Allostasis and allostatic load

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In the biology of the human living system, 'allostasis' refers to physiological mechanisms that enable the system to adjust beneficially to diverse perturbing, stressful, and potentially harmful external and internal circumstances, and thereby maintain system viability, specifically through changes in the system’s properties, its bodily state — viz., by 'adapting' the system to the stressor. Allo refers to variability; stasis, to stability — so that allostasis frequently colloquializes as "stability through change", or homeostasis through change. Allostatic mechanisms appear prominently in the central nervous system’s regulation of (a) the behavior of the system-as-a-whole (e.g., eating behavior in response to hunger stress), and (b) the physiological behavior of subsystems of the system-as-a-whole (e.g., cardiovascular function in response to predator stress). Allostatic mechanisms contribute to system homeostasis, not by restoring physiological or behavioral variables to within a fixed set-point range, but in effect by changing the optimal set-point range, at least temporarily, thereby adapting the system to the potentially harmful circumstances it currently faces. However, if the stimulus to the allostatic re-set persists, the resulting so-called allostatic load can lead to dysfunction or disease of the system.

Jeongok Logan and Debra Barksdale at the University of North Carolina Chapel Hill articulate a succinct definition of allostasis and allostatic load:

Allostasis is the extension of the concept of homeostasis and represents the adaptation process of the complex physiological system to physical, psychosocial and environmental challenges or stress. Allostatic load is the long-term result of failed adaptation or [failed] allostasis, resulting in pathology and chronic illness.

Bruce McEwen and Teresa Seeman, in collaboration with the Allostatic Load Working Group, elaborate and give specific examples:

For each system of the body, there are both short-term adaptive actions (allostasis) that are protective and long-term effects that can be damaging (allostatic load). For the cardiovascular system, a prominent example of allostasis is the role of catecholamines in promoting adaptation by adjusting heart rate and blood pressure to sleeping, waking, physical exertion (citation). Yet, repeated surges of blood pressure in the face of job stress or the failure to shut off blood pressure surges efficiently accelerates atherosclerosis and synergizes with metabolic hormones to produce Type II diabetes, and this constitutes a type of allostatic load (see (citation)). Closely related to this is the role of adrenal steroids in metabolism. Whereas adrenal steroids promote allostasis by enhancing food intake and facilitating the replenishment of energy reserves, the overactivity of this system involving repeated HPA activity in stress or elevated evening cortisol leads to allostatic load in terms of insulin resistance, accelerating progression towards Type II diabetes, including abdominal obesity, atherosclerosis, and hypertension (citations). In the brain, actions of adrenal steroids and catecholamines that are related to allostasis include promoting retention of memories of emotionally-charged events, both positive and negative. Yet, overactivity of the HPA axis together with overactivity of the excitatory amino acid neurotransmitters promotes a form of allostatic load, consisting of cognitive dysfunction by a variety of mechanisms that involve reduced neuronal excitability, neuronal atrophy and, in extreme cases, death of brain cells, particularly in the hippocampus (citations).

McEwen and Seeman divide allostatic load into several distinct types of scenarios:

• Stress overload, such as that caused by severe and repeated economic burdens, which potentially leads physical and mental dysfunctions;
• Stress adaptation failure, where mediators of a stress response fail to diminish in response to repeated similar stress events, such as repeated taking of exams during course work;
• Stress response persistence following cessation of the stressor;
• Stressors that chronically disturb normal circadian rhythms, such as sleep deprivation;
• Stress response inadequacy that leads to overreaction of other systems.

References

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