Caspi Avshalom, Sugden Karen, Moffitt Terrie E, Taylor Alan, Craig Ian W, Harrington HonaLee, McClay Joseph, Mill Jonathan, Martin Judy, Braithwaite Antony, Poulton Richie
Medical Research Council Social, Genetic, and Developmental Psychiatry Research Centre, Institute of Psychiatry, King's College London, PO80 De Crespigny Park, London, SE5 8AF, UK.
Science. 2003 Jul 18;301(5631):386-9. doi: 10.1126/science.1083968.
In a prospective-longitudinal study of a representative birth cohort, we tested why stressful experiences lead to depression in some people but not in others. A functional polymorphism in the promoter region of the serotonin transporter (5-HT T) gene was found to moderate the influence of stressful life events on depression. Individuals with one or two copies of the short allele of the 5-HT T promoter polymorphism exhibited more depressive symptoms, diagnosable depression, and suicidality in relation to stressful life events than individuals homozygous for the long allele. This epidemiological study thus provides evidence of a gene-by-environment interaction, in which an individual's response to environmental insults is moderated by his or her genetic makeup.
在一项针对具有代表性的出生队列的前瞻性纵向研究中，我们探究了为什么压力经历会导致一些人患上抑郁症，而另一些人却不会。研究发现，血清素转运体（5-HTT）基因启动子区域的功能性多态性会调节压力性生活事件对抑郁症的影响。与携带5-HTT启动子多态性长等位基因纯合子的个体相比，携带一个或两个短等位基因拷贝的个体在面对压力性生活事件时表现出更多的抑郁症状、可诊断的抑郁症和自杀倾向。因此，这项流行病学研究提供了基因与环境相互作用的证据，即个体对环境伤害的反应受到其基因构成的调节。
