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Chronic stress is the response to emotional pressure suffered for a prolonged period of time in which an individual perceives he or she has no control. It involves an endocrine system response in which corticosteroids are released. While the immediate effects of stress hormones are beneficial in a particular short-term situation, 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, suppression of the immune system,[1] and damage to mental health.

V. acute stress

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Acute stress is stress caused by homeostatic changes that trigger adaptive responses, which include various physiological changes that occur to better prepare the natural immune system for any immediate harm. The stress responses that stimulate the affected organism can either result from physical or psychological stressors.[2] Most of the physiological changes that occur during acute stress take place in the cardiovascular system, where blood pressure, arterial pressure, heart rate, and cardiac output levels are all increased. After the stimulus has occurred, several cardiovascular functions including arterial pressure and heart rate decrease and return to regular levels within 30 to 60 minutes of the end of stress.[3] These adaptive responses aimed to maintain homeostasis are beneficial in dealing with acute stress, however, continuous activation of and exposure to these acute stressors can then result in several of the negative effects of chronic stress.

Chronic stress is thus the stress that results from a chronicle persistence of stress responses after continuous exposure to these acute stressful events or continued failure to generate adequate responses to these events. Elevated levels of cardiovascular functions become maladaptive if they persist for too long. If prolonged, chronic stress often leads to several psychiatric and cardiovascular diseases along with overall worsened physical health.[3]

Historical development

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Hans Selye (1907–1982), known as the "father of stress",[4] 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.[4] 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.[5] Selye considered these conditions to be "diseases of adaptation", or the effects of chronic stress caused by heightened hormonal and chemical levels.[4] His research on acute and chronic stress responses introduced stress to the medical field.[4]

Physiology

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Animals exposed to distressing events over which they have no control respond by releasing corticosteroids.[6][7] The sympathetic branch of the nervous system is activated, also releasing epinephrine and norepinephrine.[1] These, if prolonged, lead to structural changes in the brain. Changes happen to neurons and their synapses in the hippocampus[8] and medial prefrontal cortex.[9] These produce impairments in working memory[10] and spatial memory,[10] as well as increased aggression.[11]

Linked to impairment of the medial prefrontal cortex are deficits in the part of the striatum with which it is linked.[12] This can bias decision-making strategies, as affected individuals shift from flexible behavior to one dominated by habit.[12] Changes also occur to dopaminergic activity in the prefrontal cortex.[10]

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.[13]

The release of these hormones is evolved to be temporary. If someone is under stress for long periods of time they may have adverse health effects later on, such as hypertension and increased risk of cardiovascular disease.[14]

Different factors may prolong this "fight or flight" reaction in the body. Chronic stress can be rooted in prolonged psychological stressors, for example, some studies have looked at the health effects of social discrimination in African Americans. This demographic has markedly higher hypertension levels that are attributed to higher levels of social discrimination. This phenomenon has been coined John Henryism by sociologist Sherman James.[15]

Chronic Stress and Telomeres

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Chronic stress has been associated with shortened telomeres. The following are the hypothesized mechanisms through which chronic stress results in the shortening of telomeres:

Decreasing telomerase activity : Chronic stress results in elevated levels of the stress hormone cortisol for prolonged periods of time. The elevated levels of cortisol are hypothesized to repress the expression of telomerase promoters and reduce the production of telomerase. Telomerase is an essential enzyme responsible for repairing, lengthening and maintaining telomeres. Thus low levels of this enzyme result in degraded and shortened telomeres over time.[16][17]

Making people more susceptible to adopting unhealthy lifestyles : Prolonged exposure to stress has been linked to several detrimental lifestyle choices such as increased substance abuse, poor dietary dietary choices, and reduced physical exercise.[18][19] All these unhealthy behaviors have a known association to telomere shortening and cellular aging.[20]Chronic stress is also known to be associated with an accelerated loss of telomeres in most but not all studies.[21][22]

Response

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Different types of stressors, the timing (duration) of the stressors, and personal characteristics all influence the response of the hypothalamic–pituitary–adrenal axis to stressful situations.[23]

Resilience in chronic stress is defined as the ability to deal and cope with stresses in a healthy manner.[24] There are six categories of resources that affect an individual's coping resources:[24]

Symptoms

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Symptoms of chronic stress can vary from anxiety, depression,[25] social isolation, headache, abdominal pain or lack of sleep to back pain and difficulty concentrating. Other symptoms include panic attacks or a panic disorder[25] and cardiovascular diseases.[25]

