Can family cohesion and parent-child relationship quality buffer the effects of parental adverse childhood experiences on adolescent epigenetic age acceleration?

Introduction: Parental adverse childhood experiences (ACEs), or adversities parents experience when they are children, significantly impact their children's biobehavioral outcomes. Maternal ACEs are associated with epigenetic age acceleration (EAA; faster biological aging) in infants (Sosnowski et al., 2024) and young children (Nwanaji-Enwerem et al., 2021). While the effects of paternal ACEs and EAA have not been directly examined, emerging studies indicate that paternal ACEs correlate with DNA methylation in their infants, and these methylated CpG (genetic) were associated with externalizing outcomes three years later (Merrill et al., 2021). Family factors (e.g., positive parenting practices) can buffer the association between maternal ACEs and EAA (Sullivan et al., 2023). However, it is unclear if family factors buffer the effects of both maternal and paternal ACEs and EAA; and whether the associations between parental ACEs and EAA are observed later in development, like adolescence. Hypotheses: To examine whether parental ACEs and youth’s EAA are moderated by family factors (i.e., family cohesion, parent-child relationship quality). We hypothesized that both fathers’ and mothers’ family-level (e.g., maltreatment, family dysfunction) and community-level (e.g., discrimination, community violence) ACEs would be associated with EAA, but that family factors would mitigate this effect. Sample: Participants were from the ENLACEs study. Participating families had to be of Mexican descent, and youth had to be between the ages of 12 and 15 at baseline. Our study included family triads recruited from northern Indiana: youth (n = 120), mothers (n = 120), and fathers (n = 120). Study Methods: Participants were recruited with the help of community-based partners. Bilingual and bicultural assistants administered surveys to parents in English or Spanish, while youth surveys were self-administered on tablets. Surveys assessing parental ACEs were collected during Wave 1, youth-reported questionnaires of parent-child relationships and family cohesion were collected in Wave 2, and salivary DNA for epigenetic analysis was collected in Wave 2. Epigenetic age acceleration was estimated from two clocks: the Pediatric Buccal Epigenetic (PedBE) and Horvarth. We employed path analysis and maximum likelihood estimations with robust standard errors in R. Results Consistent with our hypothesis, the association between fathers' family-level ACEs and youth EAA was moderated by parent-child relationship in both clocks: PedBE (beta=-0.03; p=0.086) and Horvath (beta=-0.173; p=0.004). Similarly, the association between mothers’ community-level ACEs and EAA was moderated by family cohesion: PedBE (beta=-0.009; p=0.041) and Horvath (beta=-0.045; p=0.001). In contrast to hypothesized directions, family cohesion moderated the association between fathers and mothers’ family-level ACEs and EAA: PedBE (beta=0.021; p=0.008) and Horvath (beta=0.018; p=0.036), respectively. Conclusion Consistent with previous mother-child dyadic studies, fathers’ ACEs can similarly impact their children’s EAA, and these observations can also be noted during adolescence. While seemingly counterintuitive, this finding points to family cohesion as an element by which family factors can strongly affect their children's biology, whether positively or negatively. Future research will be necessary to elucidate the nuanced impact of family factors on the potential intergenerational biological consequences of parental ACEs, but these findings lay a foundation for future family-based interventions.