Article ID Journal Published Year Pages File Type
10454374 Biological Psychology 2011 8 Pages PDF
Abstract
Studies of cardiovascular disease risk have explored the idea that exaggerated physiological responses to stress may signal increased risk of cardiovascular disease. We describe a neurophysiological model of brain structures and peripheral structures that may contribute to exaggerated reactivity. Level I in this model includes the limbic system and its interactions with the prefrontal cortex that determine stress appraisals and coping responses. Level II addresses the hypothalamus and brainstem that contribute outputs to the body and which also includes brainstem nuclei that feed back to Level I to modulate its functioning. Level III includes the peripheral tissues themselves. We then suggest that stress reactivity ranging from very low to very high has a normative midrange of intensity and present evidence that negative health outcomes may be associated with both exaggerated and diminished stress reactivity since both tendencies imply a loss of homeostatic regulation. In particular, dysregulation at Levels I and II in our heuristic model signify altered motivational function and an attendant alteration in outflow to the periphery and poor behavioral homeostasis. In consequence, poor affective and behavioral regulation would be expected to contribute to poor health behaviors therefore additionally impairing health. In conclusion, diminished as well as exaggerated physiological reactivity should be seen as nonoptimal functioning that can contribute to poor health outcomes. This conceptualization places physical health into the context of behavioral and physiological processes that contribute to homeostasis.
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Life Sciences Neuroscience Behavioral Neuroscience
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