Citation

Finegood ED, Miller GE. Curr. Top. Behav. Neurosci. 2021; ePub(ePub): ePub.

Copyright

(Copyright © 2021, Holtzbrinck Springer Nature Publishing Group)

DOI

10.1007/7854_2021_283

PMID

34935115

Abstract

Exposure to interpersonal violence during childhood, a severe and often traumatic form of social stress, is an enduring problem that an emerging body of work suggests may be relevant to cardiometabolic health and the progression of cardiovascular disease (CVD) across the life course. Less is known about this association causally, and consequently, the biological mechanisms that may confer risk for, and resilience to, poor health outcomes in the aftermath of violence are not well understood. Drawing on recent theoretical insights and empirical research in both humans and non-human animal models, the current paper articulates a hypothesis for one way that childhood violence could get "under the skin" to influence CVD. Based on this emerging literature, one plausible way that childhood violence exposure could increase susceptibility to CVD in later life is by sensitizing stress-response neurobiology and immune processes that regulate and promote inflammation, which is a key pathogenic mechanism in CVD. This is inherently a developmental process that begins in early life and that unfolds across the life course, although less is known about the specific mechanisms through which this occurs. The goal of this paper is to articulate some of these plausible mechanisms and to suggest areas for future research that aims to reduce the burden of disease among individuals who are exposed to violence.

Language: en

Keywords

Cardiovascular disease; Child development; Childhood violence; Inflammation; Monocytes