Author:
Prom-Wormley E. C.,Eaves L. J.,Foley D. L.,Gardner C. O.,Archer K. J.,Wormley B. K.,Maes H. H.,Riley B. P.,Silberg J. L.
Abstract
BackgroundRecent studies among males have reported a genotype–environment interaction (G×E) in which low-activity alleles at the monoamine oxidase A (MAOA) locus conferred greater sensitivity to the effects of childhood adversity on risk for conduct disorder (CD). So far, few studies of females have controlled for gene–environment correlation or used females heterozygous for this X-linked gene.MethodLogistic regression analysis of a sample of 721 females ages 8–17 years from the longitudinal Virginia Twin Study of Adolescent Behavioral Development (VTSABD) assessed the additive effects ofMAOAgenotypes on risk for CD, together with the main effect of childhood adversity and parental antisocial personality disorder (ASP), as well as the interaction ofMAOAwith childhood adversity on risk for CD.ResultsA significant main effect of genotype on risk for CD was detected, where low-activityMAOAimparted the greatest risk to CD in girls while controlling for the significant effects of maternal ASP and childhood adversity. Significant G×E with weak effect was detected when environmental exposure was untransformed, indicating a higher sensitivity to childhood adversity in the presence of the high-activityMAOAallele. The interaction was no longer statistically significant after applying a ridit transformation to reflect the sample sizes exposed at each level of childhood adversity.ConclusionsThe main effect ofMAOAon risk for CD in females, its absence in males and directional difference of interaction is suggestive of genotype–sex interaction. As the effect of G×E on risk for CD was weak, its inclusion is not justified.
Publisher
Cambridge University Press (CUP)
Subject
Psychiatry and Mental health,Applied Psychology
Cited by
67 articles.
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