atherosclerotic plaques in the Americans were attributed to the fact that they ate high-fat diets and the Koreans ate low-fat. But the Americans were also eating high-sugar diets, while the Koreans, like the Japanese, were not.”
As Yudkin put it, “It may turn out that [many factors, including sugar] ultimately have the same effect on metabolism and so produce coronary disease by the same mechanism.” What is that mechanism? Fingers are beginning to point suspiciously to an
overload of insulin
as a common culprit at the root of at least some of these metabolic and negative health effects, such as heart disease; controlling insulin was the main purpose of the original Atkins diet and has become the raison d’être of the low-carb approach to living. Though the Atkins diet is certainly not the only way to control insulin, Atkins—who was after all a cardiologist—is to be commended for being prescient when it comes to identifying carbohydrates and insulin resistance as causative factors in diabetes, obesity, hypertension, and, you guessed it, heart disease.
CHOLESTEROL INSANITY
Yudkin’s warnings against sugar and Atkins’s early low-carb approach to weight loss were mere whispers lost in the roar of anti-fat mania. By the mid-1980s, fat had been utterly and completely demonized, and fat phobia was in full bloom, with hundreds of cholesterol-free foods being foisted on a gullible public. 16 In November 1985, the National Heart, Lung, and Blood Institute launched the National Cholesterol Education Program with the stated goal of “reducing illness and death from coronary heart disease in the United States by
reducing the percent of Americans with high blood cholesterol
[italics ours].” 17
In 1976, Nathan Pritikin opened his Pritikin Longevity Center in Santa Barbara, California, and for the next decade preached the super-low-fat dogma to all who would listen, which included most of the country. Pritikin died in 1985, but his mantle was quickly taken up by Dr. Dean Ornish. Ornish’s reputation—and much of the public’s faith in the low-fat diet approach—was fueled by his famous five-year intervention study, the Lifestyle Heart Trial, which demonstrated that intensive lifestyle changes may lead to regression of coronary heart disease. Ornish took forty-eight middle-aged white men with moderate to severe coronary heart disease andassigned them to two groups. One group received “usual care,” and the other group received a special, intensive, five-part lifestyle intervention consisting of (1) aerobic exercise, (2) stress-management training, (3) smoking cessation, (4) group psychological support, and (5) a strict vegetarian, high-fiber diet with 10 percent of the calories coming from fat.
When Ornish’s study showed some reversal of atherosclerosis and fewer cardiac events in the twenty men who completed the five-year study, the public perception—reinforced by Ornish himself—was that the results largely stemmed from the low-fat diet. This conclusion is an incredible leap that is in no way supported by his research. The fact is that
there’s no way to know
whether the results were because of the low-fat diet portion of the experiment (highly unlikely in our view), the high fiber, the whole foods, the lack of sugar, or some combination of the interventions. It is entirely possible that Ornish would have gotten the same or better results with a program of exercise, stress management, smoking cessation, and group therapy plus a whole foods diet high in protein and fiber and low in sugar.
Yet low-fat eating managed to remain the dietary prescription of every major mainstream health organization. This recommendation was built on a foundation of two basic beliefs: that low-fat diets will reduce cholesterol, and that reducing cholesterol will actually reduce heart disease and extend life.
Although some studies have shown that low-fat diets do reduce overall cholesterol, many have shown nothing of the sort.
As Yudkin put it, “It may turn out that [many factors, including sugar] ultimately have the same effect on metabolism and so produce coronary disease by the same mechanism.” What is that mechanism? Fingers are beginning to point suspiciously to an
overload of insulin
as a common culprit at the root of at least some of these metabolic and negative health effects, such as heart disease; controlling insulin was the main purpose of the original Atkins diet and has become the raison d’être of the low-carb approach to living. Though the Atkins diet is certainly not the only way to control insulin, Atkins—who was after all a cardiologist—is to be commended for being prescient when it comes to identifying carbohydrates and insulin resistance as causative factors in diabetes, obesity, hypertension, and, you guessed it, heart disease.
CHOLESTEROL INSANITY
Yudkin’s warnings against sugar and Atkins’s early low-carb approach to weight loss were mere whispers lost in the roar of anti-fat mania. By the mid-1980s, fat had been utterly and completely demonized, and fat phobia was in full bloom, with hundreds of cholesterol-free foods being foisted on a gullible public. 16 In November 1985, the National Heart, Lung, and Blood Institute launched the National Cholesterol Education Program with the stated goal of “reducing illness and death from coronary heart disease in the United States by
reducing the percent of Americans with high blood cholesterol
[italics ours].” 17
In 1976, Nathan Pritikin opened his Pritikin Longevity Center in Santa Barbara, California, and for the next decade preached the super-low-fat dogma to all who would listen, which included most of the country. Pritikin died in 1985, but his mantle was quickly taken up by Dr. Dean Ornish. Ornish’s reputation—and much of the public’s faith in the low-fat diet approach—was fueled by his famous five-year intervention study, the Lifestyle Heart Trial, which demonstrated that intensive lifestyle changes may lead to regression of coronary heart disease. Ornish took forty-eight middle-aged white men with moderate to severe coronary heart disease andassigned them to two groups. One group received “usual care,” and the other group received a special, intensive, five-part lifestyle intervention consisting of (1) aerobic exercise, (2) stress-management training, (3) smoking cessation, (4) group psychological support, and (5) a strict vegetarian, high-fiber diet with 10 percent of the calories coming from fat.
When Ornish’s study showed some reversal of atherosclerosis and fewer cardiac events in the twenty men who completed the five-year study, the public perception—reinforced by Ornish himself—was that the results largely stemmed from the low-fat diet. This conclusion is an incredible leap that is in no way supported by his research. The fact is that
there’s no way to know
whether the results were because of the low-fat diet portion of the experiment (highly unlikely in our view), the high fiber, the whole foods, the lack of sugar, or some combination of the interventions. It is entirely possible that Ornish would have gotten the same or better results with a program of exercise, stress management, smoking cessation, and group therapy plus a whole foods diet high in protein and fiber and low in sugar.
Yet low-fat eating managed to remain the dietary prescription of every major mainstream health organization. This recommendation was built on a foundation of two basic beliefs: that low-fat diets will reduce cholesterol, and that reducing cholesterol will actually reduce heart disease and extend life.
Although some studies have shown that low-fat diets do reduce overall cholesterol, many have shown nothing of the sort.
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