For years we have been told that lower cholesterol levels are associated with a lower risk of death.

But it turns out that this is not true!

Research shows that the exact opposite is true!

When cholesterol levels fall, people are at a greater risk of death, not a lower risk of death!

This is noted a new review paper by independent researchers Uffe Ravnskov, MD, PhD, author of The Cholesterol Myths, Dr. Malcolm Kendrick, author of The Great Cholesterol Con, and other independent researchers.

In the review paper, they note:

“If high [total cholesterol] was the major cause of CVD [cardiovascular disease], people with high [total cholesterol] should have a higher risk of dying from CVD.

“The hypothesis that high [total cholesterol] causes CVD [cardiovascular disease] was introduced in the 1960s by the authors of the Framingham Heart Study.

“However, in their 30-year follow-up study published in 1987, the authors reported that ‘For each 1 mg/dl drop in [total cholesterol] per year, there was an eleven percent [11%] increase in coronary and total mortality’.

“Three years later the American Heart Association and the US National Heart, Lung and Blood Institute published a joint summary [8] concluding “a one percent reduction in an individual’s [total cholesterol] results in an approximate two percent reduction in CHD [coronary heart disease] risk”.

“The authors fraudulently referred to the Framingham publication to support this widely quoted false conclusion.”

In other words, they’ve been lying to us for 30 years!

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There is no association between total cholesterol and the degree of atherosclerosis notes a new review paper by independent researchers Uffe Ravnskov, MD, PhD, author of The Cholesterol Myths, Dr. Malcolm Kendrick, author of The Great Cholesterol Con, and others.

“If high [total cholesterol] causes atherosclerosis, people with high [total cholesterol] should have more atherosclerosis than people with low [total cholesterol]. In 1936 Landé and Sperry found that corrected for age, unselected people with low [total cholesterol] were just as atherosclerotic as people with high [total cholesterol]. Since then their seminal observation has been confirmed in at least a dozen studies,” they note.

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In people over 60, those with the highest LDL cholesterol levels were at a lower risk of dying over some number of years than those with the lowest LDL levels in 16 of 19 studies according to a new review paper by Uffe Ravnskov, MD, PhD, author of The Cholesterol Myths, Dr. Malcolm Kendrick, author of The Great Cholesterol Con, and others.

One-fourth with highest LDL levels 29-59% less likely to die over next 3-9 years

In 12 of those studies, the one-fourth of people with the highest LDL levels were 29% to 59% less likely to have died over the next 3-9 years than the one-fourth of people with the lowest LDL levels.

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Whether diet plus plays a major role in heart disease is a question that interests us all. Author Ravnskov has a mission. To inform his readers that there is a side to this question other than the view usually presented to us.

Government and health authorities never tire of remaining those of us who live in industrialized countries that heart disease is a major cause of death. They go further and tell us that heart disease is eminently preventable. While conceding that genetic background interacts with numerous environmental factors to influence each individuals risk of succumbing to heart attack, they insist that diet is foremost among these factors as a cause of heart disease, and that modifying diet provides a straightforward means of preventing heart attacks. If only people would do what they are advised—reduce their intake of fats, especially those rich in saturated fatty acids—then the high toll of death and disability from this disease could be readily reduced. If only!

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When the cholesterol campaign was introduced in Sweden in 1989 I became much surprised. Having followed the scientific literature about cholesterol and cardiovascular disease superficially I could not recall any study showing a high cholesterol to be dangerous to the heart or the vessels, or any type of dietary fat to be more beneficial or harmful than another one. I became curious and started to read more systematically.

Anyone who reads the literature in this field with an open mind soon discovers that the emperor has no clothes, and so did I. But I also learned that the critical analyses or comments, that I sent to various medical journals, were most often met with little interest from the editors and mocking answers from the reviewers. Besides, the inaccuracies, the misinterpretations, the exaggerations and the misleading quotations in this research area were so numerous that to question them all demanded a book.

