This is a contribution from a member of THINCS,
The International Network of Cholesterol Skeptics


Letter to the editor of JAMA as a comment to  a paper by Hu FB and Willett WC. Optimal diets for prevention of coronary heart disease. Jama 2002;288:2569-78 sent on Jan 22, 2003.

No evidence that dietary cholesterol or saturated fat has importance for cardiovascular disease.
     I agree with Dr. Hu and Professor Willett1 that dietary recommendations should be based on the results from controlled and randomised clinical trials, not on surrogate endpoints such as lipid levels. But then, why do the authors themselves argue with such results?
     I also agree that there is no scientific evidence that dietary cholesterol has any importance; this has been shown in many previous studies also.2 Considering the widespread fear of dietary cholesterol the authors should have put more stress on that finding, not even mentioned in the abstract of their paper.
     What I disagree about is the demonising of the saturated fatty acids (SFA). Hu and Willett claim that two of the nine cohort studies found an increased coronary risk associated with an overconsumption of SFA. But in one of them3 the significance disappeared after correction for other fatty acids, and they did not mention either that in one of the other cohort studies a low consumption of SFA was significantly associated with a higher risk of coronary disease.4
     There is no support from the dietary trials either. The multifactorial Oslo study cannot be used as an argument, because we do not know, whether it was the reduction of the smoking habits, the difference in body weight (6-7 kg), or the reduction of SFA that were of benefit. That leaves us with three trials where SFA was reduced, the Dayton trial (10 cal% vs. 17 cal%), the Minnesota trial (9.2 cal% vs. 18.3 cal%) and the Lorgeril trial (8.3 cal% vs. 11.7 cal%). In the latter total and CVD mortality was lowered significantly, but which of the dietary measures that was of benefit is unknown. It is doubtful that it was the decrease of dietary SFA because it was only a small dedcrease and blood cholesterol was identical in the two groups. In the Dayton trial total mortality was unchanged and coronary mortality decreased nonsignificantly; and in the Minnesota trial coronary and total mortality increased nonsignificantly. Furthermore, the authors had excluded Woodhill et al.s trial (9.8 cal% vs 13.5 cal%) where total and coronary mortality increased nonsignificantly.5 These findings are in accordance with two previous meta-analyses of all controlled, randomised, unifactorial dietary trials, showing no effect, neither on coronary or total mortality.6,7

Uffe Ravnskov, MD, PhD
Magle Stora Kyrkogata 9
S-22350 Lund, Sweden

  1. Hu FB, Willett WC. Optimal diets for prevention of coronary heart disease. JAMA 2002;288:2569-2578.
  2. Ravnskov U. A hypothesis out-of-date: The diet-heart idea. J Clin Epidemiol 2002;55:1064-1072.
  3. Hu FB, Stampfer MJ, Manson JE, et al. Dietary saturated fats and their food sources in relation to the risk of coronary heart disease in women. Am J Clin Nutr 1999;70:1001-1008.
  4. Pietinen P, Ascherio A, Korhonen P, et al. Intake of fatty acids and risk of coronary heart disease in a cohort of Finnish men. The alpha-tocopherol, beta-carotene cancer prevention study. Am J Epidemiol 1997;145:876-887.
  5. Woodhill JM, Palmer AJ, Leelarthaepin B, McGilchrist C, Blacket RB. Adv Exp Med Biol 1978;109:317-330.
  6. Ravnskov U. The questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease. J Clin Epidemiol 1998;51:443-460.
  7. Hooper L, Summerbell CD, Higgins JPT, et al. Dietary fat intake and prevention of cardiovascular disease: systematic review. BMJ 2001;322:757-763

Edotor´s answer:

February 14, 2003

Uffe Ravnskov, MD, PhD
Magle Stora Kyrkogata 9
S-22350 Lund,
RE: Letter # JLE30142
Dear Dr Ravnskov:
Thank you for your recent letter to the editor. Unfortunately, in view of the many submissions we receive and our space limitations in the Letters section, we are unable to publish your letter in THE JOURNAL.
After considering the opinions of our editorial staff, we determined your letter did not receive a high enough priority rating for publication in JAMA. We are able to publish only a small fraction of the several thousand letters submitted to us each year, which means that published letters must have an extremely high rating.
However, we are forwarding a copy of your letter to the author of the article. The author may or may not reply to you personally. We do appreciate your taking time to write to us and thank you for the opportunity to look at your letter.
Stephen J. Lurie, MD, PhD
Senior Editor, JAMA