See also

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  1. ^ a b Carlson, Neil (2013). Physiology of Behavior. Pearson. pp. 602–606. ISBN 9780205239399.
  2. ^ Eisenmann, Eric D.; Rorabaugh, Boyd R.; Zoladz, Phillip R. (25 April 2016). "Acute Stress Decreases but Chronic Stress Increases Myocardial Sensitivity to Ischemic Injury in Rodents". Frontiers in Psychiatry. doi:10.3389/fpsyt.2016.00071. PMC 4843048. {{cite journal}}: |access-date= requires |url= (help)CS1 maint: unflagged free DOI (link)
  3. ^ a b Crestani, Carlos C. (24 June 2016). "Emotional Stress and Cardiovascular Complications in Animal Models: A Review of the Influence of Stress Type". Frontiers in Physiology. doi:10.3389/fphys.2016.00251. PMC 4919347. {{cite journal}}: |access-date= requires |url= (help)CS1 maint: unflagged free DOI (link)
  4. ^ a b c d Russel, John (15 September 2012). "The legacy of Hans Selye and the origins of stress research" (PDF). Stress (15(5)): 472–478. doi:10.3109/10253890.2012.710919.
  5. ^ "Hans Selye". Encyclopaedia Britannica. Encyclopaedia Britannica. Retrieved 8 November 2016..
  6. ^ Sapolsky RM. (1998). Why Zebras Don't Get Ulcers: An Updated Guide To Stress, Stress Related Diseases, and Coping. 2nd Rev Ed, W. H. Freeman ISBN 978-0-7167-3210-5
  7. ^ McEwen BS (2007). "Physiology and neurobiology of stress and adaptation: central role of the brain". Physiol Rev. 87 (3): 873–904. doi:10.1152/physrev.00041.2006. PMID 17615391.
  8. ^ Sousa N, Lukoyanov NV, Madeira MD, Almeida OF, Paula-Barbosa MM (2000). "Reorganization of the morphology of hippocampal neurites and synapses after stress-induced damage correlates with behavioral improvement". Neuroscience. 97 (2): 253–266. doi:10.1016/S0306-4522(00)00050-6. PMID 10799757.
  9. ^ Radley JJ, Sisti HM, Hao J, Rocher AB, McCall T, Hof PR, McEwen BS, Morrison JH (2004). "Chronic behavioral stress induces apical dendritic reorganization in pyramidal neurons of the medial prefrontal cortex". Neuroscience. 125 (1): 1–6. doi:10.1016/j.neuroscience.2004.01.006. PMID 15051139.
  10. ^ a b c Mizoguchi K, Yuzurihara M, Ishige A, Sasaki H, Chui DH, Tabira T (2000). "Chronic stress induces impairment of spatial working memory because of prefrontal dopaminergic dysfunction". J Neurosci. 20 (4): 1568–74. PMID 10662846.
  11. ^ Mineur YS; Prasol DJ; Belzung C; Crusio WE (September 2003). "Agonistic behavior and unpredictable chronic mild stress in mice" (PDF). Behavior Genetics. 33 (5): 513–519. doi:10.1023/A:1025770616068. PMID 14574128. Retrieved 2009-08-16.
  12. ^ a b Dias-Ferreira E, Sousa JC, Melo I, Morgado P, Mesquita AR, Cerqueira JJ, Costa RM, Sousa N (2009). "Chronic Stress Causes Frontostriatal Reorganization and Affects Decision-Making". Science. 325 (5940): 621–625. doi:10.1126/science.1171203. PMID 19644122.
  13. ^ Tsigos C.; Chrousos G.P. (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.
  14. ^ Blascovich J.; Spencer S. J.; Quinn D. M.; Steele C. M. (2001). "African Americans and high blood pressure: The role of stereotype threat". Psychological Science. 12 (3): 225–229. doi:10.1111/1467-9280.00340. PMID 11437305.
  15. ^ James S. A.; Hartnett S. A.; Kalsbeek W. D (1983). "John Henryism and blood pressure differences among black men". Journal of Behavioral Medicine. 6 (3): 259–278. doi:10.1007/bf01315113.
  16. ^ "CHRONIC SLEEP DEPRIVATION AND ITS EFFECT ON THE LENGTH OF HUMAN TELOMERES: ...: Start Your Search!". eds.a.ebscohost.com. Retrieved 2016-11-13.
  17. ^ Effros, Rita B. (2016-11-15). "Telomere/telomerase dynamics within the human immune system: effect of chronic infection and stress". Experimental Gerontology. 46 (2–3): 135–140. doi:10.1016/j.exger.2010.08.027. ISSN 1873-6815. PMC 3246363. PMID 20833238.
  18. ^ "Organismal Stress and Telomeric Aging: An Unexpected Connection on JSTOR" (PDF). www.jstor.org. Retrieved 2016-11-13.
  19. ^ "Telomeres in a Life-Span Perspective: A New "Psychobiomarker"? on JSTOR" (PDF). www.jstor.org. Retrieved 2016-11-13.
  20. ^ Shalev, Idan; Entringer, Sonja; Wadhwa, Pathik D.; Wolkowitz, Owen M.; Puterman, Eli; Lin, Jue; Epel, Elissa S. (2013-09-01). "Stress and telomere biology: a lifespan perspective". Psychoneuroendocrinology. 38 (9): 1835–1842. doi:10.1016/j.psyneuen.2013.03.010. ISSN 1873-3360. PMC 3735679. PMID 23639252.
  21. ^ Notterman DA, Mitchell C (2015). "Epigenetics and Understanding the Impact of Social Determinants of Health". Pediatric Clinics of North America (Review). 62 (5): 1227–40. doi:10.1016/j.pcl.2015.05.012. PMID 26318949.
  22. ^ Quinlan J, Tu MT, Langlois EV, Kapoor M, Ziegler D, Fahmi H, Zunzunegui MV (2014). "Protocol for a systematic review of the association between chronic stress during the life course and telomere length". Syst Rev (Review). 3 (40). doi:10.1186/2046-4053-3-40. PMC 4022427. PMID 24886862.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  23. ^ Miller, Gregory E.; Chen, Edith; Zhou, Eric S. (January 2007). "If it goes up, must it come down? Chronic stress and the hypothalamic-pituitary-adrenocortical axis in humans". Psychological Bulletin. 133 (1): 25–45. doi:10.1037/0033-2909.133.1.25. PMID 17201569.
  24. ^ a b Schetter, Christine Dunkel; Dolbier, Christyn (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.
  25. ^ a b c Cohen S, Janicki-Deverts D, Miller GE (2007). "Psychological stress and disease". JAMA. 298 (14): 1685–1687. doi:10.1001/jama.298.14.1685. PMID 17925521.
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