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“The great tragedy of Science—the slaying of a beautiful hypothesis by an ugly fact.”
— Thomas Huxley (1825-1895)

Did you know…

• Cholesterol is not a deadly poison, but a substance vital to the cells of all mammals?
• Your body produces three to four times more cholesterol than you eat?
• This production increases when you eat only small amounts of cholesterol and decreases when you eat large amounts?
• The “prudent” diet, low in saturated fat and cholesterol, cannot lower your cholesterol more than a small percentage?
• The only effective way to lower cholesterol is with drugs?
• The cholesterol-lowering drugs are dangerous to your health and may shorten your life?
• The cholesterol-lowering drugs, called statins, do lower heart-disease mortality a little, but this is because of effects other than cholesterol lowering? Unfortunately, they also stimulate cancer.
• You may become aggressive or suicidal if you lower your cholesterol too much?
• Polyunsaturated fatty acids, those which are claimed to prevent heart attacks, stimulate infections and cancer in rats?
• If you eat too much polyunsaturated oil you will age faster than normal? You will see this on the outside as wrinkled skin. You can’t see the effects of premature aging on the inside of your body, but you will certainly feel them.
• People whose blood cholesterol is low become just as atherosclerotic as people whose cholesterol is high?
• More than thirty studies of more than 150,000 individuals have shown that people who have had a heart attack haven’t eaten more saturated fat or less polyunsaturated oil than other people?
• Old people with high cholesterol live longer than old people with low cholesterol?
• High cholesterol protects against infections?
• Many of these facts have been presented in scientific journals and books for decades but proponents of the diet-heart hypothesis never tell them to the public?
• The diet-heart idea and the cholesterol campaign create immense prosperity for researchers, doctors, drug producers and the food industry?

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“Some circumstantial evidence is very strong, as when you find a trout in the milk.”
—Henry David Thoreau (1817-1862)

A challenge

In 1953 Ancel Keys, director of the Laboratory of Physiological Hygiene at the University of Minnesota published a paper, which, looking back seems to have been an early kick-off for the cholesterol campaign.[2]

The horizon for the US Public Health Service is too limited, he wrote; any major disease should be prevented, not only those of infectious or occupational origin.

It doesn’t matter that the necessary measures are not yet known. The mere hope that the incidence of a disease may be altered is sufficient reason to invest money and manpower.

What Dr. Keys had in mind was coronary heart disease. This disease is a threat, he continued. While all other diseases are decreasing in the United States, there has been a steady upward trend in the death rate from coronary heart disease. On this particular point the Americans are inferior to other countries; in the US, for instance, four to five times more die from a heart attack than in Italy.

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Most of the fatty acids in the diet and in the blood are bound to a type of alcohol called glycerol. Usually each glycerol molecule is attached to three fatty acids, and this molecule complex is called a triglyceride. Often shortened to TG. As with cholesterol, high TG levels in the blood have been found to be associated with a higher risk of coronary heart disease. Does that mean that we should lover the level of TG in our blood?

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“In our need to understand, to explain, and to treat, the temptation to impute causality to association is pervasive and hard to resist. It is the most important reason for error in medicine.”
— Petr Skrabanek and James McCormick
, Authors of Follies and Fallacies in Medicine

Large and small percentages

Framingham is a small town near Boston, Massachusetts. Since the early-1950s a large number of Framingham citizens have taken part in a study surveying all factors that may play a role in the development of atherosclerosis and heart disease. Among other things their cholesterol was measured frequently.[30]

After five years the researchers made an observation, which should become one of the cornerstones in the cholesterol issue. When they classified the citizens into three groups with low, medium and high cholesterol values they saw that in the latter group more had died from heart attacks than in the two other groups. A high cholesterol level predicted a greater risk of a heart attack, they said; high cholesterol is a risk factor for coronary heart disease.

The predictive value of blood cholesterol levels was confirmed in the greatest medical experiment in history, the Multiple Risk Factor Intervention Trial, also called MR.FIT. In that trial researchers measured the blood cholesterol of more than 300.000 American middle-aged men.

Six years later the director of MR.FIT, professor Jeremiah Stamler and his coworkers from Chicago asked how many of these men had died and from what.[31] The participants were then divided into ten groups of equal size, so-called deciles, according to their cholesterol values. The first decile thus consisted of the tenth of the men with the lowest cholesterol, the tenth decile of the tenth with the highest cholesterol.[32]

The researchers analysis showed that in the tenth decile four times more men had died of a heart attack than in the first decile. Professor Stamler’s team put it in another way: “the risk of dying from a heart attack with cholesterol above 265 mg/dl (6.8 mmol/l) was 413 percent greater than with cholesterol below 170.”

With statistics you can change black to white, or vice versa; as any politician will tell you. Four hundred and thirteen percent! A frightening figure.

But let us look at the real figures and not only at the percentages. How many men had, in fact, died from a heart attack?

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Many doctors believe that most patients with familial hypercholesterolemia (shortened FH) die from CHD at a young age. Obviously they do not know the surprising finding of a Scientific Steering Committee at the Department of Public Health and Primary Care at Ratcliffe Infirmary in Oxford, England.[83] For several years, these researchers followed more than 500 FH-patients between the ages of 20 and 74 for several years and compared patient mortality during this period with that of the general population.

