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SLC6A4 methylation modifies the effect of the number of traumatic events on risk for posttraumatic stress disorder

Authors

  • Karestan C. Koenen Ph.D.,

    Corresponding author
    1. Departments of Society, Human Development, and Health and Epidemiology, Harvard School of Public Health, Boston, Massachusetts
    2. Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York
    • Harvard School of Public Health, Kresge 613, 677 Huntington Avenue, Boston, MA 02115
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  • Monica Uddin Ph.D.,

    1. Center for Social Epidemiology and Population Health and Department of Epidemiology, University of Michigan School of Public Health, Ann Arbor, Michigan
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  • Shun-Chiao Chang D.Sc.,

    1. Departments of Society, Human Development, and Health and Epidemiology, Harvard School of Public Health, Boston, Massachusetts
    2. Center on the Developing Child, Harvard University, Cambridge, Massachusetts
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  • Allison E. Aiello Ph.D. M.S.,

    1. Center for Social Epidemiology and Population Health and Department of Epidemiology, University of Michigan School of Public Health, Ann Arbor, Michigan
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  • Derek E. Wildman Ph.D.,

    1. Center for Molecular Medicine and Genetics & Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, Michigan
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  • Emily Goldmann M.P.H.,

    1. Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York
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  • Sandro Galea M.D. Dr. PH.

    1. Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York
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Abstract

Background: Posttraumatic stress disorder (PTSD) is a common and debilitating mental disorder that occurs following exposure to a traumatic event. However, most individuals do not develop PTSD following even a severe trauma, leading to a search for new variables, such as genetic and other molecular variation, associated with vulnerability and resilience in the face of trauma exposure. Method: We examined whether serotonin transporter (SLC6A4) promoter genotype and methylation status modified the association between number of traumatic events experienced and PTSD in a subset of 100 individuals from the Detroit Neighborhood Health Study. Results: Number of traumatic events was strongly associated with risk of PTSD. Neither SLC6A4 genotype nor methylation status was associated with PTSD in main effects models. However, SLC6A4 methylation levels modified the effect of the number of traumatic events on PTSD after controlling for SLC6A4 genotype. Persons with more traumatic events were at increased risk for PTSD, but only at lower methylation levels. At higher methylation levels, individuals with more traumatic events were protected from this disorder. This interaction was observed whether the outcome was PTSD diagnosis, symptom severity, or number of symptoms. Conclusions: Gene-specific methylation patterns may offer potential molecular signatures of increased risk for and resilience to PTSD. Depression and Anxiety, 2011.  © 2011 Wiley-Liss, Inc.

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