# Life-course Psychosocial Adversity and Biological Aging in the Hispanic Community Health Study / Study of Latinos: A Life-course Model Analysis

## TL;DR

The study explores how psychosocial adversity throughout life affects biological aging in a Hispanic population using DNA methylation data.

## Contribution

The research introduces a modified Bayesian life-course model to assess how adversity in childhood and adulthood uniquely influences biological aging markers.

## Key findings

- Adversity is linked to increased GrimAge acceleration, with adulthood adversity having a stronger effect.
- Childhood adversity indirectly affects GrimAge acceleration through adulthood adversity.
- The impact of adversity on DunedinPACE is minimal and less influenced by childhood adversity.

## Abstract

Psychosocial adversity over the life course may impact the aging process. However, life-course models have yet to fully explain the biological embedding of psychosocial adversity in aging. A subsample of participants from the Hispanic Community Health Study/Study of Latinos with DNA methylation (DNAm) data (N=970) was used to evaluate the effect of adversity on biological aging and the most compatible life-course model. Epigenetic age was estimated from GrimAge and DunedinPACE. We modified a current Bayesian life-course model to estimate the effect of adversity from childhood to adulthood on epigenetic age acceleration and the weights contributed by childhood (Wchildhood) and adulthood (Wadulthood), which sum to one. The model was also used to evaluate the compatibility with the sensitive period (Wchildhood ≠ Wadulthood) and accumulation models (Wchildhood ≈ Wadulthood). Causal mediation analysis assessed the pathway model by estimating the indirect effect of childhood adversity through adulthood adversity. Per-unit increase in adversity was associated with 0.91 years (95% credible interval [CrI]: 0.28, 1.53; Wadulthood = 82%, 95% CrI: 36%, 99%) increased GrimAge acceleration (AgeAccelGrim) and 0.013 years/calendar year (95% CrI: −0.005, 0.032; Wchildhood = 49%, 95% CrI: 3%, 97%; Wadulthood = 51%, 95% CrI: 3%, 97%) increased DunedinPACE. A pronounced indirect effect of childhood adversity was found in AgeAccelGrim (0.23 years, 95% CI: 0.09, 0.37) but minimal in DunedinPACE (0.003 years/calendar year, 95% CI: −0.001, 0.006). Psychosocial adversity from childhood to adulthood may affect biological aging, with distinct life-course models explaining its effects on different aging markers.