During a three-to-four-year period, six of 214 FH-patients below age 40 died from CHD. This may not seem particularly frightening, but as it is rare to die from CHD before the age of 40, the risk for these FH patients was almost 100 times that of the general population.

During a four-to-five-year period, eight of 237 FH-patients between ages 40 and 59 died, which was five times more than in the general population. But during a similar period of time, only one of 75 FH-patients between the ages of 60 and 74 died from CHD.

If these results are typical for FH, you could say that, between ages 20 and 59, about three percent of the patients with FH died from CHD, and between ages 60 and 74, less than two percent died from CHD, fewer than in the general population.

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“Ye shall eat the fat of the land.”
— Genesis 45:18

Food and fat in various populations

Why do levels of cholesterol vary in different people? Because of their food! This is the answer from Ancel Keys, stated over and over again in his papers. No alternative explanations are ever mentioned; Keys’s hand never trembles when he writes about the influence of diet on blood cholesterol.

One of his arguments is that the average blood cholesterol is high in countries where people eat lots of high-fat food, especially foods high in animal fat, and low in countries where people eat little fat. And, asserts Keys, if an individual with low cholesterol moves to an area where people’s cholesterol is high, then his cholesterol will also rise.

In 1958 Keys illustrated his idea with a diagram demonstrating the relationship between the amount of fat in the food and the cholesterol level of the blood in various populations (fig. 3A).[86]

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“Theorists almost always become too fond of their own ideas, often simply by living with them for so long. It is difficult to believe that one’s cherished theory, which really works rather nicely in some respects, may become completely false.”
—Francis Crick, Nobel Prize laureate together with James Watson for discovering the structure of DNA

Cholesterol: Villain or Innocent Bystander?

Although scientists should do more questioning, in cholesterol research one statement never gets questioned because it is considered just as self-evident as the law of gravity. Even many opponents of the diet-heart idea neglect to question this statement. And what is this statement? It is that, when its level is high in the blood, cholesterol passes through the vessel walls, transforming arteries from smooth canals to rocky rapids.

Doctors and scientists may debate whether cholesterol leaks in passively or is actively transported by cells. But there is a general agreement about the importance of the cholesterol level of the blood; the higher it is, the faster the arteries become sclerotic.

As early as 1953, Ancel Keys wrote: “It is a fact that a major characteristic of the sclerotic artery is the presence of abnormal amounts of cholesterol in that artery. And he added: this cholesterol is derived from the blood.”[101]

No proofs, and no arguments, not from Keys and not from his followers. Cholesterol comes from the blood, and that’s the end to it. Scientists discuss how high the cholesterol level has to be for atherosclerosis to start, but they do not discuss whether the cholesterol level by itself has any importance. The role played by cholesterol in the process of atherosclerosis is no longer under discussion; it has been settled forever, or so we are led to believe. Let us have a closer look at the facts.

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“Rabbit tricks are positive successes.”
—Henry Houdini

Animals eat the wrong food

Perhaps you’re finding the cholesterol question in man a little complicated and it is. But it’s nothing compared to the situation in the animal kingdom, although, if it will comfort you, I’ll say now that cholesterol studies just don’t apply to man.

None of the mammals of the world are exactly like us as regards cholesterol. They have other amounts of it in their blood, they rarely eat as we do, and most of them do not become arteriosclerotic.

Many mammals never eat food containing cholesterol. If they are force-fed a cholesterol-rich diet, the cholesterol level of their blood rises to values many times higher than ever seen in normal human beings. And since such animals cannot dispose of the cholesterol they have eaten, every organ soaks up the cholesterol as a sponge soaks up water.

If animals are so different from us, how can we use them to prove that fat food and cholesterol are dangerous to human beings? Using cholesterol-rich fodder, it is possible to induce in rhesus monkeys arterial changes that vaguely resemble human arteriosclerosis, but it is not possible in baboons. How do we know if man reacts like a rhesus monkey or like a baboon or in some very different way?

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Zealous proponents of the cholesterol hypothesis argue that we should begin cholesterol-lowering measures in childhood. They say that atherosclerosis starts in the early years; therefore, all parents should test their children’s cholesterol and teach them to eat “properly,” beginning at the age of two. This age limit was chosen because, in spite of their clever persuasions, diet-heart proponents would have difficulty convincing parents that whole milk, an allegedly poisonous food for adults, is harmful to babies. So “intervention” is held off until the tender age of 24 months, when most youngsters in the US are put on skimmed milk, milk substitutes and low-fat foods.

