New cholesterol guidelines for converting healthy people into patients

    Uffe Ravnskov, MD, PhD

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In the May 16 issue of the Journal of the American Medical Association an expert panel from the National Cholesterol Education Program has published new guidelines for "the detection, evaluation, and treatment of high blood cholesterol" (read the paper). Their writing seems to be an attempt to put most of mankind on cholesterol-lowering diets and drugs. To do that, they have increased the number of risk factors that demands preventive measures, and expanded the limits for the previous ones. 

But  not only does the panel exaggerate the risk of coronary disease and the relevance of high cholesterol, it also ignores a wealth of contradictory evidence. The panel statements reveal that its members have little clinical experience and lack basic knowledge of the medical literature, or worse, they ignore or misquote all studies that are contrary to their view.

Here come a few examples of the panel’s false statements.

As an argument for using cholesterol-lowering drugs the panel claims that twenty percent of patients with coronary heart disease have a new heart attack after ten years. But to reach that number any minor symptom without clinical significance is included. 

Most people survive even a major heart attack, many with few or no symptoms after recovery. What matters is how many die and this is much less than twenty percent.

The panel also recommends cholesterol-lowering drugs to all diabetics above 20, and to people with the metabolic syndrome. If you have at least three of the "risk factors" mentioned below, you are suffering from the metabolic syndrome:

Test yourself and your family! I guess that most of you "suffer" from the metabolic syndrome. And this combination, says the panel, conveys a similar risk for future heart disease as for people who already have coronary heart disease. 

Luckily, it is not true.

It is not true either, that cholesterol has a strong power to predict the risk of a heart attack in men above 65. In the 30 year follow-up of the Framingham population for instance, high cholesterol was not predictive at all after the age of  forty-seven, and those whose cholesterol went down had the highest risk of having a heart attack! To cite the Framingham authors: ”For each 1 mg/dl drop of cholesterol there was an 11 % increase in coronary and total mortality (115).”

It is not true either, that high cholesterol is a strong, independent predictor for other individuals. 

In most studies of women and of patients who already have had a heart attack, high cholesterol has little predictive power, if any at all. 

In a large study of Canadian men high cholesterol did not predict a heart attack, not even after 12 years, and in Russia, low, not high cholesterol level, is associated with future heart attacks (read summary of paper).

Most interesting is the fact, that in some families with the highest cholesterol levels ever seen in human beings, so-called familial hypercholesterolemia, the individuals do not get a heart attack more often than ordinary people, and they live just as long (read the paper and my comment).

Taken together such observations strongly suggest that high cholesterol is only a risk marker, a factor that is secondary to the real cause of coronary heart disease. It is just as logical to lower cholesterol to prevent a heart attack, as to lower an elevated body temperature to combat an underlying infection or cancer.

It has also escaped the panel’s attention that the effect of the new cholesterol-lowering drugs, the statins, goes beyond a lowering of cholesterol. The question is whether their cholesterol-lowering effect has any importance at all because the statins exert their effect whether cholesterol goes down a little or whether it goes down very much.

No doubt, the statins lower the risk of dying from a heart attack, at least in patients who already have had one, but the size of the effect is unimpressive. In one of the experiments for instance, the CARE trial, the odds of escaping death from a heart attack in five years for a patient with manifest heart disease was 94.3 %, which improved to 95.4 % with statin treatment

For healthy people with high cholesterol the effect is even smaller. The WOSCOPS trial studied that category of people and here the figures were 98.4 % and 98.8 %, respectively.

In the scientific papers and in the drug advertisements these small effects are translated to relative effect. In the mentioned WOSCOPS trial for instance, it is said that the mortality was lowered by 25 %, because the difference between a mortality of 1.6 % in the control group and 1.2 % in the treatment group is 25 %.

When presented with accurate statistics on the value of statins, almost all my patients have rejected such treatment. To claim that the statins dramatically reduce a persons risk for CHD, as was stated in the press by Claude Lenfant, the director of the National Heart, Lung and Blood Institute, is a misuse of the English language.

The figures above do not take into account possible side effects of the treatment. In most animal experiments the statins, as well as most other cholesterol-lowering drugs, produce cancer (90), and they may do it in human beings also. 

In one of the statin trials there were 13 cases of breast cancer in the group treated vid pravastatin (Pravachol^®), but only one case in the untreated control group, a scaring fact that is never mentioned in the advertisements or the guidelines.

It is also an alarming fact that in one of the largest experiments, the EXCEL trial, total mortality after just one year's treatment with lovastatin (Mevacor^®) was significantly higher among those receiving statin treatment. Unfortunately (or happily?) the trial was stopped before further observations could be made.

In human beings the effects of cancer-producing chemicals are not seen before the passage of decades. If the statins produce cancer in human beings, their small positive effect may eventually be transformed to a much larger negative one, because side effects usually appear in much higher percentages than the small positive ones noted in the trials.

Whereas possible serious side effects of the statins are hypothetical, those from the previous cholesterol-lowering drugs, still recommended by the panel, are real. Taking all experiments together, mortality from heart disease after treatment with these drugs was unchanged and total mortality increased, a fact that has given researchers outside the National Cholesterol Education Program and the American Heart Association much reason for concern.

The panel’s dietary recommendations represent the seventh major change since 1961. For instance, the original advice from the American Heart Association to eat as much polyunsaturated fat as possible has been reduced successively to the present “up to ten per cent”. 

But why this limit? Seven years ago the main author of the new guidelines, Professor Scott Grundy, suggested an upper limit of only seven per cent, because, as he argued, an excess of  polyunsaturated fat is toxic to the immune system and stimulates cancer growth in experimental animals and may also provoke gall stones in human beings. These warnings have never reached the public.

Furthermore, the panel ignores that a recent systematic review of all studies concerning the link between dietary fat and heart disease found no evidence that a manipulation of dietary fat has any effect on the development of atherosclerosis or cardiovascular disease (read summary of the paper -this paper won the Skrabanek Award 1998). 

For instance, in a large number of studies, including the incredible number of more than 150,000 individuals, none of them found the predicted pattern of dietary fats in patients with heart disease. 

No supportive association has been found either between the fat consumption pattern and the degree of atherosclerosis (arteriosclerosis) after death.

Most important, the mortality from heart disease and from all causes was unchanged in nine trials with more radical changes of dietary fat than ever suggested by the National Cholesterol Education Program, a result that was confirmed recently in another review (read the paper and my comment)

To suggest that diabetic patients should obtain more than 50 percent of their caloric intake from carbohydrates seems unusually bad advice. Many carbohydrates are quickly transformed into sugar inducing rapid changes in blood sugar and insulin levels and thus stimulating a rapid conversion of blood sugar to depot fat and chronic feelings of hunger. Diabetic patients should eat more fat. 

Is it a coincidence that the Americans’ decreasing intake of fat during the last decade has been followed by a steady increase of their mean body weight and an epidemic increase of diabetes?

Instead of preventing cardiovascular disease the new guidelines may increase the mortality of other diseases, transform healthy individuals into unhappy hypochondriacs obsessed with the chemical composition of their food and their blood, reduce the income of producers of animal fat, undermine the art of cuisine, destroy  the joy of eating, and divert health care money from the sick and the poor to the rich and the healthy. The only winners are the drug and imitation food industry and the researchers that they support.

Uffe Ravnskov, MD,

If you lack the scientific evidence for something written above you will find it in my book, The Cholesterol Myths. Exposing the fallacy that saturated fat and cholesterol cause heart disease.

Extracts from the book are presented on my website: 
The Cholesterol Myths