Allostatic load

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The graph represents the effect of increased stress on the performance of the body. The lower the stress levels are in the body, the less likely the allostatic load model will have a significant effect on the brain and health. Although, an increase in stress levels results in an increase in stress on the brain and the health of individuals, making it more likely for the body to have significant effects on homeostasis and cause breakdown of the body systems. Allostatic Load Model.png
The graph represents the effect of increased stress on the performance of the body. The lower the stress levels are in the body, the less likely the allostatic load model will have a significant effect on the brain and health. Although, an increase in stress levels results in an increase in stress on the brain and the health of individuals, making it more likely for the body to have significant effects on homeostasis and cause breakdown of the body systems.

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.

Contents

Regulatory model

The term allostatic load is "the wear and tear on the body" which accumulates as an individual is exposed to repeated or chronic stress. [1] It was coined by McEwen and Stellar in 1993. [2]

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. [3] Allostasis involves the regulation of homeostasis in the body to decrease physiological consequences on the body. [4] [5] Predictive regulation refers to the brain's ability to anticipate needs and prepare to fulfill them before they arise. [3]

Simplified sketch showing the pathophysiological evolution of allostatic load in relation to childhood exposure, post-traumatic stress disorder (PTSD), resilience, and outcome measures. Allostatic load sketch.svg
Simplified sketch showing the pathophysiological evolution of allostatic load in relation to childhood exposure, post-traumatic stress disorder (PTSD), resilience, and outcome measures.

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. [6] 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. [6]

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." [6] All long-standing effects of continuously activated stress responses are referred to as allostatic load. Allostatic load can result in permanently altered brain architecture and systemic pathophysiology. [6] [7]

Allostatic load minimizes an organism's ability to cope with and reduce uncertainty in the future. [6]

Types

McEwen and Wingfield propose two types of allostatic load with different etiologies and distinct consequences:

Type 1 allostatic load occurs when energy demand exceeds supply, resulting in activation of the emergency life history stage. This serves to direct the animal away from normal life history stages into a survival mode that decreases allostatic load and regains positive energy balance. The normal life cycle can be resumed when the perturbation has passed. Typical situations ending up in type 1 allostasis are starvation, hibernation and critical illness. Of note, the life-threatening consequences of critical illness may be both cause and consequences of allostatic load. [8] [9] [10]

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. [11]

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. [10] This may result from an interaction of type 2 allostatic load with the set point of thyroid function. [12]

Special situations may involve a blend of both type 1 and type 2 allostatic load. Examples include exhausting exercise and adaptation to antarctic conditions. [10] [13]

Measurement

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. [14]

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. [14] The rat cumulative allostatic load measure (rCALM) is a marker for allostatic load in rodents. [15]

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. [5] The Hypothalamic–pituitary–adrenal axis is the central stress response system responsible for the modification of inflammatory responses throughout the body. Prolonged stress levels can 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 in stress levels causes a shortening of dendrites in a neuron. Therefore, the shortening of dendrites causes a decrease in attention. [5] Chronic stress also causes greater response to fear of the unlearned in the nervous system, and fear conditioning. [16]

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. [5] The impairment of cell-mediated acquired immunity is also a factor resulting in the immune system due to chronic stress. [5]

The R package pscore [17] provides functions for simplified and automated calculation and statistical evaluation of physiological components of the metabolic syndrome symptom score (MSSS) and allostatic load.

Relationship to allostasis and homeostasis

The largest contribution to the allostatic load is the effect of stress on the brain. Allostasis is the system which helps to achieve homeostasis. [18] Homeostasis is the regulation of physiological processes, whereby systems in the body respond to the state of the body and to the external environment. [18] 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. [18]

Allostasis and allostatic load are related to the amount of health-promoting and health-damaging behaviors like for example cigarette smoking, consumption of alcohol, poor diet, and physical inactivity. [18]

Three physiological processes cause an increase in allostatic load:

  1. Frequent stress: the magnitude and frequency of response to stress is what determines the level of allostatic load which affects 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, excess levels of inflammation due to inadequate endogenous glucocorticoid responses.