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“But besides real diseases we are subject to many that are only imaginary, for which the physicians have invented imaginary cures; these have then several names, and so have the drugs that are proper for them.”
—Jonathan Swift (1667-1745)

Time for truth

As one scientific study after another has shown, people can gorge on animal fat for many years and still keep their blood cholesterol low. What we have learned also is that atherosclerosis and heart attacks may occur whether one’s food is meager or fat, and most surprisingly, whether cholesterol is high or low. Given these facts, is there any reason to think that lowering blood cholesterol with diet or medicine can prevent heart attacks?

Based on what I have presented so far, the answer is no. In fairness, however, it still may be possible that high-fat food contains something other than cholesterol and saturated fatty acids that might be dangerous to the heart, or that high blood cholesterol slows the coronary circulation in some way other than by stimulating atherosclerosis. It might just be possible to reach the correct conclusion from the wrong premises.

The diet-heart idea itself is invalid, as I have already demonstrated in several ways. But the best way to know for sure if fat food and a high cholesterol level are dangerous is to use human beings as guinea pigs, to see if coronary heart disease can be induced by feeding these people animal fat or by elevating their blood cholesterol, or to see if heart attacks can be prevented by feeding the experimental subjects a low-fat diet or by lowering their blood cholesterol.

The idea to raise blood cholesterol during several years by dietary means is stillborn no matter how interesting it seems. The ethical committees that must approve all experiments on living creatures should certainly condemn the idea. Fortunately the Masais and other populations already have performed the experiment for us with well-known result.

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An expedient byproduct

Parallel with the mentioned study of healthy men the Finnish researchers performed another experiment on men who already had had a heart attack. About 600 such individuals participated, all of them worked at the same companies as those in the original Helsinki study.[157]

The result after five year was disheartening. Seventeen of those who took gemfibrozil had died from a heart attack; compared to only eight in the placebo group.

Dr. Frick and his coauthors were eager to stress, that this difference was most probably a product of chance. In the summary of the paper they wrote: the number of fatal and non-fatal heart attacks did not differ significantly between the two groups.

They were right, because in contrast to their fellow-directors of the other trials they used the correct formula for determining the effect of a treatment, the two-sided t-test. If they had used the one-sided test as diet-heart supporters usually do when the allegedly positive effects are measured, significantly more had died in the treatment group.

But they had modified the result in another way. In the group “cardiac deaths” they had included a small group called “unwitnessed death.” That death is unwitnessed means that we do not know the cause of the death. It is not self-evident that an unwitnessed death is due to a heart attack and such deaths should of course have been classified otherwise.

If they had excluded the unwitnessed deaths there were more than three times more fatal heart attacks in the treatment group; sixteen against five. And this difference was indeed statistically significant.

The directors of the study admitted that the result was not “in accord with previous experience,” but they had a number of explanations.

As the trial was only “an expedient byproduct” of the original trial the number of individuals had been too small to give reliable results, they said. They were especially concerned about the low number of heart attacks in the control group. It was unlikely that it reflected the incidence in the general population. Most probably the individuals in the control group by chance had been less affected by coronary atherosclerosis than those in the treatment group.

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“It’s easier to fool people than to convince them they have been fooled.”
—Mark Twain

In the late 1980s, the pharmaceutical companies introduced a new type of cholesterol-lowering drug called the “statins.” These drugs inhibit the body’s production of many important substances, one of which is cholesterol.

Sold as Zocor®, Mevacor®, Pravachol®, Lipitor® and Lescol® these new drugs have received wide acclaim because of their supposed lack of serious side effects and, in particular, because of the substantial cholesterol they can achieve. Whereas the earlier drugs could lower cholesterol by 15-20 percent at most, the statins can lower it by 30-40 percent or more. As of January 2000, the results from the large controlled, randomized and double-blind studies, including more than 30,000 test individual, and numerous angiographic trials have been published. More data will come.

Most doctors believe that the outcome of these trials is a victory for the cholesterol hypothesis. However, a closer look reveals that the cholesterol lowering effects are unimportant and actually rather a drawback. Furthermore, the benefits are trivial and if present, only apply to certain patient groups. In addition, by process of statistical manipulation, ingenious criteria for selecting the test individuals, and generous limits to what are considered as normal laboratory results, the directors of the trials and the drug companies have succeeded in belittling the side effects and thus presenting the statins as harmless.

