Effect of Diet on Coronary-Heart-Disease Mortality

Miettinen, M; Turpeinen, Osmo; Karvonen, M J; Elosuo, Reino; Paavilainen, Erkki

doi:10.1016/s0140-6736(73)91009-x

Cited by 7 publications

(4 citation statements)

References 2 publications

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“…At almost the same time that the Wadsworth VA study was getting under way in Los Angeles, a group in Finland was planning a study using a very similar approach (44,45). However, instead of two separate dining halls in a single institution, they would use two separate psychiatric hospitals, leaving the diet at one hospital (Hospital N) unchanged but introducing a polyunsaturated fat-rich diet at the other (Hospital K).…”

Section: The Results Of Three Well-designed Pre-1970 Studiesmentioning

confidence: 99%

“…By 1972, the importance of diet in determining serum cholesterol levels was well established, and the results of several dietary intervention trials were available. Three studies in particular-the Leren Oslo Study (42), the Wadsworth Veterans Administration Study (43), and the Finnish Mental Hospital Study (44,45)-showed that diets rich in polyunsaturated fat could significantly lower serum cholesterol levels, and collectively provided very strong evidence for the lipid hypothesis, as pointed out in a recent historical perspective by Grundy (46). Before reviewing the data from these and other dietary intervention trials, it is instructive to reexamine the scientific basis for dietary treatment of hypercholesterolemia.…”

Section: Dietary Intervention Trialsmentioning

confidence: 95%

“…This is true across a wide spectrum of blood cholesterol levels and holds on comparison of populations from different countries (37) and also within populations (40, 41), 4 ) Blood cholesterol level is increased when dietary saturated fat intake is increased, as shown by carefully controlled metabolic ward studies (49,50). Moreover, populations with dietary habits that include a high saturated fat intake have higher blood cholesterol levels and a higher CHD incidence than populations with lower saturated fat intake (37), 5 ) The wide differences in blood cholesterol levels and CHD risk between populations of different countries are due largely to environmental factors (probably diet) rather than genetic factors, as shown, for example, by the Japanese migration studies (39), 6 ) Dietary intervention to lower blood cholesterol by decreasing saturated fat intake in favor of polyunsaturated fat intake reduces blood cholesterol levels and decreases risk of CHD and other atherosclerotic complications (42)(43)(44)(45)(62)(63)(64)(65)(66)(67)(68)(69)(70). 7 ) We should be treating hypercholesterolemia.…”

Section: A Possible Catechism For 1970 "Believers"mentioning

confidence: 99%

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Thematic review series: The Pathogenesis of Atherosclerosis. An interpretive history of the cholesterol controversy: part II:the early evidence linking hypercholesterolemia to coronary disease in humans

Steinberg

2005

Journal of Lipid Research

159

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The first in this series of historical reviews dealt with the pioneering animal model work of Anitschkow, implicating blood cholesterol in the pathogenesis of atherosclerosis, and the pivotally important work of Gofman, providing evidence that lipoprotein-bound cholesterol was a major factor in the human disease. This second installment reviews the early lines of evidence linking hypercholesterolemia in humans to the progression of atherosclerosis and the risk of coronary heart disease. The argument is made that by 1970, the evidence was already strong enough to justify intervention to lower blood cholesterol levels if all the available lines of evidence had been taken into account. Yet, it would be almost two decades before lowering blood cholesterol levels became a national public health goal. Some of the reasons the "cholesterol controversy" continued in the face of powerful evidence supporting intervention are discussed. The first in this series of reviews of the history of the "cholesterol controversy" focused on two early developments (1). The first was the groundbreaking studies of Anitschkow and others, showing that inducing hypercholesterolemia in rabbits was sufficient to produce arterial lesions closely resembling those in the human disease. A major, and legitimate, criticism of Anitschkow's work initially was that the rabbit, a strict herbivore, could hardly be considered a suitable model for man, an omnivore. Indeed, dogs and cats, carnivores, did not develop atherosclerosis on cholesterol feeding, as Anitschkow had himself recognized and reported (2). However, this was not because their arteries were somehow immune but simply because, despite the large increase in dietary cholesterol, their blood cholesterol levels did not rise high enough. These species have very effective systems for converting dietary cholesterol to bile acids and excreting it. The demonstration that lesions could also be readily produced in guinea pigs (3, 4), goats (5), hens and parrots (2), and, ultimately, in almost every animal species, including nonhuman primates (6), went a long way toward rebutting this criticism. Nevertheless, the extrapolation from animals to humans, in the absence of supporting evidence, was not and could not be automatically accepted. Evidence in humans was needed.The second focus in the preceding review was on the work of Gofman and coworkers (7), which revealed the complexity of the plasma lipoproteins in humans and also demonstrated, albeit with only relatively small numbers of subjects, good correlations between elevated concentrations of plasma lipoproteins and relative risk of clinical coronary heart disease (CHD). Much larger surveys involving hundreds or thousands of cases would be needed to define the association convincingly.The findings of these two pioneers suggested a causal relationship but fell short of proving the case. In the present review, we describe the several additional lines of evidence that over the ensuing two decades increasingly strengthened the case. By the late ...

