# Epigenomic mechanisms of risk and resilience: The role of parenting

> **NIH NIH R01** · FLORIDA INTERNATIONAL UNIVERSITY · 2020 · $473,525

## Abstract

Project Summary
Hispanic youth are nearly three times more likely to be at high risk for developmental, behavioral, or social
delays compared to white non-Hispanic children. Contributing to this risk disparity is disproportionate rates of
Hispanic children living in poverty and heightened risk for exposure to early-life environmental adversity, all of
which confers substantial risk for the development of psychopathology and a lifelong risk for chronic diseases.
A critical process by which disproportionate experiences of early adversity might influence risk for the
development of later psychopathology is through the biological embedding of adversity exposure via epigenetic
changes in genes involved in neuroendocrine and inflammatory responses to stress response. Despite
promise and progress of social epigenomic research on risk processes, a significant limitation of the extant
literature is that a basic understanding of how biological embedding of adversity can be prevented or reversed
has yet to be achieved, with little knowledge of the role of protective factors that impact these developmental
trajectories. In fact, prior work in humans has been almost exclusively cross-sectional and focused on
detrimental environmental impacts, greatly constraining our understanding of epigenomic processes over time
and its positive malleability to interventions. The proposed research will leverage an on-going NIH-funded R01
(#HD084497) to evaluate, via a randomized controlled trial of a home-based behavioral parent training
intervention, how changing social context (i.e., dysfunctional parenting) alters the epigenome among at-risk
Hispanic preschoolers and potentially establishes a biological foundation that promotes resiliency and
potentially ameliorates the biological embedding of adversity. In the current proposal, we propose to use a
balanced analytical approach that includes (1) a hypothesis-driven pathway analyses for genes involved in
neuroendocrine and inflammatory responses to stress, (2) a targeted design that pulls sites previously
identified in well-powered EWAS studies to create poly-epigenetic risk scores, and (3) a hypothesis-free
epigenome-wide association study. In addition to examining trajectories of change in child DNA methylation,
we will determine if exposure to a protective factor (positive parenting) buffers the impact of adversity on
biomarkers of accelerated aging during a sensitive developmental stage. Lastly, we will explore epigenomic
biosignatures of response to early intervention based on both child and parent DNA methylation. For all aims,
we will use a multi-informant, multi-method design that includes observations of parenting, task-based
measures of child self-regulation, standardized assessments of child developmental and clinical outcomes,
independent clinical evaluators, and both child and parent DNA methylation. This research will facilitate the
application of precision medicine and prevention approaches by identifying ep...

## Key facts

- **NIH application ID:** 10053496
- **Project number:** 1R01MD015401-01
- **Recipient organization:** FLORIDA INTERNATIONAL UNIVERSITY
- **Principal Investigator:** Justin Parent
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $473,525
- **Award type:** 1
- **Project period:** 2020-07-25 → 2025-02-28

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10053496

## Citation

> US National Institutes of Health, RePORTER application 10053496, Epigenomic mechanisms of risk and resilience: The role of parenting (1R01MD015401-01). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10053496. Licensed CC0.

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