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Early Life Adversity Predicts an Accelerated Cellular Aging Index Through Early Timing of Puberty

Sat, March 25, 10:00 to 11:30am, Salt Palace Convention Center, Floor: 3, Meeting Room 355 D

Abstract

Introduction: The current study examines if early life adversity is associated with accelerated biological aging, and if effects are mediated by pubertal timing. This is the first study to assess accelerated aging using a latent variable approach to examine the association with early life adversity.

Hypotheses: The aims of the current study were to establish there if there were a) an indirect effect of early adversity on accelerated aging through pubertal timing and/ or b) an indirect effect of race on accelerated aging through pubertal timing.

Study population: In early mid-life, 385 (187 Black and 198 White) women retrospectively reported on early life adversity and age at first menstruation (menarche).

Methods: Women provided saliva and blood to assess epigenetic aging, telomere length (TL), and C-Reactive Protein (CRP). Using structural equation modeling, we created a latent variable of adult biological aging using epigenetic aging, TL, and CRP as indicators. We created a latent variable of early adversity consisting of indicators of abuse/ threat events before age 13, physical abuse, and sexual abuse. We estimated the indirect effect of early adversity on accelerated aging through pubertal timing. Adversity, menarche, and accelerated aging were regressed on race.

Results: There was a significant indirect effect of early adversity on accelerated aging through age at menarche (b = 0.16, 95% CI [0.02, 0.39]), in that women who experienced more early adversity were younger at menarche, which was associated with greater accelerated aging in adulthood. There was also a significant indirect effect of race on accelerated aging through age at menarche (b = 0.21, 95% CI [0.03, 0.38]), in that Black women were younger at menarche, which was associated with greater accelerated aging. Integrating multiple biomarkers may allow a more complete understanding of multisystem-level aging and its role in health disparities.

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