Maternal adverse childhood experiences and epigenetic aging in pediatric populations: a scoping review

Abstract

Maternal exposure to adverse childhood experiences (ACEs) may influence aging biomarkers in pediatric populations, as estimated using epigenetic clocks or other measures of aging, such as telomere length. This scoping review aimed to identify and map the available evidence on the association between maternal ACEs and biomarkers of epigenetic aging in offspring from birth to 18 years of age. A systematic search of MEDLINE, Embase, APA PsycINFO, CINAHL, Scopus, and ProQuest Dissertations and Theses Global was conducted on 26 May 2025 and updated on 28 April 2026. The inclusion criteria were epigenetic clock studies that included pediatric populations (0–18 years of age) born to mothers who self-reported ACEs during gestation or within 1 year after childbirth using a standard questionnaire. DNA methylation analysis was conducted using biospecimens, and offspring aging biomarkers were examined. Three reviewers independently screened 1,441 articles, of which 38 underwent full-text review. Four studies met our inclusion criteria. The geographic scope of the studies was limited; three studies were conducted in the United States and one in the United Kingdom. Sample sizes ranged from 80 to 883 maternal-child dyads. The age at the time of biological sample collection ranged from birth to 8 years. Measures of epigenetic aging were examined across diverse tissue types, including blood, saliva, and umbilical vein endothelial cells. Some evidence has been found for an association between maternal ACEs and offspring epigenetic aging; however, the findings were often limited to specific conditions or ACE subtypes. Total maternal ACE scores were not significantly associated with newborn gestational epigenetic age acceleration or child symptoms. However, more specific associations emerged for maternal experiences of parental divorce, sexual abuse, and neglect. In addition, sex-specific associations were also noted. Racial disparities were also evident with maternal childhood abuse linked to increased epigenetic aging in Black but not White maternal-child dyads. Some associations emerged only when considering moderators such as maternal restless sleep during pregnancy. Maternal ACEs may influence offspring epigenetic aging; however, these associations are complex, context-dependent, and supported by a limited body of evidence. Longitudinal studies with greater demographic diversity and methodological consistency, alongside mechanistic investigations of the biological pathways linking maternal adversity and offspring epigenetic aging, are needed.