Abstract

Background Alcohol-related physical violence (ARPV) can be a causal consequence of alcohol consumption, but only for specific individuals (e.g., those predisposed to violence). Studies have not accounted for the shared etiology explaining comorbidity between alcohol use and violent behavior as a potential third-variable explanation of ARPV. The current study examined genetically-informed associations between ARPV, heavy alcohol use (HAU) and overall physical violence (OPV) in adolescence and young adulthood, by testing two proposed theories of ARPV processes (HAU causes ARPV, causal relationships depend upon OPV) and how overarching shared covariance may account for these associations. Methods Using the twin and sibling subsample from the National Longitudinal Study of Adolescent to Adult Health (Add Health), a series of biometric models tested hypotheses individually in adolescence and young adulthood. This included estimating bivariate Cholesky and direction-of-causality models, and trivariate Cholesky, independent pathway, and common pathway models. Results HAU had a causal effect on ARPV in adolescence and young adulthood. This effect was not moderated by OPV at either developmental stage. A shared etiology or common latent factor did not explain associations between ARPV, OPV, and HAU, even though ARPV strongly covaried independently with HAU and with OPV. Finally, OPV also had a causal effect on ARPV in adolescence, and in young adulthood for adolescent-onset drinkers. Conclusions Causal theories of ARPV still hold when accounting for shared genetic and environmental variance. Further research on the exact role of violence (predispositions, environmental contexts) is required, as both phenotypes substantially (and separately) explain influences driving ARPV. Supplemental data for this article is available online at https://doi.org/10.1080/10826084.2021.1887244.

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