawaii showroom located on S. Beretania St. in Honolulu. You can see and touch our vinyl slider and other styles before making a decision. |
For most, death is followed by one of two options: burial or cremation. But both of those options pose serious environmental risks to the living. Burial is preceded by embalming, and the main chemical used to embalm a body is the known-carcinogen formaldehyde. Cremation is energy intensive and releases massive amounts of greenhouse gases and heavy metals into the atmosphere. Visual artist and human-environment researcher Jae Rhim Lee imagines a third way to rest in peace that is more in harmony with our planet: donning a fungi-laced death shroud that consumes corpses.
Lee calls her outré idea The Infinity Burial Project. (Or, “A Modest Proposal for the Postmortem Body.”) Here’s how it works. Lee has been cultivating shiitake and oyster mushrooms on her own fingernail clippings and strands of hair, hoping to find a strain of fungi that is quick to grow on decaying human tissue. When she finds a suitable strain, she plans to embroider a “Mushroom Death Suit” with spore-infused threads. The spores may be added to a “decompiculture kit” that can be used in funeral make-up and non-toxic embalming fluids—speeding the process along. Next, when Lee (or whoever) is buried, the fungi get to work—Lee also chose mushrooms for their innate ability to break down industrial toxins in bodies and the surrounding soil. Not only does the Infinity Mushroom prevent further damage to the environment from burial practices, it also helps clean up existing pollution.
Environmental stewardship isn’t Lee’s only motivation. Learning to accept death is psychologically and socially healthy, and modern people can use a little help in that department, she argues. “I am interested in cultural death denial,” Lee told New Scientist’s CultureLab blog after a recent talk at TED Global,
and why we are so distanced from our bodies, and especially how death denial leads to funeral practices that harm the environment—using formaldehyde and pink make-up and all that to make your loved one look vibrant and alive, so that you can imagine they’re just sleeping rather than actually dead . . . So I was thinking, what is the antidote to that? For me the answer was this mushroom.
Embalming isn't practiced all over the world. In many places, it is required a a type of mortician's income guarantee plan.
PHIL BROWN
8/6/2011 2:00:34 AM
Agreed. Even a mushroom sarcophagus seems over the top. We just aren't that special.
steve eatenson
8/1/2011 11:25:38 AM
Why bother? Every other animal just dies and is consumed by other animals and microorganisms. Why not us? Why not bury us deep enough in rich organic soil without the coffin or embalming so that we can return readily to the natural environment? We could compost ourselves like we do rotting vegetables. |
The Portal games are funny, intelligent, and just plain fun. If you even have a passing interest in videogames, they're an absolute must-play.
Plus, they're old enough that they'll run amazingly well on a toaster, but they still look great even by today's standards, thanks in part to the overall design and how very effective the Source engine was at the time. Almost any Source-based game has aged well.
The comparison to Half-Life doesn't really work other than they're both first-person games and take place in the same shared universe, storyline-wise. Half-Life has some puzzle elements but is way more about combat, whereas Portal is a straight-up puzzle/strategy game. |
Religious oppression
Note:
Wikipedia, the free encyclopedia, lists brief descriptions of events
considered by some to be examples of religious discrimination by governmental,
social, and educational policies.
The ReligiousTolerance.org web site does not normally publish extensive
passages from other web sites. However, the following is a wide-ranging list of
events that may be deleted from the Wikipedia web site at any time. Wikipedia's
policy is that "Lists
of miscellaneous information should be avoided" and relocated elsewhere.
Excerpt from Wikipedia:
The Eagle Feather Law, which governs the possession and
religious use of eagle feathers, was officially written to protect then
dwindling eagle populations while still protecting traditional
Native American spiritual and religious customs,
of which the use of eagles are central. The Eagle Feather Law later
met charges of promoting racial and religious discrimination due to the
law’s provision authorizing the possession of eagle feathers to members of
only one ethnic group, Native Americans, and forbidding Native Americans
from including non-Native Americans in indigenous customs involving eagle
feathers—a common modern practice dating back to the early 1500s.
