Allostatic load

Wear and tear on the body due to stress

Allostatic load is "the wear and tear on the body" which accumulates as an individual is exposed to repeated or chronic stress. The term was coined by Bruce McEwen and Eliot Stellar in 1993. It represents the physiological consequences of chronic exposure to fluctuating or heightened neural or neuroendocrine response which results from repeated or prolonged chronic stress.

The term allostatic load is "the wear and tear on the body" which accumulates as an individual is exposed to repeated or chronic stress. It was coined by McEwen and Stellar in 1993. The term is part of the regulatory model of allostasis, where the predictive regulation or stabilization of internal sensations in response to stimuli is ascribed to the brain. Allostasis involves the regulation of homeostasis in the body to decrease physiological consequences on the body. Predictive regulation refers to the brain's ability to anticipate needs and prepare to fulfill them before they arise. But it takes a considerable amount of the brain's energy to do this, and if it fails to resolve the uncertainty, the situation may become chronic and result in the accumulation of allostatic load. Allostatic load minimizes an organism's ability to cope with and reduce uncertainty in the future. Type 2 allostatic load results from sufficient or even excess energy consumption being accompanied by social conflict or other types of social dysfunction. The latter is the case in human society and certain situations affecting animals in captivity. In all cases, secretion of glucocorticosteroids and activity of other mediators of allostasis such as the autonomic nervous system, CNS neurotransmitters, and inflammatory cytokines wax and wane with allostatic load. If allostatic load is chronically high, then pathologies may develop. Type 2 allostatic overload does not trigger an escape response, and can only be counteracted through learning and changes in the social structure. Whereas both types of allostatic load are associated with increased release of cortisol and catecholamines, they differentially affect thyroid homeostasis: Concentrations of the thyroid hormone triiodothyronine are decreased in type 1 allostasis, but elevated in type 2 allostasis. Special situations may involve a blend of both type 1 and type 2 allostatic load. Examples include exhausting exercise and adaptation to antarctic conditions.

Allostatic load is generally measured through a composite index of indicators of cumulative strain on several organs and tissues, primarily biomarkers associated with the neuroendocrine, cardiovascular, immune, and metabolic systems. Indices of allostatic load are diverse across studies and are frequently assessed differently, using different biomarkers and different methods of assembling an allostatic load index. Allostatic load is not unique to humans and may be used to evaluate the physiological effects of chronic or frequent stress in non human primates as well. In the endocrine system, the increase or repeated levels of stress results in elevated levels of the hormone Corticotropin Releasing Factor (CRH), which is associated with activation of the HPA axis. In the immune system, the increase in levels of chronic stress results in the elevation of inflammation. The increase in inflammation levels is caused by the ongoing activation of the sympathetic nervous system. provides functions for simplified and automated calculation and statistical evaluation of physiological components of the metabolic syndrome symptom score (MSSS) and allostatic load.

The largest contribution to the allostatic load is the effect of stress on the brain. Allostasis is the system which helps to achieve homeostasis. Homeostasis is the regulation of physiological processes, whereby systems in the body respond to the state of the body and to the external environment.

Type 1 allostatic load represents the adaptive response to an absolute lack in energy, glutathione, and several macronutrients. It also includes predictive responses (e. g., hibernation, infection, and depression). Socio cultural mechanisms tend to augment this relation by perpetuating disparity even in the quality of health care, which tends to be inferior in socially disadvantaged population strata. When the cumulation of stressful experiences leads to chronic exposure to fluctuations in neural or neuroendocrine responses, which surpass the individual's coping ability, the result is considered to be an allostatic load. Causing factors of allostatic load include the following: continual physiological arousal due to chronic stress, inadequate coping mechanisms, stress response continuing past the completion of a stressor, and an insufficient allostatic response to a stressor. A typical allostatic response has been initiated by a stressor and then continues for the duration of the stressor, in which it shuts off as the stressor has ended. Allostatic load is the accumulation of stressors and maladaptive responses that may result in an extreme state, where the stress response does not terminate. The long term impact of childhood adversity (e. g., abuse, neglect) has been shown to have lasting effects, including the increased risk for allostatic load in adulthood. Regardless of the type, an association between discrimination and allostatic load in adulthood has been found. Health risk behaviors, such as poor eating habits and obesity, physical inactivity, substance use, and sleep deprivation are also considered to be risk factors of allostatic load. Extended activation of the hypothalamic pituitary adrenal axis (HPA), as well as the autonomic nervous system, can lead to negative impacts on biological health. Similarly, when the structural remodeling (e. g., cellular and molecular processes from the nucleus of a cell to the surface of a cell) of neural architecture, which is a key result of stress, continues past the termination of a stressor, the body is no longer maintaining a status of homeostasis and the extended stress response has negative implications. to surrogate markers of cardiovascular health and to hard endpoints, including cause specific and all cause mortality. Mediators connecting allostatic load to morbidity and mortality include the function of the autonomic nervous system, cytokines, and stress hormones (e. g., catecholamines, cortisol, and thyroid hormones). Biological implications of allostatic load include impacts on both cognitive and physical functioning, with the prefrontal cortex, hippocampus, and amygdala being regions that may be specifically impacted by it.

To reduce and manage high allostatic load, an individual should pay attention to structural (e. g., social environment, access to health care) and behavioral factors (e. g., diet, physical health, and tobacco smoking, which can lead to chronic disease). Support from the community and the social environment can manage high allostatic load. Empowering financial help from the government allows people to gain control and improve their psychological health. Providing cleaner and safer environments and the incentive towards a higher education will reduce the chance of stress and improve mental health significantly, therefore, reducing the onset of high allostatic load. Allostatic load differs by sex, age, and the social status of an individual. Protective factors could, at various times of an individual's life span, be implemented to reduce stress and, in the long run, eliminate the onset of allostatic load. Protective factors include parental bonding, education, social support, healthy workplaces, a sense of meaning towards life and choices being made, and positive feelings in general.