The effects of child maltreatment on early signs of antisocial behavior: Genetic moderation by tryptophan hydroxylase, serotonin transporter, and monoamine oxidase A genes

Abstract

<jats:title>Abstract</jats:title><jats:p>Gene–environment interaction effects in predicting antisocial behavior in late childhood were investigated among maltreated and nonmaltreated low-income children (<jats:italic>N</jats:italic>= 627,<jats:italic>M</jats:italic>age = 11.27). Variants in three genes were examined: tryptophan hydroxylase 1 (<jats:italic>TPH1</jats:italic>), serotonin transporter linked polymorphic region (<jats:italic>5-HTTLPR</jats:italic>), and monoamine oxidase A (<jats:italic>MAOA</jats:italic>) 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<jats:italic>TPH1</jats:italic>,<jats:italic>5-HTTLPR</jats:italic>, and<jats:italic>MAOA</jats:italic>were each related to heightened self-report of antisocial behavior; the interaction of<jats:italic>5-HTTLPR</jats:italic>and developmental timing of maltreatment also indicated more severe antisocial outcomes for children with early onset and recurrent maltreatment based on genotype.<jats:italic>TPH1</jats:italic>and<jats:italic>5-HTTLPR</jats:italic>interacted with maltreatment subtype to predict peer reports of antisocial behavior; genetic variation contributed to larger differences in antisocial behavior among abused children. The<jats:italic>TPH1</jats:italic>and<jats:italic>5-HTTLPR</jats:italic>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,<jats:italic>TPH1</jats:italic>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.</jats:p>

Molecular genetics and antisocial behavior: Where do we stand?

“…[2][3][4] The hypothesis that a close linkage between behavior and genetics may exist comes from studies on twins and adoptees, 5 and is supported by several pieces of evidence recently generated by scientific research. 6 A number of candidate genes have been indeed investigated in association with antisocial behavior, especially genes involved in serotonergic [7][8][9][10][11] and dopaminergic [12][13][14] circuits.…”

Social skills and psychopathic traits in maltreated adolescents

“…Despite the severity of victimization suffered by the MTA group participants, the mean of their PCL: YV total scores did not characterize them as psychopaths (even though it was statistically higher than CG score), and the correlations between maltreatment and antisocial traits were relatively mild or moderate. Further studies should also investigate if other variables might influence the development of psychopathic traits in MTA, such as genetic inheritance, period of onset, duration and intensity of maltreatment [48].…”

A Neural Perspective of Immoral Behavior and Psychopathy

“…However, genetic factors alone may not be sufficient, and some gene-environment interaction is necessary. In a study by Cicchetti, Rogosch, and Thibodeau (2012) maltreated and abused children with specific polymorphisms of serotonin transporter gene 5-HTTLPR, serotonin synthesis gene TPH1, and neurotransmitter (serotonin, dopamine, and norepinephrine) degrader monoamine oxidase A (MAOA) demonstrated higher levels of antisocial behavior, yet differences in antisocial behavior could not be explained by genotype in children who had not experienced abuse and maltreatment. That is, all effects of genotype occurred only within the context of gene-environment interactions.…”