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Cholesterol Myths by Uffe Ravnskov MD PhD: Myth 9: The Cholesterol Campaign is Based on Good Science
Wednesday, November 12, 2014 9:55 am Email this article
”… 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)
“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. 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.
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.
The inherited disorders prove that high blood cholesterol by itself can induce coronary heart disease.
This is pure speculation. What we do know is that people with inherited disorders have high cholesterol because the passage of cholesterol from blood to cell is slowed down. What we also know is that atherosclerosis is more widespread and more severe in these individuals. But is it true atherosclerosis? And is it really caused by t heir high cholesterol?
What is special for individuals with familial hypercholesterolemia is best seen in the rare homozygous form, the form that appears when both parents have the deficient gene for the LDL-receptor. Autopsy studies of such individuals show that cholesterol deposition is increased, not only in their vessels, but generally, throughout their bodies. Many other organs are impregnated with cholesterol, just as is seen in cholesterol-fed rabbits.
The vascular changes seen in people with the more common heterozygous form of familial hyper?cholesterolemia are more difficult to analyze because these changes must partly be due to the metabolic error and partly to common atherosclerosis. And how do we know if possible effects of treatment stem from reduction of the changes caused by the inborn error or from reduction of atherosclerosis? Thus, any conclusion, which may be true for individuals with familial hypercholesterolemia, cannot possibly be valid for the rest of mankind.
Animals become atherosclerotic when they are fed diets that raise their blood cholesterol, and the atherosclerosis disappears when their cholesterol is lowered again with diet or drugs.
What the animal experiments are worth as evidence is seen in chapter 5. The fact that vascular changes, produced by an extremely unnatural diet, disappear when the diet is terminated cannot prove anything about human atherosclerosis. The fact that vascular changes produced by an extremely unnatural diet forced down in a stressed rabbit’s stomach by catheter disappear when the diet is terminated cannot prove anything about human atherosclerosis. Weird John’s gastric ulcer, caused by his swallowing iron nails, disappeared when John ceased eating hardware. But this is no proof that other patients’ gastric ulcers are caused from eating building materials.
Wisely, nothing was said in the report about coronary heart disease, because it is not possible to produce this disease in animals only by increasing blood cholesterol.
There is a direct connection between blood cholesterol and the occurrence of coronary heart disease in various populations.
Look at this diagram. It is based on data from WHO and FAO and shows the association between cardiovascular mortality and serum cholesterol in various countries. If anything, low mortality is seen more often in countries where mean cholesterol is highest.
People who have emigrated to another country with a higher average blood cholesterol level gradually acquire the dietary habits, blood cholesterol concentrations, and CHD rates of their new country of residence.
The Masai people, the Polynesians and many more were ignored; nothing was said either about Marmot’s studies of the Japanese emigrants.
Severity and frequency of raised plaques in the aorta and coronary arteries are strongly correlated with blood cholesterol levels.
Amazing, isn’t it? Maintain any delusion again and again, no matter how far from reality it may be, and it may finally be taken for the truth. See chapter 5 for the facts.
Populations experiencing severe dietary (especially fat) limitations and weight loss have been shown to have less atherosclerosis and CHD and fewer heart attacks.
Many other factors than lack of dietary fat are different in severely deprived people; no conclusions can be drawn from such observations.
Epidemiological studies have shown that elevated blood cholesterol levels in healthy people predict the future occurrence of coronary heart disease.
… except for Maoris, Stockholmers, Greeks, Finns and Canadians, except for women and men after forty-seven, and except for those who already have had a coronary.
Evidence emerging from multiple clinical trials clearly indicates that lowering blood cholesterol levels in patients with a high blood cholesterol level decreases the likelihood of fatal and nonfatal coronary heart disease.
A few lines after the above statement, the consensus report said that none of the previous dietary trials had proven that a lowering of blood cholesterol can diminish the incidence of coronary heart disease. In both the “proving” trials (LRC and CLAS), cholesterol had been lowered with drugs because diet was considered insufficient. Thus, the panel admitted, that no trial with diet had proven beneficial. At that time no drug trial either had lowered fatal coronary heart disease with statistical significance.
Thus, the evidence obtained from genetic, experimental, epidemiological, and clinical intervention investigations overwhelmingly supports a causal relationship between blood cholesterol levels and coronary heart disease.
This was all of it. This is the scientific foundation of the cholesterol campaign, the numerous proofs that do not suffice one by one but that, taken together, are so “overwhelming.”