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

Dysfunctional allostasis causes allostatic load to increase which may, over time, lead to disease, sometimes with decompensation of the problem controlled by allostasis. 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. [19]

Causes of allostatic load

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). [8] [9] [10]

Type 2 allostatic load results from an expected mismatch of energy demand and supply. It is triggered by psychosocial stressors such as low socioeconomic status, major life events, and environmental stressors. [19] This association explains the increased risk for cardiovascular disease and chronic conditions like obesity, diabetes, hypertension, and psychotic conditions in subjects that were exposed to psychosocial trauma, social disadvantage, and discrimination. [3] [20] 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. [21] [22]

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. [23] [24] 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. [25] 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. [26]

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. [27] Regardless of the type, an association between discrimination and allostatic load in adulthood has been found. [28] 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. [29]

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. [26] The human body regulates itself to maintain a status of homeostasis by utilizing allostatic mechanisms, but when there are extended stress responses that continue past the duration of the stressor's termination, it leads to the failure of these systems. [29] [26]

Implications of allostatic load on health

Increased allostatic load constitutes a significant health hazard. Several studies documented a strong association of allostatic load to the incidence of coronary heart disease, [30] to surrogate markers of cardiovascular health [31] [32] [33] [34] and to hard endpoints, including cause-specific and all-cause mortality. [35] [36] Mediators connecting allostatic load to morbidity and mortality include the function of the autonomic nervous system, [37] cytokines, and stress hormones (e.g., catecholamines, [38] [39] cortisol, [40] [41] [42] [43] and thyroid hormones). [44] 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. [45]

Reducing risk

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). [4]

Low socio-economic status (SES) affects allostatic load and therefore, focusing on the causes of low SES may reduce allostatic load levels. Reducing societal polarization, material deprivation, and psychological demands on health assists to manage allostatic load. [46] Support from the community and the social environment can manage high allostatic load. [46] In addition, healthy lifestyle that encompasses a broad array of lifestyle change including healthy eating and regular physical exercise may reduce allostatic load. [47] Empowering financial help from the government allows people to gain control and improve their psychological health. [46] Improving inequalities in health decreases the stress levels and improves health by reducing high allostatic load on the body. [46]

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. [48] 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. [48]

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. [4] Protective factors include parental bonding, education, social support, healthy workplaces, a sense of meaning towards life and choices being made, [48] and positive feelings in general. [4]

See also

Related Research Articles

<span class="mw-page-title-main">Stress (biology)</span> Organisms response to a stressor such as an environmental condition or a stimulus

Stress, whether physiological, biological or psychological, is an organism's response to a stressor such as an environmental condition. When stressed by stimuli that alter an organism's environment, multiple systems respond across the body. In humans and most mammals, the autonomic nervous system and hypothalamic-pituitary-adrenal (HPA) axis are the two major systems that respond to stress. Two well-known hormones that humans produce during stressful situations are adrenaline and cortisol.

<span class="mw-page-title-main">Hypothalamic–pituitary–adrenal axis</span> Set of physiological feedback interactions

The hypothalamic–pituitary–adrenal axis is a complex set of direct influences and feedback interactions among three components: the hypothalamus, the pituitary gland, and the adrenal glands. These organs and their interactions constitute the HPS axis.

<span class="mw-page-title-main">Cortisol</span> Human natural glucocorticoid hormone

Cortisol is a steroid hormone in the glucocorticoid class of hormones and a stress hormone. When used as medication, it is known as hydrocortisone.

Psychoneuroimmunology (PNI), also referred to as psychoendoneuroimmunology (PENI) or psychoneuroendocrinoimmunology (PNEI), is the study of the interaction between psychological processes and the nervous and immune systems of the human body. It is a subfield of psychosomatic medicine. PNI takes an interdisciplinary approach, incorporating psychology, neuroscience, immunology, physiology, genetics, pharmacology, molecular biology, psychiatry, behavioral medicine, infectious diseases, endocrinology, and rheumatology.