Charges of religious and racial discrimination have also been found in
the education system. In a recent example, the dormitory policies at Boston
University and The University of South Dakota were charged with racial and
religious discrimination when they forbade a university dormitory resident
from smudging while praying. The policy at The University of South Dakota
was later changed to permit students to pray while living in the university
dorms.
Religious organizations such as the Seventh-day
Adventist Church make it clear in their university catalog that they
have the right to discriminate on the basis of religion. They discriminate
against non-Adventists in hiring practices, disciplinary action, and
promotions. The Seventh-day Adventist Church has made many anti-Catholic
statements stating that the Bible identifies the Pope as the Anti-Christ.
Today, the church has softened these statements, explaining that they
interpret the biblical passages as referring to the papal institution and
not to a specific person. Recently, they have also taken measures against
church members who have publicly attacked the pope, especially those who
claim that it is in the name of the church.
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During 1995-1998 Newfoundland [in Canada] had only Christian schools
(four of them, Pentecostal, Roman Catholic, Seventh-day Adventist, and
inter-denominational (Anglican, Salvation Army and United Church)). The
right to organize publicly supported religious schools was only given to
certain Christian denominations, thus tax money used to support a selected
group of Christian denominations. The denominational schools could also
refuse admission of a student or the hiring of a qualified teacher on purely
religious grounds.
Quebec has used two school systems, one Protestant and the other
Roman Catholic ... [until 1998 when this system was]... replaced with two
secular school systems: one French and the other English.
In Greece since the independence from the Muslim Ottomans rule in the
1800s, the Greek Orthodox church has been given
privileged status and only the Greek Orthodox church, Roman Catholic, some
Protestant churches, Judaism and
Islam are recognized religions. The Muslim minority
alleges that Greece persistently and systematically discriminates against
Muslims.
According to a Human Rights Practices report by the U.S. State
Department on Mexico note that "some local officials infringe on religious
freedom, especially in the south". There is conflict between Catholic/Mayan syncretists and Protestant evangelicals in the Chiapas region.
In 2004, a case involving five Ohio prison inmates (two followers of
Asatru, a minister of the
Church of Jesus Christ Christian, a
Wiccan witch and a
Satanist) protesting
denial of access to ceremonial items and opportunities for group worship was
brought before the Supreme Court.
The Boston Globe
reports on the 2005 decision of
Cutter v.
Wilkinson
in favor of the claimants as a notable case. Among the denied objects was
instructions for runic writing requested by an Asatruer.
Inmates of the "Intensive Management Unit" at
Washington State Penitentiary who are adherents of Asatru in 2001 were
deprived of their
Thor's Hammer medallions.
In 2007, a federal judge confirmed that Asatru adherents in US prisons have
the right to possess a Thor’s Hammer pendant. An inmate sued the Virginia
Department of Corrections after he was denied it while members of other
religions were allowed their medallions.
Religious discrimination has also been documented in employment,
such as an
Equal Employment Opportunity Commission (EEOC) law suit alleging
discrimination against an Iranian-Muslim employee by the Merrill Lynch
company in US.
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As the government of Canada offers its support to the United 2026 Bid, it revealed that Canada is going to co-host the 2026 FIFA World Cup, soon be happened in Canada, Mexico, and the United States. This news has been announced by the Honorable Kirsty Duncan, who is the Minister of Science and Minister of Sport and Persons with Disabilities.
This FIFA world cup is held after every four years and it is one of the most liked and enjoyed tournament of the Fédération Internationale de Football Association (FIFA). Canada, as a co-host, will be benefited by it as this showcase the country itself with advantaged in sports, social, community, cultural and economic.
Though Canada never been able to host such a prestigious tournament watched by billions, the country has hosted other tournaments like FIFA Women's World Cup Canada 2015. This was played in 6 cities with 24 teams across different coasts of Canada, allowed 1.35 million people to watch the game which eventually expanded country’s economy to around half-a-billion dollars.
Both the three countries i.e. Canada, Mexico, United States joint hand to hand on April 10, 2017, for the 2026 FIFA World Cup bid.
As Canada is a multifaceted country, this bid will highly likely to develop good relations among the countries, flourishing diplomatic, cultural, educational, and commercial relations. This relationship in collaboration with the United Bid for the 2026 FIFA World Cup shows how dynamic the three countries are when they are all set to pursue the same objective and goals as a team.