The panel considered the conclusive power so great that they had no doubts when it came to recommendations.
More than a dozen randomized trials of the effects of fat-controlled diets or drugs permit the conclusion that reduction of blood cholesterol levels in people with relatively high initial levels will reduce the rate of coronary heart disease. This has been shown most convincingly in men with a high cholesterol level, but although direct intervention studies have not been conducted in women, there is no reason to propose a separate treatment schedule for women.
Nothing was said about the fact that most trials did not demonstrate any benefit (in fact both the number of deaths and the number of heart attacks had increased in some of them); or that in most studies high cholesterol has not been associated with an increased coronary mortality for women.
Individuals in the high-risk group (above 6.2 mmol/l (242 mg/dl) at an age of 30-39; above 6.7 mmol/l (261 mg/dl) at an age above 40) should primarily have intensive dietary treatment requiring a major effort on the part of physicians, nutritionists, dieticians, and other health professionals. If this treatment does not work, drug therapy should be used.
Thus, only in the United States, tens of millions of healthy individuals should be on a diet. Let’s hope that there are enough health professionals to carry out this daring project.
The drug producers and their stock holders should be happy, because, as you now know, it is extremely difficult to lower blood cholesterol with diet alone. The panel also knew it: after all, the control individuals in the LRC trial had eaten the recommended diet, and their cholesterol decreased less than one percent. No doubt about it—drugs would be necessary.
Individuals with moderate-risk blood cholesterol (above 5.7 mmol/l (220 mg/dl) at an age of 30-39; above 6.2 mmol/l (240 mg/dl) at an age above 40), — the upper 25 percent on the cholesterol scale — should also have intensive dietary treatment, and if other risk factors were present, drug therapy should be considered.
Further tens of millions of Americans on drab diet and dangerous drugs! In the LRC trial those from the upper 0.8 percent on the cholesterol scale were treated, and with drugs. And only after enormous effort could the trial directors come up with a result that nobody but a statistical incompetent could see as positive.
If it is that difficult with drugs to improve the prognosis for people with the most extreme cholesterol levels, how can diet alone produce a benefit for those with no more than a moderately high cholesterol?
Blood cholesterol is too high in most Americans because they eat too much saturated fat, too many calories, and too much cholesterol.
To avoid conflicts between the proponents, the recommendations included all the suggested diets.
Therefore, all Americans except children below the age of two are recommended a diet with no more than 250-300 mg cholesterol per day, and a reduction of total saturated fat intake to 10% or less of total calories, and an increase of polyunsaturated fat intake but to no more than 10% of total calories. The goal is to reduce blood cholesterol in the entire population to less than 5.0 mmol/l (195 mg/dl).
Here everybody is urged to eat what was originally advised for the high-risk group, except that people with normal cholesterol do not get help from health professionals. These people, the majority, have to judge for themselves when the magical ten per cent limit for polyunsaturated fat has been reached, the limit between harmless and dangerous amount. Nobody knows how the panel members found just that limit as crucial; nor why they chose a cholesterol limit of 195 mg/dl (5 mmol/l). (Every authority sees to have his own limit; the chosen value was probably determined by a vote).
There is no direct evidence of the benefit to be expected in the elderly, but dietary treatment may still be helpful.
Apart from the fact that there is no evidence either for the rest of mankind, why should we sour the lives of the elderly with an unpleasant diet if its benefit has never been proven? And remember you belong to the elderly as soon as you reach the age of forty-seven.
Also children should have treatment but not before the age of two. If blood cholesterol is above 4.4 mmol/l (172 mg/dl) diet is recommended; if it is above 5.2 mmol/l (203 mg/dl), drugs should be given, for instance, cholestyramine.
Poor kids! Remember that two out of three trial subjects given cholestyramine had gas, heartburn, belching, bloating, abdominal pain, nausea, vomiting, constipation or diarrhea.
If the American population follow the recommendations of the National Cholesterol Education Program, substantial improvements are in sight. For instance, if the cholesterol is lowered by five percent, the risk of having a heart attack will be reduced by ten percent.
These figures, which are cited in all official papers on cholesterol and diet, are grossly misleading. The risk of having a heart attack in the LRC trial was lowered from 9.8 to 8.1 percent, a difference of only 1.7 percentage point. This equals 0.2 percentage point for each percent of cholesterol lowering, which means a total of only one percentage point if blood cholesterol is lowered by 5 percent. But this whole line of reasoning is absurd because, after all, the LRC trial did not lower the number of heart attacks more than could be explained by chance.
