[Low cortisol production in chronic stress. The connection stress-somatic disease is a challenge for future research].
There is a general assumption that distressing events or situations (stress) evoke the hypothalamic-pituitary-adrenal (HPA) system, with a resulting increase in cortisol secretion. However, our increasing understanding of the complexity of the HPA axis physiology raises questions as to the validity of this model. An increasing number of studies imply that after long-term exposure to stress, the HPA axis will eventually become dishabituated, resulting in a disruption of central regulatory systems and a net decrease of cortisol output. These findings have major implications for the interpretation of stress-induced neuroendocrine response patterns.
Rosmond
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Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, USA.
Björntorp
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P
D000208:Acute Disease; D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000818:Animals; D002908:Chronic Disease; D003163:Competitive Behavior; D006801:Humans; D006854:Hydrocortisone / Q000096:biosynthesis* / Q000378:metabolism; D007030:Hypothalamo-Hypophyseal System / Q000378:metabolism*; D010913:Pituitary-Adrenal System / Q000378:metabolism*; D011602:Psychophysiologic Disorders / Q000209:etiology* / Q000378:metabolism*; D012307:Risk Factors; D013315:Stress, Psychological / Q000150:complications* / Q000378:metabolism*
D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone