Department of Psychiatry, University of North Carolina at Chapel Hill, NC, USA.
Depress Anxiety. 2011 Apr;28(4):282-96. doi: 10.1002/da.20810.
It is increasingly axiomatic that depression has widespread adverse physiological effects, and conversely that a variety of physiological systems impact the risk for developing depression. This convergence of depression and altered physiology is particularly dramatic during midlife-a time during which reproductive failure presages dramatic increases in prevalence of both heart disease and depression. The potentially meaningful and illuminating links between estrogen (E2) deficiency, cardiovascular disease (CVD), and depression have largely been obscured, first by assertions, subsequently repudiated that the perimenopause was not a time of increased risk of depression, and more recently by the denegration of hormone replacement therapy by initial reports of the Women's Health Initiative. Increasingly, however, research has led to unavoidable conclusions that CVD and depression share common and mediating pathogenic processes and that these same processes are dramatically altered by the presence or absence of E2. This review summarizes data supporting this contention with the intent of placing depression and E2 therapy in their proper physiologic context.
越来越多的事实表明，抑郁具有广泛的不良生理影响，相反，各种生理系统也会影响抑郁的发病风险。这种抑郁和生理改变的趋同，在中年时期尤为明显——此时生殖功能衰竭预示着心脏病和抑郁症的发病率都将大幅上升。雌激素（E2）缺乏、心血管疾病（CVD）和抑郁症之间可能具有重要意义和启示性的联系，在很大程度上被掩盖了，首先是有观点声称，随后又否认绝经期不是抑郁风险增加的时期，最近则是妇女健康倡议的初步报告贬低了激素替代疗法。然而，越来越多的研究得出了不可避免的结论，即 CVD 和抑郁症有共同的、中介的致病过程，而这些相同的过程会因 E2 的存在与否而发生显著改变。这篇综述总结了支持这一观点的数据，旨在将抑郁症和 E2 治疗置于适当的生理环境中。
