Christchurch Health and Development Study, University of Otago, Christchurch, PO Box 4345, Christchurch, New Zealand.
Br J Psychiatry. 2011 Feb;198(2):129-35. doi: 10.1192/bjp.bp.110.085993.
Recent meta-analyses have raised concerns about the replicability of gene × environment interactions involving the serotonin transporter gene (5-HTTLPR) in moderating the associations between adverse life events and mental disorders.
To use data gathered over the course of a 30-year longitudinal study of a New Zealand birth cohort to test the hypothesis that the presence of short ('s') alleles of 5-HTTLPR are associated with an increased response to life stress.
Participants were 893 individuals from the Christchurch Health and Development Study who had complete data on: the 5-HTTLPR genotype; psychiatric disorders up to the age of 30; and exposure to childhood and adult adverse life events.
A series of 104 regression models were fitted to four mental health outcomes (depressive symptoms, major depression, anxiety disorder and suicidal ideation) observed at ages 18, 21, 25 and 30 using 13 measures of life-course stress that spanned childhood and adult stressors. Both multiplicative and additive models were fitted to the data. No evidence was found that would support the hypothesis that 's' alleles of 5-HTTLPR are associated with increased responsivity to life stressors.
The present findings add to the evidence suggesting that it is unlikely that there is a stable gene × environment interaction involving 5-HTTLPR, life stress and mental disorders.
最近的荟萃分析对涉及血清素转运体基因（5-HTTLPR）的基因-环境相互作用在调节不良生活事件与精神障碍之间的关联的可重复性提出了担忧。
利用新西兰出生队列 30 年纵向研究中收集的数据，检验 5-HTTLPR 的短（'s'）等位基因的存在是否与对生活压力的反应增强相关的假设。
参与者为基督城健康与发展研究中的 893 名个体，他们有完整的数据：5-HTTLPR 基因型；30 岁之前的精神障碍；以及童年和成年期不良生活事件的暴露情况。
使用跨越童年和成年压力源的 13 项生命历程压力测量指标，对四个心理健康结果（抑郁症状、重度抑郁症、焦虑障碍和自杀意念）进行了 104 个回归模型的拟合，这些结果分别在 18、21、25 和 30 岁时观察到。对数据进行了乘法和加法模型的拟合。没有证据表明 5-HTTLPR 的's'等位基因与对生活压力源的反应增强相关的假设成立。
本研究结果增加了证据，表明不太可能存在涉及 5-HTTLPR、生活压力和精神障碍的稳定的基因-环境相互作用。
