Center for Research on Child Wellbeing and Office of Population Research, Princeton University, Princeton, NJ 08544, USA.
Proc Natl Acad Sci U S A. 2011 May 17;108(20):8189-93. doi: 10.1073/pnas.1014129108. Epub 2011 May 16.
Most studies of human molecular genetics and social environment interactions on health have relied heavily on the classic diathesis-stress model that treats genetic variations and environments as being either "risky" or "protective." The biological susceptibility model posits that some individuals have greater genetic reactivity to stress, leading to worse outcomes in poor environments, but better outcomes in rich environments. Using a nontruncated measure of a chronic environmental stressor--socioeconomic status--measured by education, and two polymorphisms (5-HTTLPR and STin2 VNTR) of the serotonin transporter gene (5-HTT), we find strong evidence that some women are genetically more reactive to the environment, resulting in a crossover of risks of postpartum depression for the most reactive groups. We discuss how our approach and findings provide a framework for understanding some of the confusion in the gene-environment interaction literature on stress, 5-HTT, and depression.
大多数关于人类分子遗传学和社会环境对健康影响的研究都严重依赖于经典的素质-应激模型,该模型将遗传变异和环境视为“风险”或“保护”。生物易感性模型假设,某些个体对压力的遗传反应性更强,导致在恶劣环境下的结果更差,但在丰富的环境下的结果更好。我们使用一种非截断的慢性环境应激源——社会经济地位的衡量标准(通过教育来衡量),以及两个 5-羟色胺转运体基因(5-HTT)的多态性(5-HTTLPR 和 STin2 VNTR),发现了强有力的证据表明,一些女性的遗传对环境的反应性更强,导致最易受影响的群体产后抑郁风险的交叉。我们讨论了我们的方法和发现如何为理解应激、5-HTT 和抑郁的基因-环境相互作用文献中的一些困惑提供了一个框架。