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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)
References
1. Pedersen JI, James PT, Brouwer IA et al. (2011) The importance of reducing SFA to limit CHD. Br J Nutr
doi:10.1017/S000711451100506X
2. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. (2010) Meta-analysis of prospective cohort studies evaluating
the association of saturated fat with cardiovascular disease. Am J Clin Nutr 91, 535-546.
3. Takeya Y, Popper JS, Shimizu Y et al. (1984) Epidemiologic studies of coronary heart disease and stroke
in Japanese men living in Japan, Hawaii and California: incidence of stroke in Japan and Hawaii. Stroke 15,
15-23.
4. McGee D, Reed D, Stemmerman G et al. (1985) The relationship of dietary fat and cholesterol to mortality
in 10 years: the Honolulu Heart Program. Int J Epidemiol 14, 97-105.
5. Gillman MW, Cupples LA, Millen BE et al. (1997) Inverse association of dietary fat with development of
ischemic stroke in men. JAMA 278, 2145-2150.
6. Seino F, Date C, Nakayama T et al. (1997) Dietary lipids and Incidence of cerebral infarction in a Japanese
rural community. J Nutr Sci Vitaminol 43, 83-99.
7. Iso H, Stampfer MJ, Manson JE et al. (2001) Prospective study of fat and protein intake and risk of intra-
parenchymal hemorrhage in women. Circulation 103, 856-863.
8. Iso H, Sato S, Kitamura A et al. (2003) Fat and protein intakes and risk of intraparenchymal hemorrhage
among middle-aged Japanese. Am J Epidemiol 157, 32-39.
9. Mann GV, Spoerry A, Gary M et al. (1972) Atherosclerosis in the Masai. Am J Epidemiol 95, 26-37.
10. Renaud S, de Lorgeril M. (1992) Wine, alcohol, platelets, and the French paradox for coronary heart disease.
Lancet 339, 1523-1526.
11. Stout C, Marrow J, Brandt EN Jr, Wolf S. (1964) Unusually Low Incidence of Death From Myocardial Infarction.
Study of an Italian American Community in Pennsylvania JAMA 188, 845-849.
12. Prior IA, Davidson F, Salmond CE, Czochanska Z. (1981) Cholesterol, coconuts, and diet on Polynesian
atolls: a natural experiment: the Pukapuka and Tokelau island studies. Am J Clin Nutr 34, 1552-1561.
13. Salonen JT, Puska P, Mustaniemi H (1979) Changes in morbidity and mortality during comprehensive
community programme to control cardiovascular diseases during 1972-7 in North Karelia. BMJ 2, 1178-1183.
14. Samuelson G, Bratteby LE, Mohsen R, Vessby B (2001) Dietary fat intake in healthy adolescents: inverse
relationships between the estimated intake of saturated fatty acids and serum cholesterol. Br J Nutr 85:333-
341.
15. Kark JD, Kaufmann NA, Binka F et al. (2003) Adipose tissue n-6 fatty acids and acute myocardial infarction
in a population consuming a diet high in polyunsaturated fatty acids. Am J Clin Nutr 77:796-802.
16. Scott RF, Daoud AS, Gittelsohn A et al. (1962) Lack of correlation between fatty acid patterns in adipose
tissue and amount of coronary arteriosclerosis. Am J Clin Nutr 10, 250-256.
17. Lang PD, Degott M, Heuck CC et al. (1982) Fatty acid composition of adipose tissue, blood, lipids, and
glucose tolerance in patients with different degrees of angiographically documented coronary arteriosclerosis.
Res Exp Med 180, 161-168.
18. Wood DA, Butler S, Riemersma RA et al. (1984) Adipose tissue and platelet fatty acids and coronary heart
disease in Scottish men. Lancet 2, 117-121.
19. Pedersen JI, Ringstad J, Almendingen K et al. (2000) Adipose tissue fatty acids and risk of myocardial
infarction–a case-control study. Eur J Clin Nutr 54, 618-625.
20. Yli-Jama P, Meyer HE, Ringstad J, Pedersen JI (2002). Serum free fatty acid pattern and risk of myocardial
infarction: a case-control study. J Intern Med 251, 19-28.
21. Clifton PM, Keogh JB, Noakes M (2004) Trans fatty acids in adipose tissue and the food supply are associated
with myocardial infarction. J Nutr 134, 874-879.
22. Smedman AE, Gustafsson IB, Berglund LG, Vessby BO (1999) Pentadecanoic acid in serum as a marker for
intake of milk fat: relations between intake of milk fat and metabolic risk factors. Am J Clin Nutr 69, 22-29.
