Commentary: Stress and the heart, 50 years of progress?

John Macleoda and George Davey Smithb

a Department of Primary Care and General Practice, University of Birmingham, B15 2TT, UK.
b Department of Social Medicine, University of Bristol, BS8 2PR, UK.

Ian Stewart’s essay in the 1950 Christmas edition of the Lancet, on the possible psychosocial origins of coronary heart disease (CHD),1 preceded the publication of Hans Selye’s The Stress of Life by 6 years.2 Selye is still widely credited with inventing (or discovering) ‘modern stress’, although clearly the construct, and a reasonably sophisticated conception of its possible relation to cardiovascular health, already had widespread currency in 1950. Indeed a causal association between heightened ‘stress’ and heart disease was suggested at least as long ago as the 18th century.3

Whether in its observations on medical registrars, Birmingham teenagers, charwomen or other blue-collar workers, Stewart’s essay belongs to an era when doctors were not shy of displaying the assumptions and prejudices of their class. However, it is not epidemiologically naïve. The need for any aetiological explanation of CHD to be congruent with epidemiological understanding is explicitly recognized. In 1950 the epidemiology of CHD was understood in fairly simple terms. Coronary heart disease was increasing, this increase appeared to follow increases in industrialization and urbanization and appeared particularly to affect more industrialized and urbanized populations. Middle class men (particularly ‘professionals’) appeared to be the most affected social group within these populations. In terms of physiological risk factors, hypertension seemed a good candidate and in terms of behaviour, diet was implicated. Hereditary factors were recognized as important, but were also seen to provide an incomplete explanation.

In other words then, as now, psychosocial explanations for heart disease appeared to arise for two principal reasons. First, they accorded with popular assumptions; second, they filled an apparent explanatory gap.

Stewart’s explanations of why middle class professional men experienced more ‘modern stress’ than any other section of society may now seem slightly patronising. However, it reflects a general conceptual problem that has yet to be resolved in psychosocial epidemiology (a problem that, to be fair, Stewart appeared aware of himself). Psychological ‘stress’ is conceptualized as the physiological or behavioural response to any threat to emotional homeostasis. In physiological terms this is indistinguishable from ‘excitement’—the negative connotations put on particular types of ‘stress’ are socially constructed. Positive constructions of excitement appear to have broadly the same physiological consequences (and neurophysiology is still only understood in broad terms) as negative ones. The excitement of watching football matches appears to have similar cardiovascular consequences to the stress of a missile bombardment.4,5 Thus anybody with the capacity to get excited (about anything) also has the capacity to be ‘stressed’. This universal nature of ‘stress’ does not fit well with the candidature of stress as an explanation for the disease experience of particular social groups. For such explanations to be viable, stress, or particular sub-types of stress, must be constructed and associated with particular kinds of people. The general construct stressis too general to usefully explain any social patterns of disease.6,7

So Stewart argued that ‘modern stress’, a form of middle class, male angst (not dissimilar to what Rosenman and Friedman subsequently operationalized as Type A behaviour8) experienced amongst ‘workers by brain’ rather than ‘workers by hand’ was the toxic component of stress. He further argued that although manual workers experienced greater material deprivation than non-manual workers, the latter experienced more ‘modern stress’. It is interesting to contrast this viewpoint with current assertions that the material deprivation experienced by manual workers is essentially irrelevant in developed societies, while ‘manual worker stress’—lack of control over work—is an important determinant of health inequalities.9 As Elianne Riska points out, there ‘is a certain irony involved in the stress literature of the past 30 years. During the heyday of the research on Type A men, the Type A factor was a marker of men who tried to control everything, while today work-related stress considered to have lethal effects is found in men and women who have no control over work’.10

Some categorizations of ‘stress’ are perhaps social, rather than biological. Contemporary examples are the (generally data-driven) shifts in conceptualizations of work stress and Type A behaviour, towards more ‘specific’ constructs such as job control and hostility.11,12 There is no apparent neurophysiological or endocrinological basis to assume a different effect of these types of ‘stress’ (they are not equivalent to different sub-types of lipids, although some researchers talk about them as though they were), but perhaps because they fit more closely with the social distribution of heart disease they appear better candidates for an aetiological role.

