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Although our organism adapts to stress responses, chronic (long-lasting) stress may lead to tissue damage and disease. Selye,(1950) identified 3 phases of stress, namely, alarm, resistance and exhaustion phase. The last phase appears, when the body is not able to cope with the stressor. That is a stage when the pathological symptoms, which threaten homeostasis appear (Green,1994). Stress depicts any stimuli that have negative effect on homeostasis of the organism. Stressor is the real or imagined threat. (Selye, 1956). Alternations of various areas of the brain structure can be caused by stress. The number and strength of these changes vary, depending on stress level and how long the stress occurs. (Lupien et al., 2009). Furthermore, immune system may be affected by stress. It can adjust processes in neuroendocrine and Central Nervous System (CNS). For instance, it alters secretion of hormones that are crucial for the proper functioning of the immune system (Khansari et al., 1990). This essay will discuss the relationship between stress and susceptibility to illness.
Cohen, Tyrrell, & Smith. (1993) have studied 420 participants, both males and females to check, if psychological stress increases the likelihood of developing illness. Subjects were assessed by filling up questionnaires, which were measuring perceived stress, major stressful life events as well as negative emotions associated with them. After that they were quarantined for 2 days before and 6 days after administering, 394 participants or control group of 26, either dose of one of five respiratory viruses or saline respectively. In order to avoid the bias of how participants present their symptoms, clinicians were measuring their temperature and mucus twice daily. The findings showed that 82% of volunteers who received virus were infected, whereas 38% of them developed clinical cold. By contrast, nobody from the control group developed cold, only 19% were infected. Both questionnaire results and susceptibility of developing cold were analysed and compared. It showed that negative life events were associated with higher risk of infected volunteers to develop illness. In addition, perceived stress and emotional distress were associated with higher risk of infection. The study successfully describes the connection between negative life events, perceived stress, negative affect and either susceptibility to cold or infection. It also emphasizes the difference between infection and cold. Although, it does not specify what type of stressors affect our susceptibility to illness. In order to raise more detailed understanding of stress and specify types of stressors which cause susceptibility to the common cold in adults Cohen et al. (1998) study will be further discussed. The study measured types of stressors which increase possibility of developing common cold, 276 participants went through life stressor interview, completed psychological questionnaire, provided urine and blood samples. Each of them measured different variables. Life stressors interview was conducted on the basis of Life Events and Difficulties Schedule (LEDS); it rates the severity of each of life stressor and its duration. Psychological questionnaire assessed 5 personality factors along with social network. Moreover, urine samples were needed to examine the level of three major hormones, such as epinephrine, norepinephrine and cortisol. Blood samples were collected to measure total number of white blood cells along with natural killer (NK) cell activity; NK cell is vital for restricting viral infection. All volunteers attended eligibility screenings in hospital; they were conducted to make sure that all of them are free from any diseases. Participants returned 4 and 5 weeks after the screening to have a blood drawn, needed for assessing NK cell activity. Also, participants completed personality questionnaire as well as life stressor interview. Afterwards they went through quarantine; within first 24 hours of their stay, they had their nose checked by a clinician; in the end of that period of time, volunteers received low dose of infectious rhinovirus. For the next 5 days they were quarantined and their nasal secretion was examined. After 28 days, in order to test the blood serologically, the blood sample was collected. The study found that infected were 99% of participants who did not have antibody to the virus which they received and 58% of them developed a cold; 69% of volunteers who had antibody were also infected, whereas 19% developed cold .It resulted in 84% of total infection rate and 40% of cold rate. Participants without antibody to the virus and with a chronic stressor lasting 1,3 or 6 months developed a cold at average of 74%,79% and 78% respectively; that study group without chronic stress had chance of developing cold on average 53%, 52% and 54% respectively. The group with antibody was unaffected by induced cold. It suggests that volunteers with a chronic stressor were more likely to develop cold than these without it. It has been found that participants who experienced work related chronic stressor, such as unemployment or underemployment, lasting over 3 months had greater chances of developing cold. The similar