“Diet-Heart: A Hypothesis in Crisis? Part 1: From Proposal to Paradigm to Policy.” by Kenneth W. Krause. In the January 4, 1985 issue of Science, Gina Kolata covered the 47th consensus panel report from the National Institutes of Health, published some three weeks earlier. Since 1961, the American Heart Association had asked Americans to reduce their intake of saturated fats and cholesterol, and recommended its “prudent diet” emphasizing fruits, vegetables, and vegetable oils. The NIH had been hesitant to take a firm position on the diet-heart hypothesis, according to Kolata, because the scientific literature focusing on the connection between dietary cholesterol and saturated fatty acids (SFA) on the one hand, and heart disease on the other, did “not show that lowering cholesterol makes a difference” (Kolata 1985). But the NIH’s reticence was finally overcome by the results of a then-new study conducted by the National Heart, Lung and Blood Institute on the effects of a cholesterol-reducing diet and drug, cholestyramine, on about 4000 middle-aged men with elevated serum (blood) cholesterol levels (LRCP 1984). On average, the intervention group’s cholesterol had dropped by 13.4 percent since the investigation began in 1973, or 8.5 percent better than the average decrease found among placebo-treated controls. According to the NHLBI, its researchers had provided not only “strong evidence” of a “causal role” for low-density lipoprotein cholesterol, or LDL-C, in the pathogenesis of coronary heart disease (CHD), but good reason as well to extend its findings to “other age groups and women” along with “others with more modest elevations of serum cholesterol.” Others were less impressed. In an interview with Kolata, University of Chicago and frequent NIH statistician, Paul Meier, deemed the new study’s findings “weak,” referring to the disappointing and statistically insignificant distinction between the intervention and control groups in terms of deaths from all causes. And although incidences of angina, bypass surgery, and abnormal exercise electrocardiograms all fell in the modified diet-drug group, Kolata judged that the new study had “failed, as every other trial did, to prove that lowering blood cholesterol saves lives.” But most controversial were the panel’s recommendation that all Americans from the age of two should reduce their consumption of SFA and cholesterol. Also interviewed by Kolata, Thomas Chalmers of the Mt. Sinai Medical School argued that the report “made an unconscionable exaggeration of the data,” emphasizing that “there is absolutely no evidence that it’s safe for children to be on a cholesterol-lowering diet.” In a subsequent letter to Science, Daniel Steinberg, who had chaired the NIH consensus development conference, criticized Kolata for devoting the lion’s share of her article to “no more than a handful among some 600 conferees” (Steinberg 1985). “The panel’s recommendation,” he countered, “is sound when all of the evidence is taken into account.” Such evidence also led quickly in 1985 to the National Cholesterol Education Program, a new NIH administration created to instruct physicians how to identify and treat “at-risk” patients. In fact, there was much agreement among the conferees. But dissent in 1984 was both loud and determined, as it remains at the dawn of 2015. The differences between the debates then and now are as multifactorial as heart disease itself. While television continues to manipulate viewer emotions and bombard them with highly-varied and always simplistic scientific interpretations and dietary advice, internet bloggers now flood every recess of the popular consciousness with harsh, often tactically ruthless diatribes against their nutritional adversaries. Journalists and popular authors publish infuriated texts alleging conspiracies between researchers, big food, and government agencies to intentionally mislead the public for personal gain. And as new studies and reviews have lately called the very foundations of the diet-heart hypothesis into question, some leading scientists have entrenched themselves as well, separating into mutually antagonistic nutritional camps. It might sound too melodramatic to be true. But the most regrettable result is unmistakable—the American public is bewildered and incredulous. What kind of diet will help us not only lose weight, but remain healthy and safe as well? Should we cast our lots with the low-fat or low-carbohydrate paradigm? Do saturated fats really raise the risk of heart disease, and, if so, are the officially endorsed replacements perhaps even more dangerous? Worst of all, Americans wonder if nutrition science has anything at all of substance to offer them. The classic diet-heart hypothesis (D-Hh) posits simply that diets high in SFA and cholesterol (and low in polyunsaturated fatty acids [PUFA]) raise serum total and LDL cholesterol levels and lead to the accumulation of atheromatous plaques. These plaques gradually narrow coronary arteries, reduce blood flow to the heart, and can eventuate in myocardial infarction. Early evidence linking heart disease to foods rich in cholesterol (and SFA), including red meat, eggs, and shellfish, derived from animal experiments. In 1913, for example, a Russian pathologist reported the ability to induce atherosclerotic-like lesions in rabbits by feeding them copious amounts of cholesterol (Anitschkow 1913). Others soon replicated these results, mainly with other herbivorous animals. Many researchers objected, however, that such creatures were naturally ill-suited to metabolize cholesterol. And when similar experiments were carried out on non-herbivorous (and more human-like) dogs, they added, the animals appeared to tolerate cholesterol much better. But the D-Hh wasn’t formally articulated until University of Minnesota physiologist Ancel Keys presented the concept in 1952 at Mt. Sinai in New York. Also published in a famous paper the following year, Keys’ employed a simple yet powerful graph correlating in precise curvilinear fashion total fat intake as a percentage of all calories with death rates from heart disease among men in six