Gene-Environment Correlations Underlying Genetic Predisposition for Middle Childhood Aggression and Peer Deviancy and Rejection

• In Event: 1-072 - Gene-Environment Correlations As Critical Influences on Children’s Social Relationships

Integrative Statement

Negative peer relationships form through reciprocal transactions between a child’s behavior and his/her peers. In particular, aggression in middle childhood can lead to affiliating with deviant peers but also evoke peer rejection (Chen, Drabick, & Burgers, 2014). Additionally, these peer transactions may be genetically mediated such that children’s genetic predispositions are associated with the quality of their peer relationships. These genetic-environment associations are known as gene-environment correlations (rGEs). Thus, a child’s genetic predisposition, operating through rGE, may lead to active selection into deviant peer groups but also may evoke peer rejection via offensive behavior (Brendgen & Boivin, 2015). Thus, it is important to understand the direction of effect and etiology underlying the development of negative peer relationships. The present study addressed this by examining how genetic predisposition for aggression, and possible rGE, contributed to aggressive behavior, peer rejection, and deviant peer affiliation from ages 7.5 to 10.5.

Participants were from a longitudinal randomized prevention trial to improve parenting (n-intervention=252; n-control=250), and consisted of 49% female, 45% Caucasian, 31% African American, 12% Hispanic, 10% Biracial, 2% Other. The current study used annual assessments from child ages 7.5 to 10.5. Primary caregivers reported on their child’s aggression using the CBCL (Achenbach, 2001), and deviant peer affiliation (DP) and peer rejection (PR) using the Peer Acceptance and Social Affiliation scale (Dishion & Kavanagh, 2003). Polygenic risk scores (PRSs) were used to capture genetic predisposition by aggregating across genetic polymorphisms, extending previous twin and candidate gene studies. Genetic polymorphisms for the current PRS were informed by a meta-genome wide association study of childhood aggression (Pappa et al., 2016), and filtered using gene-set enrichment analyses to retain functional genetic variants at a p < .01 cutoff. A cross-time cross-lagged model included all within-time correlations across constructs, autoregressive paths within constructs across time, and cross-lagged paths across constructs and time. The PRS was considered a distal predictor of all constructs across time. Analyses controlled for child age, sex, ethnicity, intervention group, demographic risk factors, and genetic ancestry (using principal components analysis).

Results are presented in Figure 1. The PRS was associated with age 7.5 DP, age 9.5 DP, aggression, and PR, and age 10.5 aggression. In terms of cross-lagged paths, from age 7.5 to 8.5, DP and aggression were associated with PR, and PR was associated with DP. From age 8.5 to 9.5, aggression was associated with DP and PR, and PR was associated with DP. From age 9.5 to 10.5, aggression was associated with DP and PR.

Broadly, the PRS was associated with aggression and DP, which may represent a child selecting into deviant peer groups based on genetic predisposition operating via aggressive behavior. The PRS was also associated with PR, which could be due to genetic evocation of peer behavior. These rGEs exist within a larger pattern of DP and aggression contributing to PR over time, with PR also reinforcing DP. Collectively, these bidirectional transactions indicate that negative peer relationships are driven in part by children’s genetic predisposition for aggression operating via rGE.

Authors

• Kit Elam, Arizona State University
  Presenting Author

• Kathryn Lemery-Chalfant, Arizona State University
  Non-Presenting Author

• Sierra Clifford, Arizona State University
  Non-Presenting Author

• Ariana Ruof, Arizona State University
  Non-Presenting Author

• Thomas Dishion, Arizona State University
  Non-Presenting Author

• Daniel S. Shaw, University of Pittsburgh
  Non-Presenting Author

• Melvin N. Wilson, University of Virginia
  Non-Presenting Author