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New guidelines

EXCEL, the Expanded Clinical Evaluation of Lovastatin

This trial was performed by Dr. Reagan H. Bradford and his team from a large number of American clinics and research institutions, including the Merck Sharp & Dohme Research Laboratories at West Point, NY, where the drug was produced where the drug was produced. More than 8,000 healthy individuals (called “patients” in the trial reports) with cholesterol levels between 240 and 300 mg/dl (6.2-7.7 mmol/l) received one of four different doses of lovastatin (Mevacor®) or a placebo.[225]

With a view to reporting on possible adverse effects of the treatment, preliminary study results were published after only one year of the trial. No significant side effects were reported, but in the fine print the authors were obliged to mention that death due to all causes was 0.5 percent in the four lovastatin groups combined (32 or 33 individuals out of a group of about 6,600—no exact figures were given in the report) compared to 0.2 percent in the placebo group (three or four individuals out of a group of 1,650). By taking all the lovastatin groups together, the difference would have been statistically significant if the number of deaths in the treatment groups were 33, but not if it were 32. Even if the difference wasn’t statistically significant after one year, it would certainly have become significant if the tendency to a higher mortality in the treatment groups had continued throughout the trial. In any case, the aim of the treatment was to lower mortality and most certainly no lowering was achieved.

Today at least 20 reports from the EXCEL trial have been published in various medical journals. These reports tell us how well lovastatin is tolerated and how effective it is in lowering blood cholesterol levels in various populations, but not one of them has reported the final outcome of the trial, although more than ten years have passed since it began. Therefore, we do not know whether the increased mortality, seen after just one year of treatment, has continued throughout the trial.

Why have we never heard about this outcome of the first statin trial, which was one of the largest? I asked that question in a letter to Merck, Sharp & Dohme. They answered that, “the trial was not designed to measure the clinical outcome, only to test whether the drug was tolerable and did not produce any serious side effects.”

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The figures from the MR.FIT study included both the 12,000 participating men, but also the more than 300,000 men who were excluded for various reasons. A large number of studies concerning the follow-up of these screenees has been published in well-known international medical journals, and these studies are cited again and again as the strongest proof that there is a linear association between blood cholesterol concentrations and the risk of future heart disease.

Unfortunately, the data presented in the MR.FIT reports have been carelessly produced. In a systematic search of the literature on the MR.FIT study, Professor Lars Werkö, then director of the Swedish Council on Technology Assessment in Health Care, an independent governmental agency known for its integrity, found 34 papers reporting the relationship between serum cholesterol and mortality. He asked himself whether it really was necessary to publish all these reports as their results were so similar.

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Intervening is a way of causing trouble.
—Lewis Thomas

Risk at both ends of the scale

The smaller number of heart deaths in the soybean trial of Dr. Dayton and his team, mentioned in chapter 6, was offset by a larger number of cancer deaths. Does it mean that soybean oil causes cancer?

Diet-heart proponents would argue that Dr. Dayton’s soybean trial was an anomaly, and that other trials with polyunsaturated fat have not resulted in more cancer. However, never before had such huge amounts of polyunsaturated fat been eaten over such a long period of time. Dr. Dayton’s patients were also much older than in the other trials, and thus more susceptible to cancer, which means that a possible cancer-provoking effect could be detected more easily.

Another disquieting fact is that many studies have reported a low cholesterol to be a risk factor for cancer. The purpose of these studies was to follow a great number of individuals for many years to see if the Framingham researchers were right when they claimed that high cholesterol means a high risk of a heart attack. Surprisingly, these more recent studies revealed that it was just as dangerous to have a very low cholesterol level, as it was to have a very high one. Those who had very low cholesterol levels had a greater incidence of cancer while those with very high cholesterol suffered more heart attacks.

Most investigators thought that low cholesterol levels were not the cause but the result of the cancer since cancer cells need cholesterol, just as any other cells do. Perhaps their rapid growth and greater need for cholesterol reduced the cholesterol levels in the blood?

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Coronary heart disease is a multifactorial disease that requires multifactorial intervention. This is the view of Dr. Dean Ornish and his group at the Preventive Medicine Research Institute, Sausalito, California, a view they share with many other doctors and researchers. Dr. Ornish and his group chose to intervene with a low-fat, low-cholesterol vegetarian diet, smoking cessation, stress-management training and moderate exercise. They selected 94 patients with a diagnosis of coronary artery disease according to a previous coronary angiogram. Fifty-three were randomly assigned to the experimental group and 43 to the control group, but when told about the design of the study only 28 and 20, respectively, agreed to participate.

