All participants were given a punch biopsy, which is a cut of 3.5mm just below the elbow. The wounds were dressed and treated by a nurse in the same way for each participant. In addition, a second measure of immune response was taken. The researchers assessed levels of cytokines – biochemical substances involved in regulating the body’s immune response. They were also given a 10 item perceived stress scale to check how stressed they felt.
Thirteen women who were engaged in stressful dementia care giving activities took an average of 9 days longer to completely heal a 3.5-mm punch biopsy wound than 13 well-matched control subjects, i.e., 24% longer to heal a small, standardized wound. In addition, caregivers' mononuclear cells produced lower levels of the pro-inflammatory cytokine interleukin-1 in response to lipopolysaccharide stimulation, providing evidence of one possible immunological mechanism. Stress-related alterations in wound repair could have important clinical implications, particularly for surgical recovery. Furthermore, on the perceived stress scale, the carers did actually indicate that they were feeling more stressed.
The findings support the view that chronic stress depresses the functioning of the immune system because wound healing was slower in individuals who experienced chronic stress. The lower levels of cytokines in chronically stressed individuals support the view that stress lowers immune response directly.
However, this investigation used an inexact matching of participants. The matching of the participants was not really clear, for example more of the carers were married and non-smokers, while the controls were not matched on this also. However, both of these participants’ variables are related to lower stress. Social support is known to reduce stress, and non-smoking is related to better immune functioning. Therefore this sample bias would suggest carers, should have a better immune functioning. This strengths the validity of the finding of the study.
On the other hand, these findings have important implications for treating people with infections, particularly for those recovering from surgery. Clearly it would be important to reduce stress as far as possible in such patients and thus speed their recovery.
This study was a field experiment. In field experiments the researcher is testing hypotheses in a similar way to the way it would be done in the laboratory. The main difference is that many of the extraneous variables the researcher would be able to control in the laboratory, are not able to be controlled in the field. One obvious advantage of the field study is that it is able to overcome the criticism that findings from laboratory settings are not general sable to the "real world". Field studies take place in this real world, so generalization is therefore not a problem - field studies are said to have high external or ecological validity.
Some alternative studies include Cohen et al. (1993) used the ‘viral-challenge’ technique to study the effects of stress on over 400 volunteers. Individuals were exposed to the common cold virus and also given a questionnaire to access their levels of stress. Cohen et al found a positive correlation between the levels of stress and the likelihood of catching a cold.
Shockingly, a study proved that the effects of stress may sometimes enhance the immune system - Evans et al (1994) looked at the activity of one particular antibody, sign, which coats the mucous surfaces of the mouth, lungs and stomach and helps protect against infection. They arranged for students to give talks to other students (mild but acute Stress). These students showed an increase in sign, whereas levels of sign decreased during examination periods that stretched over several weeks. Evans et al. (1997) propose that stress appears to have two effects on the immune system: up-regulation for very short-term acute stress, and down-regulation for chronic stress. This fits with the SAM/HPA distinction, and the essence of the GAS model.
A number of suggestions have been put forward to explain how stress might cause cardiovascular problems. For example,
- Stress increases the heart rate which may wear out the lining of the blood vessels.
- Stress increases blood pressure and this causes damage as high pressure would cause to any pipe
One cause of cardiovascular disorders is a condition called myocardial ischemia, which occurs when the heart muscles does not get enough oxygen. This can happen during physical exertion. However research has found that it can be brought on by psychological stress.
A study was carried out by a psychologist called Krantz et al (1991). The aim of the study is to show the extent to which mental stress could be shown to increase myocardial ischemia. Also, to see if patients with coronary artery disease reacted differently from patients with no cardiovascular problems.
39 patients and 12 controls were studied while they performed 3 mental tasks: an arithmetic task, a stroop task and a task were they stimulated public speaking. Each of these tasks was designed to create mild stress. Measurement were taken of the participants blood pressure and the extent to which blood vessels around the heart contracted (high, medium or low ischemia).
The cardiovascular patients who displayed greatest myocardial ischemia during the mental tasks also had the highest increases in blood pressure while the controls showed the lowest levels of both myocardial ischemia and blood pressure when performing the mental tasks. There was an intermediate group of patients who had either mild ischemia or none at all when performing the mental tasks. Also had only moderate increases in blood pressure.
These findings support the idea that there is a direct link between performing a mildly stressful cognitive task and physiological activity that damage the cardiovascular system. However not all cardiovascular patients responded in the same way, which leads us to conclude that way which leads us to conclude that there are important individual differences in responsiveness.
One could ask whether the mild stress given here is acceptable, especially to cardiovascular patients. The justification offered would be that the patients gave their informed consent and they were not subjected to stress greater than they would experience in everyday life.
A control group was used in order to see if the behaviour of cardiovascular patients was different from that of normal’ individuals, but no controls were used to compare a patient’s behaviour when stressed and not stressed. It is possible that the cardiovascular patients might show signs of muscle ischemia and raised blood pressure when relaxed as well as when mildly stressed, and this would mean that stress was not the cause of the ischemia or raised blood pressure. In this case, the conclusions of the study would not be justified.
Recent research suggests that the sympathetic branch of the ANS in some individuals is more reactive than in others (Rozanski et al., 1999). This would mean that some people (described as ‘hyper responsive’) respond to stress with greater increases in blood pressure and heart rate than others, and this would lead to more damage to the cardiovascular system in hyper responsive individuals. Later in this module we will look further at research into the relationship between individual differences and stress — at evidence that some types of people get more stressed and that they are more likely to have heart attacks and other cardiovascular disorders.
Russek and Zohman (1958) looked at heart disease in medical professionals. One group of doctors was designated as high-stress (GPs and anaesthetists), while others were classed as low-stress (pathologists and dermatologists), Russek found heart disease was greatest among GPs (11.9% of the sample) and lowest in dermatologists (3.2% of the sample). This supports the view that stress is linked to heart disease, but it does not indicate whether the link is direct or indirect.
