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John Macleod, Reader in Clinical Epidemiology and Primary Care Department of Social Medicine, University of |Bristol, Bristol, BS8 2PR, George Davey Smith
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For the past 100 years, considerable research activity has been directed at the question of a causal relation between psychological factors and physical disease. [1] A particular focus of this industry has been on the possible influence of psychological exposures on risk of heart disease, predicated partly on the assumption that risk of heart disease is substantially unexplained. [2] Associations between a series of psychological constructs with negative social connotations, hostility; low job control and depression for example, and increased risk of heart disease have been reported in observational studies. None of these factors have subsequently formed the basis of an intervention able to effectively reduce heart disease when assessed in experimental studies. [3] In this context, “negative affectivity” has long been considered to be one explanation for spurious associations between psychological stresses and physical disease outcomes in observational data. [4] People who view the world negatively tend to overestimate both their exposure to psychological adversity and their experience of heart disease symptoms. [5] Other non-causal mechanisms will also link negative emotions to heart disease. [3] Heart disease is strongly associated with social disadvantage and it is hardly surprising that the disadvantaged sometimes feel negative, for several good reasons. The experience of heart disease symptoms, or the knowledge of ones own increased risk of getting heart disease are also things that people are unlikely to feel positive about. All these will lead to predictable, non-causal, associations between negative affectivity, and other markers of dissatisfaction, and heart disease. The Whitehall II study originally suggested that low job control was the missing link between social disadvantage and heart disease risk. [6] Recent evidence suggests that this is probably not the case. [7] This latest report from Whitehall published in the BMJ posits that, rather than a “noise factor” whose non-causal relation to disease is well known, negative affectivity may in fact be a cause of heart disease. [8] How strong is the evidence presented in support of this hypothesis? Negative affectivity was higher, the lower an individual’s employment grade (paper, table 1). We know that lower employment grade predicts heart disease in Whitehall and that identifying “independent” effects through statistical adjustment is problematic. [3] Residual confounding by factors associated with social position is therefore likely. Further, negative affectivity may have been associated with higher baseline cardiovascular morbidity and risk such that reverse causality contributed to its association with subsequent heart disease. Exclusion of events in the first five years of follow up will not address this issue as it allows only for those at the very highest baseline risk (Framingham based risk prediction, for example, considers “high” risk to be those with a 20% or greater risk of experiencing a cardiovascular event within 10 years). Perhaps the most obvious possibility, however, is that these associations arose through reporting bias. We have previously discussed this problem in relation to the Whitehall study. [5] The composite cardiovascular outcome used (based on angina symptoms and doctor diagnoses) is likely to have been substantially influenced by individual perceptions and reports of symptoms whether to a researcher or a health professional. The Whitehall investigators could address this question of reporting bias quite simply through presenting associations between negative affectivity and two completely objective outcomes they have data on, ECG ischaemia and all cause mortality. We predict that the associations with negative affectivity seen with these outcomes would be much weaker than those with “heart disease” as measured in the paper; they would still be influenced by reverse causality and confounding, but not by reporting bias. These questions are not trivial; heart disease is still responsible for over a third of adult mortality in the UK and is the main morbid driver of health inequalities. [9] If we are to ameliorate this sorry situation we must focus on causes. Evidence that negative affectivity causes heart disease is currently very weak. Psychological theories of health inequality may be attractive to many because they shift the focus from disadvantage itself to how people feel about their disadvantage. This is unfortunate; the most consistent “independent” predictor of the small proportion of health inequality not explained by the social distribution of established behavioural and physiological risk factors is disadvantage itself. [10,11] Moreover, these established risk factors are themselves substantially created and reinforced by disadvantage and the material conditions associated with it. [10] In her accompanying editorial, Chang suggests that, “negative affect could exacerbate the consequences of disadvantage or positive affect could act as a buffer”. [12] The clear subtext (clear enough, for example, to any politician) is that if poor people could only be more positive in their outlook their health would improve. Whilst this may be true on some philosophical level we suspect that telling people to cheer up, without addressing the social structural reasons that underlie their negative feelings and adverse risk profiles, will do little to reduce inequalities in heart disease. References 1. Cannon WB. De La Paz D. The stimulation of adrenal secretion by emotional excitement. JAMA 1911;56:742. 