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From the Department of Epidemiology (Suglia), Rollins School of Public Health, Emory University, Atlanta, Georgia; School of Global Integrative Studies (Clausing) and Center for Brain, Biology, and Behavior (Clausing), University of Nebraska-Lincoln, Lincoln, Nebraska; Department of Sociomedical Sciences (Shelton), Mailman School of Public Health, New York, New York; Department of Human Genetics (Conneely, Baccarelli), School of Medicine, Emory University, Atlanta, Georgia; Department of Environmental Health (Prada-Ortega), Mailman School of Public Health, New York, New York; Department of Epidemiology (DeVivo), Harvard T. H. Chan School of Public Health; Channing Division of Network Medicine (DeVivo), Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; Department of Epidemiology (Factor-Litvak), Mailman School of Public Health, New York, New York; Child Health and Development Studies (Cirillo, Cohn), Public Health Institute, Berkeley; and Department of Sociology (Link), University of California Riverside, Riverside, California.
Published: April 2024
AI Article Synopsis
Article Abstract
Objective: Psychosocial stressors have been linked with accelerated biological aging in adults; however, few studies have examined stressors across the life course in relation to biological aging.
Methods: In 359 individuals (57% White, 34% Black) from the Child Health and Development Studies Disparities 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 time points (birth and ages 9, 15, and 50 years). Experiences of major discrimination were assessed at age 50. Life period stress scores were then assessed as childhood (birth-age 15 years) and adulthood (age 50 years). At age 50 years, participants provided blood samples, and DNA methylation was assessed with the EPIC BeadChip. Epigenetic age was estimated using six 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 quantitative polymerase chain reaction-based methods.
Results: In linear regression models adjusted for race and gender, total life stress, and 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.
Conclusions: We found that cumulative stressors across the life course 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.
