Allostasis and allostatic load

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 lethal external and internal circumstances in a manner differing from that achieved through homeostatic mechanisms. Allostatic physiological mechanisms help maintain system viability in threatening circumstances through changes in the system’s properties — its bodily state — viz., by 'adapting' the system to the stressor, achieving a kind of stability/viability through change. Allostasis achieves adaptative adjustment by resetting the body's homeostasic set-points for a requisite set of physiological measures, thereby sustaining viability as a different type of homeostasis than Bernard-Cannon homeostasis.

Allo refers to 'other' or 'different'; stasis, to stability — so that allostasis refers to a way of achieving stability (or viability) in a way different from that achieved by Bernard-Cannon homeostasis. 'Allostasis' frequently colloquializes as "stability through change", or "homeostasis through change". Homeostatic flexibility.

According to Bernard Cannon homeostasis, homeostatic mechanisms target maintenance of critical biological variables (e.g., blood glucose concentations) to within a set, ideal range, in part through action of the sympathetic nervous system and regulation of adrenal cortical secretions. Further studies of the sympathico-adrenal systems indicates that they act continuously and respond to many different effects on the body by establishing new and different ideal ranges of system variables. As Goldstein and McEwen express it:

It is by now clear that the sympathico-adrenal system is active tonically and contributes to “basal” levels of key internal variables such as blood pressure and glucose. Moreover, activities of daily life, such as meal ingestion, speaking, changing posture, and movement—i.e., not only emergencies—are associated with continual alterations in sympathetic nervous system outflows, maintaining appropriate body temperature, delivery of metabolic fuel to body organs, and so forth. Each of these activities is associated with a somewhat different set of “normal” apparent steady-states, directed by the brain and determined by coordinated actions of a variety of effector systems.

Allostatic mechanisms appear prominently in the central nervous system’s response to stress, manifesting by regulation of:

• the behavior of the system-as-a-whole (e.g., eating behavior in response to hunger stress), and
• 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 viability, not by restoring physiological or behavioral variables to within a fixed set-point range, as in Bernard-Cannon homeostasis, but in effect by changing their optimal set-point range, at least temporarily, in a way that adapts the system to the potentially harmful circumstances it currently faces. However, if the stimulus to the allostatic re-set persists for long periods, or recurs too frequently, or if the re-set turns on inadequately or turns off inefficiently, the resulting so-called allostatic load causes wear-and-tear that can lead to operational dysfunction of the system.

Allostasis reflects active, adaptive processes that maintain apparent steady states, via multiple, interacting effectors regulated by homeostatic comparators—“homeostats.” “Allostatic load” refers to the consequences of sustained or repeated activation of mediators of allostasis. From the analogy of a home temperature control system, the temperature can be maintained at any of a variety of levels (allostatic states) by multiple means (effectors), regulated by the thermostat (homeostat). Allostatic load and risks of system breakdown increase when, for example, the front door is left open in the winter. Applying these notions can aid in understanding how acute and chronic stress can exert adverse health consequences via allostatic load.

Elaborated definitions and examples

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 to 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.

In their book on the endocrine factors in aging, Derek Chadwick and Jamie Goode characterize allostasis as follows, and contrast it with homeostasis:

Speaking generally, allostasis is distinct from homeostasis in maintaining a compensated equilibrium rather than a physiological equilibrium: stability is maintained at a price. The allostatic set point is abnormal relative to the homeostatic set point, the system is inherently less stable, and it has a relatively narrow dynamic range. Finally, a system in allostasis leads to pathology whereas a system in homeostasis does not.

Chadwick and Goode go on to compare the pathology and regulatory dysfunctions caused by chronic stress (allostatic load) and by the aging process. The consider the findings supportive of the notion that allostatic load plays a role in determining longevity. They point to evidence that similar disturbances in aging and chronic stress occur in the daily rhythm of the brain's interactions between its hypothalamus and pituitary gland, and in body temperature regulation, drawing attention to allostatic load as a factor in aging.

Role of brain in the physiology and neurobiology of stress

Holding refs:

References

Citations and notes

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