countries—Japan, Italy, England and Wales, Australia, Canada, and the United States (Keys 1953). Critics claimed that Keys intentionally ignored data from twenty-two other countries. And when researchers scrutinized this additional data, they found not only that Keys’ correlation was greatly diminished, but that no association whatsoever existed between dietary fats and death from all causes (Yerushalmy 1957). Nevertheless, according to James DiNicolantonio, cardiovascular researcher at St. Luke’s Mid America Heart Institute, Keys’ early data “seemingly led us down the wrong ‘dietary-road’ for decades to follow” (DiNicolantonio 2014). Regardless, the most convincing early evidence for the D-Hh may have originated from Keys’ Seven Countries Study of sixteen cohorts (12,763 rural males age 40-59) in Greece, Italy, the former Yugoslavia, the Netherlands, Finland, the U.S., and Japan. By this time, Keys had refined his intial proposal to impugn primarily SFA and animal products. Indeed, in this, the first multi-country epidemiological undertaking in history, coronary mortality and five-year incidence of CHD was positively correlated only with SFA and not total fat or PUFA intake (Keys 1970). The cross-cultural results were striking. Upon 25-year follow-up, inter-population death rates from CHD had differed dramatically. In East Finland, for example, 268 per 1000 lumberjacks and farmers living on diets high in meat and dairy had died. By contrast, of the Greeks of Crete who in terms of dietary fats subsisted on olive oil and very little meat, only 25 per 1000 had perished. Perhaps most notably, however, SFA accounted for twenty-two percent of the Finns’, but only eight percent of the Cretans’ total calories. But Keys was and continues to be criticized for having “cherry-picked” his Seven Countries data. Some argue that populations in countries like France, Switzerland, Germany, Norway, or Sweden, for example, might have challenged Keys’ idea. Some, like journalist Nina Teicholz, go so far as to charge that he deliberately selected “only those nations … that seemed likely to confirm it” (Teicholz 2014). Indeed, Keys’ data was not chosen randomly. But Henry Blackburn, Keys’ colleague in Seven Countries, sees no reason why the populations should have been selected by chance. “Demonstrating a lack of understanding of how scientists approach new questions,” he explains, the critics ignore the fact that “any savvy scientist at an early phase of questioning knows to look first not randomly but across wide variations of the cause under consideration, in this case diet” (Blackburn 2014). Others observed of Keys’ results that CHD mortality varied widely within certain countries. “Despite similar risk factors and diet,” Danish independent researcher Uffe Ravnskov found that “the 5-year incidence of fatal CHD in Crevalcore, Italy, was more than twice that in Montegiorgio, while in Karelia it was five times higher than in West Finland; and on Corfu, 6-7 times higher than on Crete” (Ravnskov 1998). Thus, for these and other dissenters, the supposed correlation between diet and heart disease was little more than a well-staged illusion. On May 28, 1980—only five years previous to the NIH’s consensus report on the same subject—the Food and Nutrition Board of the National Academy of Sciences issued a far more controversial paper, “Toward healthful diets,” finding no clear evidence that reducing serum cholesterol through dietary intervention could prevent CHD. Therein, the fifteen-member Board reproved those “who seek to change the national diet” for assuming a nominal risk in widespread dietary adjustment and for relying so heavily on epidemiological rather than experimental evidence. Critics of the Board accused its members of maintaining inappropriately cozy relationships with big food organizations like the American Egg Board. In response to the report itself, Robert Levy, director of the NHLBI, offered the following faint-hearted guidance: “Existing information indicates that Americans should hedge their bets and seek a diet lower in saturated fats and cholesterol, at least until more evidence is available” (Broad 1980). At that point, only the Academy and the American Medical Association stood in defiance of the U.S. government and at least eighteen distinguished health organizations. America had officially become a low-fat, low-cholesterol nation. References: Anitschkow, N., S. Chalatov, C. Muller, et. al. 1913. Uber experimentelle cholesterinsteatose: Ihre bedeutung fur die entehung einiger pathogischer prozessen. Zentralblatt fur Allgemeine Pathologie und Pathologiche Anatomie 24:1-9. Blackburn, H. 2014. In defense of U research: The Ancel Keys legacy. The Star Tribune (July 17). Online at startribune/opinion/commentaries/267581481.html Broad, W.J. 1980. Academy says curb on cholesterol not needed. Science 208:1354-55. DiNicolantonio, J. 2014. The cardiometabolic consequences of replacing saturated fats with carbohydrates or omega-6 polyunsaturated fats: Do the dietary guidelines have it wrong? Open Heart 2014;1:e000032. doi:10.1136/openhrt-2013-000032. Keys, A. 1953. Atherosclerosis: a problem in newer public health. Journal of Mt. Sinai Hospital, New York 20(2):118-139. Keys, A. 1970. Coronary heart disease in seven countries. Circulation 41(Suppl. 1):1-211. Kolata, G. 1985. Heart panel’s conclusions questioned. Science 227:40-41. Lipid Research Clinics Program. 1984. The Lipid Research Clinics Coronary Primary Prevention Trial. 1. Reduction in incidence of coronary heart disease. Journal of the American Medical Association 251(3):351-364. Ravnskov, U. 1998. The questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease. Journal of Clinical Epidemiology 51(6):443-460. Steinberg, D. 1985. Heart panel’s conclusions. Science 227:582. Teicholz, N. 2014. The big fat surprise: why butter, meat & cheese belong in a healthy diet. NY: Simon & Schuster. Yerushalmy, J. and H. Hilleboe. 1957. Fat in the diet and mortality from heart disease. A methodological note. New York State Journal of Medicine 57:2343-54.
Posted on: Sun, 05 Oct 2014 03:47:00 +0000
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