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Salt and smoking: a role for interventional epidemiology?
The World Congress of Epidemiology was held in Bangkok at the end of August 2005 and presented a challenge to epidemiologists around the globe. The explicit objectives of the Congress were: to develop a new agenda for epidemiology in the 21st century; to move from a closed, inward looking field to a dynamic, outward looking one, relevant to equity in health; to encourage greater engagement of partners and people from Low and Middle Income Countries; to promote scientific discussions and regional common agendas; and to explore the possibility of linking the International Epidemiology Association (IEA) with other international partners to enhance the role of epidemiology towards equity in health for development. Epidemiologists are no strangers to examining the associations between markers of socioeconomic position and various health outcomes and postulating reasons for the gradients observed—the study of social inequalities in health. However, as was repeatedly observed by speakers at the Congress, epidemiologists tend to be much less engaged in the business of attempting to redress the avoidable injustice and unfairness—the health inequity—that exists throughout the world. Epidemiologists who belong to the IEA are a minority and to make progress with our objectives to raise the profile of ‘interventional’ epidemiology we need your involvement. Join the IEA, or at least go to a regional IEA meeting, and definitely do come to the next World Congress of Epidemiology that will be held in Porto Alegre, Brazil in 2008.
Severe dietary salt restriction causes blood pressure to fall—a first-year medical student experiment in which I was forced to endure the Kempner plain rice diet1 for a week demonstrated this to me directly. The most difficult part of the protocol was remembering to measure the volume of urine voided and to keep an aliquot for sodium assay. Our historic reprint is Dahl's 1960 paper on the role of salt intake in the development of essential hypertension.2 Making use of animal and human metabolic studies, and ecological population studies (but not Kempner's observations), he makes the case that groups consuming <5 g salt a day will have less hypertension than those consuming more salt. His graph correlating salt consumption and the proportion of hypertensives among Eskimos, Pacific Islanders, Americans, and people from northern and southern Japan demonstrates a very nice linear relationship. Paul Elliott, commenting on Dahl's work, traces the subsequent attempts to conduct larger ecological studies, culminating in the establishment of INTERSALT in 1982.3 Niels Graudal highlights Dahl's reliance on self-citation, uncontrolled observations, and his failure to cite earlier work. Graudal's group conducted an important systematic review and meta-analysis of the effects of dietary salt restriction for blood pressure reduction demonstrating the really rather small effect size of 1 mm Hg in systolic blood pressure achievable by dietary advice,4 a finding that remains robust in an updated systematic review,5 which includes the optimistic findings of DASH-sodium study, described at some length by Elliott. So after 100 years of research effort demonstrating the association between sodium and blood pressure, the blood pressure distributions of most populations remain stubbornly high, causing Graudal to ask whether it has all been worth the effort for an effect size of 1 mm Hg. In part this reflects two decades of reliance on misplaced individual clinical intervention for what is, of course, socially and culturally determined, and requires political action supported by interventionally minded epidemiologists.
Our theme in this issue is respiratory disease and smoking. Using the Norwegian twin study and structural equation modelling to examine genetic and environmental variance components, Nystad and colleagues have compared differences in aetiology among twins with disease diagnoses (asthma, hay fever, and eczema) with the respective symptoms (wheeze, sneezing, and itch).6 They find that genetic effects account for greater variation in diagnosed diseases than symptoms, with co-occurrence of both diseases and symptoms largely explained by genetic effects.
Using data from two cohorts of 1.6 million and 1.9 million New Zealanders, Hunt and colleagues examined trends in the smoking-mortality relative risk between 1981–84 and 1996–99 for ethnic groups, demonstrating a pattern of increasing relative risks over time, with the largest relative risks for non-Maori, non-Pacific men, after controlling for socioeconomic factors.7 The authors conclude that accurate definition of the tobacco-attributable mortality in a country requires up-to-date and ethnicity-specific data.
Also from the Pacific region, a new report on the effects of smoking and, importantly, quitting on cardiovascular disease risk has been produced by the Asia Pacific Cohort Studies Collaboration.8 Individual participant data from 40 cohort studies were pooled to give precise estimates of effects on coronary heart disease, haemorrhagic stroke, and ischaemic stroke. Perhaps surprisingly, an increased hazard ratio was found for haemorrhagic stroke, but no adjustment for alcohol consumption was possible, which may be responsible. Reductions in risk of 
20–30% were found in those who had stopped smoking, pointing to the importance of attempting to reduce and stop smoking in the very high proportions of people in the Asia-Pacific region who smoke. The data also debunk the notion that Asian men are less susceptible to the harmful effects of tobacco—a misbelief that gets in the way of effective health promotion.
References
1 Kempner W. Treatment of heart and kidney disease and of hypertensive and arteriosclerotic vascular disease with the rice diet. Ann Intern Med 1949;31:821–56.
2 Dahl LK. Possible role of salt intake in the development of essential hypertension. In: Cottier P, Bock KD (eds). Essential Hypertension—An International Symposium. Berlin: Springer, 1960, pp. 53–65. (Reprinted Int J Epidemiol 2005;34:967–72.)
3 Elliott P. Commentary: Role of salt intake in the development of high blood pressure. Int J Epidemiol 2005;34:975–78.
4 Graudal NA, Galloe A, Garrad P. Effects of sodium restriction on blood pressure, rennin, aldosterone, chatecholamines, cholesterols, and triglyceride. A meta-analysis. JAMA 1998;279:1383–91.
5 Hooper L, Bartlett C, Davey Smith G, Ebrahim S. Systematic review of long term effects of advice to reduce dietary salt in adults. BMJ 2002;325:628.
6 Nystad W, Roysamb E, Magnus P, Tambs K, Harris JR. A comparison of genetic and environmental variance structures for asthma, hay fever and eczema with symptoms of the same diseases: a study of Norwegian twins. Int J Epidemiol doi:10.1093/ije/dyi061.
7 Hunt D, Blakely T, Woodward A, Wilson N. The smoking–mortality association varies over time and by ethnicity in New Zealand. Int J Epidemiol 2005;34:1020–28.
8 Asia Pacific Cohort Studies Collaboration. Smoking, quitting and the risk of cardiovascular disease among women and men of the Asia-Pacific region. Int J Epidemiol 2005;34:1036–45.
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