Scientific Examination of Stress and Illness Relationship - Coursework Example

? THE LINK BETWEEN STRESS AND ILLNESS: REVIEW OF LITERATURE Introduction The role of stress in exacerbating and precipitating illness is a well-established concept. Research through the decades has continued to demonstrate various ways in which psychological and physical stress can damage the physiologic functioning of various body organs and tissues, as well as affect the working of the mind. This paper shall provide a review of contemporary scientific knowledge on the relationship between stress and illness. It will also critically analyze a few sample studies on this topic. Discussion A general definition of stress can be given as a ‘negative emotional experience resulting from a mismatch between the individual’s appraisal that the stressor is stressful and their ability to cope with and therefore reduce their response to it’ (Hewstone, Fincham and Foster, 2005, p. 420). This basic definition recognizes stress as a negative sensation. However, researchers as long ago as in the early twentieth century recognized that that there is more to stress than simply a ‘negative emotional experience’, and that it involves biochemical and physiological changes along with behavioural and psychological effects. In 1932, the psychologist Cannon proposed with his ‘fight-or-flight’ model that stress is a rimarily physiologic event, which produces changes meant to help escape from the stressful situation, or fight the stressor (Hewstone, Fincham and Foster, 2005, p. 420). Adding to this model, Selye (1950) introduced the concept of the ‘General Adaptation Syndrome’, which divided the stress response into three stages. These included ‘alarm’, the immediate increase in activity upon exposure to the stressor; changes that were identified at that time to occur during the alarm phase include sympathetic nervous system overactivity, tissue catabolism, hypoglycemia, gastro-intestinal erosions, discharge of secretory granules from the adrenal cortex, and hemoconcentration. The next stage is ‘resistance’, where the body attempts to reverse the detrimental effects of the first stage. The final stage is ‘exhaustion’, when the body no longer has resources left to produce resistance. Selye also discussed that the general adaptation syndrome involves endocrine changes and corticosteroid disregulation, and that it invariably leads to organ damage, including the cardiovascular and renal systems. Further research since then has elucidated the effect of stress on various organ systems. The link between psychological stress and physiological changes takes place in the higher cortical centres of the brain. When psychological stress occurs, the cerebral cortex sends nerve impulses to the hypothalamus (a lower brain centre), stimulating the release of endocrine hormones. The target organ of these hormones is the adrenal gland, which is stimulated to release the adrenergic neuro-hormone norepinephrine (NE) as well as cortisol, a steroid hormone. These are the major ‘stress hormones’ (Gu, Tang and Yang, 2012). They induce physiologic changes – for example, NE causes an increase in heart rate, so oxygen can be delivered to the muscles more rapidly to facilitate strength and speed. Cortisol mobilizes glucose from body reserves, to deliver it to muscles for action. However, prolonged stress produces detrimental effects on the body. Researchers have identified stress as a risk factor for cardiovascular, respiratory, neurologic, and infectious diseases. The release of NE and cortisol stimulates cerebral neurons to form memories of the event for future protection. However, under repeated stress over a period of time, these stimulated neurons undergo atrophy, leading to memory impairment – a detrimental effect (McEwen, 2005). Psychological stress alters various arms of the immune system in different ways. The release of NE during acute stress - during, for instance, public speaking - activates inflammatory cells including macrophages, and causes the release of pro-inflammatory cytokines, such as interleukin 1, 6, and C-reactive protein. This response is aimed at fighting infection. However, when prolonged stress persists during states such as depression and chronic illness, the low-grade inflammation continues via NE, but immune functions of the body become suppressed (McEwen, 2005). Neuropeptide release during chronic stress, particularly in depression, may be responsible for immunosuppression, through inhibitory effects on T lymphocytes. This makes the body vulnerable to infections such as tuberculosis, while also setting the background for atherosclerosis to take place. The steps in the pathophysiology of atherosclerosis – injury to endothelial cells of blood vessels, activation of macrophages, oxidation of LDLs, and deposition of inflammatory debris in the sub-endothelial vessel wall – are all up-regulated by chronic inflammation. Inflammatory cytokines cause endothelial damage, and the activated macrophages contribute to forming atheromatous plaques (Gu, Tang and Yang, 2012). Stress may contribute to cardiovascular disease in ways other than through atherosclerosis as well. Friedman and Rosenman were cardiologists who in 1974 identified a correlation between risk of coronary artery disease and a type A personality- whose individuals experience intense reactions to stress. This relationship was found to be robust even after excluding other factors, such as smoking and obesity. The emotions of anger and hostility among people with type A personality – that produce stronger sympathetic responses – may play a dominant role in increasing the cardiovascular risk (Weiten, Dunn, and Hammer, 2011, p. 142). The stress hormone cortisol normally has an inhibitory effect on inflammatory cells, to counteract and stabilize the heightened inflammation during stress. However, during prolonged stress, this effect of cortisol is diluted and inflammation continues. Cortisol inhibits the effects of insulin and stimulates glucose production by the liver. The resultant high blood glucose levels lead to increased fat deposition in the body. During depression and chronic illnesses, when cortisol secretion is greater than normal, this leads to obesity in these patients (Chrousos, 2000). To critically review some of the research done on the relationship between stress and illness, a few studies were selected. Kiecolt-Glaser (1986) studied the effect of acute stress on the immune system. Medical students were made study subjects, and an examination was the stressful situation. They measured the number and activity of lymphocytes in the subjects’ blood samples at two events: first, one