Long-term molecular embedding of early life adversity: leukocyte DNA methylation and gene expression associations from childhood to young adulthood
Year: 2026
Type: dataset
Abstract: Early life adversity is associated with increased cardiometabolic risk across the life course, potentially via epigenetic mechanisms. However, few studies have prospectively examined how distinct domains of early life adversity influence molecular profiles and cardiometabolic health. In the CHAMACOS cohort, a longitudinal study of rural Latino youth, we measured adversity prospectively from pregnancy through age 7 across six domains: Learning Environment, Parent-Child Interaction, Maternal Adversity, Family Dysfunction, Economic Adversity, and Stressful Life Events. Leukocyte DNA methylation (DNAm) was measured at four timepoints between ages 7 and 18, gene expression (RNA transcripts) at age 14, and body mass index (BMI) and insulin resistance (HOMA-IR) at age 18. Early life adversity was associated with differential DNAm at ages 7, 14, and 18, with 14 Bonferroni- and 101 FDR-significant differentially methylated probes (DMPs) across all timepoints. Economic adversity was the domain most strongly associated with DMPs (4 Bonferroni- and 38 FDR-significant). Methylation changes at several DMPs were significantly associated with BMI and HOMA-IR at age 18. These findings provide longitudinal evidence that early life adversity, particularly economic adversity, becomes biologically embedded via DNAm, with functional and cardiometabolic consequences, highlighting potential targets for early interventions to reduce lifelong disease risk. Difficult experiences in early childhood may raise the risk of heart and metabolic disease later in life, possibly by changing how genes are switched on or off. This study followed a group of Latino children in rural California from before birth through age 18, measuring six types of hardship experienced between the prenatal period and age 7: home learning environment, parent-child relationship quality, mother’s own stress, family dysfunction, economic hardship, and stressful life events. Chemical tags on DNA (called DNA methylation) that control gene activity were measured at four time points between ages 7 and 18, along with gene activity at age 14, and body mass index and insulin resistance at age 18. Children who experienced more early hardship showed measurable differences in DNA methylation at ages 7, 14, and 18. Economic hardship had the strongest influence on these molecular changes. Several of those changes were linked to higher body mass index and worse insulin regulation at age 18. The study suggests that childhood hardship — especially financial hardship — becomes physically embedded in the body at a molecular level, in ways that affect metabolic health into young adulthood. This points to early childhood as a key window for interventions that could reduce metabolic disease risk across a person’s lifetime.
Source: Figshare
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W7166328792
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