Allostasis (/ˌɑːloʊˈsteɪsɪs/) is a physiological mechanism of regulation in which an organism anticipates and adjusts its energy use according to environmental demands. First proposed by Peter Sterling and Joseph Eyer in 1988, the concept of allostasis shifts the focus away from the body maintaining a rigid internal set-point, as in homeostasis, to the brain's ability and role to interpret environmental stress and coordinate changes in the body using neurotransmitters, hormones, and other signaling mechanisms. Allostasis is believed to be not only involved in the body's stress response and adaptation to chronic stress; it may also have a role in the regulation of the immune system as well as in the development of chronic diseases such as hypertension and diabetes.

Stress hormones are secreted by endocrine glands to modify one's internal environment during the times of stress. By performing various functions such as mobilizing energy sources, increasing heart rate, and downregulating metabolic processes which are not immediately necessary, stress hormones promote the survival of the organism. The secretions of some hormones are also downplayed during stress. Stress hormones include, but are not limited to:

Euthyroid sick syndrome (ESS) is a state of adaptation or dysregulation of thyrotropic feedback control wherein the levels of T3 and/or T4 are abnormal, but the thyroid gland does not appear to be dysfunctional. This condition may result from allostatic responses of hypothalamus-pituitary-thyroid feedback control, dyshomeostatic disorders, drug interferences, and impaired assay characteristics in critical illness.

Chronic stress is the physiological or psychological response induced by a long-term internal or external stressor. The stressor, either physically present or recollected, will produce the same effect and trigger a chronic stress response. There is a wide range of chronic stressors, but most entail relatively prolonged problems, conflicts and threats that people encounter on a daily basis. Several chronic stressors have been identified as associated with disease and mortality including "neighbourhood environment, financial strain, interpersonal stress, work stress and caregiving."

<span class="mw-page-title-main">Cortisol awakening response</span> Physiological response

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<span class="mw-page-title-main">Effects of stress on memory</span> Overview of the effects of stress on memory

The effects of stress on memory include interference with a person's capacity to encode memory and the ability to retrieve information. Stimuli, like stress, improved memory when it was related to learning the subject. During times of stress, the body reacts by secreting stress hormones into the bloodstream. Stress can cause acute and chronic changes in certain brain areas which can cause long-term damage. Over-secretion of stress hormones most frequently impairs long-term delayed recall memory, but can enhance short-term, immediate recall memory. This enhancement is particularly relative in emotional memory. In particular, the hippocampus, prefrontal cortex and the amygdala are affected. One class of stress hormone responsible for negatively affecting long-term, delayed recall memory is the glucocorticoids (GCs), the most notable of which is cortisol. Glucocorticoids facilitate and impair the actions of stress in the brain memory process. Cortisol is a known biomarker for stress. Under normal circumstances, the hippocampus regulates the production of cortisol through negative feedback because it has many receptors that are sensitive to these stress hormones. However, an excess of cortisol can impair the ability of the hippocampus to both encode and recall memories. These stress hormones are also hindering the hippocampus from receiving enough energy by diverting glucose levels to surrounding muscles.

<span class="mw-page-title-main">Psychological stress</span> Feeling of strain and pressure

In psychology, stress is a feeling of emotional strain and pressure. Stress is a type of psychological pain. Small amounts of stress may be beneficial, as it can improve athletic performance, motivation and reaction to the environment. Excessive amounts of stress, however, can increase the risk of strokes, heart attacks, ulcers, and mental illnesses such as depression and also aggravation of a pre-existing condition.

Early childhood is a critical period in a child's life that includes ages from birth to five years old. Psychological stress is an inevitable part of life. Human beings can experience stress from an early age. Although stress is a factor for the average human being, it can be a positive or negative molding aspect in a young child's life.

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Marriage and health are closely related. Married people experience lower morbidity and mortality across such diverse health threats as cancer, heart attacks, and surgery. There are gender differences in these effects which may be partially due to men's and women's relative status. Most research on marriage and health has focused on heterosexual couples, and more work is needed to clarify the health effects on same-sex marriage. Simply being married, as well as the quality of one's marriage, has been linked to diverse measures of health. Research has examined the social-cognitive, emotional, behavioral and biological processes involved in these links.

