bioRxivGenomicsPreprint
Maternal psychosocial risk factors and offspring gestational epigenetic age acceleration in a South African birth cohort study
Nastassja KoeniD, Meaghan J. JonesiD, Raymond T. NhapiiD, Kirsten Ann DonaldiD, Whitney BarnettiD, Nadia HoffmaniD, Julia L. MacIsaaciD, Alexander M. MoriniD, David T S LiniD, Michael Steffen KoboriD, Karestan Chase KoeneniD, Heather Joy ZariD, Dan Joseph SteiniD
Abstract
Epigenetic age (EA) acceleration is associated with higher risk of chronic disease and mortality in adults. However, little is known about whether and how in utero exposures might shape gestational EA acceleration at birth. We aimed to explore associations between maternal psychosocial risk factors and offspring gestational EA acceleration at birth in a South African birth cohort study - the Drakenstein Child Health Study. Maternal psychosocial risk factors included trauma/stressor exposure; posttraumatic stress disorder (PTSD); depression, psychological distress; and alcohol/tobacco use. Offspring gestational EA acceleration at birth was calculated using an epigenetic clock previously devised for neonates. Bivariate linear regression was used to explore unadjusted associations between maternal risk factors and offspring gestational EA acceleration at birth. A stepwise regression method was then used to determine the best multivariable model for adjusted associations. Data from 272 maternal-offspring dyads were included in the current analysis. In the stepwise regression model, maternal trauma exposure ({beta}=7.92; p<0.01) or PTSD ({beta}=7.46; p<0.01) were significantly associated with offspring gestational EA acceleration at birth, controlling for ethnicity, offspring sex, head circumference at birth, maternal HIV status, and prenatal tobacco or alcohol use. In site-stratified models, these associations retained statistical significance and direction of effect. Maternal trauma exposure or PTSD may thus be associated with offspring gestational EA acceleration at birth. Given the novelty of this preliminary finding, and its potential translational relevance, further studies to delineate underlying biological pathways and to explore clinical implications of EA acceleration are warranted.
- organism: human
- assay: DNA methylation
- research focus: differential expression
- approach: statistical model
- Citations
- 1
Reproducibility ledger
Nobody has reported trying to reproduce this paper yet. Did you replicate an experiment or run the code? Your report saves the next lab a week.
Sign in to file a reproducibility report.
Related papers
- Epigenome-wide association study of posttraumatic stress disorder in a South African population
Sylvanus Toikumo, Şeyma Katrinli, … Sian M. J. Hemmings·medRxiv·May 7, 2025
- Childhood adversity in mothers is associated with accelerated epigenetic aging in pregnancy and in male newborns
Christian K. Dye, Haotian Wu, … Pamela Scorza·bioRxiv·Mar 2, 2023
- Prenatal exposure to genocide accelerates epigenetic aging as measured in second-generation clocks among young adults
Glorieuse Uwizeye, Luisa Maria Rivera, … Zaneta M. Thayer·medRxiv·Oct 1, 2024
- Intergenerational epigenetic signatures of prenatal adversity and their role in emerging child psychopathology
Anna M. Constantino-Pettit, Alexandre A. Lussier, … Joan L. Luby·bioRxiv·Jul 24, 2026
- Amplification of the epigenetic (gestational) age acceleration signal
Yunsung Lee, Jon Bohlin·bioRxiv·Feb 2, 2021
- Immune pathways and perinatal environmental exposures contribute to epigenetic gestational age prediction and acceleration
Amy Eapen, Ian M. Loveless, … Albert M. Levin·EpigeneticsPeer-reviewed·Jan 20, 2026