Allostasis

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Allostasis proposes that efficient regulation requires anticipating needs and preparing to satisfy them before they arise,[1] as opposed to homeostasis, in which the goal is a steady state.

Etymology[edit]

Allostasis /ˌɑːlˈstsɪs/ from the Greek prefix ἄλλος, állos, "other," "different" + the suffix στάσις, stasis, "standing still".

Nature of concept[edit]

The concept was named by Sterling and Eyer in 1988. Allostasis was coined from the Greek allo, which means "variable;" thus, "remaining stable by being variable".[2][3] Allostatic regulation reflects, at least partly, cephalic involvement in primary regulatory events, in that it is anticipatory to systemic physiological regulation.[2][4] This is different from homeostasis, which occurs in response to subtle ebb and flow. Both homeostasis and allostasis are endogenous systems responsible for maintaining the internal stability of an organism. Homeostasis is formed from the Greek adjective homoios, meaning "similar," and the noun stasis, meaning "standing;" thus, "standing at about the same level."[2]

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).[5]

Wingfield states:

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.[6]

Sterling (2004) proposed six interrelated principles that underlie allostasis:[7]

  1. Organisms are designed to be efficient
  2. Efficiency requires reciprocal trade-offs
  3. Efficiency also requires being able to predict future needs
  4. Such prediction requires each sensor to adapt to the expected range of input
  5. Prediction also demands that each effector adapt its output to the expected range of demand
  6. Predictive regulation depends on behavior whilst neural mechanisms also adapt.

Mechanism[edit]

Allostasis 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.[8] Allostasis is essential in order to maintain internal viability amid changing conditions.[2][9][10][4]

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.

Types[edit]

McEwen and Wingfield propose two types of allostatic overload 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.[8][2]

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.[11] This may result from type 2 allostatic load increasing the set point of pituitary-thyroid feedback control.[12]

Allostatic load[edit]

In the long run, 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.[citation needed]

Controversy[edit]

In 2005, Trevor A. Day has argued that the concept of allostasis is no more than a renaming of the original concept of homeostasis.[13]

See also[edit]

References[edit]

  1. ^ Sterling, Peter (April 2012). "Allostasis: A model of predictive regulation". Physiology & Behavior. 106 (1): 5–15. doi:10.1016/j.physbeh.2011.06.004.
  2. ^ a b c d e Sterling, P.; Eyer, J. (1988). "Allostasis: A new paradigm to explain arousal pathology". In Fisher, S.; Reason, J. T. (eds.). Handbook of life stress, cognition, and health. Chicester, NY: Wiley. ISBN 9780471912699. OCLC 17234042.
  3. ^ Klein, Robyn (2004). "Chapter 3" (PDF). Phylogenetic and phytochemical characteristics of plant species with adaptogenic properties (MS). Montana State University. Archived from the original (PDF) on October 17, 2006.open access
  4. ^ a b Schulkin, Jay (2003). Rethinking homeostasis : allostatic regulation in physiology and pathophysiology. Cambridge, MA: MIT Press. ISBN 9780262194808. OCLC 49936130.
  5. ^ Selye, H. (1973). "Homeostasis and Heterostasis". Perspectives in Biology and Medicine. 16 (3): 441–445. doi:10.1353/pbm.1973.0056.
  6. ^ 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.closed access
  7. ^ Sterling, Peter (2004). "Chapter 1. Principles of Allostasis". In Schulkin, Jay (ed.). Allostasis, homeostasis, and the costs of physiological adaptation. New York, NY: Cambridge University Press. ISBN 9780521811415. OCLC 53331074.
  8. ^ a b 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. PMID 12614627.closed access
  9. ^ McEwen, Bruce S. (1998). "Protective and Damaging Effects of Stress Mediators". Seminars in Medicine of the Beth Israel Deaconess Medical Center. N. Engl. J. Med. 338 (3): 171–9. CiteSeerX 10.1.1.357.2785. doi:10.1056/NEJM199801153380307. PMID 9428819.closed access
  10. ^ McEwen, Bruce S. (1998). "Stress, Adaptation, and Disease: Allostasis and Allostatic Load". Ann. N. Y. Acad. Sci. 840 (1): 33–44. Bibcode:1998NYASA.840...33M. doi:10.1111/j.1749-6632.1998.tb09546.x. PMID 9629234.closed access
  11. ^ 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: 163. doi:10.3389/fendo.2017.00163. PMC 5517413. PMID 28775711.
  12. ^ Dietrich, Johannes Wolfgang; Hoermann, Rudolf; Midgley, John E. M.; Bergen, Friederike; Müller, Patrick (26 October 2020). "The Two Faces of Janus: Why Thyrotropin as a Cardiovascular Risk Factor May Be an Ambiguous Target". Frontiers in Endocrinology. 11: 542710. doi:10.3389/fendo.2020.542710.
  13. ^ 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. PMID 16213079.closed access

Further reading[edit]