2. Macleod J, Davey Smith G. Stress and the heart: 50 years of progress? International Journal of Epidemiology 2002 31: 1111-1113. 3. Macleod J, Davey Smith G. Psychosocial factors and public health: a suitable case for treatment? J Epidemiol Community Health 2003;57:565- 70. 4. Watson D, Pennebaker JW. Health complaints, stress and distress: exploring the central role of negative affectivity. Psychological Review 1989;96:234-54. 5. Macleod J, Davey Smith G, Heslop P, Metcalfe C, Carroll D, Hart C. Psychological stress and cardiovascular disease: empirical demonstration of bias in a prospective observational study on Scottish men. BMJ 2002;324:1247-51. 6. Marmot MG. Bosma H. Hemingway H, Brunner E, Stansfeld S. Contribution of job control and other risk factors to social variations in coronary heart disease incidence. Lancet. 1997;350:235-9. 7. Huisman M, Van Lenthe F, Avendano M, Mackenbach J. The contribution of job characteristics to socioeconomic inequalities in incidence of myocardial infarction. Soc Sci Med. 2008;66:2240-52. 8. Nabi H, Kivimaki M, De Vogli R, Marmot MG, Singh-Manoux A. Positive and negative affect and risk of coronary heart disease: Whitehall II prospective cohort study. BMJ 2008; doi: 10.1136/bmj.a118 9. Department of Health Vascular Programme. Putting prevention first. London: Department of Health, 2008. 10. Beaglehole R, Magnus P. The search for new risk factors for coronary heart disease: occupational therapy for epidemiologists? Int J Epidemiol 2002;31:1117–22. 11. Macleod J, Davey Smith G, Metcalfe C, Hart C. Is subjective social status a more important determinant of health than objective social status? Evidence from a prospective observational study of Scottish men. Social Science and Medicine 2005 ;61:1916-29. 12. Chang VW. Affect and heart disease. BMJ 2008 337: a177 Competing interests: None declared |
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Hermann Nabi, Research Fellow INSERM U687, France; University College London, UK, Archana Singh-Manoux, Mika Kivimäki
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We read with interest the comment by Macleod and Davey Smith on our paper entitled “Positive and negative affect and risk of coronary heart disease: Whitehall II prospective cohort study”.1 The central aim of our paper is to understand the links between psychological factors and coronary heart disease (CHD) in order to add to previous research.2 The editorial accompanying our paper picks up this issue and places our research in the wider research context by highlighting some of the unresolved issues relating to the stability of negative affect (state or trait?) and its role as a higher order psychological construct.3 Macleod and Davey Smith suggest that our results might be biased due to the inclusion of “subjective” measures of coronary heart disease (CHD). We would like to reassure all readers that the BMJ reviewers were thorough and this issue was raised during the review process. We were hoping that the text in the published paper was clear in stating that ascertainment of angina included “…corroboration in medical records or abnormalities on a resting electrocardiogram, an exercise electrocardiogram, or a coronary angiogram”. Thus, angina cases based on self-report data only were not included in the analyses. We have now undertaken further analysis on “objective” CHD (fatal CHD and non fatal myocardial infarction) by excluding “objective angina”, possible only in men due to low numbers of CHD in women, and the results show that after adjustment for all covariates, negative affect in the top tertile was associated with a 1.39 times greater hazard of CHD (p=0.056). We also examined this association using negative affect scores as a continuous variable (fractional rank, ranging from 0 to 1); these results suggest a relative index of inequality of 1.57, p=0.082. These estimations are consistent with those reported in our paper. In response to our paper, Macleod and Davey Smith write that “Psychological theories of health inequality may be attractive to many because they shift the focus from disadvantage itself to how people feel about their disadvantage”. Surely, this is an error. Our paper does not deal with social inequalities in health or theories on social inequalities in health. We are interested in the main effects of psychological factors on health, CHD being the outcome examined in this case. Hermann Nabi
Mika Kivimaki
References 1. Nabi H, Kivimaki M, De Vogli R, Marmot MG, Singh-Manoux A. Positive and negative affect and risk of coronary heart disease: Whitehall II prospective cohort study. BMJ 2008;337:a118. 2. Rosengren A, Hawken S, Ounpuu S, Sliwa K, Zubaid M, Almahmeed WA, Blackett KN, Sitthi-amorn C, Sato H, Yusuf S. Association of psychosocial risk factors with risk of acute myocardial infarction in 11119 cases and 13648 controls from 52 countries (the INTERHEART study): case-control study. Lancet 2004;364:953-962. 3. Chang VW. Affect and heart disease. BMJ 2008;337:a177. Competing interests: None declared |
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