Goering · Developmental psychology 2025 · prospective longitudinal cohort study · n=350

Pubertal timing as a predictor of epigenetic aging and mortality risk in young adulthood.

Level 3 - non-randomized controlled study

Prospective longitudinal cohort study evaluating developmental timing and adulthood epigenetic markers

PubMed 39818920 · doi:10.1037/dev0001903 · record verified 2026-08-26

What was done

This longitudinal cohort study followed 350 individuals (58% female, 42% male; 80% Black, 19% non-Hispanic White) from early adolescence (mean age 13) into young adulthood (mean age 27). Adolescent pubertal timing was measured via perceived timing relative to peers and self-reported phenotypic timing based on age-adjusted Tanner scores. In adulthood, blood DNA methylation was used to evaluate epigenetic mortality risk and epigenetic aging clocks (GrimAge, DunedinPACE, and PhenoAge). Analyses adjusted for smoking, body mass index, family income, early-life stress, race/ethnicity, sex, and parenthood.

What was found

After adjusting for covariates, both early perceived and early phenotypic pubertal timing predicted higher epigenetic mortality risk in adulthood. Early phenotypic timing predicted accelerated DunedinPACE, and both perceived and phenotypic early timing correlated with accelerated GrimAge. Off-time phenotypic pubertal timing (early or late) predicted accelerated PhenoAge in males only, whereas perceived off-time timing was unexpectedly associated with lower PhenoAge acceleration. Specific numerical effect sizes, test statistics, and p-values were not reported in the abstract.

Why it matters

These findings suggest that the long-term health consequences of early pubertal development may operate through accelerated biological and cellular aging pathways detectable by young adulthood, particularly in predominantly Black populations.

Limits

The abstract reports no numerical effect sizes, confidence intervals, or exact significance levels. Pubertal timing was based on self-reported Tanner staging and subjective peer comparison rather than physician exams or hormonal assays. The observational design cannot rule out residual confounding, and findings come from a single cohort of 350 individuals.

Cited by