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- All Subjects: parenting
- Creators: Lemery-Chalfant, Kathryn
Prior research has established a relation between parenting behaviors and symptoms of child psychopathology, and this association may be influenced by both genetic and environmental factors. Gene-environment correlation, or the influence of a child’s genes on the environment they receive, represents one possible mechanism through which genes and environment combine to influence child outcomes. This study examined evocative gene-environment correlation in the relation between parenting and symptoms of child psychopathology in a sample of 676 twins (51.5% female, 58.5% Caucasian, 23.7% Hispanic/Latinx, primarily middle class, MAge=8.43, SD=.62) recruited from Arizona birth records. Using univariate ACE twin biometric models, genetic influences were found to moderately contribute to internalizing symptoms (A=.47, C=.25, E=.28), while externalizing (A=.86, E=.14) and ADHD (A=.84, E=.16) symptoms were found to be highly heritable. The genetic influences for positive (C=.54, E=.46) and negative (C=.44, E=.56) parenting were smaller and found to be nonsignificant. The correlations between parenting and types of psychopathology were examined and bivariate Cholesky decompositions were conducted for statistically significant correlations. Negative parenting was moderately positively correlated with externalizing and ADHD symptoms; the relation between externalizing symptoms and negative parenting was found to be due to shared genetics, whereas the relation between negative parenting and ADHD symptoms was due to the shared environment. The mixed results regarding the role of gene environment correlation in relations between parenting and child psychopathology indicate that further research on the mechanisms of this relation is needed.
Analyses were performed in a path analysis framework. To test these research questions, the current study employed two polygenic risk scores. The first, a theory-based score, was formed using single-nucleotide polymorphisms (SNPs) from receptor systems implicated in the amplification of positive effects in the presence of new/exciting stimuli and/or pleasure derived from using substances. The second, an empirically-based score, was formed using a data-driven approach that explained a large amount of variance in SUDs. Together, these scores allowed the present study to test explanations for the relations among parent AUD, parental knowledge, peer substance use, and SUDs.
Results of the current study found that having parents with less knowledge or an AUD conferred greater risk for SUDs, but only for those at higher genetic risk for behavioral undercontrol. The current study replicated research findings suggesting that peer substance use mediated the effect of parental AUD on SUD. However, it adds to this literature by suggesting that some mechanism other than increased behavioral undercontrol explains relations among parental AUD, peer substance use, and emerging adult SUD. Taken together, these findings indicate that children of parents with AUDs comprise a particularly risky group, although likelihood of SUD within this group is not uniform. These findings also suggest that some of the most important environmental risk factors for SUDs exert effects that vary across level of genetic propensity.