부산대학교 도서관

OBJECTIVES: Psychosocial stressors have been linked with accelerated biological aging in adults; however, few studies have examined stressors across the lifecourse in relation to biological aging. METHODS: In 359 individuals (57% White; 34% Black) from the Child Health and Development Studies (CHDS) Disparities (DISPAR) Study, economic (income, education, financial strain), social (parent-child relations, caretaker responsibilities) and traumatic (death of a sibling or child, violence exposure) stressors were assessed at multiple timepoints (birth, age 9, 15 and 50). Life period stress scores were then assessed as childhood (birth-age 15) and adulthood (age 50). At age 50, participants provided blood samples, and DNA methylation was assessed with the EPIC BeadChip. Epigenetic age was estimated using 6 epigenetic clocks (Horvath, Hannum, Skin and blood Age, PhenoAge, GrimAge, Dunedin Pace of Aging). Age acceleration was determined using residuals from regressing chronologic age on each of the epigenetic age metrics. Telomere length was assessed using the qPCR-based methods. RESULTS: In linear regression models adjusted for race and gender, total life stress, childhood and adult stress independently predicted accelerated aging based on GrimAge and faster pace of aging based on the DunedinPace. Associations were attenuated after adjusting for smoking status. In sex-stratified analyses, greater childhood stress was associated with accelerated epigenetic aging among women but not men. No associations were noted with telomere length. CONCLUSION: We found that cumulative stressors across the lifecourse were associated with accelerated epigenetic age, with differences by sex (e.g., accelerated among women). Further research of this association in large and diverse samples is needed.