BMJ 2008;337:a1681

British Journal of Nutrition (2012), 107, 455–457

Letter to the Editor

No scientific support for linking dietary saturated fat to CHD

(First published online 14 December 2011)

Uffe Ravnskov,
Magle Stora Kyrkogata 9. 22350 Lund, Sweden
email ravnskov@tele2.se

David Diamond
Departments of Psychology Molecular Pharmacology and Physiology.
Center for Preclinical and Clinical Research on PTSD.
J.A. Haley Veterans Hospital, University of South Florida.
Tampa, FL 33612, USA

M. Canan Efendigil Karatay.
Medical Faculty, Istanbul Science University.
Moda Cad 120 Kadikoy, Istanbul 34710, Turkey

Donald W. Miller
Division of Cardiothoracic Surgery. University of Washington School of Medicine
Seattle. WA USA

Harumi Okuyama
Open Research Center for Lipid Nutrition
Kinjo Gakuin University, Nagoya, Japan

doi:10.1017/S000711451100660X

Pedersen et al.(1) express concern that recently published research had downplayed the importance of SFA
consumption as a risk factor for CHD.(2) Their main argument is that prospective cohort studies are unreliable.
There are of course uncertainties in such studies, but it is difficult to ignore that more than thirty cohort studies
have shown that patients with cardiovascular disease did not eat more SFA than had heart-healthy people; in six
of them(3-8) stroke patients had actually eaten less.
To make their case, Pedersen et al. presented a small and biased subset of ecologic studies apparently
linking reduced consumption of SFA to a low incidence of CHD. However, they neglected to mention the many
ecological studies that have documented findings from groups with a high consumption of SFA, but with low
rates of  CHD, including Masai people,(9) French,(10) Italian-Americans,(11) and Polynesians.(12)  They also
claim that the association  between the decline of CHD     mortality in Finland and the lowered intake of SFA
was causal. However, the decline began in North Karelia three years before the start of the cholesterol campaign,
and it occurred also in the districts where no advice was given.(13)
    Pedersen et al. asserted that SFA with 12-16 carbon atoms are the most potent LDL and total-cholesterol-
raising fatty acids. However, other researchers reported that the serum content of these fatty acids is inversely
associated with serum cholesterol,(14) and in seven studies, two of which had Pedersen as author or co-author,
the content of C12:0-C16:0 in the blood or the fat cells was similar or lower in patients with acute CHD than in
healthy people.(15-21) The number of short-chain SFA in the serum reflects the intake of dairy fat,(22,23) and such
intake is inversely associated with BMI, waist circumference, LDL/HDL ratio and fasting glucose concentration,
and positively associated with HDL and apolipoprotein A-I. (22-25) In accordance, a meta-analysis of twenty-five
cohort studies showed that the lowest total mortality, cardiovascular incidence and mortality, and incidence of
diabetes were seen among those with the highest intake of dairy fat.(26)
Pedersen et al. endorse the many reports emphasising the importance of increasing the intake of PUFA. This
advice is not based on randomised, controlled dietary trials, because no such trial has ever succeeded in lowering
cardiovascular or total mortality by exchanging SFA with PUFA.(27) Rather, the advice is based on statistical
calculations using data from unreliable cohort studies. Pedersen et al. refer to a meta-analysis of such trials (ref 9),
the authors of which claimed benefit, but they had excluded two trials, where CHD mortality had increased in the
treatment groups,(28,29) and included a trial, where a decreased risk was seen only in the participants who
increased their intake of fish,(30) and also the Finnish Mental Hospital Study,(31) a trial which does not satisfy
the quality criteria for a correctly performed randomised  controlled trial.  A reduction of SFA was part of the
intervention in three multifactorial trials, but these trials were unsuccessful as well;(32-34) in one of them, total
mortality was twice as high in the treatment group.(33)
Numerous studies on laboratory animals and human subjects have also shown that an increased intake of PUFA,
in particular of the n-6 type, is associated with many adverse health effects such as allergy, asthma, immuno-
suppression, decreased fertility, pre-eclampsia, encephalopathy and cancer.(35-41) In accordance with this, Israeli
Jews have a high intake of the recommended n-6 type of PUFA (from grains and soybean oil) and they exhibit a
high incidence of cancer and CHD mortality compared with other western countries.(42)
     In conclusion, Pederson et al. do not provide sufficient evidence to implicate SFA in CHD risk. There is
increasingly strong evidence that SFA are not involved.(2,28,43-46)

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