The Diet Heart Hypothesis

"The diet-heart hypothesis has been repeatedly shown to be wrong, and yet, for complicated reasons of pride, profit and prejudice, the hypothesis continues to be exploited by scientists, fund-raising enterprises, food companies and even governmental agencies. The public is being deceived by the greatest health scam of the century. "

- Dr. George V. Mann, participating researcher in the Framingham study

"...there's no connection whatsoever between cholesterol in food and cholesterol in the blood. None. And we've known that all along. "
- Dr. Ancel Keys, Eating Well, 1997

The Lipid Hypothesis (or diet-heart hypothesis) states that there is a direct relationship between the amount of fat and cholesterol in the diet and the incidence of coronary heart disease. It was originally proposed by a researcher named Ancel Keys in the late 1950's and has led to the popular dogma "reducing fat in your diet, will lower your chances of chronic heart disease." Despite Key's statement in a paper published in 1956 that
"... the serum cholesterol level is essentially independent of the cholesterol intake over the whole range of human diets" the dogma has been extended to eating a low-cholesterol diet.

Popularity notwithstanding, the Lipid Hypothesis remains a hypothesis because, despite numerous studies costing millions of dollars, the statement that reducing fat in your diet will lower your chances of CHD has never been scientifically proven. Furthermore, many studies have failed to demonstrate any linkage between a low-fat diet and heart disease.

As science has taught us more about the different kinds of fat and different types of cholesterol, the Lipid Hypothesis has necessarily become more specific - dealing in terms of "bad" (saturated) fat and "bad" (LDL) cholesterol - and fragmented into two components, which have been addressed independently. The subhypoteheses currently are:

Eating less saturated fat lowers cholesterol levels (particularly LDL)
Lower LDL cholesterol leads to a reduced chance of heart disease

Although a definitive trial of serum cholesterol reduction by diet and its effect on CHD has never been conducted, a number of epidemiological clinical studies have provided some support for subhypothesis 1, though a notable exception, demonstrated by these studies, is that stearic acid (the saturated fatty acid found in beef and cocoa) has a neutral or lowering effect on serum cholesterol. Furthermore, the body of supporting research consistently shows that saturated fat increases both LDL and HDL, and that replacing saturated fat with carbohydrates lowers HDLs and raises levels of triglycerides. Low HDL and high triglycerides are both risk factors for heart disease.

Subhypothesis 2 has also been difficult to prove, and has been the subject of much controversy. The only support for demonstrating item 2 has involved the use of cholesterol-lowering medications. This evidence is suspect, as we shall see below, but even if it were perfectly valid, there is still a problem:

Evidence that a certain class of people who take a certain drug have a reduced risk of cardiac events over those who take a placebo, does not prove that cholesterol causes heart disease, or that any method of lowering cholesterol (i.e. diet) reduces the risk of heart disease for everyone, since the drug has other other effects. As we shall she with statins, reduction of inflamation may be the heart-healthy effect. But first, let's look at the studies.

One of the most often-cited studies, the Lipid Research Clinics Coronary Primary Prevention Trial (LRC) studied 3,806 asymptomatic middle-aged men, half of which were given a cholesterol-lowering medication. Those on medication reduced their total cholesterol by 8.6% more than the control group (i.e., for a baseline level of 200, a drop of 27 points vs 25 points) and had only 7% chance of a cardiac event versus 8.6%. This 19% reduction in risk led many to claim that "For each 1% reduction in cholesterol, we can expect a 2% reduction in CHD events."

This somewhat misleading extrapolation is not in any way supported by the data. What the data says is that, for men with high cholesterol, taking the cholesterol reducing medicine may improve your chances of going five years without an event from 91.4% to 93%. It also says that it won't improve your chances of living at all. Other studies cited by proponents of the lipid hypothesis show similarly marginal reductions in risk and no reduction in overall mortality.

If it improves chances of surviving even slightly, why not take the drug anyway? For one thing, the cost of medication, both in terms of money and health. Cholesterol medicine costs everyone, as, based on the most optimistic numbers, you would still have to treat 25 patients over 5 years to prevent 1 death. Cholesterol medications may have adverse effects, which may explain why several studies do not show any significant difference in event or survival rate. Just one example of many, the Framingham Study found that there was virtually no difference in coronary heart disease (CHD) events for individuals with cholesterol levels between 205 mg/dL and 294 mg/dL - the vast majority of the US population.

The studies that most consistently show a survival benefit are those done using statins. The statins do appear to protect against cardiovascular disease, but apparently not due to cholesterol-lowering. The statins protected against coronary heart disease whether the cholesterol was high, normal, or low although normal or low. The statins were effective for women, old people, patients who already have had a coronary - all groups in which high cholesterol is not a risk factor. The number of strokes was reduced after statin treatment, although no studies have shown that a high cholesterol is a risk factor for stroke. Clearly the statins do more than just lower cholesterol.

Experiments have shown that statins make smooth muscle cells less inclined to produce thromboxane, a substance that promotes the clogging of blood. Moreover, lab experiments have shown that no amount of cholesterol (good or bad) can affect thromboxane production.

More than 40 trials have been performed to test if cholesterol-lowering can prevent a heart attack. In some of the trials the number of fatal heart attacks were lowered a little, in other trials the number of fatal heart attacks increased. Overviews of the trials have shown that when all results were taken together, just as many died in the treatment groups (e.g. those whose cholesterol was lowered) as in the untreated control group. The following table (from Uffe Ravnskov's site) gives the accumulated results. None of the differences were statistically significant.

	Treatment groups	Control groups
Number of individuals on trial Non-fatal heart attacks; per cent	59,514 2.8	53,251 3.1
Number of individuals on trial Fatal heart attacks; per cent	60,824 2.9	54,403 2.9
Number of individuals on trial Total number of deaths; per cent	60,456 6.1	53,958 5.8

Click here for details on these studies

References

The Oiling of America

Know Your Fat by Mary Enig PhD

Modern thinking on the causes of heart disease

The Cholesterol Myths by Uffe Ravnskoff

The International Network of Cholesterol Skeptics

The Soft Science of Dietary Fat by Gary Taubes

1998 Ginsberg study

Lots of convincing evidence that Saturated Fat has been given a bad rap

Effect of dietary fatty acids on serum lipids and lipoproteins. A meta-analysis of 27 trials by Mensink RP, Katan MB.

Effect of monounsaturated fatty acids versus complex carbohydrates on high-density lipoproteins in healthy men and women by Mensink RP, Katan MB.

Liu S, Willett WC, Stampfer MJ, et al. A prospective study of dietary glycemic load, carbohydrate intake, and risk of coronary heart disease in US women. Am J Clin Nutr 2000;71:1455-61

Dietary fat intake and risk of coronary heart disease in women: 20 years of follow-up of the nurses' health study by Oh K, Hu F, Stampfer M, Manson J, Willett WC