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Section: The Results Of Three Well-designed Pre-1970 Studiesmentioning

confidence: 99%

Section: Dietary Intervention Trialsmentioning

confidence: 95%

Section: A Possible Catechism For 1970 "Believers"mentioning

confidence: 99%

See 1 more Smart Citation

Thematic review series: The Pathogenesis of Atherosclerosis. An interpretive history of the cholesterol controversy: part II:the early evidence linking hypercholesterolemia to coronary disease in humans

Steinberg

2005

Journal of Lipid Research

159

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show abstract

“…Epidemiological evidence suggests that the replacement of saturated fatty acids (SFA)' in the diet by polyunsaturated fatty acids (PUFA) reduces the incidence of coronary heart disease (1)(2)(3). Recently, studies of Greenland Eskimos (4,5) and men from the Netherlands (6) indicated that polyunsaturates of the w-3 fatty acid series, which are enriched in some types of fish oil, may be even more beneficial than polyunsaturates of the w-6 fatty acid series, commonly found in vegetable oils.…”

Section: Introductionmentioning

confidence: 99%

Dietary polyunsaturated fats of the W-6 and W-3 series reduce postprandial lipoprotein levels. Chronic and acute effects of fat saturation on postprandial lipoprotein metabolism.

Weintraub

Zechner²,

Brown³

et al. 1988

J. Clin. Invest.

322

121

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The chronic and acute effects of different types of dietary fat on postprandial lipoprotein metabolism were studied in eight normolipidemic subjects. Each person was placed for 25 d on each of three isocaloric diets: a saturated fat (SFA), a w-6 polyunsaturated fat (w-6 PUFA) and a w-3 polyunsaturated fat (w-3 PUFA) diet. Two vitamin A-fat loading tests were done on each diet. The concentrations in total plasma and chylomicron (Sf > 1,000) and nonchylomicron (Sf < 1,000) fractions of retinyl palmitate (RP) were measured for 12 h postprandially. Compared with the SFA diet, the w-6 PUFA diet reduced chylomicron and nonchylomicron RP levels 56 and 38%, respectively, and the w-3 PUFA diet reduced these levels 67 and 53%, respectively. On further analysis, the main determinant of postprandial lipoprotein levels was the type of fat that was chronically fed, which appeared to mediate its effect by changing the concentration of the endogenous competitor for the system that catabolizes triglyeride-rich lipoproteins. However, there was a significant effect of the acute dietary fat load, which appeared to be due to a differential susceptibility to lipolysis of chylomicrons produced by SFA as opposed to PUFA fat loads. The levels of postprandial lipoproteins are determined by the interaction of these chronic and acute effects.

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Distribution, Metabolism, and Excretion

Nabi

2014

Toxic Effects of Mercury

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Effect of Diet on Coronary-Heart-Disease Mortality

Cited by 7 publications

References 2 publications

Thematic review series: The Pathogenesis of Atherosclerosis. An interpretive history of the cholesterol controversy: part II:the early evidence linking hypercholesterolemia to coronary disease in humans

Thematic review series: The Pathogenesis of Atherosclerosis. An interpretive history of the cholesterol controversy: part II:the early evidence linking hypercholesterolemia to coronary disease in humans

Dietary polyunsaturated fats of the W-6 and W-3 series reduce postprandial lipoprotein levels. Chronic and acute effects of fat saturation on postprandial lipoprotein metabolism.

Distribution, Metabolism, and Excretion

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