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This review synthesises current evidence on how pregnancy, postpartum stressors, and reproductive history shape maternal biological ageing, integrating findings from telomere biology and emerging epigenetic ageing measures. Pregnancy represents a period of substantial metabolic, hormonal, and immunological demand and is increasingly conceptualised as a transient state of accelerated biological ageing. While telomere shortening is not consistently detectable during gestation, epigenetic clocks indicate a temporary increase in biological age, which is only partially reversible postpartum. Across the life course, higher parity is associated with shorter TL, with evidence suggesting a cumulative effect that becomes most apparent in later life and around the menopausal transition. However, this relationship is heterogeneous and modified by factors including age at last birth, breastfeeding, and socioeconomic context. Postpartum represents a critical and underexplored window in which sleep deprivation, psychological stress, and social factors converge to influence telomere dynamics. In particular, poor sleep quality and postpartum depression (PPD) are consistently linked to accelerated telomere attrition and epigenetic ageing, with emerging evidence of a bidirectional relationships whereby shorter TL may also predispose to PPD. Overall, evidence supports a model in which reproductive events impose are associated with measurable transient and cumulative costs to cellular ageing biomarkers. These findings highlight the importance of incorporating postpartum health, particularly sleep and mental health support, into life-course models of ageing and underscore the need for longitudinal, mechanistic, and intervention-focused research in maternal populations.<\/jats:p>","DOI":"10.1007\/s10522-026-10487-0","type":"journal-article","created":{"date-parts":[[2026,8,10]],"date-time":"2026-08-10T12:53:42Z","timestamp":1786366422000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Maternal biological ageing and telomere attrition across parity, pregnancy, and the postpartum period"],"prefix":"10.1007","volume":"27","author":[{"given":"Laura","family":"Collopy","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yana","family":"Kolenichenko","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,8,10]]},"reference":[{"key":"10487_CR1","doi-asserted-by":"publisher","DOI":"10.7554\/eLife.73420","author":"D Belsky","year":"2022","unstructured":"Belsky D, Caspi A, Cocoran D, Sugden L, Poulton R, Arseneault L, Baccarelli A, Chamarti K, Gao X, Hannon E, Lee H, Harrington H, Houts R, Kothari M, Kwon D, Mill J, Scwartz J, Vokonas P, Wang C, Williams B, Moffitt T (2022) DunedinPACE, a DNA methylation biomarker of the pace of aging. 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