We expand upon prior work (Gibbons et al., 2012) relating childhood stressor effects, particularly harsh childhood environments, to risky behavior and ultimately physical health by adding longer-term outcomes – deoxyribonucleic acid (DNA) methylation-based measures of accelerated aging (DNAm-aging). Further, following work on the effects of early exposure to danger (McLaughlin et al., 2014), we also identify an additional pathway from harsh childhood environments to DNAm-aging that we label the danger/FKBP5 pathway, which includes early exposure to dangerous community conditions that are thought to impact glucocorticoid regulation and pro-inflammatory mechanisms. Because different DNAm-aging indices provide different windows on accelerated aging, we contrast effects on early indices of DNAm-aging based on chronological age with later indices that focused on predicting biological outcomes. We utilize data from Family and Community Health Study participants (N = 449) from age 10 to 29. We find that harshness influences parenting, which, in turn, influences accelerated DNAm-aging through the risky cognitions and substance use (i.e., behavioral) pathway outlined by Gibbons et al. (2012). Harshness is also associated with increased exposure to threat/danger, which, in turn, leads to accelerated DNAm-aging through effects on FKBP5 activity and enhanced pro-inflammatory tendencies (i.e., the danger/FKBP5 pathway).

The National Institute of Mental Health (NIMH) Research Domain Criteria (RDoC) initiative aims to understand the mechanisms influencing psychopathology through a dimensional approach. Limited research thus far has considered potential racial/ethnic differences in RDoC constructs that are influenced by developmental and contextual processes. A growing body of research has demonstrated that racial trauma is a pervasive chronic stressor that impacts the health of Black Americans across the life course. In this review article, we examine the ways that an RDOC framework could allow us to better understand the biological embedding of racial trauma among Black Americans. We also specifically examine the Negative Valence System domain of RDoC to explore how racial trauma is informed by and can help expand our understanding of this domain. We end the review by providing some additional research considerations and future research directives in the area of racial trauma that build on the RDoC initiative.

Identifying the mechanisms linking early experiences, genetic risk factors, and their interaction with later health consequences is central to the development of preventive interventions and identifying potential boundary conditions for their efficacy. In the current investigation of 412 African American adolescents followed across a 20-year period, we examined change in body mass index (BMI) across adolescence as one possible mechanism linking childhood adversity and adult health. We found associations of childhood adversity with objective indicators of young adult health, including a cardiometabolic risk index, a methylomic aging index, and a count of chronic health conditions. Childhood adversities were associated with objective indicators indirectly through their association with gains in BMI across adolescence and early adulthood. We also found evidence of an association of genetic risk with weight gain across adolescence and young adult health, as well as genetic moderation of childhood adversity's effect on gains in BMI, resulting in moderated mediation. These patterns indicated that genetic risk moderated the indirect pathways from childhood adversity to young adult health outcomes and childhood adversity moderated the indirect pathways from genetic risk to young adult health outcomes through effects on weight gain during adolescence and early adulthood.

We examined the prospective relations between a cultural risk factor, perceived racial discrimination (PRD), and subsequent negative affect and health behavior (smoking) in a panel of 889 African American children (part of the Family and Community Health Study). Cultural moderators (protective factors) of these relations were also examined. PRD was assessed six times from ages 10.5 (Wave 1) to 24.5 (Wave 6), and negative affect (anger and depressive symptoms) was assessed at Wave 2 (age 12.5) and Wave 6 (age 24.5). Results indicated that Wave 1 PRD predicted Wave 6 smoking, controlling for multiple factors related to smoking and/or PRD, including smoking at age 15.5. Structural equation models indicated that these relations between Wave 1 PRD and smoking were mediated by both early and later negative affect. The models also indicated that Wave 1 PRD had a direct impact on Wave 6 anger (assessed 14 years later), controlling for the effects of PRD on early affect. Cultural socialization was associated with lower rates of adolescent smoking, and it buffered the relation between PRD and Wave 6 anger. The impact of early PRD experiences along with suggestions for culturally informed interventions and preventive interventions that might buffer against early PRD effects are discussed.