Cohen concluded that life stress and negative emotions reduce the effectiveness of our immune system, leaving participants less able to resist viral infections. With no direct immune function measurements, this conclusion posed methodological flaws – it is inaccurate to state that the colds were caused as a direct result of reduction in immune function. Previous studies by Evans and Edgington (1991) however, found that the probability of developing a cold was significantly correlated with negative events in preceding days, supporting the findings of Cohen et al’s study, 2 years later. A second problem with Cohen’s study is that there is no direct manipulation of the independent variable (the stress index), like in Kiecolt-Glaser’s study (details of this study will be provided). As it was correlation only, a cause and effect relationship cannot be confirmed.
No indication of which stressor was the most important in relation to the formation of the illness is given, therefore it is impossible to determine what core number of stressors act as major stressors. An individual’s cognitive process varies from one person to the next, and so by accounting for individual differences we cannot know for certain how genuine the answers given by participants were; some may have exaggerated to appear more dramatic, whilst others maybe have down-played the effect the stressor(s) had on their level of negative emotions.
Interest in naturalistic life stressors and their impact on measures of the immune function inspired earlier psychological research by Kiecolt-Glaser et al (1984). Her study consisted of seventy-five medical students preparing for their finals. The focus of the immune function was Natural Killer (NK) cell activity. Measurements of NK were taken from blood samples of the participants one month before exams and during the exam period were stress levels would have been raised from low to high. The students also completed questionnaires on experience of negative life events and social isolation. It was found that NK cell activity was significantly reduced in the high stress samples, compared to the low stress samples. The greatest reductions were in students reporting higher levels of social isolation. Kiecolt-Glaser concluded that (a brief naturalistic stressor) examination stress reduces immune function, making people potentially more vulnerable to illness and infections. The effects of this stressor are more noticeable in students who are more socially isolated.
One of the main drawbacks of the Kiecolt-Glaser study is there is no apparent assessment of whether participants became ill, therefore, not fully concluding the study. Unlike Cohen et al’s study however, there were appropriate measures in place to measure direct immune function, and therefore the results (reduction of NK cells) of the study are reliable. It could be argued however that this reduction is too small to increase the chances of stress related illnesses and therefore insignificant. Furthermore, the narrow size of the cohort (medical students) means the study lacks ecological validity and it is therefore difficult to generalize. Perhaps for this reason, it led the K-G researches group to delve into further studies several years later.
Despite these obstacles, in 1995, K-G were able to conduct studies that revealed small wounds take longer to heal in highly stressed groups such as carers for Alzheimer patients, due to reduced immune function caused by stress. Although the initial study had been limited to measuring blood samples of medical students alone, the fact that further studies were carried out using new groups, (carers for Alzheimer’s and women involved in divorce proceedings, K-G et al 1987, 1991) and immune function was found to be reduced in these highly-stressed groups too suggests that a link between stress and health outcomes exists. Despite the participant group changing, the procedure used was the same- measurements of Natural Killer cells, excluding the rest of the complex immune system and the effects that stress may have on it. Stress has the potential to alter more that the number of NK cells; from natural reduced immunity, leaving specific immunity unchanged or increased to shifting the balance from cellular to humoral immunity, K-G’s group limited themselves to basing their judgement on one single type of measurement.
Nevertheless, there seems to be a correlation between exam stress and the reduction of NK cells, however has there was no manipulation of examinations stress (the independent variable) a cause and effect relationship could not be confirmed. It is imperative to note that further studies were carried out, for example in short-term martial conflict. Marlarkey et al 1994 also found a reduction of immune function occurs, with the effect being more noticeable in women than men.
The effects of stress are influenced by several factors, i.e. the type of stress, the duration of it, and individual differences (Cox & Mackey 1978, Lazarus & Folkman 1984) such as age, life-style, typical copying style. Although a single study may not be able to account for all these factors, by observing a range of studies related to finding whether a link between stress and reduced immune function exists, we can see generally consistent results. Meta-reviews consist of collaborating data in order to produce a more reliable overall result, (which reduces the reliance on a single study where methodological limitations occurred) and look at results across many studies. This is exactly how Segerstrom & Miller worked in their 2004 meta-review of 293 studies that have been carried out on the effects of different stressors on measures on immune system functioning. By categorisation of the stressors, they were able to see clearly what the results of the studies indicated about the effects of stressors on the immune system function.
“Acute time-limited stressors” (which include very brief experiences such as public speaking or mental arithmetic) lead to an up-regulation of natural immunity, measured as an increase in natural killer cells. This activation of natural immunity is logical from what scientists already know about this fast response mechanism and how it is triggered from the immediate onset of stressors. “Chronic (long term) stressors” were actually observed as having the most consistent effects on immune function, despite significant findings from K–G et al (1984) into brief naturalistic stressors reducing immune function. The meta-analysis revealed no overall effects on immune function from B.N.S whereas nearly all measures of natural and specific immunity showed a significant down-regulation. This global immunosuppression spanned gender and age groups, eliminating the possibility of bias.
Questionnaires on “Non-specific life events” were also analysed by Segerstrom and Miller who assessed the frequency and intensity of a range of life events, for instance, over the previous year. Although no significant changes to the immune function were found, participants’ over the age of 55 who were looked at reported reductions in natural killer cell activity around the time of a life event stressor, demonstrating what Cohen et al and K-G claimed: that life stress has potential to reduce or impair immune function.
Overal, the meta-review was important in allowing Segerstrom and Miller to come to educated conclusions about links between life-stressors and the effects they have on immune system function. The case-studies analysed do suggest that there is a link between stress, reduction in immune function, and illness. We were able to establish that acute-time limited stressors result in an increased number of natural killer cells. Brief naturalistic stressors have no over effect despite Kiecolt-Glasers findings, but there is evidence to show a shift from cellular to humoral activity. Chronic stressors lead to a down regulation in Natural and Specfic Immunity across participants, despite age and gender differences. Non-specific life events measured using the SRRS rating scale, show no significant relationship between stressful life events and reduced immune function. Acute time-limited stressors stimulate a fight of flight response and Selye’s GAS and can be seen as adaptive, however, chronic stressors push the system beyond this adaptive position , to global immunosupression, leaving an individual vulnerable to stress-related illness and infection. An important mechanism linking stress to down regulation of the immune system is the release of corticosteroids’ in the bloodstream reduce T-lymphocyte production and shrinks the thymus gland. This effect of this hormone suppresses the immune system function and has actually led to them being used therapeutically. People suffering from Autoimmune diseases can be relieved of condition from steroid treatment, although it does run the risk of leaving patients vulnerable to external infections.
Nonetheless, immune changes due to stress are not simplistic; there are shifts from natural to specific immunity and sometimes imbalances between cellular and humoral immunity. There was no real evidence of gender differences but in another study conducted by Kiecolt-Glaser et al (1998), it was shown that there was greater reduced immune function in women encountering martial conflict.
These studies, however, did pose many limiting factors, which resulted in indefinite answers. This was due to the studies being correlation studies, so no specific cause and effect could be established. There were also limitations in the participants, which were very specific, hindering us from generalising and applying results to a whole population (hence the importance of meta-reviews in collecting specific data in order to gain an overall idea).
Ethical issues in these studies are problematic as Kiecolt-Glasers group inflicted wounds from blood samples to her participants (leading to distraction over the important exam period) and Cohen et al’s study did not protect participants from the risk of catching a cold. Participants however, were made aware of potential consequences and they all gave their consent, so there was no real evidence of deception involved. Nevertheless, who would be held liable should anything go wrong, in these circumstances?
