Adversity exposure during sensitive periods predicts accelerated epigenetic aging in children.
Level 3 - non-randomized controlled study
Prospective longitudinal cohort study
PubMed 31918390 · doi:10.1016/j.psyneuen.2019.104484
What was done
Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC; n = 973), researchers prospectively evaluated the relationship between repeated measures of seven types of childhood adversity and epigenetic aging measured at age 7.5. Epigenetic age acceleration was estimated using both the Horvath and Hannum DNA methylation clocks. A Least Angle Regression variable selection procedure was applied to test for sensitive period effects relative to cumulative or recent exposure models.
What was found
Exposure to abuse, financial hardship, or neighborhood disadvantage during sensitive periods in early and middle childhood best explained Hannum-based epigenetic age acceleration, remaining significant after accounting for adversity accumulation and recency. Secondary sex-stratified analyses also identified sensitive period effects. These associations were missed when analyzing adversity as a binary (exposed vs unexposed) measure. No associations were identified using the Horvath epigenetic clock. The abstract reports no numerical effect sizes, test statistics, or p-values.
Why it matters
This study provides prospective evidence that the developmental timing of adversity influences biological aging markers in children, while showing that different epigenetic clocks capture distinct biological signatures of stress.
Limits
The abstract reports no numerical values, effect sizes, confidence intervals, or p-values. Findings were discordant across measurement tools, appearing only with the Hannum clock and not the Horvath clock. As an observational cohort study, residual confounding cannot be ruled out. Epigenetic age was assessed at only a single time point (age 7.5).
Cited by
- supports Severe psychological stress such as childhood sexual abuse and PTSD has been shown in the literature to affect epigenetic age acceleration.