Just got the December issue of the American Journal of Clinical Nutrition (AJCN), which prints a letter debate on the harmful effects (or lack thereof) of saturated fats. I’m going to print the debate in its entirety below so that you can listen in. I want to you see first hand the narrow mindedness of a true believer of the lipid hypothesis.

The inspiration for this debate came from an editorial written by Martijn Katan about a paper published last May by Ronald Krauss and his group. (I wrote a fairly extensive post on this same paper as soon as it came out.) Katan is a fervent advocate of the lipid hypothesis who writes editorials espousing it whenever he gets the chance. Since these editorials seem always to advance the same issues despite any evidence to the contrary I’ve begun referring to them as the Katanic Verses.

A taste of this (typical) Katanic Verse:

This study is valuable because it extends our knowledge of dietary protein and blood lipids. Evidently, proteins lack the triacylglycerol-elevating effect of carbohydrates. However, lipoproteins are now a less pressing problem than is obesity. Low-fat, high-carbohydrate diets have failed to produce long-term weight loss, but we should not be overly optimistic about the alternatives. Obesity is a societal disease caused by an overabundance of food and mechanization, and diets high in protein or fat are unlikely to reverse the trend. We also do not know whether the consumption of large amounts of protein is safe for the kidneys and bones; trials to determine this are urgently needed. We have a way to go before we know as much about protein as we do about unsaturated fats. Clinical trials have shown that high intakes of unsaturated fatty acids reduce the risk of heart attacks, a finding that is consistent with their favorable effects on lipoproteins and with the inverse associations between unsaturated fat intake and heart disease. In comparison, the evidence that high-protein diets prevent heart disease is still slim.

Dr. Uffe Ravnskov wrote a letter to the editor of the AJCN about this editorial and the article to which it referred. Before we get to the actual letters, let me tee up the informal ground rules for such letter exchanges in academic journals. Typically it goes this way: Professor A publishes a paper. Professor B has a question or takes exception to a conclusion that Professor A has drawn. Professor B writes a letter to the editor of the journal saying something along the lines of: I read Professor A’s paper with great interest and wondered if he had considered blah blah blah. Professor A responds to Professor B’s letter by saying: I appreciate Professor B bringing this to my attention. What I perhaps didn’t make clear was blah blah blah. It’s all very clubby and congenial.

Dr. Ravskov’s letter is in such a congenial spirit.

LETTER TO THE EDITOR

Saturated fat does not affect blood cholesterol

Uffe Ravnskov
Magle Stora Kyrkogata 9
S-22350 Lund
Sweden

Dear Sir:

The most striking observation from the study by Krauss et al (1) is the finding that a diet rich in saturated fatty acids (SFAs)results in a lower or a steady state concentration of total and LDL cholesterol and an increase in the concentration of HDL cholesterol, regardless of whether the diet has a reduced energy content. Similar effects on blood lipids have been observed in 4 weight-reducing trials with high intakes of SFAs (2-5)(Table 1) and in many similar trials with unrestricted intakes of SFAs.

[Table 1 goes here. I don't have enough technical know-how to copy it from the paper. It is a summary of the above references 2-5 presenting data showing the lack of cholesterol elevation brought about by dietary saturated fat in doses of up to 50 percent of calories consumed.]

In 1973, Reiser (6) questioned the effects of SFA intake on serum cholesterol. In a thorough review of the relevant experiments, he noted several methodologic and interpretational errors. The most important errors are probably the attribution of differences between SFAs and polyunsaturated fatty acids to the former, when the effect could have been due to the latter, and the use of vegetable oils saturated by hydrogenation instead of natural SFAs.

A possible reason why the effects were more pronounced before weight reduction than after weight reduction in the study by Krauss et al was the difference in metabolism between the normal-weight and overweight subjects. Cornier et al (7) recently found that total and LDL-cholesterol concentrations decreased more with a low-carbohydrate than with a low-fat, calorie-restricted diet. Interestingly, the overweight subjects with reduced insulin sensitivity, but not those with normal insulin sensitivity, had an increase in cholesterol with the low-fat diet but a decrease with the low-carbohydrate diet. In both groups, the changes in lipids were more beneficial with a low-carbohydrate diet than with a low-fat diet. Therefore, the different lipid responses before and after weight reduction in the study by Krauss et al may have been because the loss of weight may have improved the participants’ insulin sensitivity and thus their lipid response.

