Abstract
Although genetic and environmental factors are separately implicated in the development of antisocial behavior (ASB), interactive
models have emerged relatively recently, particularly those incorporating molecular genetic data. Using a large sample of
male Caucasian adolescents and young adults from the National Longitudinal Study of Adolescent Health (Add Health), the association
of deviant peer affiliation, the 30-base pair variable number tandem repeat polymorphism in promoter region of the monoamine
oxidase-A (MAOA) gene, and their interaction, with antisocial behavior (ASB) was investigated. Weighted analyses accounting
for over-sampling and clustering within schools as well as controlling for age and wave suggested that deviant peer affiliation
and MAOA genotype were each significantly associated with levels of overt ASB across a 6-year period. Only deviant peer affiliation
was significantly related to covert ASB, however. Additionally, there was evidence suggestive of a gene-environment interaction
(G × E) where the influence of deviant peer affiliation on overt ASB was significantly stronger among individuals with the
high-activity MAOA genotype than the low-activity genotype. MAOA was not significantly associated with deviant peer affiliation,
thus strengthening the inference of G × E rather than gene-environment correlation (rGE). Different forms of gene-environment
interplay and implications for future research on ASB are discussed.
models have emerged relatively recently, particularly those incorporating molecular genetic data. Using a large sample of
male Caucasian adolescents and young adults from the National Longitudinal Study of Adolescent Health (Add Health), the association
of deviant peer affiliation, the 30-base pair variable number tandem repeat polymorphism in promoter region of the monoamine
oxidase-A (MAOA) gene, and their interaction, with antisocial behavior (ASB) was investigated. Weighted analyses accounting
for over-sampling and clustering within schools as well as controlling for age and wave suggested that deviant peer affiliation
and MAOA genotype were each significantly associated with levels of overt ASB across a 6-year period. Only deviant peer affiliation
was significantly related to covert ASB, however. Additionally, there was evidence suggestive of a gene-environment interaction
(G × E) where the influence of deviant peer affiliation on overt ASB was significantly stronger among individuals with the
high-activity MAOA genotype than the low-activity genotype. MAOA was not significantly associated with deviant peer affiliation,
thus strengthening the inference of G × E rather than gene-environment correlation (rGE). Different forms of gene-environment
interplay and implications for future research on ASB are discussed.
- Content Type Journal Article
- Pages 1-12
- DOI 10.1007/s10802-010-9474-2
- Authors
- Steve S. Lee, Department of Psychology, University of California, Los Angeles (UCLA), 1285 Franz Hall, Box 951563, Los Angeles, CA 90095-1563, USA
- Journal Journal of Abnormal Child Psychology
- Online ISSN 1573-2835
- Print ISSN 0091-0627