Commentary: The problem with stress: minds, hearts and disease

Stephen A Stansfeld

Department of Psychiatry, Barts and the London, Queen Mary’s School of Medicine and Dentistry, Queen Mary, University of London, London, UK.

Correspondence: Professor Stephen Stansfeld, Department of Psychiatry, Medical Sciences Building, Queen Mary, University of London, Mile End Road, London E1 4NS, UK. E-mail: S.A.Stansfeld{at}qmul.ac.uk

The problem with stress as a cause of illness is that it has too much face validity. Most people experience stress responses, where their resources are exceeded by environmental demands, at some time. Under these circumstances they may feel anything from annoyance, disappointment and frustration to severe anxiety, panic, fear, anger or depression. This is unpleasant and it is easy to extrapolate from this a belief that such emotional stress responses may give rise to illness; everyone has a personal hypothesis about this. As such, stress is a conveniently amorphous notion conjured up to explain anomalous findings that has both societal and personal resonance for a scientific readership and a medical author. It is in this light that Stewart, writing in 1949, invokes stress, together with eating fatty foods, as the major explanation of the social gradient in heart disease at the time where those, largely men, in non-manual social class groups had higher rates of coronary heart disease (CHD) than men working in manual occupations.1

The shift in the social distribution of CHD in the middle of last century has only partly been explained. In the first half of the 20th century, as Stewart reports, CHD was more prevalent in non-manual than manual occupational groups, while in the second half of the century a social gradient emerged in which CHD was more prevalent in manual groups. Moreover, in an occupational cohort, the Whitehall Study2 set up in the late 1960s, there was a gradient of increasing mortality risk with decreasing occupational status. Stewart’s contention that there was more stress among people in professional, middle class occupations than in working class occupations does not seem plausible. Perhaps working class solidarity and a priority given to satisfactions outside work, rather than focussing on competitive striving at work (which rather crudely sums up his argument), might be considered protective of the heart. On the other hand this is to discount the effects of poverty (or lesser degrees of material disadvantage), job insecurity, unemployment, inadequate nutrition, poor housing, and monotonous and repetitive work then, and now, current in working class populations, that would be likely to have far more negative effects on health and be more stressful than the occupational concerns of professional men.3 Explanations for this gradient must be sought elsewhere. Differential diagnostic practice by social class, with an increased tendency to diagnose CHD in middle class groups as opposed to working class groups, may provide part of the explanation. Additionally, the gradient may relate to differences in health behaviours as Stewart hints in his article. Middle class people may have had a diet higher in sugar and lower in cereal fibre, and to have smoked more cigarettes than working class people in the early years of the last century when the risk for CHD manifesting itself in the 1940s was laid down.4 Later on in the century, the working class population adopted the same dietary preferences as the middle classes had earlier espoused and hence the increased coronary risk. At the same time the middle class groups were tending to give up smoking and lead healthier lives in terms of exercise and diet, thus reducing their coronary risk and contributing to the reversal of the gradient.4

One problem with research on stress and health which tends to discredit the whole area, is the very non-specific nature of much of the research, the lack of clear specification of hypotheses, and in some areas the clinging to stress-related beliefs of causation despite little evidence to support them. Stewart, to his credit, does seem to support medical knowledge based on evidence, citing Witts5 ‘the role of the mind in the pathogenesis of organic illness is more difficult to assess thanis popularly supposed, and that in those few maladies, suchas thyrotoxicosis, in which its influence has been establishedthe demonstration has been achieved only as a result of elaborate laboratory research, never (according to Witts) from the recesses of an armchair.’ And he goes on to suggest somewhat unkindly, but memorably, ‘And seldom, I suggest, from within the curtained closets of the psychiatrists’. In contrast to 1949, academic psychiatry has changed enormously and psychiatrists have pulled back the curtains and are more active in basic aetiological research themselves, both in the laboratory and in epidemiological field studies.

