did.
As for the coronary arteries—the ones involved in heart attacks—the Japanese have less atherosclerosis in these arteries than do Americans, which may be why they are less prone to heart attacks.
But if high cholesterol is what causes atherosclerosis, this should occur in all types of arteries, since the amount of cholesterol in the blood is the same in all parts of the body. It seems much more likely that something other than cholesterol causes atherosclerosis. Blood pressure, for example, does vary in different arteries and at different times, for example when you are under stress. But few scientists seem willing to look at these complicated details.
Cholesterol Lowering: No Effect on Plaque Buildup
A recent study, published in the American Journal of Cardiology , 2003, found that patients who successfully lowered their cholesterol levels did not reduce plaque buildup in their arteries. One group took a strong dose of a cholesterol-lowering drug while the other took a lower dose of the same drug. Researchers then measured the amount of blockage in their arteries. After more than one year, both groups showed a 9.2 percent increase in plaque buildup, suggesting that plaque buildup is not related to cholesterol level.
If This Is All True…Why Does the Lipid Hypothesis Still Rule?
In science, the burden of proof rests on the scientist. If even one study contradicts a hypothesis, then we must at the very least be open to reevaluating the hypothesis, even if many studies support it. We’ve just described many studies that contradict the lipid hypothesis, yet it remains the ruling theory of heart disease in modern medicine.
Why? Consider the fact that the widespread credence given to the lipid hypothesis certainly has helped a number of industries. For example, the hypothesis provides the pharmaceutical industry with a rationale for selling cholesterol-lowering drugs, which today is a multibillion-dollar business. The hypothesis has also been a boon for the food industry, since it justifies the use of inexpensive vegetable oils in processed food products, rather than more expensive coconut oil and animal fats.
The following pages tell the story of how, due in part to the exertions of these industries, the lipid hypothesis became the basis of government policy. Going back 60 years, we’ll trace the evolution of this idea and the huge impact it has had on what Americans are eating today. And we’ll tell the tale partly from a personal perspective, for an important participant in the struggle was Dr. Mary Enig.
The Lipid Hypothesis Gets Rolling
David Kritchevsky’s 1954 studies, published in the American Journal of Physiology, July through September 1954, attracted the attention of scientists concerned about the emerging epidemic of heart disease because they appeared to support the lipid hypothesis. Kritchevsky’s studies demonstrated that
cholesterol caused atherosclerosis in vegetarian rabbits;
polyunsaturated fatty acids could lower blood cholesterol levels in humans.
Kritchevsky’s work appeared to show that by reducing the levels of animal products in their diet, Americans could avoid heart disease—as long as scientists ignored the many studies (including those we’ve described above) that contradicted Kritchevsky’s findings. In fact, Kritchevsky’s studies had no relevance to the lipid hypothesis for two reasons. First, the kind of plaque the rabbits developed was completely different from the kind of plaque humans develop. Second, the rabbits were fed purified cholesterol that was oxidized (damaged by processing), not the kind contained in ordinary food.
The lipid hypothesis was introduced to the American people in 1956, when the American Heart Association (AHA) aired a fund-raiser on all three major television networks. The panelists presented the hypothesis as the cause of heart disease and recommended the Prudent Diet, in which corn oil, margarine, chicken, and cold cereal replaced
As for the coronary arteries—the ones involved in heart attacks—the Japanese have less atherosclerosis in these arteries than do Americans, which may be why they are less prone to heart attacks.
But if high cholesterol is what causes atherosclerosis, this should occur in all types of arteries, since the amount of cholesterol in the blood is the same in all parts of the body. It seems much more likely that something other than cholesterol causes atherosclerosis. Blood pressure, for example, does vary in different arteries and at different times, for example when you are under stress. But few scientists seem willing to look at these complicated details.
Cholesterol Lowering: No Effect on Plaque Buildup
A recent study, published in the American Journal of Cardiology , 2003, found that patients who successfully lowered their cholesterol levels did not reduce plaque buildup in their arteries. One group took a strong dose of a cholesterol-lowering drug while the other took a lower dose of the same drug. Researchers then measured the amount of blockage in their arteries. After more than one year, both groups showed a 9.2 percent increase in plaque buildup, suggesting that plaque buildup is not related to cholesterol level.
If This Is All True…Why Does the Lipid Hypothesis Still Rule?
In science, the burden of proof rests on the scientist. If even one study contradicts a hypothesis, then we must at the very least be open to reevaluating the hypothesis, even if many studies support it. We’ve just described many studies that contradict the lipid hypothesis, yet it remains the ruling theory of heart disease in modern medicine.
Why? Consider the fact that the widespread credence given to the lipid hypothesis certainly has helped a number of industries. For example, the hypothesis provides the pharmaceutical industry with a rationale for selling cholesterol-lowering drugs, which today is a multibillion-dollar business. The hypothesis has also been a boon for the food industry, since it justifies the use of inexpensive vegetable oils in processed food products, rather than more expensive coconut oil and animal fats.
The following pages tell the story of how, due in part to the exertions of these industries, the lipid hypothesis became the basis of government policy. Going back 60 years, we’ll trace the evolution of this idea and the huge impact it has had on what Americans are eating today. And we’ll tell the tale partly from a personal perspective, for an important participant in the struggle was Dr. Mary Enig.
The Lipid Hypothesis Gets Rolling
David Kritchevsky’s 1954 studies, published in the American Journal of Physiology, July through September 1954, attracted the attention of scientists concerned about the emerging epidemic of heart disease because they appeared to support the lipid hypothesis. Kritchevsky’s studies demonstrated that
cholesterol caused atherosclerosis in vegetarian rabbits;
polyunsaturated fatty acids could lower blood cholesterol levels in humans.
Kritchevsky’s work appeared to show that by reducing the levels of animal products in their diet, Americans could avoid heart disease—as long as scientists ignored the many studies (including those we’ve described above) that contradicted Kritchevsky’s findings. In fact, Kritchevsky’s studies had no relevance to the lipid hypothesis for two reasons. First, the kind of plaque the rabbits developed was completely different from the kind of plaque humans develop. Second, the rabbits were fed purified cholesterol that was oxidized (damaged by processing), not the kind contained in ordinary food.
The lipid hypothesis was introduced to the American people in 1956, when the American Heart Association (AHA) aired a fund-raiser on all three major television networks. The panelists presented the hypothesis as the cause of heart disease and recommended the Prudent Diet, in which corn oil, margarine, chicken, and cold cereal replaced
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