Gene-environment interactions predict cortisol responses after acute stress: Implications for the etiology of depression
Gene-environment interactions predict cortisol responses after acute stress: Implications for the etiology of depression
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DOI：
10.1016/j.psyneuen.2009.03.017
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发表时间：
2009-10-01
影响因子：
3.7
通讯作者：
Hennig, Juergen
中科院分区：
文献类型：
--
作者：
Alexander, Nina;Kuepper, Yvonne;Hennig, Juergen
背景资料：越来越多的证据表明，5-羟色胺转运体多态性（5-HTTLPR）与不良环境影响相互作用，产生抑郁症的发展风险增加，而这种关联的潜在机制仍然在很大程度上未被探索。作为一个潜在的中间表型，我们调查了改变下丘脑-垂体-肾上腺（HPA）轴的反应，以压力在个人没有精神病理学的历史依赖于5-HTTLPR和压力lifeevents.Methods：健康的伴侣成年人（N = 100）进行基因分型，并完成了问卷调查严重的压力生活事件（生活事件清单）。为了测试基因与环境的相互作用对内分泌应激反应的影响，受试者接受了标准化的实验室应激任务（公开演讲）。唾液皮质醇水平在6个时间点前的压力和在延长恢复period.Results：主题纯合子的S-等位基因与显着的历史紧张的生活事件表现出显着升高的皮质醇分泌的压力相比，所有其他组，表明显着的基因环境相互作用的内分泌应激反应。无论是5-HTTLPR（双等位基因和三等位基因）或紧张的生活事件对皮质醇分泌patterns appeared.Conclusion：这是第一个研究报告，5-HTTLPR和紧张的生活事件相互作用，以预测内分泌应激反应在非临床样本。我们的研究结果支持潜在的调节作用，HPA轴高反应性作为一个发病前的危险因素，以增加受试者的抑郁症的脆弱性与低血清素转运体的效率和严重的生活事件的历史。(C)2009爱思唯尔有限公司保留所有权利。
Background: Growing evidence suggests that the serotonin transporter polymorphism (5-HTTLPR) interacts with adverse environmental influences to produce an increased risk for the development of depression while the underlying mechanisms of this association remain largely unexplored. As one potential intermediate phenotype, we investigated alterations of hypothalamic-pituitary-ad renal (HPA) axis responses to stress in individuals with no history of psychopathology depending on both 5-HTTLPR and stressful life events.Methods: Healthy mate adults (N = 100) were genotyped and completed a questionnaire on severe stressful life events (Life Events Checklist). To test for gene-by-environment interactions on endocrine stress reactivity, subjects were exposed to a standardized laboratory stress task (Public Speaking). Saliva cortisol levels were obtained at 6 time points prior to the stressor and during an extended recovery period.Results: Subjects homozygous for the s-allele with a significant history of stressful life events exhibited markedly elevated cortisol secretions in response to the stressor compared to all other groups, indicating a significant gene-by-environment interaction on endocrine stress reactivity. No main effect of either 5-HTTLPR (biallelic and triallelic) or stressful life events on cortisol secretion patterns appeared.Conclusion: This is the first study reporting that 5-HTTLPR and stressful life events interact to predict endocrine stress reactivity in a non-clinical sample. Our results underpin the potential moderating role of HPA-axis hyper-reactivity as a premorbid risk factor to increase the vulnerability for depression in subjects with tow serotonin transporter efficiency and a history of severe life events. (C) 2009 Elsevier Ltd. All rights reserved.