Miller GE, Chen E, Zhou ES. If it goes up, must it comd down? Chronic stress and thet hypothalamic-puitary-adrenocortical axis in humans. Psychol Bull 113: 25-45

Department of Psychology, University of British Columbia (UBC), Vancouver, BC, Canada.
Psychological Bulletin (Impact Factor: 14.76). 02/2007; 133(1):25-45. DOI: 10.1037/0033-2909.133.1.25
Source: PubMed


The notion that chronic stress fosters disease by activating the hypothalamic-pituitary-adrenocortical (HPA) axis is featured prominently in many theories. The research linking chronic stress and HPA function is contradictory, however, with some studies reporting increased activation, and others reporting the opposite. This meta-analysis showed that much of the variability is attributable to stressor and person features. Timing is an especially critical element, as hormonal activity is elevated at stressor onset but reduces as time passes. Stressors that threaten physical integrity, involve trauma, and are uncontrollable elicit a high, flat diurnal profile of cortisol secretion. Finally, HPA activity is shaped by a person's response to the situation; it increases with subjective distress but is lower in persons with posttraumatic stress disorder.

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    • "When cortisol activates the fight and flight stress response, it also sends a signal back to the hypothalamus to inhibit CRH production and the pituitary gland to inhibit ACTH. In this feedback loop, cortisol will reduce norepinephrine activity, gradually calming the person down and creating a mutually balanced system (Engelmann, Landgraf & Wotjak, 2004; Miller, Chen & Zhou, 2007). In some people who have experienced trauma, however, this system doesn't function as it should. "
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