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Cholesterol Myths by Uffe Ravnskov MD, PhD: Myth 4: High Cholesterol Blocks Arteries
Wednesday, November 12, 2014 10:24 am Email this article
“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.”
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.
Calcium and kidney stones
A finding that has convinced many scientists is the fact that when you inject cholesterol molecules made radioactive they are found at a later time in the atherosclerotic lesions. But calcium salts of kidney stones have been circulating in the blood also, once upon a time. It isn’t possible, however, to prevent or eliminate kidney stones by lowering the calcium level in the blood, nor is it possible by lowering dietary calcium. And if we exclude a rare disease called hyperparathyroidism calcium stones are certainly not due to a high calcium level in the blood because the level in patients with kidney stones is not higher than normally. The calcium salts in kidney stones originate from the blood, but we simply do not know why and how they become organized in the kidneys as stones. Any substance in a pathological structure in our body has at some time been transported by the blood. Its presence in the structure, be it a kidney stone or a sclerotic plaque or anything else, doesn’t necessarily mean that the structure is produced by a high level of this substance in the blood. That high blood cholesterol doesn’t produce atherosclerosis is also evident from many studies.
If cholesterol molecules circulating in the blood tend to settle in the arterial wall and produce atherosclerosis only because the blood contains more of them than normal, then people with high blood cholesterol should on average be more sclerotic than people with low blood cholesterol, this is pure logic. The protagonists also claim that this is the case. Let me show that they are wrong.
There are many ways for scientists to find a false correlation, and false correlations can mislead both scientists and their readers. Good, sound science is difficult; false answers are all too easy, even for the scientist who means well.
Let us start with the situation where we have recorded the blood cholesterol and the degree of atherosclerosis in a large number of dead individuals. To see if blood cholesterol and degree of atherosclerosis are related we draw a diagram where blood cholesterol is read on the horizontal axis and the degree of atherosclerosis on the vertical axis. We may now obtain a false correlation if we have put together young and old individuals in our study, because in most studies old people on average have higher cholesterol and more atherosclerosis than have young people. Therefore, the young individuals with their somewhat lower cholesterol and their low degree of atherosclerosis will mainly be represented by the symbols in the lower, left part of the diagram, and the old ones with their somewhat higher cholesterol and much more pronounced atherosclerosis will probably be represented by the symbols in the upper, right part. Thus, if we do not know the age of the studied individuals we may think that there is a correlation between blood cholesterol and atherosclerosis, when in fact it is between cholesterol and age, and between atherosclerosis and age.
It is therefore necessary to study narrow age groups. For a scientifically valid answer, the question to ask is whether someone of sixty who has high blood cholesterol is more sclerotic than another sixty-year-old person whose blood cholesterol is low.
A false correlation may also appear if the study includes many participants with familial hypercholesterolemia. Such people always have very high cholesterol values and some of them have severe atherosclerosis early in life. All of them will therefore be represented by symbols in the right side of the diagram; many of them in the upper corner. If many of these people are studied together with normal people, the statistics will be skewed and will automatically produce a correlation between cholesterol and atherosclerosis. And if the written results of the study present only the mean statistical values and correlation coefficients, or if the symbols do not specify the participants with familial hyper?cholesterolemia, readers will not be able to see this bias or skewing effect.
I shall not discuss here whether it is the high cholesterol that causes atherosclerosis in people with familial hypercholesterolemia or not. What is certain, though, is that these people have a rare, genetic abnormality in their ability to metabolize cholesterol. And, because of that, they cannot be used as proof that high cholesterol causes atherosclerosis in the 99% or more of the normal population. Individuals with familial hypercholesterolemia should be studied separately, not mixed in with normal people, that is elementary. Nevertheless, almost all studies include both groups and in many studies people with familial hyper?cholesterolemia are heavily overrepresented.
Thus, many factors can prevent a scientist from arriving at valid statistical calculations. Let’s keep that fact in mind as we look at some of the scientific studies that have convinced the scientific community that high cholesterol causes atherosclerosis.
Landé and Sperry
The first study of a possible correlation between blood cholesterol and degree of atherosclerosis was published by the pathologist Kurt Landé and the biochemist Warren Sperry at the Department of Forensic Medicine of New York University. The year was 1936. To their surprise, they found absolutely no correlation between the amount of cholesterol in the blood and the degree of atherosclerosis in the arteries of a large group of individuals, who had died violently. In age group after age group their diagrams looked like the starry sky. Because Landé and Sperry were cautious and methodical, they should have wrecked the diet-heart idea before it ever began years later. Or, more accurately, if those who promoted the diet-heart idea had read Landé and Sperry’s paper, they would probably have dropped the idea at once.
