# Early Life Adversity, Cumulative Life Stress, Race, and Cellular Aging in Midlife Women and Offspring

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · 2021 · $396,701

## Abstract

Early Life Adversity, Cumulative Stress, Race, & Cell Aging in Midlife Women & Offspring
BACKGROUND: There is an increasingly recognized role of stress in elevating disease risk, especially among
women, minorities and socioeconomically disadvantaged groups. Few prospective studies follow individuals
from childhood to adulthood, leaving critical unanswered questions such as which types of adversity, and life
periods (childhood, adolescence, adulthood, or cumulative) have the greatest impact on biological aging and
can help explain racial differences in health. We have a remarkable opportunity to examine types of lifespan
stress in a longitudinal cohort of black and white women who have been followed from 10 years old. We have
collected multiple sources of stress, including individual stressors (severe life events, chronic stressors, global
perceived stress) and environmental stressors (neighborhood deprivation and violence). Our broad aim is to
conduct a novel examination of adversity and links to current epigenomic markers (telomere length,
epigenetic aging) in women and their children, and to systemic inflammation in the women. In this re-
submission, we have identified archived serum samples from the womens’ childhood baseline visit and are
thus able to examine change in inflammation as well. These indices of biological aging each serve as a reliable
predictor of early disease.
METHOD: We are conducting a 30 year follow up of the prospective NHLBI Growth and Health Study (NGHS),
a biracial cohort of children to examine intergenerational transmission of obesity (R01 HD073568). Black and
white girls were initially followed prospectively from 10 to 20 years old and are now being enrolled at roughly
39 years old. Here we propose to assess indices of cellular aging in 590 NGHS women and their most recent
(index) child. Retention of sample and adherence to blood and saliva sampling are excellent and an R56
helped us ensure our target sample size. We will assess whether lifespan stress is associated with indices
of accelerated cellular aging at age 39, and for inflammation, change from childhood (Aim 1) and secondarily
whether types of stress (severe events, chronic stressors, global perceptions, neighborhood deprivation) or
time-periods (childhood, adolescence, adulthood) have differential or cumulative effects. We will assess
whether pregnancy stress or lifespan stress is associated with offspring epigenomic markers (Aim 2), and
whether race modifies these effects (Aim 3). Lastly, we will explore whether high resilience (support and self-
esteem) buffers the effects of adversity.
SIGNIFICANCE & INNOVATION: This will be the first prospective study to test lifespan stress predictors of
three distinct indices of biological aging, each representing different pathways of aging, in a biracial cohort and
to assess stress effects on offspring epigenome. This should advance our understanding of lifespan stress on
aging biology. A more granular understanding ...

## Key facts

- **NIH application ID:** 10180837
- **Project number:** 5R01AG059677-03
- **Recipient organization:** UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
- **Principal Investigator:** Elissa S. Epel
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $396,701
- **Award type:** 5
- **Project period:** 2019-09-15 → 2024-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10180837

## Citation

> US National Institutes of Health, RePORTER application 10180837, Early Life Adversity, Cumulative Life Stress, Race, and Cellular Aging in Midlife Women and Offspring (5R01AG059677-03). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10180837. Licensed CC0.

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