Combat exposure severity as a moderator of genetic and environmental liability to post-traumatic stress disorder.

Combat exposure severity as a moderator of genetic and environmental liability to post-traumatic stress disorder.
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DOI:
10.1017/s0033291713002286
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发表时间:
2014-05
影响因子:
6.9
通讯作者:
Miller MW
Miller MW
中科院分区:
医学1区
文献类型:
--
作者:
Wolf EJ;Mitchell KS;Koenen KC;Miller MW

文献摘要

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对退伍军人和成年人的双胞胎研究表明,创伤后应激障碍(PTSD)的变异中约有30-46%可归因于遗传因素。其余差异归因于非共享环境,根据定义,非共享环境包括战斗风险。本研究采用基因测量环境双胞胎设计,以检查导致PTSD病因的遗传和环境因素的影响是否依赖于战斗暴露水平。样本来自越南时代双胞胎登记处,包括620对在越南战争期间在东南亚服役的美国军队的男性双胞胎。分析是基于终生PTSD症状的临床诊断访谈和战斗暴露的自我报告测量的数据。生物统计学模型显示,遗传和非共享环境因素对PTSD的影响随战斗暴露水平的变化而变化,这些因素与PTSD之间的关联在较高水平的战斗暴露中更强。战斗暴露可能作为一种催化剂,增加了遗传和环境因素对PTSD的影响。受遗传和其他环境因素影响,最大程度暴露于战斗创伤的个体患创伤后应激障碍的风险增加。需要进一步的工作,以确定驱动这些协会的生物和环境机制。
Twin studies of veterans and adults suggest that approximately 30–46% of the variance in posttraumatic stress disorder (PTSD) is attributable to genetic factors. The remaining variance is attributable to the non-shared environment, which, by definition, includes combat exposure. This study used a gene by measured environment twin design to examine if the effect of genetic and environmental factors that contribute to the etiology PTSD were dependent on level of combat exposure. The sample was drawn from the Vietnam Era Twin Registry and included 620 male-male twin pairs who served in the U.S. Military in South East Asia during the Vietnam War era. Analyses were based on data from a clinical diagnostic interview of lifetime PTSD symptoms and a self-report measure of combat exposure. Biometric modeling revealed that the effect of genetic and non-shared environment factors on PTSD varied as a function of level of combat exposure such that the association between these factors and PTSD was stronger at higher levels of combat exposure. Combat exposure may act as a catalyst that augments the impact of hereditary and environmental contributions to PTSD. Individuals with the greatest exposure to combat trauma were at increased risk for PTSD as a function of both genetic and other environmental factors. Additional work is needed to determine the biological and environmental mechanisms driving these associations.