A new angiogram was performed after one year, but one of the angiograms disappeared; in three patients the second angiogram could not be evaluated; one patient was not studied because of unpaid bills; one died during heavy exercise; and one dropped out because of alcohol misuse. Thus, only 22 patients in the experimental group and nineteen in the control group were available for analysis.

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”… the fourth and last wrong measure of probability I shall take notice of, and which keeps in ignorance or error more people than all the other together, is… the giving up our assent to the common received opinions, either of our friends or party, neighbourhood or country. How many men have no other ground for their tenets than the supposed honesty, or learning, or number of those of the same profession? As if honest or bookish men could not err, or truth were to be established by the vote of the multitude; yet this with most men serves the turn. If we could but see the secret motives that influenced the men of name and learning in the world, we should not always find that it was the embracing of truth for its own sake, that made them espouse the doctrines they owned, and maintained.”
—John Locke (1632-1704)

“When two people share responsibility, they will each carry only one percent of the burden, at most.”
—Piet Hein 
(1906-1996; Danish poet and physicist)

The proofs

“It has been established beyond a reasonable doubt that lowering definitely elevated blood cholesterol levels…will reduce the risk of heart attacks caused by coronary heart disease.”

If you have read this book, you probably wonder if I just quoted a drug advertisement, and if the drug company got taken to court for misleading advertising practices. The statement, however, is quoted, word for word, from the summary of a consensus conference held at the National Institutes of Health in 1984[265]. The aim of this conference was to discuss how the results of the LRC trial should be translated into general recommendations for the American people.

The conference was headed by Basil Rifkind, who had been the director of the trial. Rifkind also determined who would be invited to join the panel that formulated the final recommendations.

Consensus is Latin for accord or unanimity. There were no such feelings in the audience, however. Among the many critical voices, Professor Michael Oliver from Scotland, the director of the early WHO trial, stressed that the trend towards an increased mortality from other causes was as strong as the trend towards a reduced mortality from coronary heart disease. “Why explain these results away?” he asked.

A British epidemiologist named Richard Peto admitted that in every trial “something ridiculous” had happened. But, he said, while no single trial was convincing, the trial evidence was impressive when analyzed together. (Does this sound familiar?)

Biostatistician Paul Meier from the University of Chicago opposed Rifkind’s presentation of the LRC trial. He remarked: “To call ‘conclusive’ a study which showed no difference in total mortality, and by the usual statistical criteria, an entirely non-significant difference in coronary incidents, seems to me a substantial misuse of the term.”

There was no unanimity, either, about the treatment that was going to be introduced. One speaker at the conference advised lowering dietary cholesterol; another advised lowering dietary fat of animal origin and did not think that dietary cholesterol had any importance; a third member recommended lowering the caloric intake, no matter how.

The final statement from the conference resolved the disagreements by recommending all three dietary measures. Criticism from the audience was simply swept under the rug. Some of the critics were cut off by the panel chairman, Daniel Steinberg, who cited a lack of time. Requests to write a minority report were denied as inconsistent with the conference’s goal of consensus.[266]

Let us now look at the findings, which the panel considered as the scientific support for their recommendations. Here they are at last, all the proofs, which, added to each other, supposedly speak overwhelmingly for the diet-heart idea. Knowing the radical measures, which followed, we can be confident that the panel members included all available arguments. Here they come, all the strong proofs.

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From a George Lymann Duff memorial lecture:

“A final lesson worth noting is that the current cholesterol campaign represents a rare concordance of interests on the part of many constituencies. The health professions, the pharmaceutical industry, government, the public—all should benefit from efforts to promote and implement the recommendations and guidelines in the Adult Treatment Panel report. Physicians will benefit because they will be providing better medical care to their patients and incidentally will have available a new and expanded market of patients for preventive medical care. The pharmaceutical industry will benefit from the greatly expanded market for cholesterol-lowering drugs that will result from even the most careful application of the guidelines on a national scale. The public will benefit from reductions in coronary risk and disease. And government will benefit from better health of its citizens and from reduced national expenditures that should result from reductions in coronary risk and disease.

“Moreover, this concordance of interests should promote cooperation—even collaboration—on the part of these various constituencies, something that is indeed occurring in part in quite a gratifying way.

“In closing, I’d like to acknowledge the pleasure I’ve had in playing an active role in the national cholesterol campaign. It has been a most exciting year—and a great pleasure this evening to be able to share some of my thoughts with friends and colleagues in the cholesterol and cardiovascular communities.”

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“Only dead fishes go downstream.”
— Polish proverb

At this point you may probably wonder why you haven’t heard about all this controversy before and why not even your doctor knows anything.

