"Indeed the findings have been contradictory. For example, in Framingham, Mass, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower the person's serum cholesterol."
Concerning the Possibility of a Nut...
The findings reported by Fraser et al1 from the Adventist Health Study revive our interest in looking for data from prospective studies that show diet factors associated with favorable blood cholesterol or lipoprotein levels in free-living populations eventually lead to lower rates of coronary heart disease (CHD). Most of what we know about the effects of diet factors, particularly the saturation of fat and cholesterol, on serum lipid parameters derives from metabolic ward-type studies.2,3 Alas, such findings, within a cohort studied over time have been disappointing, indeed the findings have been contradictory. For example, in Framingham, Mass, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower the person's serum cholesterol. The opposite of what one saw in the 26 metabolic ward studies, the opposite of what the equations pro- vided by Hegsted et al2 and Keys et al3 would predict. Only the international comparisons showed that the world could be lined up on choles¬ terol intake or saturated fat intake, and it would correlate with the rate of CHD.4 Of course, since these countries differed in many other ways, the possibility that some unidentified factor might explain the rate ofCHD, loomed in one's thoughts. Eventually, diet intervention trials were done, and where the follow-up got out beyond 3 years, they all show the same thing. The larger the per¬ centage fall in cholesterol, the larger the percentage fall in CHD.5 In view of this, this study fails to describe a relationship of those traditional dietary constituents, saturated fat and cholesterol, known to have an adverse effect on blood lipids, and thereby, on the subsequent development of coronary disease end points. Only the Western Electric study6 has shown dietary cholesterol to be related to the later development of CHD in a population study. However, the authors of this Adventist study did show a slight increase in definite nonfatal myocar- dial infarction with eating cheese one to two times per week (RR = 1.97; 95% confidence interval, 1.27 to 3.04) and, in men, a relationship of eating beef to fatal CHD. Whole wheat bread, thank goodness, lowered the nonfatal coronary disease rate. The big finding was nuts. Nuts, eaten five or more times a week, apparently independently (Cox proportional hazard model analysis adjusted by age, sex, smoking, exercise, relative weight, and high blood pressure) lowered the coronary fatal and nonfatal end points in half. But these are the Seventh-Day Adventists who already have a seventh of our heart attack rate, who live 7 years longer than we do. How could you cut this rate even lower, in half? Is this the first article showing a dramatic fall in coronary disease rates in men and women who are already at low risk? The first reaction of a population watcher is that there just has to be some other factor related to nut ingestion confounding this relationship. The two factors that jump to mind are exercise and weight. In Framingham, for example, we found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories, weighed the least, and were the most physically active. This article showed that the people who eat the most nuts weigh the least. However, in the Cox model, neither exercise nor weight explained the impact on coronary disease. As to what other factors associated with nut eating explain the benefit, the authors give us a preview of a feeding trial, using walnuts, that at least shows a favorable change in the blood lipids eating nuts. Is this due to the polyunsaturated or monounsaturated fat in nuts? Is it some exotic fiber component? Hopefully, this anecdote will allay speculation about some other exotic confounder like television watching, nose-picking, or any myriad number of factors not routinely measured in this study. I suppose that the Archives will be bombarded by the usual letters aboutan article such as this by those cheerful folk who will want to know if the fall in coronary death rate in the nut eaters was offset by an increase in accidental, violent, or suicidal death. Perhaps there was a social price to pay, at least from the peanuts that, after all, are legumes. Should dietitians everywhere tremble? Has the magic bullet arrived? Is it the humble nut? Should fat people eat fat-rich nuts to lose weight and atherosclerosis, or do nuts only work in vegetarians? Should nuts replace oat bran as the shield that I can load up on each day which will let those hot dogs just bounce right off my chest, no trouble.
Will this article affect the stock market sending the lipid-drugs reeling when that well-balanced report ap¬ pears in the Wall Street Journal? So many questions, so little time. In the meantime, hold the cheese, I will have my nuts (walnuts?) on whole wheat, please.
William P. Castelli, MD
Framingham Heart Study
National Heart, Lung, and Blood Institute
5 Thurber St
Framingham, MA 01701
1. Fraser GE, Sabate J, Beeson WL, Strahan TM. A possible protective effect of nut consumption on risk of coronary heart disease:The Adventist Health Study. Arch Intern Med. 1992;152:1416-1424.
2. Hegsted DM, McGandy RB, Myer ML, Stare FJ. Quantitative effects of dietary fat on serum cholesterol in man. Am J Clin Nutr. 1965;17:281-295.
3. Keys A, Anderson JT, Grande F. Prediction of serum cholesterol responses of men to changes in fats in the diet. Lancet. 1957; 2:959-966.
4. Keys A. Coronary heart disease in seven countries. Circulation. 1970;41(suppl 1):1-211.
5. Castelli W. Cholesterol and lipids in the risk of coronary artery disease: The Framing- ham Heart Study. Can J Cardiol. 1988;4(suppl A):5A-10A.
6. Stamler J, Shekelle R. Dietary cholesterol and human coronary heart disease. Arch Pathol Lab Med. 1988;112:1032-1040.
“That went over like a wet blanket with my superiors at NIH,” Mann told me, “because it was contrary to what they wanted us to find.” The NIH also generally favored the diet-heart hypothesis from the early 1960s on, and “they wouldn’t allow us to publish that data,” he says. Mann’s results lay in an NIH basement for nearly a decade. (To withhold scientific information “is a form of cheating,” Mann lamented.) And even when the findings eventually came out in 1968, they were so deeply buried that a researcher has to dig through twenty-eight volumes to find the news that variations in serum cholesterol levels could not be traced back to the amount or type of fat eaten.
Not until 1992, in fact, did a Framingham study leader publicly acknowledge the study’s findings on fat. “In Framingham, Mass, the more saturated fat one ate . . . the lower the person’s serum cholesterol . . . and [they] weighed the least,” wrote William P. Castelli, one of the Framingham directors, and he published this admission not as a formal study finding but instead as an editorial in a journal not normally read by most doctors.VII (Castelli clearly found it hard to believe that this finding could be true, and he insisted in an interview that the problem must have been one of imprecise collection of the dietary data, but the methodology Mann used was meticulous by the standards of the field, so Castelli’s explanation doesn’t seem likely.)