One of the reasons why stress has been studied so consistently is because of its potential effect on the health of the individual. Research shows that hypertension rates are more common in those with high stress jobs such as air traffic controllers (Cobb and Rose 1973) than in less stressed occupations such as nuns (Timio et al. 1988). Further, both cross-sectional and longitudinal studies show that stressful occupations are associated with an increased risk of coronary heart disease (Karasek et al. 1981; Lynch et al. 1997; Kivimaki et al. 2002). In addition, Appels and Mulder (1989) and Appels et al. (2002) indicated that ‘vital exhaustion’ is common in the year preceding a heart attack. In one study people were given nasal drops either containing viruses responsible for the common cold or placebo saline drops. Their level of stress was then assessed in terms of life events during the past year (Cohen et al. 1991). The results showed that not everyone who was given the virus contracted the virus and not everyone who did contract the virus actually exhibited cold symptoms and became ill. Stress was shown to predict first who contracted the virus and second who developed symptoms. However, these studies involved a cross- sectional, prospective or retrospective design which raises the problem of causality as it is unclear whether stress causes illness or illness causes stress (or stress ratings). To solve this problem some research has used an experimental design which involves inducing stress and assessing subsequent changes in health. Because of the ethical problems with such a design most experimental work has been done using animals. A classic series of animal studies by Manuck, Kaplan and colleagues (e.g. Kaplan et al. 1983; Manuck et al. 1986) experimentally manipulated the social groupings of Bowman Gray monkeys who have a strong social hierarchy. The results showed that the monkeys illustrated not only behavioural signs of stress but also a marked increase in the disease of their coronary arteries. In addition, stress management, which involves experimentally reducing stress has had some success reducing coronary heart disease (Johnston 1989, 1992) and at reducing recurrent cold and flu in children (Hewson-Bower and Drummond 2001).
How does stress cause illness?
Johnston (2002) argued that stress can cause illness through two interrelated mechanisms and developed his model of the stress illness link which involves chronic and acute processes.
The chronic process
The most commonly held view of the link between stress and illness suggests that stress leads to disease due to a prolonged interaction of physiological, behavioural and psycho- logical factors. For example, chronic work stress may cause changes in physiology and changes in behaviour which over time lead to damage to the cardiovascular system. In particular, chronic stress is associated with atherosclerosis which is a slow process of
arterial damage that limits the supply of blood to the heart. Further, this damage might be greater in those individuals with a particular genetic tendency. This chronic process is supported by research indicating links between job stress and cardiovascular disease (Karasek et al. 1981; Lynch et al. 1997; Kivimaki et al. 2002). Such an approach is parallel to Levi’s (1974) ‘stress-diathesis’ model of illness which is illustrated in Figure 11.2.
However, there are several problems with a purely chronic model of the stress illness link:
- Exercise protects against the wear and tear of stress with more active individuals being less likely to die from cardiovascular disease than more sedentary individuals (Kivimaki et al. 2002). However, exercise can also immediately precede a heart attack.
- The wear and tear caused by stress can explain the accumulative damage to the cardiovascular system.
In the light of these problems, Johnston (2002) argues for an acute model.
The acute process
Heart attacks are more likely to occur following exercise, following anger, upon wakening, during changes in heart rate and during changes in blood pressure(e.g. Muller et al. 1994, 1985; Moller et al. 1999). They are acute events and involve a sudden rupture and thrombogenesis. Johnston (2002) argues that this reflects an acute model of the link between stress and illness with acute stress triggering a sudden cardiac problem. This explains how exercise can be protective in the longer term but a danger for an at-risk individual. It also explains why and when a heart attack occurs.
However, the acute and chronic processes are intrinsically interlinked. Chronic stress may simply be the frequent occurrence of acute stress, acute stress may be more likely to trigger a cardiac event in someone who has experienced chronic stress and acute stress may also contribute to the wear and tear on the cardiovascular system.
Furthermore, both the chronic and acute processes highlight the central role for stress induced changes in behaviour and changes in physiology. These will now be considered.