month before the exam, and second, on the day of the exam. It was postulated that the first sample would represent immune cells’ status under a non-stress state. As a control experiment, they also provided half the subjects with relaxation techniques to reduce exam-related stress. They found significantly lower levels of T-cells and NK cell activity, signifying immunosuppression, in the subjects after the examination compared to the levels one month earlier. They also found significantly lower immune cell activity in the subject group that had not been given relaxation exercises and had thus experienced more stress. This study provided quantifiable definitive evidence of the inhibitory effect of stress on lymphocytic function. In a similar research approach, Porter et al. (1958) subjected rhesus monkeys to electric shocks in a psychological stress model. In one of the experimental setups, the animals were first trained to access food by pressing a lever, and later on the lever simultaneously delivered an electric shock along with giving access to food. Thus, the monkeys were made to anticipate the coming shocks when they needed food, and suffered an anxiety response that was manifested by intense locomotor activity, trembling, and frequent urination and defecation. Slightly different experiments were done to study avoidance behavior and conditioning. Briefly, the animals began to avoid pressing the lever in order to avoid the shocks. After the experiments, histopathological examination of the animals’ internal organs was performed. This demonstrated the development of various gastrointestinal lesions in the animals that developed anxiety, including gastric hemorrhage and erosion, duodenal ulceration, enteric intussusception, and chronic colitis. It was postulated that these occurrences were due to ‘psychosomatic’ disease. This term describes the phenomenon of somatic or organic illnesses occuring in the context of psychological stress. Beyond laboratory research on the biochemical effects of stress, researchers have also directly studied the illness-related effect of stress on human individuals. Cobb and Rose (1973) determined the prevalence of three illnesses that had been linked to stressful lifestyle in air traffic controllers: peptic ulcer disease, hypertension, and diabetes. As air-traffic controllers and airmen face significant stress during their routine, they were selected as subjects. They found high rates of hypertension and peptic ulcer disease among the study subjects. Although this correlation was strong, the authors could not prove definitively a cause-and effect relationship between stress and these illnesses, due to the nature of the study design. Stress has also been recognized as a predisposing factor for infectious diseases. Cohen, Tyrrell and Smith (1991) investigated the effect of psychological stress on the incidence of the clinical colds, to study whether stress increased vulnerability to infectious disease. They gathered healthy subjects, determined their degree of experienced stress through a questionnaire, and then exposed them to respiratory viruses in an experimental lab. They were then observed for clinical features of a respiratory infection. The results showed a significant, increase in the rate of clinical cold in subjects pre-determined to be suffering from higher psychological stress, in a dose-response manner for stress. The experiment was controlled for confounding factors such as age or allergic status. They concluded with robust evidence that psychological stress was associated in a dose-response manner with an increased risk of acute infectious respiratory illnesses. The emerging evidence on the effect of psychological factors on illness has gradually altered the scientific community’s concept of illness itself. Although it was considered as a purely biological phenomena at a point in history, a ‘biopsychosocial model’ of illness is now recognized, which states that physical illness is caused by a ‘complex interaction of biological, psychological, and socio-cultural factors’. It is also recognized that different individuals respond to stressful situations differently, individual thresholds for breaking out with stress vary. Thus, the same environment of stress under which one individual struggles with depression and consequences of chronic illness, may permit other individuals to thrive in with ease. This range of person-to-person variability in vulnerability to stress may explain the often inconclusive results of experiments on human subjects on stress (Weiten, Dunn, and Hammer, 2011, p. 139). Conclusion The review of literature discussed allows the conclusion that illness is brought about by an interaction of biological and psychological factors. Psychological stress, if experienced repeatedly, such as in individuals with type A personality, or chronically, such as in patients suffering from depression, contributes to the risk of disease in various organ systems. This review discussed scientific evidence supporting the role of stress in enhancing risk for obesity, cardiovascular disease and infectious disease, references were also found regarding its role in neurologic and chronic respiratory disease. References Chrousos, G. P. 2000. The role of stress and the hypothalamic-pituitary-adrenal axis in the pathogenesis of the metabolic syndrome: neuro-endocrine and target tissue-related causes. Int J Obes Relat Metab Disord. Suppl 2:S50-5. Cobb, S., Rose, R.M. 1973. Hypertension, peptic ulcer, and diabetes in air traffic controllers. JAMA, 224(4), p.489-92. Cohen, S., Tyrrell, D.A., Smith, A.P. 1991. Psychological stress and susceptibility to the common cold. N Engl J Med. 325(9), p. 606-12. Gu, H.F., Tang, C.K., Yang, Y.Z. 2012. Psychological stress, immune response, and atherosclerosis. Atherosclerosis [Epub ahead of print]. Hewstone, M., Fincham, F.D., Foster, J. 2005. Psychology. Oxford: Blackwell Publishing Kiecolt-Glaser, J.K., Glaser, R., Strain, E.C., Stout, J.C., Tarr, K.L., Holliday, J.E., Speicher, C.E. 1986. Modulation of cellular immunity in medical students. J Behav Med. 9(1):5-21. McEwen, B.S. 2005. Stressed or stressed out: what is the difference? J Psychiatry Neurosci, 30(5), p.315-8. Porter, R.W., Brady, J.V., Conrad, D., Mason, J.W., Galambos, R., Rioch, D.M. 1958. Some experimental observations on gastrointestinal lesions in behaviorally conditioned monkeys. Psychosom Med, 20(5), p.379-94. Selye, H. 1950. Stress and the General Adaptation Syndrome. British Medical Journal, 1(4667), p.1383–1392. Weiten, W., Dunn, D. S., Hammer, E. Y. 2011. Psychology Applied to Modern Life: Adjustment in the 21st Century. Belmont: Cengage Learning. Read More