Risky family climates presage increased cellular aging in young adulthood

Gene H Brody1, Tianyi Yu1, Edith Chen2

  • 1Center for Family Research, University of Georgia, 1095 College Station Road, Athens 30602-4527, GA, USA.

Insights

Childhood exposure to risky family environments may accelerate cellular aging. This process, linked to stress hormones, could increase the risk of chronic diseases later in life.

Area of Science:

  • Developmental Psychology
  • Molecular Biology
  • Public Health

Background:

  • A growing consensus links adverse childhood family environments to long-term health issues, including chronic diseases and early mortality.
  • Prospective data elucidating the biological mechanisms underlying these associations are limited.

Purpose of the Study:

  • To investigate the relationship between childhood risky family climates and cellular aging in a Black family cohort.
  • To explore the mediating role of stress hormone levels in this association.

Main Methods:

  • A prospective study involving 323 Black families.
  • Measurement of stress hormones (epinephrine and norepinephrine) at ages 19 and 20.
  • Assessment of cellular aging via epigenetic aging markers from ages 20 to 27.

Main Results:

  • Risky family climates were significantly associated with elevated epinephrine and norepinephrine levels in late adolescence.
  • These elevated stress hormone levels predicted accelerated cellular aging between ages 20 and 27.
  • Findings suggest a potential biological pathway linking early life adversity to later-life disease risk.

Conclusions:

  • Childhood risky family climates are associated with increased stress hormone secretion.
  • This hormonal response may mediate the link between adverse early environments and accelerated epigenetic aging.
  • These findings highlight a potential trajectory toward chronic diseases of aging for individuals exposed to risky family climates.

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