Correspondence

More on Low-Fat Diets

N Engl J Med 1998; 338:1623-1624May 28, 1998

Article

To the Editor:

Winston Churchill's tribute to the Royal Air Force in the House of Commons (“Never in the field of human conflict was so much owed by so many to so few”) could be paraphrased to apply to the Lifestyle Heart Trial (“Rarely have so many conclusions been based on so few subjects”), as discussed in the recent correspondence on low-fat diets (Jan. 8 issue).1 In this study, 94 patients were randomly assigned to the intervention group (53 patients) or the control group (43 patients).2 Only 28 intervention and 20 control patients agreed to participate. One control patient and 6 intervention patients did not have usable repeat angiograms, including 1 intervention patient who died while exercising, leaving results for only 22 treatment patients and 19 controls. Intervention patients also spent seven, eight, and three hours a week practicing stress management, attending support groups, and exercising, respectively.

Such a design makes it impossible to ascribe the “91 percent reduction in angina after one year” 1 to the low-fat diet alone. As early as 1802 William Heberden, who described angina pectoris, could offer no definitive treatment for the condition, but he did know of one patient “who set himself a task of sawing wood for half an hour every day and was nearly cured.”3 Many patients with angina after exercise training have angina after more exertion but at the same double product, whereas in some patients angina occurs at a higher rate-pressure product, implying an increase in coronary blood supply.3 Exercise training may also alter the coronary artery's vasomotor response to nitroglycerin4 and could have affected the apparent severity of coronary-artery lesions in the Lifestyle Heart Trial treatment group, depending on how nitroglycerin was used in the angiographic studies.

Consequently, before too much is attributed to low-fat diets in patients with coronary disease, such diets should be tested according to intention-to-treat principles in a sample large enough to permit examination of which components of a multifaceted intervention might be therapeutic. To do less runs the risk of misleading patients and physicians alike about the benefits of low-fat diets.

Paul D. Thompson, M.D.
Hartford Hospital, Hartford, CT 06070

4 References

1. 1

   Ornish D. Low-fat diets. N Engl J Med 1998;338:127-127
   Full Text | Web of Science | Medline

2. 2

   Ornish D, Brown SE, Scherwitz LW, et al. Can lifestyle changes reverse coronary heart disease? Lancet 1990;336:129-133
   CrossRef | Web of Science | Medline

3. 3

   Thompson PD. The benefits and risks of exercise training in patients with chronic coronary artery disease. JAMA 1988;259:1537-1540
   CrossRef | Web of Science | Medline

4. 4

   Haskell WL, Sims C, Myll J, Bortz WM, St Goar FG, Alderman EL. Coronary artery size and dilating capacity in ultradistance runners. Circulation 1993;87:1076-1082
   Web of Science | Medline

Author/Editor Response

Dr. Ornish replies:

To the Editor: Judging the quality of a clinical study solely on the basis of the number of patients is somewhat akin to judging the merits of a book only on the number of pages or a symphony on the number of notes. The precision and reproducibility of quantitative coronary arteriography make possible studies with smaller numbers of subjects than would be possible with the use of qualitative angiography. When there are fewer subjects, greater and more consistent treatment effects are necessary to achieve statistically significant differences.

Indeed, this is what we found in the Lifestyle Heart Trial.1,2 Adding to the strength of the evidence are the following: (1) improvement in the intervention group as shown by quantitative coronary arteriography after one year yet worsening in the control group; (2) more improvement after four years than after one year in the intervention group yet more progression of disease in the control group; (3) improvement as shown by cardiac positron-emission tomographic scans in the intervention group but worsening in the control group; (4) a dose–response relation between adherence to the lifestyle intervention and changes in the percent diameter of stenosis after one year and also after four years; and (5) a doubling of the frequency of cardiac events in the control group as compared with the intervention group. Angina was not the primary dependent variable, although the marked and sustained reduction in angina was very motivating.

The Lifestyle Heart Trial was not conducted in a vacuum. Our findings are consistent with a vast body of epidemiologic evidence, studies in animals, and randomized controlled trials in humans showing the strong benefits of low-fat, whole-food, vegetarian diets high in complex carbohydrates and low in simple sugars.3 For example, coronary heart disease is 20 times as common in the United States as in rural China, where a diet similar to that used in the Lifestyle Heart Trial is consumed. In contrast, most patients with coronary artery disease who follow a Step 2 diet (30 percent fat, 200 mg of dietary cholesterol per day) show worsening of coronary atherosclerosis.4

All clinical trials have limitations.5 For example, we cannot separate the relative contribution of each component of the intervention, although we found a dose–response relation between dietary fat and cholesterol intake and changes in coronary-artery stenoses. The few patients who received nitroglycerin during base-line arteriography were given nitroglycerin during subsequent arteriography. I am unaware of any studies showing that moderate exercise alone (walking, not ultradistance running) can cause improvement as assessed by coronary arteriography.

Churchill also said, “Americans will always do the right thing . . . after they've exhausted all the alternatives.”

Dean Ornish, M.D.
University of California, San Francisco, School of Medicine, San Francisco, CA 94115

5 References

1. 1

   Ornish D, Brown SE, Scherwitz LW, et al. Can lifestyle changes reverse coronary heart disease? Lancet 1990;336:129-133
   CrossRef | Web of Science | Medline

2. 2

   Gould KL, Ornish D, Scherwitz L, et al. Changes in myocardial perfusion abnormalities by positron emission tomography after long-term, intense risk factor modification. JAMA 1995;274:894-901
   CrossRef | Web of Science | Medline

3. 3

   Ornish D. Dr. Dean Ornish's program for reversing heart disease. New York: Random House, 1990.
   

4. 4

   Ornish D, Denke M. Dietary treatment of hyperlipidemia. J Cardiovasc Risk 1994;1:283-286
   CrossRef | Medline

5. 5

   Ornish D, Hart J. Intensive risk factor modification. In: Hennekens C, Manson J, eds. Clinical trials in cardiovascular disease. Boston: W.B. Saunders, 1998.
   

Citing Articles (2)

Citing Articles

1. 1

   Jose M. Ordovas, Ernst J. Schaefer. (1999) Treatment of dyslipidemia: Genetic interactions with diet and drug therapy. Current Atherosclerosis Reports 1:1, 16-23
   CrossRef

2. 2

   Jose M. Ordovas, Ernst J. Schaefer. (1999) Genes, variation of cholesterol and fat intake and serum lipids. Current Opinion in Lipidology 10:1, 15-22
   CrossRef