Criticism has been raised—a great deal of criticism. But it has been presented in journals and books that are not easily accessible to the layman, and critical voices have been drowned out in a flood of papers from the proponents. And the media, supported in large part by advertising revenues from pharmaceuticals and a food industry that has found it extremely profitable to use vegetable oils instead of animal fats, has consistently ignored the voices of dissent while hyping the recommendations for expensive drugs and dietary change.

Furthermore, as I have exemplified here and there in the previous chapters, the pontiffs of the cholesterol crusade systematically ignore the contradictory findings. And the same people are brilliant in finding the few studies that apparently are in support, and if they are not, a magic spell may change the picture. And don’t forget that if your research is in accord with the wizards view, financial support from the drug and the food industry is almost endless. If not, you may risk both your funding and your position. Let me just remind you about Kilmer McCully, the American researcher who discovered the association between homocysteine and atherosclerosis. When he published his observation that the homocysteine, not the cholesterol concentration in the blood was associated with degree of atherosclerosis, he lost his position at Harvard Medical School and Massachusetts General Hospital and for two years he wasn’t able to get a new one anywhere.[268]

And there are more brave researchers. Presented here, in alphabetic order, are a few of those who have had the courage to swim against the current. All of them have produced a large number of scientific studies of which I shall mention only the most important.

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After a lecture, a journalist asked me how she could be certain that my information was not just as biased as that of the cholesterol campaign. At first I did not know what to say. Afterwards I found the answer.

She could not be certain. Everyone must gain the truth in an active way. If you want to know something you must look at all the premises yourself, listen to all the arguments yourself, and then decide for yourself what sees to be the most likely answer. You may be easily led astray if you ask the authorities to do this work for you.

This is also the answer to those who wonder why even honest scientists are misled. And it is also the answer to those who after reading this book, ask the same question.

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These are the references for the book
The Cholesterol Myths: Exposing the Fallacy that Saturated Fat and Cholesterol Cause Heart Disease
by Uffe Ravnskov, MD, PhD.

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Low cholesterol levels increase the risk of cancer notes Uffe Ravnskov, MD, PhD in the wonderful documentary Statin Nation.

He notes that a Japanese study in which they gave roughly 40,000 men small doses of the statin, Zocor (simvastatin), and followed them for 6 or 7 years, those with the lowest cholesterol levels had 3 times more cancer deaths than in men with normal cholesterol levels.

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HIGHER cholesterol levels are associated with
- a LONGER life
- a LOWER risk of cancer
- a LOWER risk of infections
notes independent researcher Uffe Ravnskov, MD, PhD in an extended interview on the DVD for the wonderful documentary called
Statin Nation.

He also notes that cholesterol is essential for life.

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Lipoproteins including LDL, HDL and VLDL, which carry cholesterol, perform an immune function in that they bind to and inactivate bacteria and viruses notes independent researcher Uffe Ravnskov, MD, PhD in an extended interview on the DVD for the wonderful documentary called
Statin Nation.

LDL is THE MOST POTENT of the lipoproteins in humans at performing this immune function, Dr. Ravnskov notes.

People with LOW cholesterol levels have HIGHER rates of infectious disease.

Below is the exact quote of what Dr. Ravnskov says about this.

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"[T]here is no evidence that diet prevents cardiovascular morbidity or mortality," noted Uffe Ravnskov, MD, PhD.

"This effect was shown in a systematic review of eight ecological, 41 cross-sectional, 25 cohort, six case-control studies, and a meta-analysis of nine controlled randomised dietary trials." Read the entire article | Email this article

According to conventional wisdom it is wise to lower your cholesterol if it is too high.

The main reason for this advice is the observation that people with a high cholesterol more often get a heart attack than people with a normal or a low cholesterol.

The observation is correct, but it does not mean that the high cholesterol is the cause of the heart attack (see section 1). If it were, lowering of the high cholesterol by any means should prevent it, but it doesn´t (except with the new group of cholesterol-lowering drugs, the statins; see below).

[This article was written by Uffe Ravnskov, MD PhD, and is an excerpt from his book The Cholesterol Myths: Exposing the Fallacy That Saturated Fat and Cholesterol Cause Heart Disease.]

[Note: The book Fat and Cholesterol are Good for You is a shortened, simplified and updated version of Dr. Ravnskov's first book, "The Cholesterol Myths".] Read the entire article | Email this article

"f you have come to believe that you can ward off death from heart disease by altering the amount of cholesterol in your blood, whether by diet or by drugs, you are following a regime that still has no basis in fact," wrote Edward R. Pinckney, MD, editor of four medical journals and former co-editor of JAMA.
"Rather, you as a consumer, have been taken in by certain commercial interests and health groups who are more interested in your money than your life."