Perseverative cognition is a collective term in psychology for continuous thinking about negative events in the past or in the future.

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Biological inequity, also known as biological inequality, refers to the “systematic, unfair, and avoidable stress-related biological differences which increase risk of disease, observed between social groups of a population”. The term developed by Centric Lab aims to unify societal factors with the biological underpinnings of health inequities – the unfair and avoidable differences in health status and risks between social groups of a population — such that these inequalities can be investigated in a holistic manner.

References

  1. ↑ Ogden J (2004). Health Psychology: A textbook (3rd ed.). Open University Press - McGraw-Hill Education. pp.  259. ISBN   978-0335214716.
  2. ↑ McEwen BS, Stellar E (September 1993). "Stress and the individual. Mechanisms leading to disease". Archives of Internal Medicine. 153 (18): 2093–2101. doi:10.1001/archinte.153.18.2093. PMID   8379800.
  3. 1 2 3 Sterling P (April 2012). "Allostasis: a model of predictive regulation". Physiology & Behavior. 106 (1): 5–15. doi:10.1016/j.physbeh.2011.06.004. PMID   21684297. S2CID   27164469.
  4. 1 2 3 4 Schenk HM, Jeronimus BF, van der Krieke L, Bos EH, de Jonge P, Rosmalen JG (2017). "Associations of Positive Affect and Negative Affect With Allostatic Load: A Lifelines Cohort Study". Psychosomatic Medicine. 80 (2): 160–166. doi:10.1097/PSY.0000000000000546. PMID   29215457. S2CID   20121114.
  5. 1 2 3 4 5 Danese A, McEwen BS (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. S2CID   3840754.
  6. 1 2 3 4 5 Peters A, McEwen BS, Friston K (September 2017). "Uncertainty and stress: Why it causes diseases and how it is mastered by the brain" (PDF). Progress in Neurobiology. 156: 164–188. doi: 10.1016/j.pneurobio.2017.05.004 . PMID   28576664. S2CID   286501. Open Access logo PLoS transparent.svg
  7. ↑ Dolan, Eric W. (2022-10-20). "New study uncovers a troubling interaction between depression and allostatic load". PsyPost. Retrieved 2022-10-22.
  8. 1 2 Brame AL, Singer M (October 2010). "Stressing the obvious? An allostatic look at critical illness". Critical Care Medicine. 38 (10 Suppl): S600–S607. doi:10.1097/CCM.0b013e3181f23e92. PMID   21164403. S2CID   39889109.
  9. 1 2 Cuesta JM, Singer M (December 2012). "The stress response and critical illness: a review". Critical Care Medicine. 40 (12): 3283–3289. doi:10.1097/CCM.0b013e31826567eb. PMID   22975887. S2CID   7064946.
  10. 1 2 3 4 Chatzitomaris A, Hoermann R, Midgley JE, Hering S, Urban A, Dietrich B, et al. (2017). "Thyroid Allostasis-Adaptive Responses of Thyrotropic Feedback Control to Conditions of Strain, Stress, and Developmental Programming". Frontiers in Endocrinology. 8: 163. doi: 10.3389/fendo.2017.00163 . PMC   5517413 . PMID   28775711.
  11. ↑ McEwen BS, Wingfield JC (January 2003). "The concept of allostasis in biology and biomedicine". Hormones and Behavior. 43 (1): 2–15. doi:10.1016/S0018-506X(02)00024-7. PMID   12614627. S2CID   11329342.
  12. ↑ Dietrich JW, Hoermann R, Midgley JE, Bergen F, Müller P (26 October 2020). "The Two Faces of Janus: Why Thyrotropin as a Cardiovascular Risk Factor May Be an Ambiguous Target". Frontiers in Endocrinology. 11: 542710. doi: 10.3389/fendo.2020.542710 . PMC   7649136 . PMID   33193077.
