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What the Renfrew / Paisley data really tell us about tackling health inequalities: the need to refocus upstream
- Alex Scott-Samuel (28 February 2009)
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Interpeting the Renfrew/Paisley data: a mixed picture of health inequalities emerges
- Ken Judge (2 March 2009)
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Smoking, altered blood rheology and survival.
- Les O. Simpson (6 March 2009)
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Neither more reports, nor papers. It’s time to declare full war against tobacco.
- Alain Braillon (17 March 2009)
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Alex Scott-Samuel, Director, EQUAL - Equity in Health Research and Development Unit Division of Public Health, University of Liverpool, Whelan Building, Quadrangle, Liverpool, L69 3GB
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While I am wholly in accord with Gruer and colleagues regarding their main message, namely that smoking remains the major preventable threat to public health in the UK, their data also suggest additional important conclusions regarding the nature and persistence of health inequalities. Examination of the survival curves in their Figure 3 and the associated data in Tables 3 and 4 shows that after 28 years of follow-up, social class differentials in mortality among never-smokers (and also among male ex-smokers) are as great or greater than those among current smokers. If these three pairs of socioeconomic subgroups (ie social class 1+2 and 4+5 current, ex- and never-smokers) are comparable except in their smoking behaviour, the important implication is that smoking abstinence or cessation has little or no long term impact on health inequalities. This finding is consistent with the epidemiological concept of ‘competing causes of death’, which would suggest that if the total impact of smoking on mortality could somehow be eliminated, poorer people would continue to die prematurely from other ‘competing risks of death’ which would increase in importance and ‘fill the gap’ left by the elimination of smoking-related risk. Theoretical arguments supporting this positon have been elaborated and empirically verified by Phelan and colleagues(1). Essentially they argue that addressing current manifestations of inequality (be they cholera 100 years ago or smoking now) cannot have a lasting impact on health inequality, since its 'fundamental causes' remain unaffected. Only by addressing these fundamental causes of health inequality (which they list as inequalities in power, money, knowledge and beneficial social connections) can lasting reductions in inequality be achieved. The long-term persistence of health inequalities in the face of effective interventions, offers further support. A hundred years ago, one could have predicted the long term decline of health inequalities if freely available, effective treatments for infectious diseases were to be developed. In the event, antibiotics and the NHS had little or no impact on long term health inequalities. Health ministers currently make similar predictions about the potential reduction of inequalities in the context of effective smoking prevention / cessation. The survival curves in Gruer et al’s Figure 3 demonstrate that they are incorrect. My thesis could be verified epidemiologically using a cause- elimination life table approach; I would encourage government statisticians to carry out the necessary work. I should point out that I am well aware that smoking is a major cause of death in lower social classes, and that it disproportionately affects lower as compared to higher social classes. I am also aware that smoking only explains a proportion of the current class differences in mortality. But neither of these facts is relevant to my argument - which is that entirely eliminating the impact of smoking would have little or no long term impact on class inequalities in mortlaity. Application of this argument to the current public health context would suggest that smoking abstinence / cessation confers substantial benefits on those individuals concerned, but that, in the case of people in lower social classes, other competing mortality risks rapidly increase in prevalence, such that long term class inequalities in mortality are maintained (albeit at higher levels of overall life expectancy). It should be noted that while smoking is used here as the example, the need in principle to refocus policy change ‘upstream’ toward the fundamental causes, if health inequalities are to be reduced, would apply to all health inequality determinants and outcomes. References 1 Phelan JC, Link BG et al. “Fundamental Causes” of social inequalities in mortality: a test of the theory. Journal of Health and Social Behavior 2004, 45, 265–285 Competing interests: None declared |
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Ken Judge, Professor & Head, School for Health University of Bath, BA2 7AY
