Allostatic Load

Allostatic load is “the wear and tear on the body” that accumulates as an individual is exposed to repeated or chronic stress.[1] The term was coined by McEwen and Stellar in 1993.[2][non-primary source needed] It represents the physiological consequences of chronic exposure to fluctuating or heightened neural or neuroendocrine response that results from repeated or prolonged chronic stress.[medical citation needed]

The regulatory model of allostasis claims that the brain’s primary role as an organ is the predictive regulation or the stabilisation of internal sensations.[3] Allostasis involves the regulation of homeostasis in the body to decrease physiological consequences on the body.[4] Predictive regulation refers to the brain’s ability to anticipate needs and prepare to fulfill them before they arise.[3] Therefore, in this model, the brain is responsible for efficient stimuli regulation.

Part of efficient regulation is the reduction of uncertainty. Humans naturally do not like feeling as if surprise is inevitable. Because of this, we constantly strive to reduce the uncertainty of future outcomes, and allostasis helps us do this by anticipating needs and planning how to satisfy them ahead of time.[5] But it takes a significant 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 experience of “allostatic load”.[5]

The concept of allostatic load provides that “the neuroendocrine, cardiovascular, neuroenergetic, and emotional responses become persistently activated so that blood flow turbulences in the coronary and cerebral arteries, high blood pressure, atherogenesis, cognitive dysfunction and depressed mood accelerate disease progression.”[5]In other words, all of the long-standing effects of continuously activated stress responses are referred to as allostatic load. And allostatic load can even result in permanently altered brain architecture and systemic pathophysiology.[5]

Further, as a result of these physical effects, allostatic load also minimizes an organism’s ability to cope with and reduce uncertainty in the future, which cements the entire cycle.[5] There are direct and Indirect effects on health resulting in a higher allostatic load.

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.[6]

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.[6]

In the endocrine system, the increase or repeated levels of stress results in the increased levels of the hormone Corticotropin-Releasing Factor (CRH), which is associated with activation of HPA axis.[4] HPA axis is the central stress response system which is responsible for modulating inflammatory responses that occur throughout the body. The prolonged stress levels can also lead to decreased levels of cortisol in the morning and increased levels in the afternoon, leading to greater daily output of cortisol which in the long term increases blood sugar levels.

In the nervous system, structural and functional abnormalities are a result of chronic prolonged stress. The increase of stress levels causes a shortening of dendrites in a neuron. Therefore, the shortening of dendrites causes the decrease in attention.[4] Chronic stress also causes greater response to fear of the unlearned in the nervous system, and fear conditioning.

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.[4] The impairment of cell-mediated acquired immunity is also a factor resulting in the immune system due to chronic stress.[4]

The greatest contribution to the allostatic load is the effects of stress on the brain. Allostasis. therefore, is the systems in the body that help achieve homeostasis.[7]Homeostasis is the regulation of physiological processes. The systems in the body respond to the state of the body and also to the external environment.[7] The relationship between allostasis and allostatic load is the concept of anticipation. Anticipation can drive the output of mediators. Examples of mediators include hormones and cortisol. Excess amounts of such mediators will result in an increase in allostatic load, contributing to anxiety and anticipation.[7]

Another relationship between allostasis and allostatic load are the health-damaging and health-promoting behaviours which contribute to allostatic load.[7] Theses behaviours include cigarette smoking, consumption of alcohol, poor diet and physical inactivity.[7]

There are three physiological processes which cause an increase in allostatic load, these include:

  1. Frequent stress: the magnitude and frequency of response to stress is what determines the level of allostatic load which effects the body.
  2. Failed shut-down: the inability of the body to shut off while stress accelerates and levels in the body exceed normal levels, for example, elevated blood pressure.
  3. Inadequate response: the failure of the body systems to respond to challenge, for example, exceeded levels of inflammation due to inadequate endogenous glucocorticoid responses.

The importance of homeostasis, therefore, is to regulate the stress levels encountered on the body to reduce allostatic load.

