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EDITOR Mann et al 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, which was
biased by a significant higher number of heavy smokers in the control group.
Mann et al also say that there is an enormous body of descriptive
epidemiology that supports the link between dietary fat, cholesterol
concentrations, and coronary heart disease. The accumulated epidemiology actually strongly contradicts such a link, as illustrated by a systematic review.4 In a study of Japanese migrants
in the United States the cultural upbringing was the strongest
predictor of coronary heart disease. Those who were brought up in a
non-Japanese fashion but preferred the lean Japanese food had a heart
attack almost twice as often as those who were brought up in the
Japanese way but preferred fatty American food.4
Masai people probably have the highest intake of animal fat in the
world, but abnormalities on electrocardiography were far less frequent
than in Americans and raised atherosclerotic lesions were
rare.4 Mortality from coronary heart disease in southern India was seven times higher than in the north and the age at death 44 years compared with 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 10 and decreased in
23.4 In six case-control studies the diet of the coronary
patients did not differ appreciably from that of the
controls.4 In 21 cohort studies including more than 150 000 participants 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 et al have published several studies with similar findings.
But just as is the case with the analysis by Hooper et al, 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 disease hypothesis is unfalsifiable and should therefore be
classified as non-science.
Mann et al and Hu et al list several shortcomings in the trials
reviewed by Hooper et al that explain why dietary treatments for
patients with coronary heart disease were ineffective.1-3 Inferior studies with negative results are prevalent, but where is the
positive evidence that justifies the dietary recommendations?
Magle Stora Kyrkogata 9, S-22350, Lund, Sweden
uffe.ravnskov{at}swipnet.se
| 1. |
Mann J, Skeaff M, Truswell S.
Dietary fats and prevention of cardiovascular disease.
BMJ
2001;
323:
1000 |
| 2. | Hu FB, Sacks F, Willett WC. Dietary fats and prevention of cardiovascular disease. BMJ 2001; 323: 1000. (27 October.) |
| 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 |
| 4. | Ravnskov U. The questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease. J Clin Epidemiol 1998; 51: 443-460[CrossRef][ISI][Medline]. |
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