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Poster #22 - Genetic Risk for Child Psychopathology is Mitigated by Early Family Prevention

Fri, March 24, 10:30 to 11:15am, Salt Palace Convention Center, Floor: 1, Hall A-B

Abstract

As children at genetic risk for internalizing problems are more likely to develop general psychopathology in adolescence and adulthood, elucidating environmental and genetic contributions to etiology is important. Mounting evidence shows that problem behaviors are not fixed, but rather can be mitigated through family-based intervention (Shaw et al., 2009). Although the genetic contribution to internalizing problems is not well understood, recent research has shown that internalizing polygenic risk scores (PRS) are associated with childhood temperament and internalizing symptoms (Wang et al., 2020). The Early Steps Multisite study, a large randomized control trial (RCT) of the Family Check-Up, provides a rare opportunity to examine the contributions of genetic risk for internalizing symptoms and an intervention aimed at reducing youth problem behaviors by providing support to parents and families (Dishion et al., 2008). The present study builds on a small literature to examine whether early family-based prevention can buffer the association between genetic risk and psychopathology across childhood.

Racially and ethnically diverse families were recruited at child age 2 from rural, urban, and suburban low-income communities (M income = $28,993), and followed longitudinally in an RCT (N = 731, 50% female, 50% White, 28% Black, 13% biracial, 13% Hispanic, representative 515 genotyped). Primary caregivers reported children’s psychopathology symptoms with the Child Behavior Checklist at ages 2, 3, 4, and then 7.5, 8.5, 9.5, and 10.5 years. With high co-occurrence between internalizing and externalizing symptoms, we applied a bi-factor confirmatory factor analysis to the symptom data at each age, yielding a P factor representing general psychopathology. Based on the Jami et al. (2022) discovery genome-wide association meta-analysis of internalizing behavior in childhood, we formed PRS for internalizing problems at p-value thresholds of .1, .05, .01, .001, .0001, .00001, and .000001. We conducted separate analyses regressing the P factor on genetic risk, Family Check-Up, and their interaction at each age, controlling for principal components representing genetic ancestry, sex, age, and family income. Sensitivity analyses ensured that findings held for the major racial/ethnic groups.

Genetic risk interacted with Family Check-Up group to predict the P factor at ages 7.5 (b = -.12, t = -2.15, p = .033), 8.5 (b = -.13, t = -2.15, p = .032), 9.5 (b = -.16, t = -2.64, p = .009), and 10.5 (b = -.14, t = -2.22, p = .027), but not in early childhood. Genetic association was found at some p-value thresholds, but not others. Figure 1 depicts the interaction at age 9.5, suggesting that children in the intervention group with high genetic risk had the lowest P factors (simple slope for intervention group, b = -.09, t = -2.22, p = .027; control group b = .05, t = 1.41, p = .160). Family intervention may reduce psychopathology symptoms for children at higher genetic risk for internalizing behaviors. Findings have implications for intervention efficacy and resilience theory.

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