But the few who remember Landé and Sperry misquote them and claim that they found a connection, or they ignore their results by arguing that cholesterol values in the dead are not identical with those in living people.
Veterans explained away
That problem was solved by Dr. J. C. Paterson from London, Canada and his team. For many years they followed about 800 war veterans. These men were confined to a hospital because they were mentally ill or needed residential care. Over the years, Dr. Paterson and his coworkers regularly analyzed blood samples from the veterans. Because the veterans were all between the ages of sixty and seventy when they died, the scientists were informed about the cholesterol level over a large part of the time when atherosclerosis normally develops.
Blood cholesterol varied considerably from one veteran to another but for each individual it was fairly constant, so that, for example, those who had low cholesterol at the beginning of the study usually had low cholesterol just before they died.
A postmortem was performed on all the veterans who died. Changes in their degree of atherosclerosis were measured, and so was the amount of cholesterol in the walls of the arteries. Like Drs. Landé and Sperry, Dr. Paterson and his colleagues did not find any connection between the degree of atherosclerosis and the blood cholesterol level; patients with low blood cholesterol were just as sclerotic as those with high blood cholesterol.
But the studies of the veterans were also explained away. Supporters of the diet-heart idea declared that the veterans had eaten the same food and that there are much greater variations in the amount of dietary fat consumed by people living outside an institution.
Although we don’t know what each individual veteran ate, it is probably safe to assume that many supplemented the hospital diet with candy bars and potato chips and other supposedly unhealthy foods. It is probably a safe assumption, too, that some of the veterans left the fatter foods untouched on their plates in the dining hall, whereas others did not. But let us assume that all these men ate approximately the same amount of fat, confined as they were to an institution. In that case, the diet-heart idea that blood cholesterol depends on the amount and type of fat we eat must be wrong, because the blood cholesterol levels of these veterans varied considerably, just as much as in the study by Landé and Sperry.
High cholesterol and smooth arteries
In the city of Agra in India, Dr. K. S. Mathur and his coworkers have performed a similar study. Their first step was to measure blood cholesterol in twenty patients shortly before death and then a varying number of hours afterwards. They found that the cholesterol values were nearly the same if sampled before death and within sixteen hours after. Thus, they showed that blood samples taken very shortly after death are reliable; an important confirmation of the study done by Drs. Landé and Sperry. Dr. Paterson’s group in Canada did a similar test and with the same result.
Next, Dr. Mathur and his colleagues studied two hundred people who had died suddenly by accident without any preceding disease. Like Drs. Landé and Sperry, and like Dr. Paterson, the Indian researchers could find no connection between the level of cholesterol and the degree of atherosclerosis. Of the two hundred dead people, those with low blood cholesterol had just as much atherosclerosis as those whose cholesterol was high.
Similar studies have also been performed in Poland, in Guatemala and in the USA, all with the same result: no correlation between the level of cholesterol in the blood and the amount of atherosclerosis in the vessels.
We are the only good ones
But some studies did find a correlation. One of them was the famous study from Framingham, Massachusetts. The correlation in Framingham was minimal, however. In statistical terms, the correlation coefficient there was only 0.36. Such a low coefficient indicates a desperately weak relationship between variables, in this case, of course, between cholesterol and atherosclerosis. Usually, scientists demand a much higher correlation coefficient before they conclude that there is a biologically important relationship between two variables. Usually, but Framingham was not quite the usual case; it involved huge amounts of government funding.
The very low correlation coefficient was arrived at after much study. First, many of the townspeople of Framingham had their cholesterol tested several times over a period of several years. Then, Dr. Manning Feinleib of the National Heart, Lung, and Blood Institute, led a team of coworkers in studying the coronary vessels of those who had died. The researchers were eager to learn which of the many factors they had studied was most important in the development of atherosclerosis in these dead people from Framingham. Was it blood cholesterol or the number of cigarettes smoked, or something else?
After carefully describing the atherosclerosis in the coronary arteries of the dead people, Dr. Feinleib and his associates concluded that it was blood cholesterol levels that best predicted the degree of atherosclerosis. Neither age nor weight nor blood pressure nor any other factor was as good as blood cholesterol. But the correlation coefficient between cholesterol and atherosclerosis was a mere 0.36.
The written report of the study offered no diagrams and no information about cholesterol and atherosclerosis of each of the individuals whose bodies had been examined. And the report did not discuss the very low correlation coefficient; it didn’t even comment upon that matter.