The absolute magnitude of this benefit should be greater in patients at high risk from existing coronary heart disease or the presence of other risk factors such as cigarette smoking and hypertension.
This statement is preposterous. The calculations mentioned above were based on the figures from the LRC trial which studied no one but high risk individuals.
The panel had no reservations except to say that a number of problems should be investigated in the future (thus ensuring huge amounts of future government welfare for scientists and research doctors). They suggested for instance, that more information should be gained about the possible danger of eating great amounts of polyunsaturated fat. Let us hope that a diet, very high in polyunsaturated fatty acids is not harmful, but it would have been wise to perform such studies before launching a campaign to reform everyone’s diet.
The document prompted protests from many scientists, but, as we know, without any impact whatsoever. The cholesterol campaign has flourished ever since then and has spread to many other countries. Rumors are circulating that Ancel Keys has been suggested as a candidate for the Nobel prize.
Nothing was mentioned in the consensus report about the numerous unsupportive studies I have discussed in this book. And contrary to the initial statement of the consensus report many scientists have not agreed about the dangers of fat food and cholesterol. In the next chapter I shall present some of the critics and their objections.
Here are links to the other chapters in the book.
- Cholesterol Myths by Uffe Ravnskov, MD, PhD: Forward to Book by Michael Gurr, PhD
- Cholesterol Myths by Uffe Ravnskov, MD, PhD: Author’s Foreword
- Cholesterol Myths by Uffe Ravnskov MD, PhD: Introduction: The Diet-Heart Idea: A Die-Hard Hypothesis
- Cholesterol Myths by Uffe Ravnskov MD, PhD: Myth 1: High-Fat Foods Cause Heart Disease
- Cholesterol Myths by Uffe Ravnskov MD, PhD: Triglycerides
- Cholesterol Myths by Uffe Ravnskov MD, PhD: Myth 2: High Cholesterol Causes Heart Disease
- Cholesterol Myths by Uffe Ravnskov MD: Familial hypercholesterolemia—not as risky as you may think
- Cholesterol Myths by Uffe Ravnskov MD, PhD: Myth 3: High-Fat Foods Raise Blood Cholesterol
- Cholesterol Myths by Uffe Ravnskov MD, PhD: Myth 4: High Cholesterol Blocks Arteries
- Cholesterol Myths by Uffe Ravnskov MD, PhD: Myth 5: Animal Studies Prove the Diet-Heart Idea
- Cholesterol Myths by Uffe Ravnskov MD, PhD: Cholesterol lowering in children
- Cholesterol Myths by Uffe Ravnskov MD: Myth 6: Lowering Cholesterol Will Lengthen Your Life (Part 1)
- Cholesterol Myths by Uffe Ravnskov MD: Myth 6: Lowering Cholesterol Will Lengthen Your Life (Part 2)
- Cholesterol Myths by Uffe Ravnskov MD PhD: Myth 7: The Statins — Gift to Mankind (Part 1)
- Cholesterol Myths by Uffe Ravnskov MD PhD: Myth 7: The Statins — Gift to Mankind (Part 2)
- Cholesterol Myths by Uffe Ravnskov MD PhD: “The most exact data base”—the screenee
- Cholesterol Myths by Uffe Ravnskov MD PhD: Myth 8: Polyunsaturated Oils are Good for You
- Cholesterol Myths by Uffe Ravnskov MD PhD: Dr. Ornish and The Lifestyle Heart trial
- Cholesterol Myths by Uffe Ravnskov MD PhD: Myth 9: The Cholesterol Campaign is Based on Good Science
- Cholesterol Myths by Uffe Ravnskov MD PhD: Insider Insight
- Cholesterol Myths by Uffe Ravnskov MD PhD: Myth 10: All Scientists Support the Diet-Heart Idea
- Cholesterol Myths by Uffe Ravnskov MD PhD: Epilogue
- Cholesterol Myths by Uffe Ravnskov MD PhD: References
This chapter is from the book
The Cholesterol Myths: Exposing the Fallacy that Saturated Fat and Cholesterol Cause Heart Disease
by Uffe Ravnskov, MD, PhD.
Dr. Ravnskov has given me the permission to share this version of his book to help educate the world about the cholesterol campaign.
Information about Uffe Ravnskov, MD, PhD is posted here.
More information about Cholesterol Myths is posted on his website here.
Dr. Ravnskov posted his book for free here.
Uffe Ravnskov, MD, PhD is the founder of The International Network of Cholesterol Skeptics (THINCS.org) which can be found here.
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