# A neurobiological diathesis-stress model of CVD risk

> **NIH NIH P01** · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · 2020 · $296,154

## Abstract

ABSTRACT
Project 2 (Thomas Kamarck, PL)
A neurobiological diathesis-stress model of CVD risk
Psychosocial stress has been associated with risk for cardiovascular disease (CVD), and emerging evidence
suggests that individuals may differ in their susceptibility to this stress-related risk. Project 2 will examine
whether the activity of brain areas that coordinate autonomic and endocrine output to internal organs (called
`visceral control areas') may help to explain some of these individual differences in stress susceptibility during
daily life, and may also moderate the effects of psychosocial stress on preclinical CVD progression.
Importantly, growing evidence indicates that physical activity (PA) modifies the influence of visceral control
areas on peripheral physiology, and this influence may represent a source of resilience to reduce stress
susceptibility. Accordingly, Project 2 also aims to test how individual differences in the functioning of visceral
control areas may partly explain the association between PA and daily stress susceptibility effects. Specifically,
we will follow 350 midlife and community dwelling adults over a 32-month period, collecting two one-week
samples, at the beginning and at the end of this period. At each of these 2 points, we will assess daily
psychosocial stressors using multiple momentary electronic diary reports and ambulatory blood pressure
readings. We will use daily actigraphy to assess habitual PA, and we will collect biological markers of
subclinical CVD. At baseline, all participants will complete a standardized battery of stressor tasks during
fMRI. We will test whether individual differences in the functionality of visceral control areas (that is,
differences stressor-evoked functional connectivity) predict corresponding differences in susceptibility to
psychosocial stress in the natural environment. We hypothesize that people who exhibit greater stressor-
evoked functional connectivity among visceral control areas will also exhibit a) larger blood pressure reactions
to daily psychosocial stressors in the natural environment, and b) stronger associations between psychosocial
stressor exposures and 32-month preclinical CVD progression. We further hypothesize that stressor-evoked
functional connectivity will partly account for the effects of PA on daily stress-related blood pressure reactivity.
The public health significance of this novel work is that understanding the role of particular brain circuits in
stress susceptibility and CVD risk will help us to better measure and, potentially, to enhance stress resilience
through more targeted intervention efforts.

## Key facts

- **NIH application ID:** 9947985
- **Project number:** 5P01HL040962-23
- **Recipient organization:** UNIVERSITY OF PITTSBURGH AT PITTSBURGH
- **Principal Investigator:** THOMAS WILSON KAMARCK
- **Activity code:** P01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $296,154
- **Award type:** 5
- **Project period:** — → —

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9947985

## Citation

> US National Institutes of Health, RePORTER application 9947985, A neurobiological diathesis-stress model of CVD risk (5P01HL040962-23). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9947985. Licensed CC0.

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