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

Publication ,  Journal Article
Haberstick, BC; Lessem, JM; Hewitt, JK; Smolen, A; Hopfer, CJ; Halpern, CT; Killeya-Jones, LA; Boardman, JD; Tabor, J; Siegler, IC ...
Published in: Biol Psychiatry
January 1, 2014

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.

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Published In

Biol Psychiatry

DOI

EISSN

1873-2402

Publication Date

January 1, 2014

Volume

75

Issue

1

Start / End Page

25 / 30

Location

United States

Related Subject Headings

  • White People
  • Psychiatry
  • Monoamine Oxidase
  • Male
  • Humans
  • Genotype
  • Genetic Predisposition to Disease
  • Gene-Environment Interaction
  • Child Abuse
  • Child
 

Citation

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Haberstick, B. C., Lessem, J. M., Hewitt, J. K., Smolen, A., Hopfer, C. J., Halpern, C. T., … Mullan Harris, K. (2014). MAOA genotype, childhood maltreatment, and their interaction in the etiology of adult antisocial behaviors. Biol Psychiatry, 75(1), 25–30. https://doi.org/10.1016/j.biopsych.2013.03.028
Haberstick, Brett C., Jeffrey M. Lessem, John K. Hewitt, Andrew Smolen, Christian J. Hopfer, Carolyn T. Halpern, Ley A. Killeya-Jones, et al. “MAOA genotype, childhood maltreatment, and their interaction in the etiology of adult antisocial behaviors.Biol Psychiatry 75, no. 1 (January 1, 2014): 25–30. https://doi.org/10.1016/j.biopsych.2013.03.028.
Haberstick BC, Lessem JM, Hewitt JK, Smolen A, Hopfer CJ, Halpern CT, et al. MAOA genotype, childhood maltreatment, and their interaction in the etiology of adult antisocial behaviors. Biol Psychiatry. 2014 Jan 1;75(1):25–30.
Haberstick, Brett C., et al. “MAOA genotype, childhood maltreatment, and their interaction in the etiology of adult antisocial behaviors.Biol Psychiatry, vol. 75, no. 1, Jan. 2014, pp. 25–30. Pubmed, doi:10.1016/j.biopsych.2013.03.028.
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. MAOA genotype, childhood maltreatment, and their interaction in the etiology of adult antisocial behaviors. Biol Psychiatry. 2014 Jan 1;75(1):25–30.
Journal cover image

Published In

Biol Psychiatry

DOI

EISSN

1873-2402

Publication Date

January 1, 2014

Volume

75

Issue

1

Start / End Page

25 / 30

Location

United States

Related Subject Headings

  • White People
  • Psychiatry
  • Monoamine Oxidase
  • Male
  • Humans
  • Genotype
  • Genetic Predisposition to Disease
  • Gene-Environment Interaction
  • Child Abuse
  • Child