Chronic stress

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Chronic stress is the physiological or psychological response induced by a long-term internal or external stressor. [1] The stressor, either physically present or recollected, will produce the same effect and trigger a chronic stress response. [1] There is a wide range of chronic stressors, but most entail relatively prolonged problems, conflicts and threats that people encounter on a daily basis. [2] And several chronic stressors, including "neighbourhood environment, financial strain, interpersonal stress, work stress and caregiving.", have been identified as associated with disease and mortality. [3]

Contents

Stress responses, such as the fight or flight response, is fundamental. The complexity of the environment means that it is constantly changing. To navigate the surroundings, we, therefore, need a system that is capable of responding to perceived threatening and harmful situations. [4] The stress response system thus has its role as an adaptive process to restore homeostasis in the body by actively making changes. [4] [5] For instance, the body will involve in an endocrine system response in which corticosteroids are released. This process is known as allostasis, first proposed by Sterling and Eyer (1988). [6] Research has provided considerable evidence to illustrate the stress response as a short-term adaptive system. [4] The immediate effects of stress hormones are beneficial in a particular short-term situation. The system is arguably a protective defense against threats [5] and usually does not pose a health risk. [7]

However, the problem arises when there is a persistent threat. First-time exposure to a stressor will trigger an acute stress response in the body; however, repeated and continuous exposure causes the stressor to become chronic. [4] McEwen and Stellar (1993) argued there is a "hidden cost of chronic stress to the body over long time periods". [8] That is often known as allostatic load. Chronic stress can cause the allostasis system to overstimulate in response to the persistent threat. [7] And such overstimulation can lead to an adverse impact. To illustrate, the long-term exposure to stress creates a high level of these hormones. This may lead to high blood pressure (and subsequently heart disease), damage to muscle tissue, inhibition of growth, [9] and damage to mental health. Chronic stress also relates directly to the functionality and structure of the nervous system, thereby influencing affective and physiological responses to stress. [3] These subsequently can result in damage to the body.

Historical development

Hans Selye (1907–1982), known as the "father of stress", [10] is credited with first studying and identifying stress. He studied stress effects by subjecting lab mice to various physical, antigenic, and environmental stressors, including excessive exercise, starvation, and extreme temperatures. He determined that regardless of the type of stress, the mice exhibited similar physical effects, including thymus gland deterioration and the development of ulcers. [10] Selye then developed his theory of general adaptive syndrome (GAS) in 1936, known today as "stress response". He concluded that humans exposed to prolonged stress could also experience hormonal system breakdown and subsequently develop conditions such as heart disease and elevated blood pressure. [11] Selye considered these conditions to be "diseases of adaptation", or the effects of chronic stress caused by heightened hormonal and chemical levels. [10] His research on acute and chronic stress responses introduced stress to the medical field. [10]

Physiology

Animals exposed to distressing events over which they have no control respond by releasing corticosteroids. [5] The sympathetic branch of the nervous system is activated, also releasing epinephrine and norepinephrine. [9]

Stress has a role in humans as a method of reacting to difficult and possibly dangerous situations. The "fight or flight" response when one perceives a threat helps the body exert energy to fight or run away to live another day. This response is noticeable when the adrenal glands release epinephrine, causing the blood vessels to constrict and heart rate to increase. In addition, cortisol is another hormone that is released under stress and its purpose is to raise the glucose level in the blood. Glucose is the main energy source for human cells and its increase during time of stress is for the purpose of having energy readily available for over active cells. [12]

Chronic stress is also known to be associated with an accelerated loss of telomeres in most but not all studies. [13] [14]

Response

Different types of stressors, the timing (duration) of the stressors, and genetic inherited personal characteristics all influence the response of the hypothalamic–pituitary–adrenal axis to stressful situations. The hypothalamic–pituitary–thyroid axis and other endocrine axes are also involved in the stress response. Those with a wealthy background have a stronger response to stress than those in the lower strata. [15] [ citation needed ]

Resilience in chronic stress is defined as the ability to deal and cope with stresses in a healthy manner. [16] There are six categories of resources that affect an individual's coping resources: [16]

Symptoms

People may experience anxiety, [17] depression, [18] sadness, [17] anger, [17] irritability, [17] social isolation, headache, [17] menstrual problems, [19] abdominal pain, back pain and difficulty concentrating. [20]

Impacts

Chronic stress causes the body to stay in a constant state of alertness, despite being in no danger. Extensive studies have provided evidence of the association between "chronic stressors and physical health outcomes" [3] Take caregiving as an example. A review of 37 studies has suggested that dementia caregivers subjected to chronic stress are more susceptible to diseases. [21] Although the connection between stress and health requires continuous research, [7] the existing findings have suggested the potential link between the two.  

