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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.[1] Allostasis is essential in order to maintain internal viability amid changing conditions (Sterling and Eyer, 1988; McEwen, 1998a, 1998b; Schulkin, 2003).

Nature of conceptEdit

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".[2][3] Allostatic regulation reflects, at least partly, cephalic involvement in primary regulatory events, in that it is anticipatory to systemic physiological regulation (Sterling and Eyer, 1988; Schulkin 2003). 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.[4]

Sterling (2004) proposes six interrelated principles that underlie allostasis:

  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.

Contrast with homeostasisEdit

The difference between allostasis and homeostasis is popularized by Robert Sapolsky's book Why Zebras Don't Get Ulcers:

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.

TypesEdit

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.,[1][5]

Allostatic loadEdit

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.

ControversyEdit

Trevor A. Day has argued that the concept of allostasis is no more than a renaming of the original concept of homeostasis. Defining stress as a prelude to mapping its neurocircuitry: No help from allostasis

ReferencesEdit

  1. 1.0 1.1 [1]The concept of allostasis in biology and biomedicine. Horm Behav. 2003 Jan;43(1):2-15. McEwen BS, Wingfield JC. (Laboratory of Neuroendocrinology, The Rockefeller University
  2. Sterling, P. and Eyer, J., 1988, Allostasis: A new paradigm to explain arousal pathology. In: S. Fisher and J. Reason (Eds.), Handbook of Life Stress, Cognition and Health. John Wiley & Sons, New York.
  3. [2][dead link] Robyn Klein Phylogenetic and phytochemical characteristics of plant species with adaptogenic properties MS Thesis, 2004, Montana State University Chapter 3
  4. Wingfield JC (2003) Anniversary Essay: Control of behavioural strategies for capricious environments. Animal Behaviour. 66:000-000. (Department of Neuroendocrinology, University of Washington)
  5. Sterling & Eyer, 1988 op. cit.

McEwen, BS. (1998a). Protective and damaging effects of stress mediators. New England Journal of Medicine 338: 171-9.

McEwen, BS. (1998b). Stress, adaptation, and disease: Allostasis and allostatic load. Ann NY Acad Sci 840: 33-44.

Schulkin, J. (2003). Rethinking homeostasis: Allostatic regulation in physiology and pathophysiology. MIT Press: London.

Sterling, P. (2004). Principles of Allostasis: Optimal design, predictive regulation, pathophysiology, and rational therapeutics. IN: Schulkin, J. (Ed.). Allostasis, homeostasis, and the costs of physiological adaptation. Cambridge University Press: Cambridge, UK.

See alsoEdit

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