MAOA genotype, childhood maltreatment, and their interaction in the etiology of adult antisocial behaviors.

Published

Journal Article

BACKGROUND: Maltreatment by an adult or caregiver during childhood is a prevalent and important predictor of antisocial behaviors in adulthood. A functional promoter polymorphism in the monoamine oxidase A (MAOA) gene has been implicated as a moderating factor in the relationship between childhood maltreatment and antisocial behaviors. Although there have been numerous attempts at replicating this observation, results remain inconclusive. METHODS: We examined this gene-environment interaction hypothesis in a sample of 3356 white and 960 black men (aged 24-34) participating in the National Longitudinal Study of Adolescent Health. RESULTS: Primary analysis indicated that childhood maltreatment was a significant risk factor for later behaviors that violate rules and the rights of others (p < .05), there were no main effects of MAOA genotype, and MAOA genotype was not a significant moderator of the relationship between maltreatment and antisocial behaviors in our white sample. Post hoc analyses identified a similar pattern of results among our black sample in which maltreatment was not a significant predictor of antisocial behavior. Post hoc analyses also revealed a main effect of MAOA genotype on having a disposition toward violence in both samples and for violent convictions among our black sample. None of these post hoc findings, however, survived correction for multiple testing (p > .05). Power analyses indicated that these results were not due to insufficient statistical power. CONCLUSIONS: We could not confirm the hypothesis that MAOA genotype moderates the relationship between childhood maltreatment and adult antisocial behaviors.

Full Text

Duke Authors

Cited Authors

  • Haberstick, BC; Lessem, JM; Hewitt, JK; Smolen, A; Hopfer, CJ; Halpern, CT; Killeya-Jones, LA; Boardman, JD; Tabor, J; Siegler, IC; Williams, RB; Mullan Harris, K

Published Date

  • January 1, 2014

Published In

Volume / Issue

  • 75 / 1

Start / End Page

  • 25 - 30

PubMed ID

  • 23726513

Pubmed Central ID

  • 23726513

Electronic International Standard Serial Number (EISSN)

  • 1873-2402

Digital Object Identifier (DOI)

  • 10.1016/j.biopsych.2013.03.028

Language

  • eng

Conference Location

  • United States