Brain

A primary target of stress is the brain. When exposed to stress, it serves as the centre to interpret the stressors and determine the appropriate behavioural and psychological responses. [7] Therefore, exposure to chronic stress will have a direct impact on brain function. [7] For instance, chronic stress inhibits neuron growth inside the hippocampus and prefrontal cortex. [5] The neuronal atrophy in these two structures can lead to hypertrophy in amygdala, responsible for anxiety and stress. [22] In turn, this will lead to an increase of fear and aggression and impairment in learning ability. Memory and decision-making can also be negatively affected. [22] Additionally, chronic stress can suppresses neural pathways active in cognition and decision-making, speeding up aging. Also, being chronically stressed worsens the damage caused by a stroke and can lead to sleep disorders due to the overexposure of cortisol. [23]

Other systems

The alterations in brain function can have a more extensive effect on other body systems. Since chronic stress is due to a wide variety of environmental, nutritional, chemical, pathological, or genetic [24] factors, a wide range of physiological systems can be damaged. [25] Prolonged stress can disturb the immune, digestive, cardiovascular, sleep, and reproductive systems. [17] For example, it was found that:

Measurement

The advancement of the scientific study of stress will require better and more accurate measurement of the stress process. However, the complexity of stress has added difficulties to establish consistent and thorough measures. [3]

Chronic stress measures primarily comprise epidemiological studies that look at current experiences within specific life domains. Despite its significance, cumulative stress exposure from past experiences is often compromised due to practical difficulties such as limitations on time. [3] Another potential issue with measuring chronic stress is the validity. In particular for retrospective studies, the validity of the measure is strongly dependent on the accuracy of recollection. Biases and memory decay can contribute to underreporting. Similarly for prospective studies, the validity of the measures will depend on the accuracy of report and detection by the respondent and monitoring agencies. [3]

In regards to measuring stress responses, it is important to note that it can vary from person. [28] It is suggested that individual and environmental contextual factors, such as genes and culture, will contribute to one's vulnerability and resilience to stress. By contrast, protective factors, such as a supportive environment, can strengthen resilience. [3] The two factors are important as they influence the brain's judgment of the stressors. In addition, the interactions of different stressors will lead to cumulative stress exposure. These all together contribute to the differential stress responses. [3] The subjective differences thus may pose challenges for researchers.

Owing to the complexity of measuring stress processes over the lifespan, many researchers decided on measuring more assessable aspects of stress. That includes: "historic exposure, current exposure and responses across different time scale". [3] In many cases, chronic stress is measured by its duration. Yet, there can be considerable variations in the criteria. [3] For example, the Life Events and Difficulties Schedule by Brown and Harris (1978) [29] proposed that chronic difficulty is characterised by a 4-week-cut-off. Alternatively, other researchers may define chronicity with a shorter or longer period. The implication is that studies on chronic stress may not necessarily have a uniform scale for comparison.

See also

Related Research Articles

<span class="mw-page-title-main">Hans Selye</span> Austro-Hungarian scientist (1907–1982)

János Hugo Bruno "Hans" Selye was a pioneering Hungarian-Canadian endocrinologist who conducted important scientific work on the hypothetical non-specific response of an organism to stressors. Although he did not recognize all of the many aspects of glucocorticoids, Selye was aware of their role in the stress response.

<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. Stress is the body's method of reacting to a condition such as a threat, challenge or physical and psychological barrier. There are two hormones that an individual produces during a stressful situation, well known as adrenaline and cortisol. There are two kinds of stress hormone levels. Resting (basal) cortisol levels are normal everyday quantities that are essential for standard functioning. Reactive cortisol levels are increases in cortisol in response to stressors. Stimuli that alter an organism's environment are responded to by multiple systems in 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.

<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 HPA axis.

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.

Acute stress reaction and acute stress disorder (ASD) is a psychological response to a terrifying, traumatic or surprising experience. Combat stress reaction (CSR) is a similar response to the trauma of war. The reactions may include but are not limited to intrusive or dissociative symptoms, and reactivity symptoms such as avoidance or arousal. It may be exhibited for days or weeks after the traumatic event. If the condition is not correctly addressed, it may develop into post-traumatic stress disorder (PTSD).

Allostasis (/ˌɑːloʊˈsteɪsɪs/) is a physiological mechanism of regulation in which the human body 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:

<span class="mw-page-title-main">Allostatic load</span> 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.

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.