Because the main reason for restricting the intake of SFAs in all official guidelines is to change blood lipids, demonizing these nutrients seems inappropriate. In his editorial, Katan (8) claims that high intakes of unsaturated fatty acids reduce the risk of heart attacks, but his evidence is based on a meta-analysis that had ignored 4 unsuccessful trials (9). Two meta-analyses of all controlled clinical trials in which the only intervention was a change in dietary fats found no effect on coronary or total mortality (10).

ACKNOWLEDGMENTS

The author had no vested interest in the subject of this letter.

REFERENCES

1. Krauss RM, Blanche PJ, Rawlings RS, Fernstrom HS, Williams PT. Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia. Am J Clin Nutr 2006;83:1025–31.
2. Sondike SB, Copperman N, Jacobson MS. Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factor in overweight adolescents. J Pediatr 2003;142:253–8.
3. Hays JH, DiSabatino A, Gorman RT, Vincent S, Stillabower ME. Effect of a high saturated fat and no-starch diet on serum lipid subfractions in patients with documented atherosclerotic cardiovascular disease. Mayo Clin Proc 2003;78:1331–6.
4. Meckling KA, O’Sullivan C, Saari D. Comparison of a low-fat diet to a low-carbohydrate diet on weight loss, body composition, and risk factors for diabetes and cardiovascular disease in free-living, overweight men and women. J Clin Endocrinol Metab 2004;89:2717–23.
5. Sharman MJ, Gomez AL, Kraemer WJ, Volek JS. Very low-carbohydrate and low-fat diets affect fasting lipids and postprandial lipemia differently in overweight men. J Nutr 2004;134:880–5.
6. Reiser R. Saturated fat in the diet and serum cholesterol concentration: a critical examination of the literature. Am J Clin Nutr 1973;26:524–55.
7. Cornier MA, Donahoo WT, Pereira R, et al. Insulin sensitivity determines the effectiveness of dietary macronutrient composition on weight loss in obese women. Obes Res 2005;13:703–9.
8. Katan MB. Alternatives to low-fat diets. Am J Clin Nutr 2006;83:989–90.
9. Ravnskov U. The diet-heart idea is kept alive by selective citation. Rapid response. BMJ 8. December 2003.
10. Ravnskov U. Diet-heart disease hypothesis is wishful thinking. BMJ 2002;324:238.

The letter in response by Dr. Katan is the epitome of rudeness and non-collegiality. It is the standard in academic papers and letters to reference any categorical statements. Even if you say something generally accepted you do it. For example, if you wrote: ‘the incidence of obesity has risen greatly over the past 20 years in this country’ you would list a reference to one or more of the many papers showing such. If what you are saying is the least bit controversial, you always reference it. I’ll add my interjections to Dr. Katan’s response using brackets and italics.

LETTER TO THE EDITOR

Reply to U Ravnskov

Martijn B Katan
Vrije Universiteit
Faculty of Earth and Life Sciences Institute of Health Sciences
De Boelelaan 1085
1081 HV Amsterdam
Netherlands

Dear Sir:

Ravnskov’s suggestion that a reduction in the intake of saturated fat does not lower cholesterol is wrong. [Where is the citation?] At constant body weight, the replacement of saturated fat with other nutrients unequivocally lowers cholesterol concentrations; [citation?] all meta-analyses of controlled trials agree on this.[Citation?]

As for the effects of saturated fatty acids on heart disease, Ravnskov rightly notes that some clinical trials have failed to show that the replacement of saturated fat with unsaturated fat reduces heart disease. However, most clinical trials have shown a benefit. [Citation?] In addition, evidence from epidemiologic, metabolic, and laboratory studies confirms that high intakes of saturated fat do cause heart disease. [Citation?] Ignoring this evidence leads to absurd consequences. For instance, our knowledge of the ill effects of cigarette smoking rests purely on epidemiologic, metabolic, and laboratory studies, whereas evidence from clinical trials is largely lacking. The same holds true for the ill effects of physical inactivity, the failure to use seat belts, the consumption of toxic chemicals in foods, and asbestos exposure. None of these conditions has been proven to be unhealthy in clinical trials performed according to the standards for pharmaceutical drugs. I believe that, in all of these cases, we should consider the totality of the evidence, and the totality of the evidence overwhelmingly indicts saturated fat as a cause of heart disease, just as it indicts cigarettes. [If the totality of the evidence indicts heart disease, how come the Framingham data, the biggest study of all, shows no correlation. I would say that kind of blows the totality-of-the-data-overwhelmingly-indicts theory.]

