Allostasis is the process of achieving stability, or homeostasis, through physiological or behavioral change. This can be carried out by means of alteration in HPA axis hormones, the autonomic nervous system, cytokines, or a number of other systems, and is generally adaptive in the short term (McEwen & Wingfield 2003). Allostasis is essential in order to maintain internal viability amid changing conditions (Sterling & Eyer 1988; McEwen 1998a; McEwen 1998b; Schulkin 2003). Allostasis provides compensation for various problems, such as in compensated heart failure, compensated kidney failure, and compensated liver failure. However, such allostatic states are inherently fragile, and decompensation can occur quickly, as in acute decompensated heart failure.
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The concept of allostasis was proposed by Sterling and Eyer in 1988 to describe an additional process of reestablishing homeostasis, but one that responds to a challenge instead of to subtle ebb and flow. This theory suggests that both homeostasis and allostasis are endogenous systems responsible for maintaining the internal stability of an organism. Homeostasis, from the Greek homeo, means “similar,” while stasis means “stand;” thus, “standing at about the same level.” (The term was not coined as “homostasis” or “standing the same” because internal states are frequently being disturbed and corrected, thus rarely perfectly constant.) Allostasis was coined similarly, from the Greek allo, which means “variable;” thus, “remaining stable by being variable” (Sterling & Eyer 1988; Klein 2004). Allostatic regulation reflects, at least partly, cephalic involvement in primary regulatory events, in that it is anticipatory to systemic physiological regulation (Sterling & Eyer 1988; Schulkin 2003). The term Heterostasis is also used in place of Allostasis, particularly where state changes are finite in number and therefore discrete (e.g. computational processes).
The concept of allostasis, maintaining stability through change, is a fundamental process through which organisms actively adjust to both predictable and unpredictable events… Allostatic load refers to the cumulative cost to the body of allostasis, with allostatic overload… being a state in which serious pathophysiology can occur… Using the balance between energy input and expenditure as the basis for applying the concept of allostasis, two types of allostatic overload have been proposed (Wingfield 2003).
Sterling (2004) proposes six interrelated principles that underlie allostasis:
1Organisms are designed to be efficient
2Efficiency requires reciprocal trade-offs
3Efficiency also requires being able to predict future needs
4Such prediction requires each sensor to adapt to the expected range of input
5Prediction also demands that each effector adapt its output to the expected range of demand
6Predictive regulation depends on behavior whilst neural mechanisms also adapt.
Contrast with homeostasis
Homeostasis is the regulation of the body to a balance, by single point tuning such as blood oxygen level, blood glucose or blood pH. For example, if a person walking in the desert is hot, the body will sweat and they will quickly become dehydrated. Allostasis is adaptation but in regard to a more dynamic balance. In dehydration, sweat occurs as only a small part of the process with many other systems also adapting their functioning, both to reduce water use and to support the variety of other systems that are changing to aid this. In this case, kidneys may reduce urine output, mucous membrane in the mouth, nose and eyes may dry out; urine and sweat output will decrease; the release of arginine vasopressin (AVP) will increase; and veins and arteries will constrict to maintain blood pressure with a smaller blood volume.
McEwen and Wingfield propose two types of allostatic load which result in different responses:-
Type 1 allostatic overload occurs when energy demand exceeds supply, resulting in activation of the emergency life history stage. This serves to direct the animal away from normal life history stages into a survival mode that decreases allostatic load and regains positive energy balance. The normal life cycle can be resumed when the perturbation passes.
Type 2 allostatic overload begins when there is sufficient or even excess energy consumption accompanied by social conflict and other types of social dysfunction. The latter is the case in human society and certain situations affecting animals in captivity. In all cases, secretion of glucocorticosteroids and activity of other mediators of allostasis such as the autonomic nervous system, CNS neurotransmitters, and inflammatory cytokines wax and wane with allostatic load. If allostatic load is chronically high, then pathologies develop. Type 2 allostatic overload does not trigger an escape response, and can only be counteracted through learning and changes in the social structure (McEwen & Wingfield 2003; Sterling & Eyer 1988)
Whereas both types of allostasis are associated with increased release of cortisol and catecholamines, they differentially affect thyroid homeostasis: Concentrations of the thyroid hormone triiodothyronine are decreased in type 1 allostasis, but elevated in type 2 allostasis.
Main article: Allostatic load
In the long run, allostatic changes may fail to be adaptive as the maintenance of allostatic changes over a long period may result in wear and tear, the so-called allostatic load. If a dehydrated individual is helped but continues to be stressed and hence does not reinstate normal body function, the individual’s body systems will wear out. The human body is adaptable, but it cannot maintain allostatic overload for very long without consequence.
Trevor A. Day has argued that the concept of allostasis is no more than a renaming of the original concept of homeostasis (Day 2005).
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^ Selye, H. (1973) Homeostasis and Heterostasis. Perspectives in Biology and Medicine, 16, 441-445
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^ Chatzitomaris, Apostolos; Hoermann, Rudolf; Midgley, John E.; Hering, Steffen; Urban, Aline; Dietrich, Barbara; Abood, Assjana; Klein, Harald H.; Dietrich, Johannes W. (20 July 2017). “Thyroid Allostasis–Adaptive Responses of Thyrotropic Feedback Control to Conditions of Strain, Stress, and Developmental Programming”. Frontiers in Endocrinology. 8. doi:10.3389/fendo.2017.00163. PMC 5517413 . PMID 28775711.
•Day, Trevor A. (2005). “Defining stress as a prelude to mapping its neurocircuitry: No help from allostasis”. Prog. Neuropsychopharmacol. Biol. Psychiatry. 29 (8): 1195–1200. doi:10.1016/j.pnpbp.2005.08.005. ISSN 0278-5846.
•Klein, Robyn (2004). “Chapter 3”. Phylogenetic and phytochemical characteristics of plant species with adaptogenic properties (PDF) (MS). Montana State University. Archived from the original (PDF) on October 17, 2006.
•McEwen, Bruce S. (1998a). “Protective and Damaging Effects of Stress Mediators”. Seminars in Medicine of the Beth Israel Deaconess Medical Center. N. Engl. J. Med. 338: 171–9. doi:10.1056/NEJM199801153380307. PMID 9428819.
•McEwen, Bruce S.; Wingfield, John C. (2003). “The concept of allostasis in biology and biomedicine”. Horm. Behav. 43 (1): 2–15. doi:10.1016/S0018-506X(02)00024-7. ISSN 0018-506X.
•Sterling, P.; Eyer, J. (1988). “Allostasis: A new paradigm to explain arousal pathology”. In Fisher, S.; Reason, J. T. Handbook of life stress, cognition, and health. Chicester, NY: Wiley. ISBN 9780471912699. OCLC 17234042.
•Sterling, Peter (2004). “Chapter 1. Principles of Allostasis”. In Schulkin, Jay. Allostasis, homeostasis, and the costs of physiological adaptation. New York, NY: Cambridge University Press. ISBN 9780521811415. OCLC 53331074.
•Wingfield, John C. (2003). “Control of behavioural strategies for capricious environments”. Anniversary Essays. Anim. Behav. 66 (5): 807–16. doi:10.1006/anbe.2003.2298.
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