When scientists reach a result contrary to all others, it is routine—not merely usual but routine—to provide a detailed report about the result and also to discuss any possible ways in which the study may have been biased away from accuracy and truth. In the Framingham case, there was an especially great need for this routine scientific procedure to be followed. Not only was the correlation coefficient so trivial, but this study, funded with millions of taxpayers’ dollars by The National Institute of Health, could have a major impact on national health care and the American economy. If there was no connection between cholesterol and atherosclerosis, as all the previous studies had shown, then there was no reason to bother about cholesterol or the diet. And billions of taxpayers’ dollars could have been spent more wisely than in lowering cholesterol of healthy people.
But the scientists conducting the Framingham study had no reservations. They were eager to stress their own excellence and to highlight the weaknesses of Dr. Paterson’s study of Canadian war veterans. In their report, they did not mention the studies of Drs. Landé and Sperry at all, nor the study of Dr. Mathur in India, nor the studies in Poland or Guatemala and the USA. And when the Framingham study authors mentioned Dr. Paterson’s study, it was only to criticize without putting their own cards on the table. Some of those hidden cards are fascinating to wonder about.
For example, how were the dead of Framingham chosen for postmortem examination? From 914 dead individuals the researchers examined only 281. And from the 281, they selected 127 (14 percent of all dead) who became the subjects of an autopsy program especially designed to investigate the heart and its vessels.
Thus, those chosen for autopsy in the Framingham study were not a random sampling of the population, as they had been in the previous studies. The report from Framingham said nothing about the selection criteria, although scientific studies routinely do. Usually the determining factor is age. A postmortem is seldom performed on people who have died peacefully in old age, as most of us will. Primarily, a postmortem is restricted to young and middle-aged people, who have died before their time, and so it was in the Framingham study. Almost half of those autopsied were younger than 65 years. For this reason, the autopsied subjects must have included a relatively large number with familial hypercholesterolemia. Furthermore, people with this disease are of special interest to scientists studying the cholesterol problem and were probably chosen for autopsy in a program tailored to investigate coronary disease. With only 14% of the Framingham dead chosen for autopsy, the risk of preferably selecting those with this metabolic abnormality must have been great.
The ungrateful dead
Two studies with a design similar to that of the Framingham study have been published from Japan. One, led by Dr. Noriya Okumiya, took place at the Kyushu University; the other, directed by Drs. Shuichi Hatano and Toshihisa Matsuzaki, occurred at the Geriatric Hospital in Tokyo. In both studies the researchers said that the level of blood cholesterol correlated with the degree of atherosclerosis.
But in the first of these studies of dead Japanese citizens, the correlation appeared only in people with a low or normal cholesterol level; in the second, it appeared only in elderly people. The reports of the studies presented no individual figures, merely correlation coefficients, and these were as small as in the Framingham study. Moreover, the researchers did not explain the fact that the small correlation coefficient between cholesterol and atherosclerosis was present only in some groups but not in others.
More remarkably, among the dead people with high cholesterol, the degree of atherosclerosis was the same, whether these people were young or old. Logically, since atherosclerosis develops more and more as people grow old, it should develop faster in people whose cholesterol is high, or it should if the diet-heart idea were true.
Perhaps you’re thinking that the degree of atherosclerosis was the same in all age groups because death had consistently weeded out only the most arteriosclerotic. But all degrees of atherosclerosis were present among those who had died.
The fact that atherosclerosis was just as severe in people of all ages with high cholesterol must mean that the cholesterol level was unimportant. After all, if the cholesterol level had been of any importance, the old people should have been much more sclerotic than the younger ones, after living far longer with high cholesterol.
Similar peculiar results turned up in a study done in Oslo, Norway, where atherosclerotic diseases have been investigated for many years in a great number of the city’s inhabitants. The project included a study of coronary atherosclerosis, led by Dr. Lars Solberg and his coworkers in cooperation with researchers at the Louisiana State University in New Orleans. The authors of the final report from this large study claimed that in Oslo, too, the degree of atherosclerosis correlated with the level of blood cholesterol. But, as in the previous studies, the correlation was very weak. And the correlation may have stemmed from the fact that the researchers did not consider the twenty-year age difference between the youngest and the oldest of the people whom they studied.
In the investigation from Oslo, the weakness of the correlation between atherosclerosis and cholesterol appeared in many ways. For instance, many of the people who had no narrowings of the coronary vessels had cholesterol as high as in the people who had narrowings of all three coronary vessels. Furthermore, people with two narrowed coronary vessels had, on average, a lower cholesterol level than those with just one narrowed vessel. The scientific word for such results is unsystematic, which means that Mr. Chance and Mrs. Bias have determined their outcome.
If we take a solution of iodine atoms and inject them into a blood vessel of a living person, we can see, with X-rays, the inside of that vessel. This is the principle behind the medical technique called angiography. A narrow and flexible plastic tube is inserted into the femoral artery in the groin and pushed gently upwards through the aorta, the chief artery of the human body, until it reaches the vessel to be investigated; for instance those that provide the heart muscle with blood, the coronary vessels. When the tip of the catheter has been placed in the entrance of one of the coronary vessels, the iodine solution is slowly injected.
