title: MAOA, abuse exposure and antisocial behaviour: 30-year longitudinal study.
abstract: BACKGROUND
  Recent studies have raised issues concerning the replicability of gene × environment (G × E) interactions involving the monoamine oxidase A (MAOA) gene in moderating the associations between abuse or maltreatment exposure and antisocial behaviour. This study attempted to replicate the findings in this area using a 30-year longitudinal study that has strong resemblance to the original research cohort.
  
  
  OBJECTIVE
  To test the hypothesis that the presence of the low-activity MAOA genotype was associated with an increased response to abuse exposure.
  
  
  METHODS
  Participants were 398 males from the Christchurch Health and Development Study who had complete data on: MAOA promoter region variable number tandem repeat genotype; antisocial behaviour to age 30; and exposure to childhood sexual and physical abuse.
  
  
  RESULTS
  Regression models were fitted to five antisocial behaviour outcomes (self-reported property offending; self-reported violent offending; convictions for property/violent offending; conduct problems; hostility) observed from age 16 to 30, using measures of childhood exposure to sexual and physical abuse. The analyses revealed consistent evidence of G × E interactions, with those having the low-activity MAOA variant and who were exposed to abuse in childhood being significantly more likely to report later offending, conduct problems and hostility. These interactions remained statistically significant after control for a range of potentially confounding factors. Findings for convictions data were somewhat weaker.
  
  
  CONCLUSIONS
  The present findings add to the evidence suggesting that there is a stable G × E interaction involving MAOA, abuse exposure and antisocial behaviour across the life course.
authors.affiliation: Christchurch Health and Development Study, Department of Psychological Medicine, University of Otago, Christchurch, New Zealand. dm.fergusson@otago.ac.nz
authors.forename: David M
authors.initials: DM
authors.lastname: Fergusson
authors.forename: Joseph M
authors.initials: JM
authors.lastname: Boden
authors.forename: L John
authors.initials: LJ
authors.lastname: Horwood
authors.forename: Allison L
authors.initials: AL
authors.lastname: Miller
authors.forename: Martin A
authors.initials: MA
authors.lastname: Kennedy
mesh_terms: D000293:Adolescent; D000294:Adolescent Behavior / Q000523:psychology; D000328:Adult; D000987:Antisocial Personality Disorder / Q000453:epidemiology / Q000235:genetics* / Q000523:psychology; D002648:Child; D002649:Child Abuse / Q000523:psychology / Q000706:statistics & numerical data; D019955:Conduct Disorder / Q000453:epidemiology / Q000235:genetics / Q000523:psychology; D003415:Crime / Q000706:statistics & numerical data*; D019548:Crime Victims / Q000523:psychology; D004812:Epidemiologic Methods; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006791:Hostility; D006801:Humans; D008297:Male; D008995:Monoamine Oxidase / Q000235:genetics*; D009520:New Zealand / Q000453:epidemiology; D010287:Parent-Child Relations; D016133:Polymerase Chain Reaction / Q000706:statistics & numerical data; D011401:Promoter Regions, Genetic / Q000235:genetics; D012917:Social Adjustment; D012959:Socioeconomic Factors; D014754:Violence / Q000706:statistics & numerical data; D055815:Young Adult
chemical_list: D008995:Monoamine Oxidase