FIFA is going to reveal the fact if any bidder, United 2026, or Morocco will be the hosts of 2026 FIFA Men's World Cup.
Quotes about FIFA 2026:
"Hosting major sporting events allows Canadian athletes to compete at home in front of their families, friends and fans. It is also a significant opportunity for Canadians to witness, first-hand, world-class sport competitions. What better place to host the 2026 FIFA World Cup™ than in our multicultural cities where every team is a home team!"
—The Honorable Kirsty Duncan, Minister of Science and Sport and Persons with Disabilities
"On behalf of Canada Soccer, I would like to thank the Government of Canada for their support of the United Bid to host the 2026 FIFA World Cup™ in Canada, Mexico and the United States. Canada has raised the bar for women's and youth FIFA competitions including the most recent record-setting FIFA Women's World Cup Canada 2015™ and as the only G7 country to have not hosted the men's competition, we are more than ready to welcome the world along with our neighbors in Mexico and the United States."
—Steven Reed, President, Canada Soccer and Co-chair, United Bid Committee |
i am a simple girl come from a simple family..i have one son he lived with me..i am vey loving and caring person..i know im not a perfect person but all i want is to be happy with my love one ans soon to be a good father of my son.....
Interests
:
i know how to dance and sing...but im not a good singer as well...i love going beaches,camping outing with my family and friends....and specialy to my love one soon..
Message
to you
:
Not Available
Height
:
157cm,5,2"
Weight
:
50kg,110lbs
Nationality
:
Philippines
Ethnicity
:
Philippino
Marital
Status
:
Never Married
Religion
:
Christian-Catholic
Education
:
College
Work
:
at the same time i dont have work
Primary Language
:
English
English
Ability
:
Ok
Languages
:
English, Tagalog
Eyes
:
Black
Hair
:
Black
Children
:
1
,and I live with them
Living
:
I,live with my Parents/extended family
Birth Date
:
1989-02-05
Last Online
:
2009-04-20
Western
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:
Dont Know
Chinese
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Dont Know
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Dont Know
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:
Average
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:
Occasionaly
Smoke
:
No
Seeking For
My Match
:
i want to meet a person who is a family orinted person,,romantic person full of surprices,,he must love to go outings too with my family and him,,specially im looking for a life time partner who is wiling to marry me and have a happy family and he must wiling also to help my family,, |
Q:
Limite of a sequence of integrals
Find
$$\lim_{n\to\infty}\int_{0}^{\infty}\left(1+\frac{x}{n}\right)^{-n}\sin \left(\frac{x}{n}\right)dx.$$
My attempt is find a dominating function to apply the dominated convergence theorem i.e.
$f\in L_1$ such that $\left| f_n=\left(1+\dfrac{x}{n}\right)^{-n}\right|\leq f$ for all $n$.
Thanks for any suggestion.
A:
By letting $t=x/n$ and by using integration by parts we have that
$$
\begin{align}\lim_{n\to\infty}\int_{0}^{\infty}\left(1+\frac{x}{n}\right)^{-n}\sin \left(\frac{x}{n}\right)dx&=
\lim_{n\to\infty}n\int_{0}^{\infty}\frac{\sin(t)}{\left(1+t\right)^{n}}dt\\
&=\lim_{n\to\infty}\left(\frac{n}{n-1}\left[\frac{\sin(t)}{\left(1+t\right)^{n-1}}\right]_0^{+\infty}+\frac{n}{n-1}\int_{0}^{\infty}\frac{\cos(t)}{\left(1+t\right)^{n-1}}dt\right)
\\&=0+1\cdot \lim_{n\to\infty}\int_{0}^{\infty}\frac{\cos(t)}{\left(1+t\right)^{n-1}}dt=0
\end{align}$$
because for $n\geq 3$,
$$\left|\int_{0}^{\infty}\frac{\cos(t)}{\left(1+t\right)^{n-1}}dt\right|
\leq \int_{0}^{\infty}\frac{1}{\left(1+t\right)^{n-1}}dt=\frac{1}{n-2}\to 0.$$
P.S. After integration by parts, you may also use dominated convergence.
|
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