[This is an article written by Uffe Ravnskov, MD PhD, and is an excerpt from his book The Cholesterol Myths: Exposing the Fallacy That Saturated Fat and Cholesterol Cause Heart Disease.]

[Note: The book Fat and Cholesterol are Good for You is a shortened, simplified and updated version of Dr. Ravnskov's first book, "The Cholesterol Myths".] Read the entire article | Email this article

George Mann [ScD, MD], now retired, was previously a professor in medicine and biochemistry at Vanderbilt University in Tennessee. From his studies of the Masai people (see section 3) he realized that diet couldn't possibly be the main cause of high cholesterol and coronary heart disease. As long ago as 1977, in The New England Journal of Medicine he published a strong argument against the diet-heart idea citing the lack of relationship between dietary habits and blood cholesterol, the lack of correlation between this century's trends in fat consumption and death rates in the United States, and the disappointing outcome of the cholesterol lowering trials (92).

[This is an article written by Uffe Ravnskov, MD PhD, and is an excerpt from his book The Cholesterol Myths: Exposing the Fallacy That Saturated Fat and Cholesterol Cause Heart Disease.]

[Note: The book Fat and Cholesterol are Good for You is a shortened, simplified and updated version of Dr. Ravnskov's first book, "The Cholesterol Myths".] Read the entire article | Email this article

Michael F. Oliver, a former professor and director of the Wynn Institute for Metabolic Research, London, [and formerly worked at the National Heart and Lung Institute in London, England] those at a very high risk for cardiovascular risk may benefit from cholesterol lowering, but in several papers he has warned against campaigns for cholesterol lowering in the general population.

He notes that the accumulated evidence [of cholesterol-lowering in the general population] is that total mortality is unchanged or possibly even increased (94).

[This is an article written by Uffe Ravnskov, MD PhD, and is an excerpt from his book The Cholesterol Myths: Exposing the Fallacy That Saturated Fat and Cholesterol Cause Heart Disease.]

[Note: The book Fat and Cholesterol are Good for You is a shortened, simplified and updated version of Dr. Ravnskov's first book, "The Cholesterol Myths".] Read the entire article | Email this article

"The idea that saturated fats cause heart disease is completely wrong, but the statement has been “published” so many times over the last three or more decades that it is very difficult to convince people otherwise unless they are willing to take the time to read and learn what all the economic and political factors were that produced the anti-saturated fat agenda," lipid biochemist Mary Enig was quoted as saying in an interview when asked if saturated fat causes heart disease.

[This is part of an article written by Uffe Ravnskov, MD PhD, and is an excerpt from his book The Cholesterol Myths: Exposing the Fallacy That Saturated Fat and Cholesterol Cause Heart Disease.]

[Note: The book Fat and Cholesterol are Good for You is a shortened, simplified and updated version of Dr. Ravnskov's first book, "The Cholesterol Myths".] Read the entire article | Email this article

One of the most surprising facts about cholesterol is that there is no relationship between the blood cholesterol level and the degree of atherosclerosis in the vessels. If a high cholesterol really did promote atherosclerosis, then people with a high cholesterol should evidently be more atherosclerotic than people with a low. But it isn´t so.

[This article was written by Uffe Ravnskov, MD PhD, and is an excerpt from his book The Cholesterol Myths: Exposing the Fallacy That Saturated Fat and Cholesterol Cause Heart Disease.]

[Note: The book Fat and Cholesterol are Good for You is a shortened, simplified and updated version of Dr. Ravnskov's first book, "The Cholesterol Myths".] Read the entire article | Email this article

A reduction of animal fat and an increase of vegetable fat in the diet is said to lower the blood cholesterol. This is correct, but the effect of such dietary changes is very small. Ramsay and Jackson (37) reviewed 16 trials using diet as intervention. They concluded that the so-called step-I diet, which is similar to the dietary advices that are given nationwise by the health authorities in many countries, lower the serum cholesterol by 0 to 4% only. There are more effective diets, but they are unpalatable to most people.

[This article was written by Uffe Ravnskov, MD PhD, and is an excerpt from his book The Cholesterol Myths: Exposing the Fallacy That Saturated Fat and Cholesterol Cause Heart Disease.]

[Note: The book Fat and Cholesterol are Good for You is a shortened, simplified and updated version of Dr. Ravnskov's first book, "The Cholesterol Myths".] Read the entire article | Email this article