Koenen Karestan C, Fu Qiang J, Ertel Karen, Lyons Michael J, Eisen Seth A, True William R, Goldberg Jack, Tsuang Ming T
Department of Society, Human Development, and Health, Harvard School of Public Health, Boston, MA 02115, United States.
J Affect Disord. 2008 Jan;105(1-3):109-15. doi: 10.1016/j.jad.2007.04.021. Epub 2007 May 30.
Major depression (MD) and posttraumatic stress disorder (PTSD) are highly comorbid. The degree to which a common genetic liability explains the etiology of the MD-PTSD association has not been quantified and has important implications for research and prevention.
This paper presents an analysis of data from 6744 members of the Vietnam Era Twin Registry. MD and PTSD were assessed using the Diagnostic Interview Schedule-III-R in 1991-92. Bivariate twin modeling was conducted to determine the genetic and environmental etiology of the MD-PTSD association.
The best-fitting model for the MD-PTSD association included a substantial genetic correlation (r=.77; 95% CI, .50-1.00) and a modest individual-specific environmental correlation (r=.34; 95% CI, .19-.48). Common genetic liability explained 62.5% of MD-PTSD comorbidity. Genetic influences common to MD explained 15% of the total variance in risk for PTSD and 58% of the genetic variance in PTSD. Individual-specific environmental influences common to MD explained only 11% of the individual-specific environmental variance in PTSD.
Our participants were male Vietnam era veterans and our findings may not generalize to civilians, females or other cohorts.
MD-PTSD comorbidity is largely explained by common genetic influences. Substantial genetic overlap between MD and PTSD implies that genes implicated in the etiology of MD are strong candidates for PTSD and vice versa. Environmental influences on MD and PTSD explain less of their covariation and appear to be largely disorder-specific. Research is needed to identify environmental factors that influence the development of MD versus PTSD in the context of common genetic liability.
重度抑郁症(MD)和创伤后应激障碍(PTSD)高度共病。共同遗传易感性在多大程度上解释了MD - PTSD关联的病因尚未得到量化,这对研究和预防具有重要意义。
本文对越南战争时期双胞胎登记处的6744名成员的数据进行了分析。1991 - 1992年使用诊断访谈表第三版修订版对MD和PTSD进行评估。进行双变量双胞胎建模以确定MD - PTSD关联的遗传和环境病因。
MD - PTSD关联的最佳拟合模型包括显著的遗传相关性(r = 0.77;95%可信区间,0.50 - 1.00)和适度的个体特异性环境相关性(r = 0.34;95%可信区间,0.19 - 0.48)。共同遗传易感性解释了MD - PTSD共病的62.5%。MD共有的遗传影响解释了PTSD风险总方差的15%和PTSD遗传方差的58%。MD共有的个体特异性环境影响仅解释了PTSD个体特异性环境方差的11%。
我们的参与者是越南战争时期的男性退伍军人,我们的研究结果可能不适用于平民、女性或其他队列。
MD - PTSD共病在很大程度上由共同的遗传影响所解释。MD和PTSD之间大量的遗传重叠意味着与MD病因相关的基因是PTSD的有力候选基因,反之亦然。环境对MD和PTSD的影响对它们的共变解释较少,并且似乎在很大程度上是疾病特异性的。需要开展研究以确定在共同遗传易感性背景下影响MD与PTSD发展的环境因素。