Research Paper Volume 13, Issue 24 pp 25653—25669

Maternal adverse childhood experiences before pregnancy are associated with epigenetic aging changes in their children

Jamaji C. Nwanaji-Enwerem1,2,3,4, , Lars Van Der Laan3,4, , Katherine Kogut5, , Brenda Eskenazi3,4,5,6, , Nina Holland3,4,5, , Julianna Deardorff5,6, , Andres Cardenas3,4,5, ,

  • 1 Gangarosa Department of Environmental Health, Emory Rollins School of Public Health, Atlanta, GA 30322, USA
  • 2 Department of Emergency Medicine, Emory University School of Medicine, Atlanta, GA 30303, USA
  • 3 Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, CA 94720, USA
  • 4 Center for Computational Biology, School of Public Health, University of California, Berkeley, CA 94720, USA
  • 5 Center for Environmental Research of Community Health, CERCH, School of Public Health, University of California, Berkeley, CA 94720, USA
  • 6 Community Health Sciences Division, School of Public Health, University of California, Berkeley, CA 94720, USA

Received: October 1, 2021       Accepted: November 24, 2021       Published: December 18, 2021
How to Cite

Copyright: © 2021 Nwanaji-Enwerem et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Emerging research suggests associations of physical and psychosocial stressors with epigenetic aging. Although this work has included early-life exposures, data on maternal exposures and epigenetic aging of their children remain sparse. Using longitudinally collected data from the California, Salinas Valley CHAMACOS study, we examined relationships between maternal Adverse Childhood Experiences (ACEs) reported up to 18 years of life, prior to pregnancy, with eight measures (Horvath, Hannum, SkinBloodClock, Intrinsic, Extrinsic, PhenoAge, GrimAge, and DNAm telomere length) of blood leukocyte epigenetic age acceleration (EAA) in their children at ages 7, 9, and 14 years (N = 238 participants with 483 observations). After adjusting for maternal chronological age at delivery, pregnancy smoking/alcohol use, parity, child gestational age, and estimated leukocyte proportions, higher maternal ACEs were significantly associated with at least a 0.76-year increase in child Horvath and Intrinsic EAA. Higher maternal ACEs were also associated with a 0.04 kb greater DNAm estimate of telomere length of children. Overall, our data suggests that maternal preconception ACEs are associated with biological aging in their offspring in childhood and that preconception ACEs have differential relationships with EAA measures, suggesting different physiologic utilities of EEA measures. Studies are necessary to confirm these findings and to elucidate potential pathways to explain these relationships, which may include intergenerational epigenetic inheritance and persistent physical and social exposomes.


ACEs: Adverse Childhood Experiences; ALSPAC: Avon Longitudinal Study of Parents and Children; CHAMACOS: Center for the Health Assessment of Mothers and Children of Salinas; DNAm TL: DNA Methylation Telomere Length; EAA: Epigenetic Age Acceleration; EEAA: Extrinsic Epigenetic Age Acceleration; IEAA: Intrinsic Epigenetic Age Acceleration.