The impact of alcohol on aging is multifaceted. Evidence shows that alcoholism or chronic alcohol consumption can cause both accelerated (or premature) aging – in which symptoms of aging appear earlier than normal – and exaggerated aging, in which the symptoms appear at the appropriate time but in a more exaggerated form. The effects of alcohol use disorder on the aging process include hypertension, cardiac dysrhythmia, cancers, gastrointestinal disorders, neurocognitive deficits, bone loss, and emotional disturbances especially depression. On the other hand, research also shows that drinking moderate amounts of alcohol may protect healthy adults from developing coronary heart disease. The American Heart Association cautions people not to start drinking, if you are not already drinking.

Prenatal stress is exposure of an expectant mother to psychosocial or physical stress, which can be caused by daily life events or by environmental hardships. This psychosocial or physical stress that the expectant mother is experiencing has an effect on the fetus. According to the Developmental Origins of Health and Disease (DOHaD), a wide range of environmental factors a woman may experience during the perinatal period can contribute to biological impacts and changes in the fetus that then causes health risks later in the child's life.

Caregiver syndrome or caregiver stress is a condition that strongly manifests exhaustion, anger, rage, or guilt resulting from unrelieved caring for a chronically ill patient. This condition is not listed in the United States' Diagnostic and Statistical Manual of Mental Disorders, although the term is often used by many healthcare professionals in that country. The equivalent used in many other countries, the ICD-11, does include the condition.

Performance Medicine is a sub-speciality of clinical and diagnostic medicine that is focussed on the optimisation of emotional, mental, and emotional well-being and performance. It is a new and innovative medical speciality that merges the goals of internal medicine, anti-ageing medicine, functional medicine, sports medicine and preventative health care.

<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 conception 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.

Addiction vulnerability is an individual's risk of developing an addiction during their lifetime. There are a range of genetic and environmental risk factors for developing an addiction that vary across the population. Genetic and environmental risk factors each account for roughly half of an individual's risk for developing an addiction; the contribution from epigenetic risk factors to the total risk is unknown. Even in individuals with a relatively low genetic risk, exposure to sufficiently high doses of an addictive drug for a long period of time can result in an addiction. In other words, anyone can become an individual with a substance use disorder under particular circumstances. Research is working toward establishing a comprehensive picture of the neurobiology of addiction vulnerability, including all factors at work in propensity for addiction.

Caffeine-induced anxiety disorder is a subclass of the DSM-5 diagnosis of substance/medication-induced anxiety disorder.

