text_1: Estrogen Patch in Newly Postmenopausal Women May Reduce Alzheimer’s Risk
text_2: A small pilot study has found that giving recently postmenopausal women estrogen via a patch is associated with reduced depositions of amyloid in the brain (a hallmark of Alzheimer’s disease) relative to women who received estrogen orally or who took a placebo. Additionally, the study found that the association was strongest among women with a greater genetic risk of Alzheimer’s disease. The study was carefully done, and the news release offers some useful details about the study’s methods. However, the study included just 68 women, too few to make the patterns found reliable. To its credit, the release quotes the lead author about the need for larger replications. But that begs the question of why the Mayo Clinic seeks to publicize this work at all, particularly with a news release headline that emphasizes disease reduction potential, when the study only looked at amyloid levels, a risk marker. There is very active debate as to whether lowering amyloid will have any impact on actual symptoms or rates of Alzheimer’s disease. A better headline might have been: “Pilot Study Suggests Estrogen Patch in Newly Postmenopausal Women Reduces Amyloid, Marker of Alzheimer’s Risk.” Journalists certainly deserve to know about this study, but they need to keep it in their back pockets until more rigorous clinical studies have been done. Whether estrogen replacement therapy is of value to postmenopausal women is contested territory, and researchers, including those in the Kronos Early Estrogen Prevention Study from which this research stems, are trying to explore the contingencies, if any, that distinguish women who could benefit from estrogen supplementation from those who may not. This study adds to a body of work looking at the “timing hypothesis,” that is, the notion that estrogen has different effects in the heart and brain when given to younger postmenopausal woman compared to women in their 60s or 70s. Studies of effects on the heart using intermediate disease markers (carotid artery thickness, analogous to heart disease in the way that amyloid deposition is to Alzheimer disease) in lieu of clinical outcomes (heart attacks, cognitive impairment) have been appearing in journals over the past two years. Considered in this context, the research is of interest but needs to be shared with a strong dose of qualifiers.