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Uffe Ravnskov Magle Stora Kyrkogata 9, S-22350, Lund, Sweden
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Mann, Skeaff and Truswell,1 and Hu, Sacks and Willett2 list a number of shortcomings in the trials, reviewed by Hooper et al.,3 that explain why the dietary treatments were ineffective. No doubt, inferior studies with negative results are prevalent, but where is the positive evidence that justifies the dietary recommendations? Mann, Skeaff and Truswell point to the improved outcome in the subgroup analysis of the five prolonged trials. But in that analysis Hooper et al. excluded the Sydney diet-heart study, where total mortality was significantly increased, and included the Veterans Administration Trial, that was biased by a significant higher number of heavy smokers in the control group. Mann, Skeaff and Truswell also claim that there is “an enormous body of descriptive epidemiology, which supports the link between dietary fat, cholesterol, and coronary heart disease”. There is nothing of the kind; the accumulated epidemiology strongly contradicts such a link. Let me give a few examples from a systematic review.4 In a study of Japanese migrants in the US the cultural upbringing was the strongest predictor of coronary heart disease. Indeed, those who were brought up in a non-Japanese fashion but preferred the lean Japanese food had almost twice as often a heart attack compared with those who were brought up in the Japanese way but preferred the fat American food.4 Masai people probably have the highest intake of animal fat in the world. However, electrocardiographic abnormalities were far less frequent than in Americans and raised atherosclerotic lesions were rare.4 Coronary mortality in southern India was seven times higher than in the north and the age at death 44 against 52, although people in the north ate 19 times more fat, mostly animal fat, and also smoked much more.4 In 30 of 103 time periods in 33 countries fat intake increased along with coronary mortality, but in 33 periods where the intake also increased, coronary mortality was unchanged in ten and decreased in 23.4 In six case-control studies the diet of the coronary patients did not differ significantly from that of the control individuals.4 In 21 cohort studies including more than 150,000 individuals with and without coronary heart disease no study found an eating pattern in accordance with the current view on the influence of dietary fat.4 Hu, Sacks and Willett have published several studies with similar findings. But just as is the case with Hooper et al.s analysis, these findings and many other contradictions are always explained away with more or less valid arguments. As Karl Popper would have said: the diet-heart idea is unfalsifiable and should therefore be classified as non-science. 1. Mann J, Skeaff M, Truswell S. Dietary fats and prevention of cardiovascular disease. Conclusions may have been underplayed. BMJ 2001;323:1000 . [Full text] 2. Hu FB, Sacks F, Willett WC. Dietary fats and prevention of cardiovascular disease. Patient compliance should have been considered. BMJ 2001;323:1000. . [Full text] 3. Hooper L, Summerbell CD, Higgins JPT, Thompson R, Capps NE, Davey Smith G, et al. Dietary fat intake and prevention of cardiovascular disease: systematic review. BMJ 2001; 322: 757-763. [Abstract/Full Text]. 4. Ravnskov U. The questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease. J Clin Epidemiol 1998;51:443-60 [Abstract] |
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Barry Groves, Author Home
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Editor In their reply to letters at BMJ 2001;323:1000, Hooper et al say that "raised blood concentrations of cholesterol are associated with increased risk of stroke". However, studies in Japan (1-3) and the Multiple Risk Factor Intervention Trial (4) do not support this contention. A meta analysis of RCTs to look at the effects of lowering serum cholesterol on diseases other than coronary heart disease found increased risk of fatal stroke (13 trials) although these were slightly mitigated by a reduced risk of non-fatal strokes (8 trials).(5) And in a review of cholesterol- lowering RCTs that included more than 36,000 individuals, while mean reductions in cholesterol levels ranged from 6% to 23%, there were no significant reductions in either fatal or non-fatal strokes.(6) Going in hand with this, dietary interventions that concentrate on lowering fat intake while increasing dietary carbohydrates have been demonstrated to increase, rather than reduce, cardiovascular diseases.(7, 8) Yours faithfully Barry Groves
References: 1. Shimamoto T, Komachi Y, Inada H, Doi M, Iso H, Sato S et al. Trends for coronary heart disease and stroke and their risk factors in Japan. Circulation 1989;79:503-15. 2. Ueshima H, Tatara K, Asakura S, Okamoto M. Declining trends in blood pressure level and the prevalence of hypertension, and changes in related risk factors in Japan. J Chronic Dis 1987;40:137-147. 3. Kodama K Shimizu Y, Sawada H, Kato H. Incidence of stroke and coronary heart disease in the Adult Health Study sample 1958-1978. RERF Tech Rep 1984;22:1-22. 4. Iso H Jacobs DR Jr, Wentwoth D, Neaton J, Cohen J. Relationship of serum cholesterol to risk of different types of stroke. (Abstract) The 28th Conference on Cardiovascular Disease Epidemiology. CVD Epidemiol Newsletter 1988;43:40 5. Atkins D, Psaty BM, Koepsell TD, Longstreth WT, Larson EB. Cholesterol reduction and the risk of stroke in men. A meta-analysis of randomized, controlled trials. Ann Int Med 1993;119:136-45. 6. Hebert PR, Gaziano JM, Hennekens CH. An overview of trials of cholesterol lowering and risk of stroke. Arch Intern Med 1995;155:50-55. 7. J Jeppeson, et al. Effects of low-fat, high-carbohydrate diets on risk factors for ischemic heart disease in postmenopausal women. Am J Clin Nutr 1997; 65: 1027-33 8. F Abbasi, et al. High carbohydrate diets, triglyceride-rich lipoproteins and coronary heart disease risk. Am J Cardiol 2000; 85: 45- 48. |
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