The term allostasis denotes long-term adaptation processes, by which the organism maintains homeostasis in the context of chronic stressor load. This ensures survival, but also increases waste and ageing (allostatic load).
Allostasis results from a directed change in the parameters of affected information processing structures. Consequently, beneficial alterations in the behaviour of the respective system ensue, but in the long-term also setpoint diseases.
The term was first coined by Sterling and Eyer in order to sharpen the concept of stress response.
Examples for allostatic reactions are
- Increased secretion of glucocorticoids in long-term stress situations
- Hyperdeiodation (hyperdeiodination) and hypodeiodation (hypodeiodination) leading to central and peripheral components, respectively, of non-thyroidal illness syndrome
- Incomplete compensatory increase of beta-cell function in the situation of insulin resistance
- Goldstein DS. Computer models of stress, allostasis, and acute and chronic diseases. Ann N Y Acad Sci. 2008 Dec;1148:223-31. PMID 19120114
- McEwen BS. Physiology and neurobiology of stress and adaptation: central role of the brain. Physiol Rev. 2007 Jul;87(3):873-904. Review. PubMed PMID 17615391.
- Michael Stumvoll, P. Antonio Tataranni, Norbert Stefan, Barbora Vozarova and Clifton Bogardus. Glucose Allostasis. Diabetes 52:903-909, 2003. PMID 12663459
- Sterling P, Eyer J. Allostasis: a new paradigm to explain arousal pathology. In: Handbook of Life Stress, Cognition and Health, edited by Fisher S, Reason J. New York: Wiley, 1988, p. 629–649.