In recent years, allostasis and allostatic load have become proverbial terms, owing to their encompassing notion of stress and stress-related pathology. Allostasis refers to the active maintainence of stability of the internal milieu carried out via the initiation of broad shifts in hormonal, behavioral, and autonomic pathways to match a perceived or anticipated challenge (McEwen, 1998; Sterling and Eyer, 1988). Such adaptive changes work well when turned on and off efficiently. Maladaptions in restraining responses have been termed "allostatic load," which can be due to overstimulation from frequent stress, failure to turn off allostatic responses after stress, or inability to respond adequately to the initial challenge leading other systems to overreact. Thus, this concept suggests that the normal attempts of the body to adapt to adversity cost a price, reflected in the wear-and-tear of tissue and/or organ systems that may subsequently impair normal function and lead to overt pathology (McEwen,
2000). The response of the corticotropin system is a particularly good example of allostatic regulation. For example, glucocorticoids released in response to challenge mobilize energy stores and act in the brain to influence locomotion and arousal, in part by regulating corticotropin pathways in distinct nuclei. These effects are adaptive when increased activity is needed such as escape from a predator. In the event that increased glucocorticoid production continues unchecked, allostatic load may occur with the development of pathological abnormalities such as increased fat deposition, decreased immune function, or impaired cognitive function.
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