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

Published online by Cambridge University Press:  04 September 2013

E. J. Wolf*
Affiliation:
National Center for PTSD, VA Boston Healthcare System, Boston, MA, USA Department of Psychiatry, Boston University School of Medicine, Boston, MA, USA
K. S. Mitchell
Affiliation:
National Center for PTSD, VA Boston Healthcare System, Boston, MA, USA Department of Psychiatry, Boston University School of Medicine, Boston, MA, USA
K. C. Koenen
Affiliation:
Department of Epidemiology, Columbia University Mailman School of Public Health, New York, NY, USA
M. W. Miller
Affiliation:
National Center for PTSD, VA Boston Healthcare System, Boston, MA, USA Department of Psychiatry, Boston University School of Medicine, Boston, MA, USA
*
* Address for correspondence: E. J. Wolf, Ph.D., National Center for PTSD, VA Boston Healthcare System (116B-2), 150 South Huntington Avenue, Boston, MA 02130, USA. (Email: [email protected])

Abstract

Background

Twin studies of veterans and adults suggest that approximately 30–46% of the variance in post-traumatic 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 determine whether the effects of genetic and environmental factors that contribute to the etiology of PTSD are dependent on the level of combat exposure.

Method

The sample was drawn from the Vietnam Era Twin Registry (VETR) and included 620 male–male twin pairs who served in the US 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.

Results

Biometric modeling revealed that the effects 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.

Conclusions

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 environmental factors. Additional work is needed to determine the biological and environmental mechanisms driving these associations.

Type
Original Articles
Copyright
Copyright © Cambridge University Press 2013 

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