Kinney Dennis K, Tanaka Midori
Genetics Laboratory, McLean Hospital, Belmont, MA 02478, USA.
J Nerv Ment Dis. 2009 Aug;197(8):561-7. doi: 10.1097/NMD.0b013e3181b05fa8.
Major depression is an evolutionary paradox: it carries great disadvantages for survival and reproduction of both patients and their relatives, yet it is common and has significant heritability. We propose a new hypothesis to help explain many of depression's symptoms and its risk factors, most of them not explained by previous evolutionary theories. We hypothesize that the evolutionary costs of depression are offset by its benefits in combating existing infections and avoiding new ones. As our hypothesis predicts, depression can be elicited by various infections as well as by environmental stressors that compromise immune function. Moreover, many depressive symptoms tend to aid immune function and reduce exposure to new infections and stressors. The hypothesis makes many predictions about the epidemiology and physiology of depression that are supported by available evidence. The hypothesis also suggests that possible underlying infectious and immune factors deserve greater consideration in prevention and treatment of depression.
它对患者及其亲属的生存和繁殖极为不利，但却很常见且具有显著的遗传性。我们提出了一个新假说，以帮助解释抑郁症的诸多症状及其风险因素，其中大多数无法由先前的进化理论来解释。我们推测，抑郁症的进化成本被其在对抗现有感染和避免新感染方面的益处所抵消。正如我们的假说所预测的那样，各种感染以及损害免疫功能的环境应激源都可能引发抑郁症。此外，许多抑郁症状往往有助于免疫功能，并减少接触新感染和应激源的机会。该假说对抑郁症的流行病学和生理学做出了许多预测，这些预测得到了现有证据的支持。该假说还表明，在抑郁症的预防和治疗中，潜在的感染和免疫因素值得更多关注。
