Several research teams have previously traced patterns of emerging conduct problems (CP) from early or middle childhood. The current study expands on this previous literature by using a genetically-informed, experimental, and long-term longitudinal design to examine trajectories of early-emerging conduct problems and early childhood discriminators of such patterns from the toddler period to adolescence. In addition to examining child, family, and community level discriminators of patterns of emerging CP, we accounted for genetic susceptibility using polygenic scores and using the study’s experimental design, whether random assignment to the Family Check-Up (FCU) discriminated trajectory groups. In addition, in accord with differential susceptibility theory, we also tested whether effects of the FCU were stronger for those children at higher genetic susceptibility (genetic x intervention (GxI) effects).
Methods
The sample represents a cohort of 731 toddlers and diverse families recruited from Women, Infant, and Children Nutritional Supplement Programs recruited on the basis of socioeconomic, child, and family risk at three sites in the US varied in urbancity, and assessed on 9 occasions between ages 2 to 14. Polygenic risk scores were based on a recent meta-GWAS of aggression in middle childhood (Pappa et al., 2015). Parenting was coded from 50 minutes of parent-child observational tasks at age 2 to create a composite of positive behavior support (Dishion et al., 2008), with sociodemographic risk and parental depression (CES-D, Radloff, 1977) assessed using maternal report at child age 2. Child inhibitory control at age 2 was also based on maternal report using the Children’s Behavior Questionnaire (CBQ; Rothbart et al., 2001). Finally, primary caregivers reported on child oppositional and aggressive behavior from ages 2 to 14 using overlapping items from the preschool and school-age versions of the Child Behavior Checklist (oppositional-aggressive factor).
Results
Results augmented previous findings documenting the influence of child (inhibitory control, gender) and family (harsh parenting, parental depression and educational attainment) risk for those with persistently high vs. persistently low levels of CP from ages 2 to 14. In addition, children in the FCU were overrepresented in the persistent low versus persistent high CP group, but such direct effects were qualified by an interaction between the intervention and genetic susceptibility that was consistent with differential susceptibility.
Discussion
Implications are discussed for early identification and specifically, prevention efforts addressing early child and family risk, with a focus on how children at higher genetic susceptibility might be more malleable to early family-based interventions.