Childhood adversity predicts black young adults' DNA methylation-based accelerated aging: A dual pathway model

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 (DNA(m)-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 DNA(m)-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 DNA(m)-aging indices provide different windows on accelerated aging, we contrast effects on early indices of DNA(m)-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 DNA(m)-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 DNA(m)-aging through effects on FKBP5 activity and enhanced pro-inflammatory tendencies (i.e., the danger/FKBP5 pathway).

Automated summary

This study builds upon prior research on the impact of childhood stressors and harsh environments on risky behavior and physical health, by adding measures of accelerated aging based on DNA methylation. The findings suggest that harsh childhood environments influence accelerated DNA aging through risky cognition and substance use pathways, as well as through the danger/FKBP5 pathway involving early exposure to threats and enhanced pro-inflammatory tendencies.