This MedLibrary.org supplementary page on Allostatic load is provided directly from the open source Wikipedia as a service to our readers. Please see the note below on authorship of this content, as well as the Wikipedia usage guidelines. To search for other content from our encyclopedia supplement, please use the form below:
Related Sponsors
 |
The introduction to this article provides insufficient context for those unfamiliar with the subject. Please help improve the article with a good introductory style. |
The hormones and other physiological agents that mediate the effects of stress on the body have protective and adaptive effects in the short run and yet can accelerate pathophysiology when they are over-produced or mismanaged[1].
The term Allostatic load was coined by McEwan (2000) and refers to the physiological costs of chronic exposure to the neural or neuroendocrine stress response. Allostatic load specifically refers to a composite index of indicators of cumulative strain on multiple organs and tissues which accumulates via the wear and tear associated with acute shifts in physiologic activity in response to negative stimuli.
Adaptation in the face of stressful situations and stimuli involves activation of neural, neuroendocrine and neuroendocrine-immune mechanisms. This adaptation has been called "allostasis" or "maintaining stability through change", which is an essential component of maintaining homeostasis. The main hormonal mediators of the stress response, cortisol and epinephrine (adrenaline), have both protective and damaging effects on the body. In the short run, they are essential for adaptation, maintenance of homeostasis, and survival “allostasis”. Yet, over longer time intervals, when called upon frequently, they exact a cost “allostatic load” that can accelerate disease processes. Allostatic load can be measured in physiological systems as chemical imbalances in autonomic nervous system, central nervous system, neuroendocrine, and immune system activity as well as perturbations in the diurnal rhythms, and, in some cases, plasticity changes to brain structures.
Four conditions that lead to allostatic load are:
- Repeated frequency of stress responses to multiple novel stressors;
- Failure to habituate to repeated stressors of the same kind;
- Failure to turn off each stress response in a timely manner due to delayed shut down; and
- Inadequate response that leads to compensatory hyperactivity of other mediators.
The effects of these forms of dysfunctional allostasis cause allostatic load and this in turn leads over time to diseases. Allostatic load effects can be measured in the body. When tabulated in the form of allostatic load indices using sophisticated analytical methods, it gives an indication of cumulative lifetime effects of all types of stress on the body.[1]
References
- ^ a b McEwen BS (2000). "Allostasis and allostatic load: implications for neuropsychopharmacology". Neuropsychopharmacology 22 (2): 108–24. doi:. PMID 10649824.
 |
This medical article is a stub. You can help Wikipedia by expanding it. |
Wikipedia content modification information:
- This page was last modified on 12 June 2008, at 12:58.
Wikipedia Authorship and Review
Wikipedia content provided here is not reviewed directly by MedLibrary.org. Wikipedia content is authored by an open community of volunteers and is not produced by or in any way affiliated with MedLibrary.org.
Wikipedia Usage Guidelines
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article on "Allostatic load".
The URL for this specific entry is:
All Wikipedia text is available under the terms of the GNU Free Documentation License. (See Copyrights for details). Wikipedia® is a registered trademark of the Wikimedia Foundation, Inc.