Allostatic load
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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 adrenalin, 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: 1) Repeated frequency of stress responses to multiple novel stressors; 2) Failure to habituate to repeated stressors of the same kind; 3) Failure to turn off each stress response in a timely manner due to delayed shut down; and 4) 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
- ↑ McEwen BS (2000). "Allostasis and allostatic load: implications for neuropsychopharmacology". Neuropsychopharmacology. 22 (2): 108–24. doi:10.1016/S0893-133X(99)00129-3. PMID 10649824.