Stewart only briefly touched on the mechanisms linking stress and coronary disease, and did not discuss the influential work of the likes of Cannon and Selye who had already elaborated the principal neurophysiological pathways (the sympatho-adrenal and hypothalamic-pituitary-adrenal axes, respectively) through which psychological stress could plausibly lead to disease (if not to social patterns of disease).1,13–16 Although stress was already popularly linked to smoking, the further link between smoking and CHD had not yet been well established.17

Two weeks after the publication of Stewart’s essay an equally entertaining response from Robert Platt appeared in the correspondence columns of the Lancet18 (as reprinted in this issue of the International Journal of Epidemiology). Platt wondered to what extent the social distribution of diagnosed CHD was a diagnostic artefact. He pointed out that an occupational group’s standardized mortality ratio for CHD appeared directly proportional to the likelihood of a member of that group seeing a consultant cardiologist prior to their death. Coronary heart disease was a relatively new diagnosis in 1931 and therefore one only likely to be made by a specialist. Platt’s suspicion appeared to be borne out by subsequent data. By the 1961 decennial supplement, CHD (along with cardiovascular disease generally) was clearly associated with social disadvantage.19 As a consequence, plausible psychosocial explanations of social variations in CHD have, from the 1970s onwards, of necessity been couched in terms of working class, rather than middle class, psychological attributes.20,21 Intriguingly, however, the proposed mediating mechanisms remain, essentially, the same.

Other than the conceptual problems discussed above, the strength of the empirical evidence linking psychological ‘stress’ to CHD appears questionable to some.22 Confounding, particularly by socioeconomic factors, is an issue that many studies have been unable to resolve.23 Further the typical discrepancy between associations of heightened ‘stress’ with subjective disease outcomes and those with objective disease outcomes, apparent in virtually every observational study where both are available for comparison, is highly suggestive of reporting bias.24,25

Some of these interpretational problems are further illustrated in the current issue of the International Journal of Epidemiology.26 Earlier publications from the GLOBE study (a large, Dutch, prospective, observational study looking at various stress subtypes and social patterns of disease) suggested that psychosocial factors were important determinants of social patterns of subjective health.21,27 Since the same factors now appear to have no relation to objective health, a role of reporting bias must be considered. Similarly, the GLOBE investigators previously reported that ‘perceived control’ was an important determinant of mortality amongst a subset of the cohort followed for 6 years. Control now appears unrelated to mortality amongst the whole cohort followed for 7 years. This inconsistency is intriguing, and perhaps suggests that confounding produced the former results.

Stewart wrote about ‘the "stress" of modern existence’, that had increased to such a degree that the newspapers were full of references to it. His largely medical readership would have appreciated the fact that a recent committee had concluded that the ‘strain of medical practice’ shortened the life expectancy of doctors—largely through heart disease. However, he was clearly sceptical of any real increase in stress, pointing out that the ‘trials of life have usually appeared exceptional to the generation called upon to bear them’. However, the perception that stress had increased, together with the rise in CHD, would have encouraged a link between the two. Similar links were drawn at the time between stress and peptic ulcer, which was also a disease that had increased in incidence, and indeed a veritable research industry mined the stress and peptic ulcer field, to no great benefit to either individual or population health, until Helicobacter pylori was identified and both treatment and prevention became effective.28,29

Given that the evidence on stress and CHD is still far from secure—in particular with respect to the disappointing outcomes of psychosocial interventions30—why does it generate such interest and sometimes passionate advocacy?31–33 Some factors identified by Stewart are probably relevant: the general public consider that it is important; researchers feel it has relevance for their (stressful) lives, and it offers to explain currently mysterious aspects of disease distribution. In addition, as the anthropologist Allan Young has convincingly argued,34 the discourse regarding stress and health fits conveniently with ‘conventional knowledge’—in that it tends to voluntarist and individualizing strategies that do not threaten fundamental exploitative economic relations. As Viner has described, stress research has historically received some of its strongest support from the North American military-industrial complex with its preoccupation with predicting and optimizing human performance, particularly under difficult and unpleasant environmental conditions.35

Our reflections on Stewart’s essay should not suggest that psychosocial epidemiogists call it a day.36 Even if stress is not an important aetiological factor in somatic disease it certainly contributes to feelings of dissatisfaction, distress and misery—which are no less real, nor deligitimized, if found to be unimportant as contributors to other forms of pathology. Indeed, in many wealthy countries with long—and lengthening—life expectancies, the burden of such distress may be of more importance than much somatic disease. There are many questions remaining that may yet prove to have important answers. And evidence for the basic plausibility of a causal connection between the psyche and physical disease has considerably strengthened in the past 50 years.37 ‘Stress’ may be a poor candidate for explaining social inequalities in health but that does not mean it has no causal relevance to health per se.

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