Cholesterol

Dietary Fat Recommendations

1957:

• 25-30% of calories from total fat.

• “The possibility remains that the kind, rather than the amount of fat in the diet is responsible for atherosclerosis.”

A third famous clinical trial that is cited again and again is the Finnish Mental Hospital study. I first heard about this study from a top nutrition expert who assured me that it was really “the best possible proof” that saturated fat is unhealthy.

In 1958, researchers seeking to compare a traditional diet high in animal fats to a new one high in polyunsaturated fats selected two mental hospitals near Helsinki. One they called Hospital K and the other, Hospital N. For the first six years of the trial, inmates at Hospital N were fed a diet very high in vegetable fat. Ordinary milk was replaced with an emulsion of soybean oil in skim milk, and butter was replaced by a special margarine high in polyunsaturated fats. The vegetable oil content of the special diet was six times higher than in a normal diet. Meanwhile, inmates of Hospital K ate their regular fare. Then the hospitals swapped, and for the next six years, Hospital K inmates got the special diet while Hospital N returned to their normal one.

In the special-diet group, serum cholesterol went down by 12 percent to 18 percent, and “heart disease was halved.” This is how the study is remembered and is the conclusion that the study directors, Matti Miettinen and Osmo Turpeinen, themselves drew. In a population of middle-aged men, they said, a diet low in saturated fats “exerted a substantial preventive effect upon coronary heart disease.”

But a closer look reveals a different picture. Heart disease incidence (which the investigators defined as deaths plus heart attacks) did go down dramatically for the men at Hospital N: there were sixteen such cases among men on the normal diet compared to only four on the special diet. But the difference found in Hospital K was not significant. Nor was any difference observed among the women. The biggest problem with the study, however, was that, like the subjects in the LA Veterans Trial, its population was a moving target. With admissions and discharges over the years, the composition of the groups changed by half. A shifting population means that an inmate in the group who died of a heart attack might have been admitted three days earlier and the death would have had nothing to do with his diet; and, vice versa, a patient who was released might have died soon thereafter but would not have been recorded in the study.

This and other design problems were so great that two high-level NIH officials together with a professor at George Washington University felt moved to criticize the study in a letter to The Lancet asserting that the authors’ conclusions were too statistically weak to be used as any kind of evidence for the diet-heart hypothesis. Miettinen and Turpeinen acknowledged that their study design was “not ideal,” including the fact that the study population was far from stable, but asserted in their defense that a perfect trial would be “so elaborate and costly . . . [that it] may perhaps never be performed.” Their imperfect trial, meanwhile, would have to stand: “we do not see any reason to change or modify our conclusions,” they wrote. The research community accepted this “good-enough” reasoning, and the Finnish Mental Hospital study earned a spot as one of the linchpins of evidence for the diet-heart hypothesis.

Nina Teicholz - Page 77

MD Conf, May 1961: Margaret Albrink, Yale: Elevated Triglycerides (TG) - not cholesterol - were asso w/ increased risk of heart disease. Low-fat, high-carb diets raised TG. Albrink: Ancel Keys' supporters attacked me, "They were so angry," & the science bullies prevailed.

The occasional occurrence of lactescent or milky serum in patients with certain diseases caused interest and speculation at least as long ago as 1799 when Mariet described turbid sera in some patients with diabetic acidosis (1). The lightscattering fat particles or chylomicrons causing lactescence are present in modest numbers after a fat meal but become scarce in normal postabsorptive sera. In certain pathological states, however, chylomicrons occur in excessive numbers, giving rise to a characteristic milky appearance of the sera. In a previous study, lactescence was reported to be directly proportional to the total triglyceride concentration in serum (2). Turbidity was invariably present when total triglyceride fatty acid concentration exceeded 20 mEq per L. As triglyceride concentration increased further, a progressively greater proportion of cholesterol and phospholipids also occurred in the particulate lipid fraction which could be readily removed by flotation of unaltered serum at moderate speeds in the ultracentrifuge. Serum lipids are now known to exist in a spectrum of lipoproteins of varying density, from very low density particulate chylomicrons composed chiefly of triglycerides, through various classes of low density lipoproteins relatively rich in cholesterol, to high density lipoproteins in which phospholipids are prominent (3). Interest in various classes of low density lipoproteins has been stimulated because of their possible role in the etiology of coronary arterial disease (4). Studies from this laboratory (5-7) have shown serum triglyceride concentration to be intimately associated with this disease. Antonis and Bersohn have also found elevation of serum triglycerides in ischemic heart disease (8). From the known composition of very low density lipoproteins, it might be inferred that their presence in abnormally high concentrations would be associated with increased concentration of total serum triglycerides. The present study was undertaken to learn whether total triglyceride concentration might determine not only the fraction of lipids present in chylomicrons but also the partition of lipids among the various low density lipoproteins. At the same time the lipoprotein composition of the relatively clear subnatant fluid after removal of the chylomicron "cream" layer of lactescent sera could be determined. This clear fraction was previously analyzed in toto (2), but no analysis of lipoproteins was made.

* Supported (in part) by Grant H-3498(C2) from the National Heart Institute, Bethesda, Md., and by a grant from The James Hudson Brown Memorial Fund. This work was done during tenure of an established investigatorship of the American Heart Association.

The dissenting voices were fading. An “almost embarrassingly high number of researchers boarded the ‘cholesterol bandwagon,’ ” lamented the editors of the Journal of the American Medical Association in 1967, referring to the narrow, “fervent embrace of cholesterol” to the “exclusion” of other biochemical processes that might cause heart disease. In the pages of sympathetic scientific journals, Ahrens and Mann, plus their handful of like-minded colleagues, continually sent up futile cries against the relentless march of the diet-heart hypothesis, but they were powerless in the face of the elite. As George Mann wrote at the end of his career in 1978, a “heart Mafia” had “supported the dogma” and hoarded research funds. “For a generation, research on heart disease has been more political than scientific,” he declared.

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-Nina Teicholz - Page 70

In the January 4, 1985, issue of Science, Gina Kolata covered the 47th consensus panel report from the National Institutes of Health (NIH), 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).