Moderating role of the MAOA genotype in antisocial behaviour.
BACKGROUND
Recent studies have examined gene×environment (G×E) interactions involving the monoamine oxidase A (MAOA) gene in moderating the associations between exposure to adversity and antisocial behaviour. The present study examined a novel method for assessing interactions between a single gene and multiple risk factors related to environmental and personal adversity.


OBJECTIVE
To test the hypothesis that the presence of the low-activity MAOA genotype was associated with an increased response to a series of risk factors.


METHODS
Participants were 399 males from the Christchurch Health and Development Study who had complete data on: (a) MAOA promoter region variable number tandem repeat genotype; (b) antisocial behaviour (criminal offending) to age 30 and convictions to age 21; and (c) maternal smoking during pregnancy, IQ, childhood maltreatment and school failure.


RESULTS
Poisson regression models were fitted to three antisocial behaviour outcomes (property/violent offending ages 15-30; and convictions ages 17-21), using measures of exposure to adverse childhood circumstances. The analyses revealed consistent evidence of G x E interactions, such that those with the low-activity MAOA variant who were exposed to adversity in childhood were significantly more likely to report offending in late adolescence and early adulthood.


CONCLUSIONS
The present findings add to the evidence suggesting that there is a stable G x E interaction involving MAOA, a range of adverse environmental and personal factors, and antisocial behaviour across the life course. These analyses also demonstrate the utility of using multiple environmental/personal exposures to test G×E interactions.
Christchurch Health and Development Study, University of Otago, Christchurch, PO Box 4345, Christchurch, New Zealand. dm.fergusson@otago.ac.nz
David M
DM
Fergusson
Joseph M
JM
Boden
L John
LJ
Horwood
Allison
A
Miller
Martin A
MA
Kennedy
D000328:Adult; D000987:Antisocial Personality Disorder / Q000453:epidemiology / Q000235:genetics*; D002648:Child; D002649:Child Abuse / Q000706:statistics & numerical data*; D003415:Crime / Q000331:legislation & jurisprudence / Q000706:statistics & numerical data*; D004522:Educational Status; D059647:Gene-Environment Interaction; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008137:Longitudinal Studies; D008297:Male; D018598:Minisatellite Repeats / Q000235:genetics; D008995:Monoamine Oxidase / Q000235:genetics*; D015999:Multivariate Analysis; D009520:New Zealand / Q000453:epidemiology; D016133:Polymerase Chain Reaction; D011401:Promoter Regions, Genetic / Q000235:genetics; D012044:Regression Analysis; D012307:Risk Factors; D012907:Smoking / Q000453:epidemiology
D008995:Monoamine Oxidase