Ravnskov has now published approximately 58 Letters to the Editor (1-58) that address publications about lipids and heart disease. His letters have been published in the Journal of the American Medical Association, the New England Journal of Medicine, the British Medical Journal, the Lancet, Science, Annals of Internal Medicine, the Journal of Clinical Epidemiology, the Quarterly Journal of Medicine, and several Scandinavian medical journals. All his letters have argued essentially the same point, namely that lowering blood cholesterol concentrations is of unproven value. I agree with the dozens of scientists who have carefully replied to his letters and who have shown that, by and large, his arguments are faulty. [The implication here is that scientists refute all of these 58 papers, which you'll find isn't the case if you read them.]

ACKNOWLEDGMENTS

The author had no conflict of interest.

REFERENCES

2. Ravnskov U, Rosch PJ, Sutter MC, Houston MC. Should we lower cholesterol as much as possible? BMJ 2006;332:1330–2.
2. Ravnskov U, Rosch PJ, Sutter MC. High-dose statins and the IDEAL study. JAMA 2006;295:2476, 2478–9.
3. Ravnskov U. [Misleading advice on cholesterol reduction.] Lakartidningen 2006;103:568, 569 (discussion).
4. Ravnskov U. [Treatment of hypercholesterolemia—lower is not better.] Ugeskr Laeger 2006;168:1665.
5. Understrup AG, Ravnskov S, Hansen HC, Fomsgaard IS. Biotransformation of 2-benzoxazolinone to 2-amino-(³H)-phenoxazin-3-one and 2-acetylamino-(³H)-phenoxazin-3-one in soil. J Chem Ecol 2005;31:1205–22.
6. Ravnskov U, Rosch PJ, Sutter MC. Intensive lipid lowering with atorvastatin in coronary disease. N Engl J Med 2005;353:93–6.
7. Ravnskov U. [Should cholesterol levels be reduced more aggressively?] Lakartidningen 2005;102:2583–4.
8. Ravnskov U. Europe in transition: dietary fat is not the villain. BMJ 2005;331:906–7.
9. Ravnskov U, Sutter MC. Aggressive lipid-lowering therapy and regression of coronary atheroma. JAMA 2004;292:38–40.
10. Ravnskov U. Inflammation, cholesterol levels, and risk of mortality among patients receiving dialysis. JAMA 2004;291:1833–5.
11. Ravnskov U. [High cholesterol level may protect against infections and probably also atherosclerosis.] Lakartidningen 2004;101:1215–7, 1218 (discussion), 1221–2.
12. Ravnskov U. [Hasty conclusions on cardiac mortality in Norway.] Tidsskr Nor Laegeforen 2004;124:2153.
13. Ravnskov U. [Karl Popper and the cholesterol hypothesis.] Tidsskr Nor Laegeforen 2004;124:2517.
14. Ravnskov U. ASCOT-LLA: questions about the benefits of atorvastatin. Lancet 2003;361:1986.
15. Ravnskov U. Lipoproteins and cardiovascular risk. Lancet 2003;361:1988–9./li>
16. Ravnskov U. [Too many calories and too little exercise cause obesity not intake of fat.] Lakartidningen 2003;100:3255–6.
17. Ravnskov U. High cholesterol may protect against infections and atherosclerosis. QJM 2003;96:927–34.
18. Ravnskov U. Dietary fat intake and risk of stroke: allegations about dietary fat are unfounded. BMJ 2003;327:1348.
19. Ravnskov U, Allen C, Atrens D, et al. Studies of dietary fat and heart disease. Science 2002;295:1464–6.
20. Ravnskov U. Diet-heart disease hypothesis is wishful thinking. BMJ 2002;324:238.
21. Ravnskov U. [Surrogate research on heart disease and risk factors.] Lakartidningen 2002;99:1507.
22. Ravnskov U. Is atherosclerosis caused by high cholesterol? QJM 2002;95:397–403.
23. Ravnskov U. [The debate in science: dietary guidelines against myocardial infarction are defended by wrong citations.] Lakartidningen 2002;99:2673.
24. Ravnskov U. A hypothesis out-of-date. the diet-heart idea. J Clin Epidemiol 2002;55:1057–63.
25. Ravnskov U. [Millions of healthy people can be considered ill because of the American cholesterol policy.] Lakartidningen 2001;98:4574–7.
26. Ravnskov U. [Lipid lowering doesn’t affect the development of atherosclerosis in peripheral artery disease.] Lakartidningen
