Journal of affective disorders · 2007
Common genetic liability to major depression and posttraumatic stress disorder in men.
СтатьяTwin StudyНазвание и аннотация: Перевод в очереди
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Koenen Karestan C, Fu Qiang J, Ertel Karen, Lyons Michael J, Eisen Seth A, True William R, Goldberg Jack, Tsuang Ming T
Аннотация
BACKGROUND: 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.
METHODS: 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.
RESULTS: 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.
LIMITATIONS: Our participants were male Vietnam era veterans and our findings may not generalize to civilians, females or other cohorts.
CONCLUSIONS: 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.
METHODS: 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.
RESULTS: 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.
LIMITATIONS: Our participants were male Vietnam era veterans and our findings may not generalize to civilians, females or other cohorts.
CONCLUSIONS: 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.