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

• Type of Material: Article
• Authors: Jamaji Nwanaji-Enwerem, Emory University; Lars van der Laan, University of California Berkeley; Katherine Kogut, University of California Berkeley; Brenda Eskenazi, University of California Berkeley; Nina Holland, University of California Berkeley; Julianna Deardorff, University of California Berkeley; Andres Cardenas, University of California Berkeley
• Language: English
• Date: 2021-12-31
• Publisher: IMPACT JOURNALS LLC
• Publication Version: Final Published Version
• Copyright Statement: © 2021 Nwanaji-Enwerem et al.
• License: Creative Commons Attribution 3.0 Unported
• Final Published Version (URL): http://dx.doi.org/10.18632/aging.203776
• Title of Journal or Parent Work: AGING-US
• Volume: 13
• Issue: 24
• Start Page: 25653
• End Page: 25669
• Grant/Funding Information: This work was supported by the National Institutes of Health (R03AG067064; R01ES031259; R01ES026994; 1R01ES021369; P01ES009605; R01ES017054; R01DA035300; and R24ES028529) and by the Environmental Protection Agency (R82670901; RD83171001; and RD83451301).
• Keywords: Cell Biology; epigenetic age; CLOCK; mitotic clocks; Science & Technology; BIOMARKER; adversity; AGE; DNA METHYLATION; BLOOD; ACES; Life Sciences & Biomedicine; Geriatrics & Gerontology; DNA methylation
• Research Categories: Health Sciences, Medicine and Surgery; Health Sciences, Public Health

Abstract

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