results were found for interpersonal chronic stressors when the likelihood was gradually increasing with its duration 1, 3 and 6 months respectively. Based on 3 months stressors’ number of viral replication, it has been implied that higher amount of replication was linked with greater chance of developing cold. In addition, volunteers who do physical exercises two or less times per week, drink one or none drinks per day and take 85mg or less of vitamin C per day are more likely to develop cold. Cohen et al. (1998) underline that his findings investigated relationship between chronic stress and cold, and may not be applicable to different illnesses. Furthermore, despite the ability to show relationship between colds and two major hormones and neurotransmitters such as adrenaline and noradrenaline, they were unable to connect it with life stressors (Leventhal, Patrick-Miller, Leventhal, 1998), As it has been established in the previous study, that work related stressors increase the chances of getting a cold. The relation between this type of stressors and coronary heart disease (CHD) will be further examined. Marmot & Brunner (2005) have conducted longitudinal study called Whitehall II. Chandola et al. (2008) accurately describes the study. It comprised of 10308 participants between 35 and 55 years old, who were based in London and were working in 20 civil service departments. The study started in 1985 and ended in 2004. It had 7 phases; each of them measured different variables. The first and second phase assessed experience of work stress, third measured environmental risk factors at work and in personal life. Phases 2nd to 7th based on coronary heart disease death, definite angina, or myocardial infraction, diagnosed whether the participant appeared to have CHD or not. In addition, 7th phase measured morning levels of cortisol. Odd numbers of phases used postal questionnaires as well as clinical examinations, whereas even numbers used only the first measure. They found that people under 50 were more likely to have CHD while being under chronic work stress. Furthermore, the presence of work stress exposure in addition to any of these factors such as, poor dietary choices, low physical activity, metabolic syndrome and decreased heart rate variability increase the chances of developing coronary heart disease. These data suggest that incidence of work stress may be related to CHD, directly through activation of neuroendocrine responses to stressors and indirectly through unhealthy behaviours. Autonomic nervous system (ANS) is the main source of neuroendocrine response for stress. People who activate ANS frequently, in other words come across many stressful situations, may have lowered heart rate variability (HRV). The association between work stress and decreased HRV was observed in studies with men. Work related stress may cause dysregulation of the hypothalamic-pituitary-adrenal axis, which is related to disruptions in the cycle of cortisol. In the duration of the study, many participants who did not turn up for a clinical screening were more likely to have poor health choices, have incidence of work stress; this could underrate the effects of the experiment. Moreover, the study was conducted on office based employees; the findings of the experiment would have been different, if it had been examined on physical workers instead.
To conclude, each of these studies suggests that stress may have an impact on our immune system and cause illness. Based on them it is easier to specify the correlation between stress and illness. Out of three psychological stress scales presented by Cohen et al. (1993), only negative life events increase the risk of developing common cold; whereas perceived stress and emotional distress are only related to higher susceptibility to infection. Moreover, two types of stressors were associated with greater risk of developing flu, namely work related chronic stressors, interpersonal chronic stressors as well as unhealthy habits (Cohen et al. 1998). Whitehall II, longitudinal study explained direct and indirect link between coronary heart disease and work related stress such as neuroendocrine responses and unhealthy behaviours respectively.
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- Cohen, S., Tyrrell, D.A., & Smith, A.P. (1993) Negative life events, perceived stress, negative affect, and susceptibility to the common cold. Journal of Personality and Social Psychology. 64, 131-140.
- Cohen, S., Frank, E., Doyle, W.J., Skoner, D.P., Rabin, B.S., & Gwaltney, J.M. Jr. (1998). Types of stressors that increase susceptibility to the common cold in healthy adults. Health Psychology. 17(3), 214-223.
- Leventhal, H., Patrick-Miller, L., & Leventhal, E.A. (1998). It’s long-term stressors that take a toll: comment on Cohen et al. (1998). Health Psychology. 17(3), 211-213.
Marmot, M., & Brunner, E. (2005). Cohort Profile: The Whitehall II study. International Journal of Epidemiology, 34(2), 251–256.
Chandola, T., Britton, A., Brunner, E., Hemingway, H., Malik, M., Kumari, M., Badrick, E., Kivimaki, M., & Marmot, M. (2008) Work stress and coronary heart disease: what are the mechanisms?. European Heart Journal, 29(5), 640–648.
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