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Gruer at al's analysis of the impact of smoking on long- term survival by social position has encouraged Scott- Samuel (1) to suggest that smoking cessation may have no long term impact on health inequalities. This view appears to be based on the fact that inequalities in long-term survival between social classes is greater among never smokers than current smokers. For example, using the data in Table 5 of the published paper, the absolute rate gap (ARG) and the relative rate ratio (RRR) between social classes I & II and IV & V are consistently greater for never smokers than current smokers for both men and women. However, when a different measure of social position is used a more mixed picture emerges. Table 5 in the supplementary tables provided by Gruer et al compares long-term survival by smoking status and gender by deprivation category of residence rather than social class. Using these data, the ARG and the RRR between deprivation categories 1 & 3 and 6 & 7 are both greater for current smokers than never smokers among women. Using the same basis for comparison, the ARG for men is lower but the RRR is higher. These differences in the pattern of health inequalities that emerge across different measures of social position suggest that one should be cautious in drawing strong conclusions from the paper by Gruer et al about the wider implications for health inequality policy. References 1 Scott-Samuel A. What the Renfrew/Paisley data really tell us about tackling health inequalities: the need to focus upstream. BMJ, letters, 28 February 2009. Competing interests: None declared |
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Les O. Simpson, retired experimental pathologist Dunedin, New Zealand 9077
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In 1975, Leopold Dintenfass (1)reported that cigarette smokers aged between 45 and 55 years had, "...elevated haematocrit values, fibrinogen levels and blood viscosity." Those observations have been confirmed by many others on an international basis. Such changes in blood rheology have been linked to cardiovascular and cerebrovascular morbidity. In addition the aging process is asssociated with increased blood viscosity and elevated levels of fibrinogen and those changes would be additive to the changes in blood rheology associated with cigarette smoking. High dietary intakes of saturated fats, as in junk foods would add to the blood viscosity burden, but this would have a smaller contribution in the higher social classes. Galea and Davidson (2) in 1985 reported that after 2 weeks of not smoking, whole blood viscosity and carboxyhaemoglobin levels had improved significantly. Similar findings were reported in 1987 by Ernst and Matrai (3) who reported that after abstaining from smoking for 8 weeks, "...chronic cigarette smokers show a gradual normalisation of blood and plasma viscosity, haematocrit, blood cell filterability, plasma fibrinogen levels as well as total white cell count." Such observations indicate that the mortality associated with smoking is a consequence of the major blood rheology factors, increased blood viscosity and reduced red cell deformability. As it is possible to use agents such as prostaglandin E1, or fish oil or pentoxifylline to lower blood viscosity and increase red cell deformability, this raises a question about the ethics of following a group for 28 years without attempting to modify the consequences of a potentially lethal lifestyle. Therefore it would have been possible to predict the general outcome (but not the detail) of the Gruer et al report on the basis of the haemorheogical changes which are known to occur with smoking and in the aging process. References. 1. Dintenfass L. Elevation of blood viscosity, aggregation of red cells, haematocrit values and fibrinogen levels with cigarette smokers. Med J Aust 1975; 1:617-20. 2. Galea G, Davidson RJ. Haematological and haemorheological changes associated with cigarette smoking. J Clin Pathol 1985; 38: 978-84. 3. Ernst E, Matrai A. Abstention from chronic cigarette smoking normalizes blood rheology. Atherosclerosis 1987; 64:75-7. Competing interests: None declared |
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Alain Braillon, Public Health 80000 Amiens FRANCE
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The Organisation for Economic Co-operation and Development (OECD) has just published a 55 pages report (where the word “smoking” appears only once) relating health inequalities to socioeconomic inequalities.1 The conclusion offers no projection towards the future but new indicators to collect, feeding the data’s graveyard. Gruer et al showed that smoking is a greater source of health inequality than social position adding evidence to obviousness.2 Indeed, smoking is the top killer, more than half the people who keep smoking will die because of it. OECD and World Health Organisation must act. 1 Gruer L, Hart CL, Gordon DS, Watt GCM. Effect of tobacco smoking on survival of men and women by social position: a 28 year cohort study. BMJ 2009; 338: b480 2 de Looper M, Lafortune G. Measuring and monitoring disparities in health status, and in health care access and use. OECD 09- Mar-2009. avalaible at :http://www.olis.oecd.org/olis/2009doc.nsf/LinkTo/NT00000DE2/$FILE/JT03260782.PDF Competing interests: None declared |
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