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Serotonin transporter 5-HTTLPR genotype moderates the effects of childhood adversity on posttraumatic stress disorder risk: a replication study

机译:血清素转运蛋白5-HTTLPR基因型激起儿童逆境对错误胁迫障碍风险的影响:复制研究

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摘要

We reported that the 5-HTTLPR polymorphism in the promoter region of the serotonin transporter gene (SLC6A4) moderates the effect of childhood adversity on posttraumatic stress disorder (PTSD)risk (). In the present study, we considered 5178 subjects (a group with generally high substance dependence comorbidity, as for our previous study) using similar methodology to replicate our previous results.We used logistic regression analyses to explore the interaction effect of 5-HTTLPR genotype and childhood adversity on PTSD risk. We found that, as reported in our previous study, in individuals with childhood adversity, the presence of one or two copies of the S allele of 5-HTTLPR increased the risk to develop PTSD. This gene-environment interaction effect was present in European Americans (EAs), but not in African Americans (AAs) (EAs, OR=1.49, 95% CI=1.07–2.08, P=0.019; AAs, OR=0.90, 95% CI=0.60–1.35, P=0.62). The statistical power to detect this interaction effect was increased when data were combined with those from our previous study ().The findings reported here replicate those from our previous work, adding to a growing body of research demonstrating that the 5-HTTLPR genotype moderates risk for anxiety and depression phenotypes in the context of stress and adverse events.
机译:我们报道,血清素转运蛋白基因(SLC6A4)的启动子区中的5-HTTLPR多态性调节儿童逆境对错误应激障碍(PTSD)风险()的影响。在本研究中,我们考虑了5178名受试者(一个群体具有一般高质物质依赖性合并的,我们以前的研究)使用类似的方法来复制我们以前的结果。我们使用的物流回归分析探索5-HTTLPR基因型的相互作用效果和儿童时期对应激障碍风险的逆境。我们发现,正如我们之前的研究中所报告的那样,在具有童年逆境的个人中,5-HTTLPR的一个或两个副本的存在增加了开发PTSD的风险。这种基因环境相互作用效果存在于欧洲美国人(EAS)中存在,但不在非洲裔美国人(AAS)(EAS)(EAS,或= 1.49,95%CI = 1.07-2.08,P = 0.019; AA,或= 0.90,95% CI = 0.60-1.35,p = 0.62)。当数据与我们以前的研究中的那些相结合时,检测这种相互作用效果的统计学力量增加了。报告的调查结果将这些结果复制了我们以前的工作,增加了越来越多的研究体验,证明了5-HTTLPR基因型适度的风险对于压力和不良事件的背景下的焦虑和抑郁表型。

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