Ancel Keys provided an answer: the "diet-heart hypothesis" (for simplicity's sake, I am calling it the "fat hypothesis").
British scientists also had long found the diet-heart hypothesis perplexing.
He found a receptive audience for his "diet-heart hypothesis" among public-health experts who faced a growing emergency: heart disease, a relative rarity three decades earlier, had skyrocketed to be a leading cause of death.
In this rebuttal to the conclusion drawn in 'Toward Healthful Diets', we review recent evidence in support of the diet-heart hypothesis.
The document, entitled 'Toward Healthful Diets' that was developed by the Food and Nutrition Board of the National Academy of Sciences last year, has again stirred major controversy among the general public and in the medical community regarding the diet-heart hypothesis as a basis for efforts to favorably modify the natural history of atherosclerotic vascular disease in the American population.
He played key roles in many of the early epidemiologic cohort studies important to resolution of the diet-heart hypothesis, produced a key monograph on the risks of smoking and health (1), and founded the Framingham Eye Study.
4 5 6 7 8 9 10 11 In 1981 the "iron-heart" hypothesis was proposed to explain differences in rates of coronary heart disease between men and premenopausal women on the basis of differences in their iron stores.
61 The traditional diet-heart hypothesis predicts that these favorable, diet induced changes in blood lipids will diminish deposition of cholesterol in the arterial wall, slow progression of atherosclerosis, reduce clinical cardiovascular risk, and eventually improve survival.
An editorial in the same issue asserted that the "final nail" had been driven into the CoQ10 for heart failure hypothesis.
This in turn implies that oxidative stress is an important modifier of the autonomic control of the heart, a hypothesis that has received little attention until recently.
However, the highly selective If channel blocker ivabradine has good tolerability, with a mean reduction in RHR of 8 10 bpm at usual doses and similar anti-ischemic benefits to atenolol 45, but without reduction in blood pressure or cardiac contractility and thus represents an intriguing agent to test the heart rate hypothesis.
