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.
Allostatic load means "the wear and tear on the body" which accumulates as an individual is exposed to repeated or chronic stress. [1] The term 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]
Part of efficient regulation is the reduction of uncertainty. Humans are naturally averse to surprise; because of this, they constantly strive to reduce the uncertainty of future outcomes, and allostasis enables 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]
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]
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.
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:
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]
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]
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]
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]
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.
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.
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."
The cortisol awakening response (CAR) is an increase between 38% and 75% in cortisol levels peaking 30–45 minutes after awakening in the morning in some people. This rise is superimposed upon the late-night rise in cortisol which occurs before awakening. While its purpose is uncertain, it may be linked to the hippocampus' preparation of the hypothalamic-pituitary-adrenal axis (HPA) in order to face anticipated stress.
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.
In psychology, stress is a feeling of emotional strain and pressure. Stress is a form of psychological and mental discomfort. 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 aggravate pre-existing conditions.
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.
Social stress is stress that stems from one's relationships with others and from the social environment in general. Based on the appraisal theory of emotion, stress arises when a person evaluates a situation as personally relevant and perceives that they do not have the resources to cope or handle the specific situation.
Alcohol and cortisol have a complex relationship. While cortisol is a stress hormone, alcoholism can lead to increased cortisol levels in the body over time. This can be problematic because cortisol can temporarily shut down other bodily functions, potentially causing physical damage.
Perseverative cognition is a collective term in psychology for continuous thinking about negative events in the past or in the future.
Attachment and health is a psychological model which considers how the attachment theory pertains to people's preferences and expectations for the proximity of others when faced with stress, threat, danger or pain. In 1982, American psychiatrist Lawrence Kolb noticed that patients with chronic pain displayed behaviours with their healthcare providers akin to what children might display with an attachment figure, thus marking one of the first applications of the attachment theory to physical health. Development of the adult attachment theory and adult attachment measures in the 1990s provided researchers with the means to apply the attachment theory to health in a more systematic way. Since that time, it has been used to understand variations in stress response, health outcomes and health behaviour. Ultimately, the application of the attachment theory to health care may enable health care practitioners to provide more personalized medicine by creating a deeper understanding of patient distress and allowing clinicians to better meet their needs and expectations.
Functional somatic syndrome (FSS) is any of a group of chronic diagnoses with no identifiable organic cause. This term was coined by Hemanth Samkumar. It encompasses disorders such as fibromyalgia, chronic widespread pain, temporomandibular disorder, irritable bowel syndrome, lower back pain, tension headache, atypical face pain, non-cardiac chest pain, insomnia, palpitation, dyspepsia and dizziness. General overlap exists between this term, somatization and somatoform. The status of ME/CFS as a functional somatic syndrome is contested. Although the aetiology remains unclear, there are consistent findings of biological abnormalities, and major health bodies such as the NAM, WHO, and NIH, classify it as an organic disease.
Angela J. Grippo is an American neuroscientist and health psychologist known for her research on stress, mood disorders, and cardiovascular disease. She is an associate professor of psychology at Northern Illinois University.
The shift-and-persist model has emerged in order to account for unintuitive, positive health outcomes in some individuals of low socioeconomic status. A large body of research has previously linked low socioeconomic status to poor physical and mental health outcomes, including early mortality. Low socioeconomic status is hypothesized to get "under the skin" by producing chronic activation of the sympathetic nervous system and hypothalamic–pituitary–adrenal axis, which increases allostatic load, leading to the pathogenesis of chronic disease. However, some individuals of low socioeconomic status do not appear to experience the expected, negative health effects associated with growing up in poverty. To account for this, the shift-and-persist model proposes that, as children, some individuals of low socioeconomic status learn adaptive strategies for regulating their emotions ("shifting") and focusing on their goals ("persisting") in the face of chronic adversity. According to this model, the use of shift-and-persist strategies diminishes the typical negative effects of adversity on health by leading to more adaptive biological, cognitive, and behavioral responses to daily stressors.
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.