Fig. 1: Conceptual model of key psychological and biological mechanisms linking trauma exposure with incident cardiovascular disease (CVD). | Translational Psychiatry

Fig. 1: Conceptual model of key psychological and biological mechanisms linking trauma exposure with incident cardiovascular disease (CVD).

From: Psychological and biological mechanisms linking trauma with cardiovascular disease risk

Fig. 1

Experiences of trauma and severe stress precede manifestations of posttraumatic psychopathology, such as posttraumatic stress disorder (PTSD) and depression. Subsequent dysregulation of biological stress response systems, including the hypothalamic-pituitary-adrenal (HPA) axis and sympathetic-adrenal-medullary (SAM) system, can contribute to further dysregulation in several interconnected biological systems, potentially leading to immune dysregulation and elevated inflammation, oxidative stress, mitochondrial dysfunction, and dysregulation of the renin-angiotensin system (RAS). Not only can these biological processes further influence one another (as indicated by the recursive arrows), but they can also contribute to accelerated biological aging. Together, these biological alterations can lead to the accumulation of intermediary cardiovascular risk factors, such as hypertension, endothelial dysfunction, and atherosclerosis, which—in turn—increase risk of developing CVD. Furthermore, these psychological and biological processes may unfold after trauma within a milieu of shared genetic risk.

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