Whitehall II

Listened to an old More or Less recently about the socioeconomic gradient in health outcomes (specifically mortality) in the UK. The presenter Andrew Dilnot, and his interviewee, referred to the Whitehall II study as showing how people's job status and sense of control in work are related to this. This is a common conclusion to draw from the Whitehall II study and, while this may be a somewhat controversial view, one that I think is utterly unfounded.

As in many other studies, Whitehall II found that coronary heart disease mortality was associated with job grade, which is obviously seriously confounded with socioeconomic status:

This gradient is somewhat due to known coronary risk factors as we would expect, but is not entirely so. Other factors that have been associated with coronary risk are height (considered a marker of early life and genetic differences) and job control - it is job control that is supposedly associated independent of socioeconomic status, and what leads people to assume that it is job status, rather than socioeconomic status per se, that is associated with heart disease.

This evidence has lead many researchers to accept that psychosocial factors have a profound influence on coronary heart disease and that it is not material deprivation but status that is important in socioeconomic health inequalities (the argument here is about direct aetiological effects of psychosocial factors on health, rather than, for example, indirect effects mediated via know risk factors such as smoking). Others have worried that this view could lead to a regressive lack of emphasis on material factors in addressing health inequality.

So we should consider the evidence base for this contention because health inequalities are a rather pressing public health concern, and policy making should be based on the best evidence. The latest update of the Whitehall II study on job control is Kuper & Marmot (following on from the Bosma et al study).

They looked at two outcomes, all coronary heart disease (all CHD; including self-reported angina) and myocardial infarction (MI; fatal or non-fatal). They find no effect for women, but for men there is a highly significant effect of job control on all CHD even adjusted for coronary risk factors (smoking, cholesterol, hypertension, exercise, alcohol, BMI). But there is no effect of job control on the harder endpoint of MI - even unadjusted for coronary risk factors. i.e. low job control is associated with angina (self-reported chest pain - it is unclear whether this is solely derived from the Rose questionnaire or whether clinically diagnosed angina is also associated, but in the original Bosma study the effect was driven largely by Rose questionnaire scores) but not more objective measures of coronary heart disease. Studies of other 'psychosocial' risk factors in Whitehall II have similar problems.

The fundamental problem with this conclusion is that most studies have tended to only find associations between subjective reports of psychosocial factors (such as sense of workplace control) and subjective measures of cardiovascular disease, rather than objective measures. Obviously it is possible, and in this case pretty likely, that people report more symptoms of angina when they feel less in control of their work (causality here may be direct, or via third factors like personality). Without an effect on objective coronary endpoints we can only assume that an explanation of this form is most likely. I can only think that the popularity of the 'psychosocial' explanation is due to its trendy image, rather than the strength of the evidence.

George Davey Smith has a good chapter on the less than successful history of psychosocial explanations of physical disease (e.g. peptic ulcers) in Biopsychosocial Medicine. In particular he points out the similarities of the findings from the Whitehall II study on CHD and job control and a study of his own where they found that perceived stress correlated with Rose angina but not more objective measures of cardiovascular disease:

"The broad categories "cardiovascular disease" and "coronary heart disease" are made up of different constituent diagnoses. Admissions for coronary heart disease did not increase with increasing stress, whereas admissions for cardiovascular disease did. We have broken down these categories to explore this discrepancy. Admissions for "coronary heart disease" are dominated by those for acute myocardial infarction, a condition where admission would normally be considered mandatory and where diagnostic classification depends primarily on objective criteria (such as the measurement of cardiac enzymes). Reporting bias will not influence these, hence admissions for myocardial infarction are not related to stress. For most classes of hospital admission the decision to admit and the classification of cause of admission depends on a combination of symptoms and signs. Where symptoms have the dominant influence, reporting bias may exert an important influence. This probably explains the weakly positive associations between angina admissions and stress and the more strongly positive association between stress and the group of admissions for cardiovascular conditions where admission was likely to be, to a substantial degree, discretionary or when diagnostic classification reflected non-specific symptoms or signs. Because of this, admissions for "cardiovascular disease" overall were positively associated with stress. Some studies have used disease diagnosed by a doctor as an "objective" outcome.19 These results suggest that it may also be influenced by reporting bias.

We are not questioning the reality of symptoms to the person experiencing them. Nor, given the strong association between angina and mortality, are we suggesting that self reported angina is, in general, a poor predictor of coronary heart disease. However, reporting tendency as well as physical disease can lead to angina being experienced and reported. This has important implications for treatment and prevention.

The weak inverse association between higher stress, ischaemia detected by electrocardiography, acute myocardial infarction, and mortality is also likely to be non-causal. In this population, socially advantaged men perceived themselves to be most stressed, leading to a confounded association between higher stress and better health. Adjustment for current occupational class attenuated but did not abolish this relation. Adjustment for other markers of social position had little additional effect (data not shown). All measures of social position are relatively crude, and statistical adjustment for them is likely to leave a residually confounded association between any socially patterned exposure and health.

In the systematic review concluding that evidence supported a causal relation between stress and cardiovascular health, these associations were most consistently observed between stress and substantially subjective end points such as self reported symptoms. 2 20-23 It seems likely that at least some of these relations are artefactual in the same way as the ones we report here. Only one study in this review reported an association between perceived stress and mortality, in a population where stress was associated with social disadvantage and therefore likely to show a confounded association with health.

Associations between "psychosocial" factors and objectively poorer health have been shown in other studies. In all of these, where the social distribution of the psychosocial factor was described, "adverse" exposure was associated with social disadvantage. It is possible that these relations were also residually confounded."