Pregnancy is linked to faster epigenetic aging in young women

Energy invested into reproduction is thought to come at the expense of bodily maintenance. Consistent with this hypothesis, women with higher fertility tend to live shorter, less healthy lives. To test whether costs of reproduction are present prior to age-related health declines, we examined the effect of reproduction on six epigenetic clock measures of biological aging in 1,735 young adults in the Philippines. Cross-sectionally, pregnancy number was associated with faster aging across all six epigenetic clocks. Longitudinally, change in pregnancy number was associated with acceleration in two epigenetic clocks. The number of pregnancies fathered was not associated with aging among same-aged cohort men. Our findings support the hypothesis that pregnancy carries a cost that is detectable even in young women. 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.