What evidence can be cited today that stress causes CHD? There are many aetiological conundrums that require explanation: the decline in CHD in Western Europe coupled with the increase in Eastern Europe, the strong social gradient in coronary disease and the tendency for the decline in incidence to be greater in groups with a higher rather than lower socioeconomic position.6 Can personality type be entirely discounted in the aetiology of CHD? Type ‘A’ behaviour pattern has been largely discredited as a coronary risk factor, despite great initial excitement, as later studies have not confirmed earlier findings.7,8 The story of this rise and fall of a risk factor is in itself interesting. In the 1960s and 1970s was there an association between Type ‘A’ behaviour and other risk factors for CHD that conferred risk at the time but that has now been lost as society has changed? Alternatively, did Type ‘A’ behaviour relate more pathogenically to certain aspects of society at the time, and these conditions no longer pertain? This is not clear but one element of Type ‘A’ behaviour has remained as a risk factor, namely hostility measured by instruments such as the Minnesota Multiphasic Personality Inventory, that has predicted incident CHD in several studies.9,10 Recently Type ‘A’ behaviour has also been shown to be associated with the precipitation of coronary events in those with existing CHD; so rather than having a primary aetiological association with CHD it may be associated with progression of disease.11

There is evidence from an increasing number of studies that psychological factors play a part in the aetiology of CHD. Depressive illness and depressive symptoms have been associated with increased risk of incident CHD morbidity and mortality.12–15 Part of this association may be explained by health behaviours, as depressed people may smoke more, take less exercise, and eat an unhealthier diet than people who are not depressed.16 However, this can only be a partial explanation as adjustment for health behaviours does not account forthe association between depression and CHD.17 Depression, independent of other mediating factors, may induce biochemical and physiological changes that may be long-lasting. These include sympathoadrenal hyperactivity, hypothalamic-pituitary-adrenal axis hyperactivity, diminished heart rate variability, ventricular instability, and alterations in platelet receptors.18 Separately, three prospective studies have shown an association between measures of phobic anxiety and increased risk of sudden death.19–21 The mechanism for this could be that a tendency to severe anxiety in some specific circumstances could be associated with increased susceptibility to ventricular arrhythmias. There is also evidence that depression post-myocardial infarction is a risk factor for mortality. This risk is maintained even after adjustment for the severity of the damage to the myocardium and impaired cardiac function.22 Part of this increased risk may be because depressed cardiac patients find more difficulty in giving up smoking or in adhering to dietary or exercise programmes than non-depressed patients.23 Also depression may confer an increased susceptibility to ventricular arrhythmias that may be potentially more serious in an already damaged heart.24

Other psychosocial factors, that is stressors with both a psychological and a social component, that are important in CHD aetiology are social relations and work characteristics. Small social networks and social isolation predict higher levels of mortality, especially from cardiac causes25–27 and also an increased risk of CHD incidence.28 In different cohort studies, different types of social relations are associated with mortality, but this may be as much to do with variation in the age structure and cultural mores of different populations for whom the salience of particular social relations may vary.29 Social integration and social participation are linked to healthy behaviours, particularly being involved in physical activity, and this may contribute to the protective effect against CHD. Nevertheless, social relations are likely to precede healthy behaviours in the causal chain. Social support from close others may be viewed partly as a form of social control.30 Nowadays this may encourage a healthier diet and more moderate alcohol intake—this may be part of the explanation for the protective effects of marital status on men’s mortality risk.31 However, this social control can work both ways, in certain subcultures heavy alcohol intake and smoking may be reinforced.

Low control at work and Karasek’s job strain, a combination of low decision latitude and high psychological demands, has been found to predict self-reported CHD morbidity and CHD mortality.32,33 High levels of imbalance between efforts applied at work and rewards received also predicts increased risk of CHD morbidity that seems to be independent of the effects of low control.34,35 These findings have been criticized as being confounded by socioeconomic position, where low control is merely an indicator of low social status.36 Low control at work is indeed strongly associated with low social position. However, although much of the CHD risk associated with low social status may be the result of the cumulative experience of material disadvantage in childhood and adulthood, it may also be the case that, for working populations, who spend much of their adult life at work, the effects of low social status on CHD risk are mediated through low control at work. It seems unrealistic to expect that all the effects of material disadvantage on health are directly on physiological systems and none is mediated through psychological perceptions coloured by feelings of hopelessness, unfairness, anxiety, insecurity, stigma, and lack of equality. Such perceptions of the workplace and the feelings they engender may be on the pathway between reports of low control and health.