With the advent of bypass surgery that allow us to replace old and roughened coronary vessels with new and smooth ones, coronary angiography has gained great importance. On the x-ray pictures, the shadows show how much the coronary vessels have been narrowed.
If we know the cholesterol values of the patients studied with coronary angiography and compare these values with the angiographic pictures we can test the cholesterol hypothesis. If blood cholesterol is the most important factor in the production of atherosclerosis, as we have been told for decades, then people with rough and irregular vessel shadows should have higher cholesterol than people with smooth artery shadows.
It seems as if every specialist in coronary angiography in America has performed his own study, funded with federal tax monies awarded by the National Heart, Lung and Blood Institute. In paper after paper published in various medical journals, using almost identical words, these medical specialists emphasize the importance of the blood cholesterol level for the development of atherosclerosis.
But the reports offer no individual figures, only correlation coefficients, and these are never above a minimal 0.36, usually even smaller. And they never mention any of the previous studies that found no association.
Studies based on coronary angiography are fundamentally flawed, or they are if their findings are meant to be applied to the general population. Coronary angiographies are performed mainly on young and middle-aged patients with symptoms of heart disease, which means that a great number of patients with familial hypercholesterolemia must have been included in all angiographic studies. Again, there is an obvious risk for the kind of bias that I have described earlier.
The fact that this objection is justified was demonstrated in a Swedish study performed by Dr. Kim Cramér and his coworkers in Gothenburg, Sweden. As in most other angiographic studies the patients with the highest cholesterol values had on average the most sclerotic coronary vessels.
But if those who were treated with cholesterol-lowering drugs were excluded, and almost certainly this group must have included all patients with familial hyper?cholesterolemia, the correlation between blood cholesterol and degree of atherosclerosis disappeared.
Another Japanese paradox
You have already heard that in Japan the food is meager, blood cholesterol is low and the risk of getting a heart attack is much smaller than in any other country. Given these facts you will most probably say that in Japan atherosclerosis must be rare.
The condition of the arteries of American and Japanese people was studied in the 1950s by Professors Ira Gore and A. E. Hirst at Harvard Medical School and Professor Yahei Koseki from Sapporo, Japan. At that time US people on average had blood cholesterol of 220 mg/dl whereas Japanese had about 170 mg/dl.
The aorta, the main artery of the body, from 659 American and 260 Japanese people were studied after death. Meticulously all signs of atherosclerosis were recorded and graded. As expected atherosclerosis increased from age 40 and upward, both in Americans and in Japanese. Now to the shocking fact.
When the degree of atherosclerosis was compared in each age group there was hardly any difference between American and Japanese people. Between age forty and sixty Americans were a little more sclerotic than Japanese; between sixty and eighty there was practically no difference, and above eighty Japanese were a little more sclerotic than Americans.
A similar study was conducted by Dr JA Resch from Minneapolis and Dr’s N. Okabe and K. Kimoto from Kyushu, Japan. They studied the arteries of the brain in 1408 Japanese and in more than 5000 American people and found that in all age groups Japanese people were more sclerotic than Americans.
Those who want us to lower our cholesterol say that heart attacks are caused by atherosclerosis in the vessels of the heart, not in the vessels of the aorta or the vessels of the brain and they are right. Curiously, the coronary arteries of Japanese people are in fact less affected by atherosclerosis than the vessels of Americans and this may explain why Japanese people rarely get a heart attack.
But why are the aorta and the vessels of the brain just as sclerotic in Japan where cholesterol is much lower than in the US? If high cholesterol causes atherosclerosis in the vessel walls it should of course do it in any vessel because the cholesterol level is identical whether the blood comes from the heart or the brain or any other organ. Isn’t it much more likely that something else causes atherosclerosis than cholesterol? Something that may vary between the vessels, for instance the blood pressure? Blood pressure may vary greatly in various arteries depending on their. For instance, the tension of the coronary vessels, but not necessarily of other vessels, increases significantly when you are mentally stressed, and mental stress varies considerably between individuals and, as Dr. Marmot argued in his Japanese migrant study, probably also between populations.
Cholesterol is innocent
That people with a low cholesterol become just as sclerotic as people with a high cholesterol is, of course, devastating for the diet-heart idea. But the names of Landé and Sperry, Paterson, and Matur do not appear in the hundreds of papers and books published every year by the proponents of this idea.
“But what about the animal experiments?” the proponents of the diet-heart idea may ask. “You cannot explain away all the animal experiments!”
What the animal experiments have taught us is the subject of the next chapter.
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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