23. Wolk A, Furuheim M, Vessby B (2001) Fatty acid composition of adipose tissue and serum lipids are valid
biological markers of dairy fat intake in men. J Nutr 131, 828-833.
24. Rosell M, Johansson G, Berglund L et al. (2004) Associations between the intake of dairy fat and calcium
and abdominal obesity. Int J Obes Relat Metab Disord 28,1427-1434.
25. Brevik A, Veierod MB, Drevon CA, Andersen LF (2005) Evaluation of the odd fatty acids 15:0 and 17:0 in
serum and adipose tissue as markers of intake of milk and dairy fat. Eur J Clin Nutr 59, 1417-1422.
26. Elwood PC, Pickering JE, Givens DI et al. (2010) The consumption of milk and dairy foods and the incidence
of vascular disease and diabetes: an overview of the evidence. Lipids 45, 925-939.
27. Ravnskov U (1998) The questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease.
J Clin Epidemiol 51, 443-460.
28. Rose GA, Thomson WB, Williams RT (1965) Corn oil in treatment of ischemic heart disease. BMJ 1, 1531-1533
29. Woodhill JM, Palmer AJ, Leelarthaepin B et al. (1978) Adv Exp Med Biol 109 317-330.
30. Watts GF, Lewis B, Brunt JN, Lewis ES, Coltart DJ, et al. (1992) Effects on coronary artery disease of lipid-
lowering diet, or diet plus cholestyramine, in the St Thomas’ Atherosclerosis Regression Study (STARS).
Lancet 339: 563–569.
31. Turpeinen O, Karvonen MJ, Pekkarinen M et al. (1979) Dietary prevention of coronary heart disease: the
Finnish Mental Hospital Study. Int J Epidemiol 8: 99–118.
32. Multiple Risk Factor Intervention Trial Research Group. Multiple risk factor intervention trial. (1982) Risk factor
changes and mortality results. JAMA 248:1465-1477.
33. Miettinen TA, Huttunen JK, Naukkarinen V. (1985) Multifactorial primary prevention of cardiovascular diseases
in middle-aged men. Risk factor changes, incidence, and mortality. JAMA, 254, 2097-2102.
34. World Health Organization European Collaborative Group. (1986) European collaborative trial of multifactorial
prevention of coronary heart disease: final report on the 6-year results. Lancet 1, 869-872.
35. Dam H, Søndergaard E (1962). The encephalomalacia producing effects of arachidonic and linoleic acids. Z
Ernahrungswiss 2, 217-222.
36. Pinckney ER (1973) The potential toxicity of excessive polyunsaturates. Do not let the patient harm himself.
Am Heart J 85, 723-726.
37. West CE, Redgrave TG (1974) Reservations on the use of polyunsaturated fats in human nutrition. Search 5,
90-95.
38. McHugh MI, Wilkinson R, Elliott RW et al. (1977) Transplantation 24, 263-267.
39. Simonsen N, van´t Veer P, Strain JJ et al. (1998) Adipose tissue omega-3 and omega-6 fatty acid content
and breast cancer in the EURAMIC study. Am J Epidemiol 147, 342-352.
40. Clausen T, Slott M, Solvoll K et al. (2001) High intake of energy, sucrose, and polyunsaturated fatty acids is
associated with increased risk of preeclampsia. Am J Obstet Gynecol 185, 451-458.
41. Leitzmann MF, Stampfer MJ, Michaud DS et al. (2004) Dietary intake of n-3 and n-6 fatty acids and the risk
of prostate cancer. Am J Clin Nutr 80, 204-216.
42. Yam D, Eliraz A, Berry EM. (1996) Diet and disease–the Israeli paradox: possible dangers of a high omega-6
polyunsaturated fatty acid diet. Isr J Med Sci 32, 1134-1143.
43. Oddy WH, de Klerk NH, Kendall GE et al. (2004) Ratio of omega-6 to omega-3 fatty acids and childhood asthma.
J Asthma 41, 319-326.
44. Weinberg SL. (2004) The diet-heart hypothesis: A critique. J Amer Coll Cardiol 43:731-733.
45. German JB, Dillard CJ. (2004) Saturated fats: what dietary intake? Am J Clin Nutr 80, 550-559.
46. Volek JS, Forsythe CE. (2005) The case for not restricting saturated fat on a low carbohydrate diet. Nutr Metab
doi:10.1186/1743-7075-2-21.
47. Kuipers RS, de Graaf DJ, Luxwolda MF et al. (2011) Saturated fat, carbohydrates and cardiovascular disease.
Neth J Med 69, 372-8
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