Increased psychological demands alone do not always seem to be associated with increased CHD risk. For instance, in the first longitudinal reports from the Whitehall II Study, psychological demands were not related to self-reported CHD although they were related prospectively to increased risk of psychological distress.37,38 This is interesting in relation to Stewart’s paper, where in essence he is suggesting the excess of coronary risk in professional as opposed to manual occupations is related to the psychological demands and expectations found in these groups. Psychological demands at work are multifarious. Although they are made up of work pace and being asked to undertake conflicting tasks which might be expected to be risky for health, they may also indicate jobs that mean you are ‘in demand’ and hence an important part of the organization, aspects of work that are likely to increase self esteem rather than impair health (these are ‘active jobs’ in Karasek’s characterization32). Thus teasing out pathogenic aspects of psychological demands at work may be difficult—they may relate to poorer mental health—but their association with poorer cardiac health is problematic.

It was an interesting time for Stewart to be writing, World War II had recently finished and the National Health Service had just started. It was a time of both hope but also world weariness, and this is reflected in the article. He is somewhat dismissive of the links made between both detailed descriptions of personality type and behaviour and subsequent disease, and the association between certain physical ‘somatotypes’ and predisposition to disease.1 Nowadays these associations have been almost entirely discredited, although there have been studies that link behavioural styles with disease; for instance, goal frustration has been linked to organic bowel disease.39

We may be apt to look scornfully on his assertion that few can doubt the link between personality and peptic ulcer in the light of studies that suggest that Helicobacter pylori is the cause of peptic ulceration—but should we be so ready to throw the baby out with the bathwater?40 It may be that personality characteristics, rather than being related to the aetiology ofthe disorder, are associated with the tendency to perceive, report, and act on symptoms. The tendency to report ‘physical’ symptoms does differ across people and may relate to neuroticism and negative affectivity.41 In this way they may be important in the presentation of an illness like peptic ulceration but not in its aetiology—this can be confusing when the assumption is made that psychological factors are involved in the causation of the condition. A similar mechanism may be involved in angina pectoris, although here it may be more complex. Angina pectoris is a symptom of CHD and a predictor of CHD mortality. Psychological distress and symptoms of anxiety predict angina pectoris measured by self-completion questionnaire.42,43 Is this sufficient further evidence that in this case psychological distress is a predictor of CHD? Probably not. Rather, in CHD, a condition with a high prevalence rate, psychological distress may influence those who notice and remember chest pain and who then go on to report chest pain on a questionnaire. This influence is likely to be more obvious in those with milder grade 1 angina because in severe CHD, chest pain on exertion may be impossible to ignore and psychological factors influencing reporting will be less important. A complicating factor is that in more severe chest pain associated with functional impairment of activities of everyday living, psychological distress, especially depression, may develop as a consequence of the pain and restriction of activities.43

A recent study from the West of Scotland using the Reeder scale44 to measure stress, found that high scores were relatedto higher socioeconomic position, and predicted angina pectoris, non-specific cardiac hospital admissions, smoking, and alcohol intake, but were inversely associated with incidence of ischaemia.45 The authors interpret the association with angina pectoris as probably being due to negative affectivity butthen appear to dismiss all associations between psychosocial factors and health as being spurious on the basis of the inverse association between the Reeder scale and ischaemia and mortality.36 The Reeder Scale bears closer examination. It is a short scale that appears to measure generalized anxiety and self-descriptions of being stressed. This old fashioned view of stress is curiously reminiscent of Stewart, a diffuse, self-defined condition expected to predict illness and mortality. But as the evidence above has shown, such a non-specific view of stressis out of date, rather the focus has shifted to more specific psychosocial factors, such as lack of social support or depression where there are both plausible biological mechanisms linking these psychosocial factors and CHD, and supportive evidence from animal studies. However, the implication of these authors’ work is right, and I think Stewart would support this,—that the field of stress and health research needs to be pursued with the utmost research rigour to discover the truth in a subtle, complex and seductive field.

Acknowledgments

I acknowledge the help of Lisa Kass in preparing this paper.

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