Abstract
•Maternal stress reported during pregnancy was prospectively associated with shortened buccal cell telomere length (an indicator of cellular aging) in the offspring at 3–5 years of age.•This study supports the theory that accelerated biological aging is a mechanism through which in utero exposure to stress may increase risk for aging-related disease and earlier death.•These findings extend previous reports by documenting that the effects of maternal stress on offspring aging biology are detectable in early childhood.
Prenatal exposure to stress increases risk for suboptimal child and adult mental and physical health outcomes, hypothesized to occur via fetal exposure to maternal stress hormones that alter growth and development. One proposed pathway through which stress exposure in utero could affect the offspring is by accelerating cellular aging in the form of telomere attrition. We tested this hypothesis in a cohort of 111 mother-child dyads, where mothers were assessed over 6 or more years, beginning prior to conception, and later during pregnancy, postpartum, and when the children were 3–5 years old. Adjusting for child age and concurrent maternal stress, we found that higher maternal perceived stress in the 3rd trimesters of pregnancy was predictive of shorter child buccal telomere length (bTL) (β = −0.24, p < .05), while maternal preconception and postpartum maternal stress were not associated with bTL (all p’s > 0.42). These findings suggest a vulnerable time period in pregnancy when maternal stress influences offspring telomere length, suggesting the early embedding of adult disease might occur through biological aging pathways.