The effects of child maltreatment on early signs of antisocial behavior: genetic moderation by tryptophan hydroxylase, serotonin transporter, and monoamine oxidase A genes.
Gene-environment interaction effects in predicting antisocial behavior in late childhood were investigated among maltreated and nonmaltreated low-income children (N = 627, M age = 11.27). Variants in three genes were examined: tryptophan hydroxylase 1 (TPH1), serotonin transporter linked polymorphic region (5-HTTLPR), and monoamine oxidase A (MAOA) upstream variable number tandem repeat. In addition to child maltreatment status, we considered the impact of maltreatment subtypes, developmental timing of maltreatment, and chronicity. Indicators of antisocial behavior were obtained from self-, peer, and adult counselor reports. In a series of analyses of covariance, child maltreatment and its parameters demonstrated strong main effects on early antisocial behavior as assessed by all report forms. Genetic effects operated primarily in the context of gene-environment interactions, moderating the impact of child maltreatment on outcomes. Across the three genes, among nonmaltreated children no differences in antisocial behavior were found based on genetic variation. In contrast, among maltreated children specific polymorphisms of TPH1, 5-HTTLPR, and MAOA were each related to heightened self-report of antisocial behavior; the interaction of 5-HTTLPR and developmental timing of maltreatment also indicated more severe antisocial outcomes for children with early onset and recurrent maltreatment based on genotype. TPH1 and 5-HTTLPR interacted with maltreatment subtype to predict peer reports of antisocial behavior; genetic variation contributed to larger differences in antisocial behavior among abused children. The TPH1 and 5-HTTLPR polymorphisms also moderated the effects of maltreatment subtype on adult reports of antisocial behavior; again, the genetic effects were strongest for children who were abused. In addition, TPH1 moderated the effect of developmental timing of maltreatment and chronicity on adult reports of antisocial behavior. The findings elucidate how genetic variation contributes to identifying which maltreated children are most vulnerable to antisocial development.
Institute of Child Development, University of Minnesota, 51 East River Road, Minneapolis, MN 55455, USA. cicchett@umn.edu
Dante
D
Cicchetti
Fred A
FA
Rogosch
Eric L
EL
Thibodeau
D000987:Antisocial Personality Disorder / Q000235:genetics* / Q000523:psychology; D002648:Child; D002649:Child Abuse / Q000523:psychology*; D002652:Child Behavior / Q000523:psychology*; D005260:Female; D059647:Gene-Environment Interaction; D005838:Genotype; D006801:Humans; D008297:Male; D008995:Monoamine Oxidase / Q000235:genetics*; D010379:Peer Group; D020641:Polymorphism, Single Nucleotide; D011203:Poverty; D050486:Serotonin Plasma Membrane Transport Proteins / Q000235:genetics*; D014365:Tryptophan Hydroxylase / Q000235:genetics*
D050486:Serotonin Plasma Membrane Transport Proteins; D014365:Tryptophan Hydroxylase; D008995:Monoamine Oxidase