title: Interaction of prenatal exposure to cigarettes and MAOA genotype in pathways to youth antisocial behavior.
abstract: Genetic susceptibility to antisocial behavior may increase fetal sensitivity to prenatal exposure to cigarette smoke. Testing putative gene x exposure mechanisms requires precise measurement of exposure and outcomes. We tested whether a functional polymorphism in the gene encoding the enzyme monoamine oxidase A (MAOA) interacts with exposure to predict pathways to adolescent antisocial behavior. We assessed both clinical and information-processing outcomes. One hundred seventy-six adolescents and their mothers participated in a follow-up of a pregnancy cohort with well-characterized exposure. A sex-specific pattern of gene x exposure interaction was detected. Exposed boys with the low-activity MAOA 5' uVNTR (untranslated region variable number of tandem repeats) genotype were at increased risk for conduct disorder (CD) symptoms. In contrast, exposed girls with the high-activity MAOA uVNTR genotype were at increased risk for both CD symptoms and hostile attribution bias on a face-processing task. There was no evidence of a gene-environment correlation (rGE). Findings suggest that the MAOA uVNTR genotype, prenatal exposure to cigarettes and sex interact to predict antisocial behavior and related information-processing patterns. Future research to replicate and extend these findings should focus on elucidating how gene x exposure interactions may shape behavior through associated changes in brain function.
authors.affiliation: Institute for Juvenile Research, Department of Psychiatry, University of Illinois at Chicago, Chicago, IL 60608, USA. lwakschlag@psych.uic.edu
authors.forename: L S
authors.initials: LS
authors.lastname: Wakschlag
authors.forename: E O
authors.initials: EO
authors.lastname: Kistner
authors.forename: D S
authors.initials: DS
authors.lastname: Pine
authors.forename: G
authors.initials: G
authors.lastname: Biesecker
authors.forename: K E
authors.initials: KE
authors.lastname: Pickett
authors.forename: A D
authors.initials: AD
authors.lastname: Skol
authors.forename: V
authors.initials: V
authors.lastname: Dukic
authors.forename: R J R
authors.initials: RJ
authors.lastname: Blair
authors.forename: B L
authors.initials: BL
authors.lastname: Leventhal
authors.forename: N J
authors.initials: NJ
authors.lastname: Cox
authors.forename: J L
authors.initials: JL
authors.lastname: Burns
authors.forename: K E
authors.initials: KE
authors.lastname: Kasza
authors.forename: R J
authors.initials: RJ
authors.lastname: Wright
authors.forename: E H
authors.initials: EH
authors.lastname: Cook
mesh_terms: D000293:Adolescent; D000294:Adolescent Behavior / Q000502:physiology; D000328:Adult; D004777:Environment; D005260:Female; D005500:Follow-Up Studies; D020022:Genetic Predisposition to Disease / Q000453:epidemiology; D005838:Genotype; D006801:Humans; D008297:Male; D008995:Monoamine Oxidase / Q000235:genetics*; D010641:Phenotype; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000453:epidemiology / Q000235:genetics*; D012307:Risk Factors; D017678:Sex Distribution; D012907:Smoking / Q000009:adverse effects* / Q000453:epidemiology / Q000235:genetics*; D012920:Social Behavior Disorders / Q000453:epidemiology / Q000235:genetics*; D055815:Young Adult
chemical_list: D008995:Monoamine Oxidase