Background: At least half a million women are victims of intimate partner violence in the United States annually, resulting in substantial harm. However, the etiology of violence to intimate partners is not well understood. Witnessing such violence in childhood has been proposed as a principal cause of adulthood perpetration, yet it remains unknown whether the association between witnessing intimate partner violence and adulthood perpetration is causal.
Method: We conducted a propensity-score analysis of intimate partner violence perpetration to determine whether childhood witnessing is associated with perpetration in adulthood, independent of a wide range of potential confounding variables, and therefore might be a causal factor. We used data from 14,564 U.S. men ages 20 and older from the 2004-2005 wave of the National Epidemiologic Survey on Alcohol and Related Conditions.
Results: Nearly 4% of men reported violent behavior toward an intimate partner in the past year. In unadjusted models, we found a strong association between childhood witnessing of intimate partner violence and adulthood perpetration (for witnessing any intimate partner violence, risk ratio [RR] = 2.6 [95% confidence interval = 2.1-3.2]; for witnessing frequent or serious violence, 3.0 [2.3-3.9]). In propensity-score models, the association was substantially attenuated (for witnessing any intimate partner violence, adjusted RR = 1.6 [1.2-2.0]; for witnessing frequent or serious violence, 1.6 [1.2-2.3]).
Conclusions: Men who witness intimate partner violence in childhood are more likely to commit such acts in adulthood, compared with men who are otherwise similar with respect to a large range of potential confounders. Etiological models of intimate partner violence perpetration should consider a constellation of childhood factors.
From the Departments of aSociety, Human Development, and Health, and bEpidemiology, Harvard School of Public Health, Boston, MA; cDepartment of Psychiatry, Harvard Medical School, Boston, MA; dDepartment of Biostatistics, Harvard School of Public Health, Boston, MA; eLaboratory for Psychiatric Biostatistics, McLean Hospital, Belmont, MA; fDepartment of Population, Family and Reproductive Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD; and gCenter on the Developing Child, Harvard University, Cambridge, MA.
Submitted 23 February 2010; accepted 21 June 2010; posted 1 September 2010.
Supported by the Harvard Training Program in Psychiatric Genetics and Translational Research T32MH017119 (AR), NIH grant R01-MH54693 (GF), NIH grant RO3DA20887 (SG), and NIH grants K08MH070627 and 5R01MH078928 (KK).
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Correspondence: Andrea L. Roberts, Harvard School of Public Health, 677 Huntington Avenue, Kresge Building, 9th Floor, Boston, MA 02115. E-mail: firstname.lastname@example.org.