  13. ↑ Spinelli, E; Werner Junior, J (13 April 2022). "Human adaptative behavior to Antarctic conditions: A review of physiological aspects". WIREs Mechanisms of Disease. 14 (5): e1556. doi:10.1002/wsbm.1556. PMID   35419979. S2CID   248156906.
  14. 1 2 Edes AN, Crews DE (January 2017). "Allostatic load and biological anthropology". American Journal of Physical Anthropology. 162 (Suppl 63): 44–70. doi: 10.1002/ajpa.23146 . PMID   28105719.
  15. ↑ McCreary, JK; Erickson, ZT; Paxman, E; Kiss, D; Montina, T; Olson, DM; Metz, GAS (January 2019). "The rat cumulative allostatic load measure (rCALM): a new translational assessment of the burden of stress". Environmental Epigenetics. 5 (1): dvz005. doi:10.1093/eep/dvz005. PMC   6500369 . PMID   31065381.
  16. ↑ Hoffman, Ann N.; Lorson, Nickolaus G.; Sanabria, Federico; Foster Olive, M.; Conrad, Cheryl D. (July 2014). "Chronic stress disrupts fear extinction and enhances amygdala and hippocampal Fos expression in an animal model of post-traumatic stress disorder". Neurobiology of Learning and Memory. 112: 139–147. doi:10.1016/j.nlm.2014.01.018. PMC   4051860 . PMID   24508064.
  17. ↑ pscore cran.r-project.org
  18. 1 2 3 4 McEwen BS (May 1998). "Stress, adaptation, and disease. Allostasis and allostatic load". Annals of the New York Academy of Sciences. 840 (1): 33–44. Bibcode:1998NYASA.840...33M. doi:10.1111/j.1749-6632.1998.tb09546.x. PMID   9629234. S2CID   20043016.[ needs update ]
  19. 1 2 McEwen BS (February 2000). "Allostasis and allostatic load: implications for neuropsychopharmacology". Neuropsychopharmacology. 22 (2): 108–124. doi: 10.1016/S0893-133X(99)00129-3 . PMID   10649824.
  20. ↑ Guidi J, Lucente M, Sonino N, Fava GA (2021). "Allostatic Load and Its Impact on Health: A Systematic Review". Psychotherapy and Psychosomatics. 90 (1): 11–27. doi: 10.1159/000510696 . PMID   32799204. S2CID   221144801.
  21. ↑ Falkentoft AC, Andersen J, Malik ME, Selmer C, Gæde PH, Staehr PB, et al. (March 2022). "Impact of socioeconomic position on initiation of SGLT-2 inhibitors or GLP-1 receptor agonists in patients with type 2 diabetes - a Danish nationwide observational study". The Lancet Regional Health. Europe. 14: 100308. doi:10.1016/j.lanepe.2022.100308. PMC   8802041 . PMID   35146474.
  22. ↑ Nauck MA, Dietrich JW (March 2022). "Understanding the restrictions in the prescription and use of potentially beneficial diabetes medications associated with low socio-economic status". The Lancet Regional Health. Europe. 14: 100318. doi:10.1016/j.lanepe.2022.100318. PMC   8819377 . PMID   35146476.
  23. ↑ Fava, Giovanni A.; Cosci, Fiammetta; Sonino, Nicoletta (2017). "Current Psychosomatic Practice". Psychotherapy and Psychosomatics. 86 (1): 13–30. doi: 10.1159/000448856 . ISSN   0033-3190. PMID   27884006. S2CID   9517439.
  24. ↑ Guidi, Jenny; Lucente, Marcella; Sonino, Nicoletta; Fava, Giovanni A. (2021). "Allostatic Load and Its Impact on Health: A Systematic Review". Psychotherapy and Psychosomatics. 90 (1): 11–27. doi: 10.1159/000510696 . ISSN   0033-3190. PMID   32799204. S2CID   221144801.
  25. ↑ Guidi, Jenny; Lucente, Marcella; Sonino, Nicoletta; Fava, Giovanni A. (2021). "Allostatic Load and Its Impact on Health: A Systematic Review". Psychotherapy and Psychosomatics. 90 (1): 11–27. doi: 10.1159/000510696 . ISSN   0033-3190. PMID   32799204. S2CID   221144801.
