Lauren S. Wakschlag , PhD 1 , 7 , Emily O. Kistner , PhD 2 , Daniel S. Pine , MD 3 , Gretchen Biesecker , PhD 1 , Kate E. Pickett , PhD 4 , Andrew Skol , PhD 5 , Vanja Dukic , PhD 2 , R. James Blair , PhD 3 , Bennett L. Leventhal , MD 1 , Nancy Cox , PhD 5 , James Burns , MS 1 , Kristen E. Kasza , MS 2 , Rosalind J. Wright , MD, MPH 6 , Edwin H. Cook , MD 1
3 March 2009
Genetic susceptibility to antisocial behavior may increase fetal sensitivity to prenatal exposure to cigarette smoke. Testing putative Gene × 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. 176 adolescents and their mothers participated in a follow-up of a pregnancy cohort with well-characterized exposure. A sex-specific pattern of gene × exposure interaction was detected. Exposed boys with the low activity MAOA 5’ untranslated region variable number of tandem repeats (uVNTR) 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 may focus on elucidating how gene × exposure interactions may shape behavior via associated changes in brain function.