Diet-heart disease hypothesis is wishful thinking
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Letters
Diet-heart disease hypothesis is wishful thinking
EDITOR
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?
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.
Uffe Ravnskov
Magle Stora Kyrkogata 9, S-22350, Lund,
Sweden
uffe.ravnskov@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 |
| 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 |
| 1: J Clin Epidemiol 1998 Jun;51(6):443-60 |
Related Articles,
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Comment in:
The questionable role of
saturated and polyunsaturated fatty acids in
cardiovascular disease.
Ravnskov U.
uffe.ravnskov@swipnet.se
A fat diet, rich in
saturated fatty acids (SFA) and low in
polyunsaturated fatty acids (PUFA), is said
to be an important cause of atherosclerosis
and cardiovascular diseases (CVD). The
evidence for this hypothesis was sought by
reviewing studies of the direct link between
dietary fats and atherosclerotic vascular
disease in human beings. The review included
ecological, dynamic population,
cross-sectional, cohort, and case-control
studies, as well as controlled, randomized
trials of the effect of fat reduction alone.
The positive ecological correlations between
national intakes of total fat (TF) and SFA
and cardiovascular mortality found in earlier
studies were absent or negative in the
larger, more recent studies. Secular trends
of national fat consumption and mortality
from coronary heart disease (CHD) in 18-35
countries (four studies) during different
time periods diverged from each other as
often as they coincided. In cross-sectional
studies of CHD and atherosclerosis, one group
of studies (Bantu people vs. Caucasians) were
supportive; six groups of studies (West
Indians vs. Americans, Japanese, and Japanese
migrants vs. Americans, Yemenite Jews vs.
Yemenite migrants; Seminole and Pima Indians
vs. Americans, Seven Countries) gave partly
supportive, partly contradictive results; in
seven groups of studies (Navajo Indians vs.
Americans; pure vegetarians vs. lacto-ovo-vegetarians
and non-vegetarians, Masai people vs.
Americans, Asiatic Indians vs. non-Indians,
north vs. south Indians, Indian migrants vs.
British residents, Geographic Study of
Atherosclerosis) the findings were
contradictory. Among 21 cohort studies of CHD
including 28 cohorts, CHD patients had eaten
significantly more SFA in three cohorts and
significantly less in one cohort than had
CHD-free individuals; in 22 cohorts no
significant difference was noted. In three
cohorts, CHD patients had eaten significantly
more PUFA, in 24 cohorts no significant
difference was noted. In three of four cohort
studies of atherosclerosis, the vascular
changes were unassociated with SFA or PUFA;
in one study they were inversely related to
TF. No significant differences in fat intake
were noted in six case-control studies of CVD
patients and CVD-free controls; and neither
total or CHD mortality were lowered in a
meta-analysis of nine controlled, randomized
dietary trials with substantial reductions of
dietary fats, in six trials combined with
addition of PUFA. The harmful effect of
dietary SFA and the protective effect of
dietary PUFA on atherosclerosis and CVD are
questioned.
Publication Types:
-
Review
-
Review, Academic
PMID: 9635993 [PubMed - indexed for MEDLINE]
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