  26. 1 2 3 Fava, Giovanni A.; McEwen, Bruce S.; Guidi, Jenny; Gostoli, Sara; Offidani, Emanuela; Sonino, Nicoletta (October 2019). "Clinical characterization of allostatic overload". Psychoneuroendocrinology. 108: 94–101. doi:10.1016/j.psyneuen.2019.05.028. hdl: 11585/717244 . PMID   31252304. S2CID   171091952.
  27. ↑ Widom, Cathy Spatz; Horan, Jacqueline; Brzustowicz, Linda (September 2015). "Childhood maltreatment predicts allostatic load in adulthood". Child Abuse & Neglect. 47: 59–69. doi:10.1016/j.chiabu.2015.01.016. PMC   4539293 . PMID   25700779.
  28. ↑ Miller, Hailey N.; LaFave, Sarah; Marineau, Lea; Stephens, Janna; Thorpe, Roland J. (July 2021). "The impact of discrimination on allostatic load in adults: An integrative review of literature". Journal of Psychosomatic Research. 146: 110434. doi:10.1016/j.jpsychores.2021.110434. PMC   8172431 . PMID   33810863.
  29. 1 2 Suvarna, Beena; Suvarna, Aditya; Phillips, Riana; Juster, Robert-Paul; McDermott, Brett; Sarnyai, Zoltan (January 2020). "Health risk behaviours and allostatic load: A systematic review". Neuroscience & Biobehavioral Reviews. 108: 694–711. doi:10.1016/j.neubiorev.2019.12.020. PMID   31846655. S2CID   209351855.
  30. ↑ Gillespie SL, Anderson CM, Zhao S, Tan Y, Kline D, Brock G, et al. (November 2019). "Allostatic load in the association of depressive symptoms with incident coronary heart disease: The Jackson Heart Study". Psychoneuroendocrinology. 109: 104369. doi:10.1016/j.psyneuen.2019.06.020. PMC   7232849 . PMID   31307010.
  31. ↑ Veronesi G, Cavicchiolo M, Ferrario MM (December 2019). "Allostatic load as a mediator of the association between psychosocial risk factors and cardiovascular diseases. Recent evidence and indications for prevention". Giornale Italiano di Medicina del Lavoro ed Ergonomia. 41 (4): 333–336. PMID   32126604.
  32. ↑ Viljoen M, Claassen N (June 2017). "Allostatic load and heart rate variability as health risk indicators". African Health Sciences. 17 (2): 428–435. doi:10.4314/ahs.v17i2.17. PMC   5637028 . PMID   29062338.
  33. ↑ Magnusson Hanson LL, Rod NH, Vahtera J, Virtanen M, Ferrie J, Shipley M, et al. (August 2020). "Job insecurity and risk of coronary heart disease: Mediation analyses of health behaviors, sleep problems, physiological and psychological factors". Psychoneuroendocrinology. 118: 104706. doi: 10.1016/j.psyneuen.2020.104706 . PMID   32460194. S2CID   218580825.
  34. ↑ Milad E, Bogg T (November 2020). "Personality Traits, Coping, Health-related Behaviors, and Cumulative Physiological Health in a National Sample: 10 Year Prospective Effects of Conscientiousness via Perceptions of Activity on Allostatic Load". Annals of Behavioral Medicine. 54 (11): 880–892. doi:10.1093/abm/kaaa024. PMC   7646150 . PMID   32359064.
  35. ↑ Borrell LN, Rodríguez-Álvarez E, Dallo FJ (2020). "Racial/ethnic inequities in the associations of allostatic load with all-cause and cardiovascular-specific mortality risk in U.S. adults". PLOS ONE. 15 (2): e0228336. Bibcode:2020PLoSO..1528336B. doi: 10.1371/journal.pone.0228336 . PMC   7018050 . PMID   32053626.
  36. ↑ Robertson T, Beveridge G, Bromley C (2017). "Allostatic load as a predictor of all-cause and cause-specific mortality in the general population: Evidence from the Scottish Health Survey". PLOS ONE. 12 (8): e0183297. Bibcode:2017PLoSO..1283297R. doi: 10.1371/journal.pone.0183297 . PMC   5559080 . PMID   28813505.
