Department of Psychology, Institute for Policy Research, Northwestern University, Evanston, IL, USA.
Curr Top Behav Neurosci. 2022;54:439-459. doi: 10.1007/7854_2021_283.
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.
儿童时期遭受人际暴力，这是一种严重且常常是创伤性的社会压力形式，是一个长期存在的问题。越来越多的研究表明，这种暴力可能与心血管代谢健康以及心血管疾病（CVD）在整个生命周期中的进展有关。人们对这种关联的因果关系知之甚少，因此，暴力事件后可能导致健康状况不佳的风险和恢复能力的生物学机制还不太清楚。本文借鉴了人类和非人类动物模型中最近的理论见解和实证研究，提出了一个假设，即儿童期暴力可能会以一种方式“深入皮肤”，从而影响 CVD。基于这一新兴文献，儿童期暴力暴露可能会增加晚年患 CVD 易感性的一种可能方式是，使调节和促进炎症的应激反应神经生物学和免疫过程变得敏感，炎症是 CVD 的一个关键发病机制。这本质上是一个始于生命早期并贯穿整个生命周期的发育过程，尽管人们对这一过程发生的具体机制知之甚少。本文的目的是阐述其中一些可能的机制，并提出未来旨在减少遭受暴力的个体疾病负担的研究领域。
