Calen P. Ryan, Nanette R. Lee, Delia B. Carba, Julie L. MacIsaac, David T.S. Lin, Parmida Atashzay, Daniel W. Belsky, Michael S. Kobor, Christopher W. Kuzawa
A central prediction of evolutionary theory is that energy invested into reproduction comes at the expense of somatic maintenance and repair, accelerating biological aging. Supporting this prediction are findings that high fertility among women predicts shorter lifespan and poorer health later in life. However, biological aging is thought to begin before age-related health declines, limiting the applicability of morbidity and mortality for studying the aging process earlier in life. Here, we examine the relationship between reproductive history and biological aging in a sample of young (20 to 22yo) men and women from the Cebu Longitudinal Health and Nutrition Survey, located in the Philippines (n = 1,735). We quantify biological aging using six measures, collectively known as epigenetic clocks, reflecting various facets of cellular aging, health, and mortality risk. In a subset of women, we test whether longitudinal changes in gravidity between young and early–middle adulthood (25 to 31yo) are associated with changes in epigenetic aging during that time. Cross-sectionally, gravidity was associated with all six measures of accelerated epigenetic aging in women (n = 825). Furthermore, longitudinal increases in gravidity were linked to accelerated epigenetic aging in two epigenetic clocks (n = 331). In contrast, the number of pregnancies a man reported fathering was not associated with epigenetic aging among same-aged cohort men (n = 910). These effects were robust to socioecological, environmental, and immunological factors, consistent with the hypothesis that pregnancy accelerates biological aging and that these effects can be detected in young women in a high-fertility context. © 2024 the Author(s). Published by PNAS.
Robert N. Butler Columbia Aging Center, Mailman School of Public Health, Columbia University, New York, 10032, NY, United States; USC-Office of Population Studies Foundation, University of San Carlos, Talamban, Cebu City, 6000, Philippines; BC Children’s Hospital Research Institute, University of British Columbia, Vancouver, V5Z 4H4, BC, Canada; Department of Epidemiology, Columbia University, Mailman School of Public Health, Columbia University, New York, 10032, NY, United States; Child and Brain Development Program, Canadian Institute for Advanced Research, Toronto, M5G 1M1, ON, Canada; Department of Medical Genetics, Faculty of Medicine, University of British Columbia, Vancouver, V6T 2A1, BC, Canada; Centre for Molecular Medicine and Therapeutics, Vancouver, V5Z 4H4, BC, Canada; Department of Anthropology, Northwestern University, Evanston, 60208, IL, United States