  37. ↑ Goldstein DS (August 2020). "The extended autonomic system, dyshomeostasis, and COVID-19". Clinical Autonomic Research. 30 (4): 299–315. doi:10.1007/s10286-020-00714-0. PMC   7374073 . PMID   32700055.
  38. ↑ Brindley DN, Rolland Y (November 1989). "Possible connections between stress, diabetes, obesity, hypertension and altered lipoprotein metabolism that may result in atherosclerosis". Clinical Science. 77 (5): 453–461. doi:10.1042/cs0770453. PMID   2684477.
  39. ↑ Rigney T (September 2010). "Allostatic load and delirium in the hospitalized older adult". Nursing Research. 59 (5): 322–330. doi:10.1097/NNR.0b013e3181ec156b. PMID   20671582. S2CID   205891002.
  40. ↑ Skinner ML, Shirtcliff EA, Haggerty KP, Coe CL, Catalano RF (November 2011). "Allostasis model facilitates understanding race differences in the diurnal cortisol rhythm". Development and Psychopathology. 23 (4): 1167–1186. doi:10.1017/S095457941100054X. PMC   3583352 . PMID   22018088.
  41. ↑ Adam EK, Heissel JA, Zeiders KH, Richeson JA, Ross EC, Ehrlich KB, et al. (December 2015). "Developmental histories of perceived racial discrimination and diurnal cortisol profiles in adulthood: A 20-year prospective study". Psychoneuroendocrinology. 62: 279–291. doi:10.1016/j.psyneuen.2015.08.018. PMC   4739843 . PMID   26352481.
  42. ↑ Price JL, Frazier IR, Lewis B, Walker R, Javors MA, Nixon SJ, Adinoff B (February 2019). "Differences in pituitary-adrenal reactivity in Black and White men with and without alcohol use disorder". Psychoneuroendocrinology. 100: 180–189. doi:10.1016/j.psyneuen.2018.10.004. PMC   6333532 . PMID   30347319.
  43. ↑ Casavant SG, Cong X, Fitch RH, Moore J, Rosenkrantz T, Starkweather A (March 2019). "Allostatic Load and Biomarkers of Stress in the Preterm Infant: An Integrative Review". Biological Research for Nursing. 21 (2): 210–223. doi:10.1177/1099800418824415. PMID   30654634. S2CID   58652915.
  44. ↑ Aweimer A, El-Battrawy I, Akin I, Borggrefe M, Mügge A, Patsalis PC, et al. (May 2021). "Abnormal thyroid function is common in takotsubo syndrome and depends on two distinct mechanisms: results of a multicentre observational study". Journal of Internal Medicine. 289 (5): 675–687. doi: 10.1111/joim.13189 . PMID   33179374.
  45. ↑ Fava, Giovanni A.; Cosci, Fiammetta; Sonino, Nicoletta (2017). "Current Psychosomatic Practice". Psychotherapy and Psychosomatics. 86 (1): 13–30. doi: 10.1159/000448856 . ISSN   0033-3190. PMID   27884006. S2CID   9517439.
  46. 1 2 3 4 Kristenson M, Eriksen HR, Sluiter JK, 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. PMID   14759694.
  47. ↑ Tan M, Mamun A, Kitzman H, Dodgen L (2019-04-18). "Longitudinal Changes in Allostatic Load during a Randomized Church-based, Lifestyle Intervention in African American Women". Ethnicity & Disease. 29 (2): 297–308. doi:10.18865/ed.29.2.297. PMC   6478040 . PMID   31057315.
  48. 1 2 3 Juster RP, McEwen BS, Lupien SJ (September 2010). "Allostatic load biomarkers of chronic stress and impact on health and cognition". Neuroscience and Biobehavioral Reviews. 35 (1): 2–16. doi:10.1016/j.neubiorev.2009.10.002. PMID   19822172. S2CID   3562563.
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