TY - JOUR
T1 - Rumination as a mediator of chronic stress effects on hypertension
T2 - A causal model
AU - Gerin, William
AU - Zawadzki, Matthew J.
AU - Brosschot, Jos F.
AU - Thayer, Julian F.
AU - Christenfeld, Nicholas J.S.
AU - Campbell, Tavis S.
AU - Smyth, Joshua M.
PY - 2012
Y1 - 2012
N2 - Chronic stress has been linked to hypertension, but the underlying mechanisms remain poorly specified. We suggest that chronic stress poses a risk for hypertension through repeated occurrence of acute stressors (often stemming from the chronic stress context) that cause activation of stress-mediating physiological systems. Previous models have often focused on the magnitude of the acute physiological response as a risk factor; we attempt to extend this to address the issue of duration of exposure. Key to our model is the notion that these acute stressors can emerge not only in response to stressors present in the environment, but also to mental representations of those (or other) stressors. Consequently, although the experience of any given stressor may be brief, a stressor often results in a constellation of negative cognitions and emotions that form a mental representation of the stressor. Ruminating about this mental representation of the stressful event can cause autonomic activation similar to that observed in response to the original incident, and may occur and persist long after the event itself has ended. Thus, rumination helps explain how chronic stress causes repeated (acute) activation of one's stress-mediating physiological systems, the effects of which accumulate over time, resulting in hypertension risk.
AB - Chronic stress has been linked to hypertension, but the underlying mechanisms remain poorly specified. We suggest that chronic stress poses a risk for hypertension through repeated occurrence of acute stressors (often stemming from the chronic stress context) that cause activation of stress-mediating physiological systems. Previous models have often focused on the magnitude of the acute physiological response as a risk factor; we attempt to extend this to address the issue of duration of exposure. Key to our model is the notion that these acute stressors can emerge not only in response to stressors present in the environment, but also to mental representations of those (or other) stressors. Consequently, although the experience of any given stressor may be brief, a stressor often results in a constellation of negative cognitions and emotions that form a mental representation of the stressor. Ruminating about this mental representation of the stressful event can cause autonomic activation similar to that observed in response to the original incident, and may occur and persist long after the event itself has ended. Thus, rumination helps explain how chronic stress causes repeated (acute) activation of one's stress-mediating physiological systems, the effects of which accumulate over time, resulting in hypertension risk.
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U2 - 10.1155/2012/453465
DO - 10.1155/2012/453465
M3 - Review article
C2 - 22518285
AN - SCOPUS:84864528799
SN - 2090-0384
VL - 2012
JO - International Journal of Hypertension
JF - International Journal of Hypertension
M1 - 453465
ER -