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. 1 2 "APA Dictionary of Psychology". dictionary.apa.org. Retrieved 20 February 2022.
  2. Pearlin LI (1989). "The Sociological Study of Stress". Journal of Health and Social Behavior. 30 (3): 241–256. doi:10.2307/2136956. ISSN   0022-1465. JSTOR   2136956. PMID   2674272.
  3. 1 2 3 4 5 6 7 8 9 10 Epel ES, Crosswell AD, Mayer SE, Prather AA, Slavich GM, Puterman E, Mendes WB (April 2018). "More than a feeling: A unified view of stress measurement for population science". Frontiers in Neuroendocrinology. 49: 146–169. doi:10.1016/j.yfrne.2018.03.001. PMC   6345505 . PMID   29551356.
  4. 1 2 3 4 Rohleder N (July 2019). "Stress and inflammation - The need to address the gap in the transition between acute and chronic stress effects". Psychoneuroendocrinology. 105: 164–171. doi:10.1016/j.psyneuen.2019.02.021. PMID   30826163. S2CID   72332925.
  5. 1 2 3 4 McEwen BS (July 2007). "Physiology and neurobiology of stress and adaptation: central role of the brain". Physiological Reviews. 87 (3): 873–904. doi:10.1152/physrev.00041.2006. PMID   17615391.
  6. Fisher S, Reason JT (1988). Handbook of life stress, cognition, and health. Chichester: Wiley. ISBN   0-471-91269-7. OCLC   17234042.
  7. 1 2 3 4 5 6 Schneiderman N, Ironson G, Siegel SD (1 April 2005). "Stress and health: psychological, behavioral, and biological determinants". Annual Review of Clinical Psychology. 1 (1): 607–628. doi:10.1146/annurev.clinpsy.1.102803.144141. PMC   2568977 . PMID   17716101.
  8. 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.1993.00410180039004. PMID   8379800.
  9. 1 2 Carlson NR (2013). Physiology of Behavior (11th ed.). Boston: Pearson. pp. 602–6. ISBN   978-0-205-23939-9. OCLC   879099798.
  10. 1 2 3 4 Szabo S, Tache Y, Somogyi A (September 2012). "The legacy of Hans Selye and the origins of stress research: a retrospective 75 years after his landmark brief "letter" to the editor# of nature" (PDF). Stress. 15 (5): 472–478. doi:10.3109/10253890.2012.710919. PMID   22845714. S2CID   16530497. Archived from the original (PDF) on 26 November 2019. Retrieved 13 November 2016.
  11. "Hans Selye". Encyclopædia Britannica. Encyclopædia Britannica, Inc. 22 July 2010. Retrieved 8 November 2016..
  12. Tsigos C, Chrousos GP (October 2002). "Hypothalamic-pituitary-adrenal axis, neuroendocrine factors and stress". Journal of Psychosomatic Research. 53 (4): 865–871. doi:10.1016/s0022-3999(02)00429-4. PMID   12377295.
  13. Notterman DA, Mitchell C (October 2015). "Epigenetics and Understanding the Impact of Social Determinants of Health". Pediatric Clinics of North America (Review). 62 (5): 1227–1240. doi:10.1016/j.pcl.2015.05.012. PMC   4555996 . PMID   26318949.
  14. Quinlan J, Tu MT, Langlois EV, Kapoor M, Ziegler D, Fahmi H, Zunzunegui MV (April 2014). "Protocol for a systematic review of the association between chronic stress during the life course and telomere length". Systematic Reviews (Review). 3: 40. doi: 10.1186/2046-4053-3-40 . PMC   4022427 . PMID   24886862. Open Access logo PLoS transparent.svg
  15. Blair C, Raver CC (April 2016). "Poverty, Stress, and Brain Development: New Directions for Prevention and Intervention". Academic Pediatrics. 16 (3 Suppl): S30–S36. doi: 10.1016/j.acap.2016.01.010 . PMC   5765853 . PMID   27044699.
  16. 1 2 Schetter CD, Dolbier C (September 2011). "Resilience in the Context of Chronic Stress and Health in Adults". Social and Personality Psychology Compass. 5 (9): 634–652. doi:10.1111/j.1751-9004.2011.00379.x. PMC   4494753 . PMID   26161137.
  17. 1 2 3 4 5 6 "NIMH » 5 Things You Should Know About Stress". www.nimh.nih.gov. Retrieved 20 November 2019.
  18. Cohen S, Janicki-Deverts D, Miller GE (October 2007). "Psychological stress and disease". JAMA. 298 (14): 1685–1687. doi:10.1001/jama.298.14.1685. PMID   17925521. S2CID   12159960.
  19. "Stress and your health: MedlinePlus Medical Encyclopedia". medlineplus.gov. Archived from the original on 11 December 2019. Retrieved 30 April 2020.
  20. "Stress and your health: MedlinePlus Medical Encyclopedia". medlineplus.gov. Archived from the original on 11 December 2019. Retrieved 25 October 2019.
  21. Fonareva I, Oken BS (May 2014). "Physiological and functional consequences of caregiving for relatives with dementia". International Psychogeriatrics. 26 (5): 725–747. doi:10.1017/S1041610214000039. PMC   3975665 . PMID   24507463.
  22. 1 2 McEwen BS, Chattarji S (December 2004). "Molecular mechanisms of neuroplasticity and pharmacological implications: the example of tianeptine". European Neuropsychopharmacology. 14 (Suppl 5): S497–S502. doi:10.1016/j.euroneuro.2004.09.008. PMID   15550348. S2CID   21953270.
  23. "BrainFacts". www.brainfacts.org. Retrieved 30 March 2019.
  24. "Chronic stress puts your health at risk". Mayo Clinic. Retrieved 30 April 2020.
  25. "Stress effects on the body". American Psychological Association. 1 November 2018. Archived from the original on 1 February 2021. Retrieved 5 May 2021.
  26. Rohleder N (2016). "Chronic Stress and Disease". Insights to Neuroimmune Biology. pp. 201–214. doi:10.1016/B978-0-12-801770-8.00009-4. ISBN   9780128017708.
  27. Henry JP, Stephens PM, Santisteban GA (January 1975). "A model of psychosocial hypertension showing reversibility and progression of cardiovascular complications". Circulation Research. 36 (1): 156–164. doi: 10.1161/01.RES.36.1.156 . PMID   1116216. S2CID   6005356.
  28. 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.
  29. Brown GW, Harri TO (2011). Social origins of depression : a study of psychiatric disorder in women. Abingdon, Oxon: Routledge. ISBN   978-0-203-71491-1. OCLC   1086555347.