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How We Came to Believe that the Low-Fat Diet is Good and Cholesterol is Bad

Posted by medconsumers on December 30, 2003

Despite decades of effort and many thousands of people randomized [into clinical trials], there is still only limited and inconclusive evidence of the effects of modification of total, saturated, monounsaturated, or polyunsaturated fats on cardiovascular morbidity and mortality.

Lee Hooper et al, British Medical Journal, March 31, 2001

Yes, the low-fat message is yet-another overrated bit of medical advice. Haven’t we been hearing for years that a low-fat diet will reduce your odds of dying of a heart attack? Yet those who assessed all the relevant studies (like the reviewers quoted above) have concluded that the evidence supporting the advice boils down to this: Eating a low-fat diet will not help you live longer, but it may slightly reduce the odds of having a non-fatal heart attack–if you are a man. 

You may wonder why we have been led to believe otherwise. It’s a long story that begins with the Korean War. Autopsies done on the young casualties, whose average age was 22 years, surprised physicians who saw early evidence of heart disease in 77% of them. Next came the Framingham Heart Study, which began in the early 1950s and followed over 5,000 healthy men and women. High blood levels of cholesterol emerged as a major risk factor for heart attack for young and middle-aged men, but not for women or the elderly. It was, however, only one of 240 risk factors identified by the Framingham Heart Study.

Though dietary cholesterol was the assumed culprit in the development of heart disease, this possibility was disproved early on, according to an historical account by Thomas J. Moore for his 1989 book, Heart Failure. Moore notes that the Framingham researchers singled out over 900 men and women to compare their blood levels of cholesterol with the amount of cholesterol in their diets. To their surprise, there was no relationship. As so often happens in other areas of medicine, opinions became fixed before definitive studies proved or disproved the hypothesis. And in this case, a medical consensus had already developed: Everyone should be concerned about the amount of cholesterol in their diets. In time, the public was told to increase intake of polyunsaturated fats (e.g., vegetable oils), reduce intake of saturated fats (e.g., meat and dairy products), and severely restrict dietary cholesterol (e.g., egg yolks, beef, pork). Total fat intake was to be kept under 30% of calories.

Many more studies confirmed the Framingham finding of an association between high blood levels of cholesterol and heart disease. It is, however, one thing to identify a factor that puts people at higher risk for heart attack–proving that a change in the risk factor will lower a person’s death rate is an entirely different matter. This was demonstrated by the failure of the Multiple Risk Factor Intervention Trial, sponsored by the National Heart, Lung, and Blood Institute. 

This ten-year, $115 million research project followed over 12,866 middle-aged healthy but high-risk men who were randomly assigned to one of two groups. The Special Intervention Group received intensive instruction on smoking cessation, reducing consumption of dietary cholesterol and saturated fats, the need for regular physical activity, and blood pressure reduction. The other half of the participants formed the Usual Care Group who received no encouragement to change their risk factors. At ten years, there was no difference between the two groups in overall death rate or in the heart disease death rate.

In three other major trials where diet was used to reduce cholesterol, the best that could be found was a barely significant reduction in non-fatal cardiovascular “events.” In cholesterol-lowering drug trials, the heart disease death rates went down among the drug-treated men, but the reduction was always offset by a higher rate of death from other causes. “All we are doing is changing what it says on the death certificate,” said researcher Dr. William C. Taylor. With several colleagues, Dr. Taylor had calculated that a lifelong program of cholesterol reduction adds about three days to three months to the life expectancy of a low-risk symptom-free adult (Annals of Internal Medicine, 4/87). 

Despite the lack of proof that lowering cholesterol in people without heart disease has a lifesaving benefit, the National Cholesterol Education Program began a nationwide “Know Your Numbers” campaign in 1987 to get all Americans to have their blood cholesterol measured regularly. In 1995, a landmark clinical trial proved for the first time that a cholesterol-lowering drug could prevent heart disease deaths in healthy but high-risk men without increasing their odds of dying of something else. The drug used in this study was from a new class of cholesterol-lowering medications called statins. Half the 6,000 middle-aged Scottish men in this trial were given pravastatin and half were given a placebo. Results showed a modest lifesaving benefit for the group taking pravastatin. At five years, there was a 3.2% heart disease death rate among the men on pravastatin (brand name: Pravachol) and a 4.1% heart disease death rate among the men on the placebo.

Several years later, another statin, lovastatin (Mevacor), became the first drug to benefit healthy men and women with normal or borderline levels of cholesterol. The heart attack rate in the placebo group was 5.4%, compared with 3.5% in the lovastatin-treated group. The overall death rate was the same for both groups. While these two trials appear to verify the benefits of lowering blood levels of cholesterol, a growing number of researchers see another explanation for the statins’ benefit. These drugs appear to have anti-coagulation, anti-inflammatory, and some other biological effects that protect the arteries. Many researchers believe that inflammation plays a role in heart attacks and some forms of stroke, but the exact mechanism is uncertain. The inflammatory theory could explain why half the heart attacks occur in people with normal cholesterol levels. 

As statin drugs move front and center in the heart attack prevention picture, the low-fat diet is now under attack because the lack of supporting evidence was brought to the public’s attention by Gary Taubes, first in a 2001 article for Science (“The Soft Science of Dietary Fat”) and later in a much-discussed 2002 article for The New York Times (“What If It’s All Been a Big Fat Lie?”).  

While researchers continue to work out the ways that heart attacks and stroke can be prevented, it should be noted that the death rates for both have been declining steadily since the late 1940s–well before Americans ever heard the low-fat, lower your cholesterol messages. The nation is experiencing an epidemic of obesity that some attribute to the low-fat message which drove people to consume more refined carbohydrates and to increase their total caloric intake. Still, the heart disease death rate has dropped dramatically in the last two decades, a period in which the nation’s fat intake dropped only a pitiful 6%. Better treatments are thought to be the reason. It could also be due to the increasing percentage of Americans entering the middle class, a trend that began after World War II. (High socioeconomic status is associated with a lower rate of premature heart disease death, especially for women.) Whatever the reason, it isn’t the low-fat diet, and it isn’t reduced intake of dietary cholesterol.

 Maryann Napoli, Center for Medical Consumers© 2003

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