The effects of these forms of dysfunctional allostasis cause increased allostatic load and may, over time, lead to the development of disease, sometimes with decompensation of the allostatically controlled problem. 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.[8]

To reduce and manage high Allostatic Load, an individual should pay attention to structural and behavioural factors. Structural factors include the social environment, and access to health services. Behavioural factors include diet, physical health and tobacco smoking, which can lead to chronic disease. Actions such as tobacco smoking are brought about from the stress levels that an individual experiences. Therefore, controlling stress levels from the beginning, for example by not leading to tobacco smoking, will reduce the chance of chronic disease development and high allostatic load.

Low SES (socio-economic status) effects allostatic load significantly and therefore, focusing on the causes of low SES will reduce allostatic load levels. Societal polarisation, material deprivation, and psychological demands on health should be reduced to manage allostatic load. [9] The increased support from the community and the social environment will manage high allostatic load. [9] A way to reduce and manage high allostatic load is to empower financial help from the government. Empowerment ensures the management of allostatic load and improve health by allowing people to gain control and improve their psychological health. [9] Therefore, the improvement of inequalities in health will increase the stress levels and improve health, while reducing the chances of high allostatic load on the body. [9]

Interventions can include encouraging sleep quality and quantity, social support, self-esteem and wellbeing, improving diet, avoiding alcohol or drug consumption and participating in physical activity.[10] 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.[10]

Allostatic load differs by sex and 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, health workplaces, and a sense of meaning towards life and choices being made.[10]

  1. ^ Jane Ogden (2004). Health Psychology: A textbook, 3rd edition. Open University Press – McGraw-Hill Education. p. 259. ISBN 978-0335214716.
  2. ^ McEwen, BS; Stellar, E (Sep 27, 1993). “Stress and the individual. Mechanisms leading to disease”. Archives of Internal Medicine. 153 (18): 2093–101. doi:10.1001/archinte.153.18.2093. PMID 8379800.
  3. ^ Jump up to: a b Sterling, P (12 April 2012). “Allostasis: a model of predictive regulation”. Physiology & Behavior. 106 (1): 5–15. doi:10.1016/j.physbeh.2011.06.004. PMID 21684297.
  4. ^ Jump up to: a b c d e Danese, A; McEwen, BS (12 April 2012). “Adverse childhood experiences, allostasis, allostatic load, and age-related disease”. Physiology & Behavior. 106 (1): 29–39. doi:10.1016/j.physbeh.2011.08.019. PMID 21888923.
  5. ^ Jump up to: a b c d e Peters, A; McEwen, BS; Friston, K (September 2017). “Uncertainty and stress: Why it causes diseases and how it is mastered by the brain”. Progress in Neurobiology. 156: 164–188. doi:10.1016/j.pneurobio.2017.05.004. PMID 28576664. open access publication – free to read
  6. ^ Jump up to: a b Edes, Ashley; Crews, Douglas (January 1, 2017). “Allostatic load and biological anthropology”. American Journal of Physical Anthropology. 162: 44–70. doi:10.1002/ajpa.23146. PMID 28105719.
  7. ^ Jump up to: a b c d e McEwen, BS (1 May 1998). “Stress, adaptation, and disease. Allostasis and allostatic load”. Annals of the New York Academy of Sciences. 840: 33–44. doi:10.1111/j.1749-6632.1998.tb09546.x. PMID 9629234. [needs update]
  8. ^ McEwen B. S. (2000). “Allostasis and allostatic load: implications for neuropsychopharmacology”. Neuropsychopharmacology. 22 (2): 108–24. doi:10.1016/S0893-133X(99)00129-3. PMID 10649824.
  9. ^ Jump up to: a b c d Kristenson, M; Eriksen, H.R; Sluiter, J.K; Starke, D; Ursin, H (April 2004). “Psychobiological mechanisms of socioeconomic differences in health”. Social Science & Medicine. 58 (8): 1511–1522. doi:10.1016/s0277-9536(03)00353-8. ISSN 0277-9536. PMID 14759694.
  10. ^ Jump up to: a b c Juster, Robert-Paul; McEwen, Bruce S.; Lupien, Sonia J. (September 2010). “Allostatic load biomarkers of chronic stress and impact on health and cognition”. Neuroscience & Biobehavioral Reviews. 35 (1): 2–16. doi:10.1016/j.neubiorev.2009.10.002. ISSN 0149-7634. PMID 19822172.
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