27. Ravnskov U. Cholesterol and all-cause mortality in Honolulu. Lancet 2001;358:1907.
28. Ravnskov U. VAT and fat. Evidence is contradictory. BMJ 2000;320:1470.
29. Ravnskov U. [Misleading cholesterol statistics.] Lakartidningen 1999;96:1947.
30. Ravnskov U. Why heart disease mortality is low in France. Authors’ hypothesis is wrong. BMJ 1999;319:255–6.
31. Ravnskov U. [Experts ask for priorities when it comes to interpretation. Ravnskov answers in the debate on dietary fats.] Lakartidningen 1998;95:1022–3.
32. Ravnskov U. The questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease. J Clin Epidemiol 1998;51:443–60.
33. Ravnskov U. [Excellence of the "Mediterranean diet" is a myth. There is no evidence that monounsaturated fats prevent myocardial infarction.] Lakartidningen 1998;95:4749–50.
34. Ravnskov U. [On honesty and monounsaturated fat.] Lakartidningen 1998;95:4966.
35. Ravnskov U. [Do cholesterol-lowering drugs cause cancer?] Lakartidningen 1996;93:2040.
36. Ravnskov U. American College of Physicians guidelines on cholesterol screening. Ann Intern Med 1996;125:1010–1.
37. Ravnskov U. [Fatty acids and confusing signals.] Ugeskr Laeger 1995;157:1534–5.
38. Ravnskov U. Quotation bias in reviews of the diet-heart idea. J Clin Epidemiol 1995;48:713–9.
39. Ravnskov U. Implications of 4S evidence on baseline lipid levels. Lancet 1995;346:181.
40. Ravnskov U. Beneficial effects of simvastatin may be due to non-lipid actions. BMJ 1995;311:1436–7.
41. Ravnskov U. Hypercholesterolemia does not cause coronary heart disease–evidence from the nephrotic syndrome. Nephron 1994;66:356–9.
42. Ravnskov U. Ischaemic heart disease and cholesterol. Optimism about drug treatment is unjustified. BMJ 1994;308:103.
43. Ravnskov U. [Do polyunsaturated fats cause male sterility?] Lakartidningen 1994;91:2308.
44. Ravnskov U. [Uncritical review of articles on cholesterol.] Ugeskr Laeger 1994;156:4479–80.
45. Ravnskov U. Is intake of trans-fatty acids and saturated fat causal in coronary heart disease? Circulation 1994;90:2568–9.
46. Ravnskov U. Doing the right thing: stop worrying about cholesterol. Circulation 1994;90:2572–3.
47. Ravnskov U. What do angiographic changes after cholesterol lowering mean? Lancet 1994;344:1297.
48. Ravnskov U. [Doubtful advices on cholesterol screening in children.] Ugeskr Laeger 1993;155:1886–7.
49. Ravnskov U. Reducing serum cholesterol. Lower cholesterol of doubtful benefit to anyone. BMJ 1993;307:125.
50. Ravnskov U. [New trends from the USA. The cholesterol campaign is questioned.] Lakartidningen 1993;90:2528–9.
51. Ravnskov U. Coronary atherosclerosis on angiography—progress or regress, and why? Circulation 1993;88:1358–60.
52. Ravnskov U. [Decreased cholesterol level shortens life.] Ugeskr Laeger 1993;155:3679–80.
53. Ravnskov U. [Stop the cholesterol campaign!] Lakartidningen 1993;90:4587–8, 4589–90 (discussion).
54. Ravnskov U. [What is the correct answer in the cholesterol debate?] Ugeskr Laeger 1992;154:1716–8.
55. Ravnskov U. Cholesterol lowering trials in coronary heart disease: frequency of citation and outcome. BMJ 1992;305:15–9.
56. Ravnskov U. Frequency of citation and outcome of cholesterol lowering trials. BMJ 1992;305:717.
57. Ravnskov U. [Are polyunsaturated fats useful?] Lakartidningen 1991;88:1058.
58. Ravnskov U. An elevated serum cholesterol level is secondary, not causal, in coronary heart disease. Med Hypotheses 1991;36:238–41.

This letter, like Katan himself, is a nasty piece of work that shouldn’t be legitimized in the pages of a prestigious scientific journal. That it is speaks volumes to the notion that the editors are on board with Katan and his anti-saturated fat jihad. At least you can see what kind of bias need be overcome in presenting an opposing viewpoint to the lipid hypothesis.