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The Cholesterol Myths
1. Cholesterol is not a deadly poison, but a substance vital to the cells of all mammals. There are no such things as good or bad cholesterol, but mental stress, physical activity and change of body weight may influence the level of blood cholesterol. A high cholesterol is not dangerous by itself, but may reflect an unhealthy condition, or it may be totally innocent.
2. A high blood cholesterol is said to promote atherosclerosis and thus also coronary heart disease. But many studies have shown that people whose blood cholesterol is low become just as atherosclerotic as people whose cholesterol is high.
3. Your body produces three to four times more cholesterol than you eat. The production of cholesterol increases when you eat little cholesterol and decreases when you eat much. This explains why the ”prudent” diet cannot lower cholesterol more than on average a few per cent.
4. There is no evidence that too much animal fat and cholesterol in the diet promotes atherosclerosis or heart attacks. For instance, more than twenty studies have shown that people who have had a heart attack haven't eaten more fat of any kind than other people, and degree of atherosclerosis at autopsy is unrelated with the diet.
5. The only effective way to lower cholesterol is with drugs, but neither heart mortality or total mortality have been improved with drugs the effect of which is cholesterol-lowering only. On the contrary, these drugs are dangerous to your health and may shorten your life.
6. The new cholesterol-lowering drugs, the statins, do prevent cardio-vascular disease, but this is due to other mechanisms than cholesterol-lowering. Unfortunately, they also stimulate cancer in rodents, disturb the functions of the muscles, the heart and the brain and pregnant women taking statins may give birth to children with malformations more severe than those seen after thalidomide.
7. Many of these facts have been presented in scientific journals and books for decades but are rarely told to the public by the proponents of the diet-heart idea.
8. The reason why laymen, doctors and most scientists have been misled is because opposing and disagreeing results are systematically ignored or misquoted in the scientific press.
9. The Benefits Of High Cholesterol
1. Cholesterol is not a deadly poison, but a substance vital to the cells of all mammals. There are no such things as good or bad cholesterol, but mental stress, physical activity and change of body weight may influence the level of blood cholesterol. A high cholesterol is not dangerous by itself, but may reflect an unhealthy condition, or it may be totally innocent.
2. A high blood cholesterol is said to promote atherosclerosis and thus also coronary heart disease. But many studies have shown that people whose blood cholesterol is low become just as atherosclerotic as people whose cholesterol is high.
3. Your body produces three to four times more cholesterol than you eat. The production of cholesterol increases when you eat little cholesterol and decreases when you eat much. This explains why the ”prudent” diet cannot lower cholesterol more than on average a few per cent.
4. There is no evidence that too much animal fat and cholesterol in the diet promotes atherosclerosis or heart attacks. For instance, more than twenty studies have shown that people who have had a heart attack haven't eaten more fat of any kind than other people, and degree of atherosclerosis at autopsy is unrelated with the diet.
5. The only effective way to lower cholesterol is with drugs, but neither heart mortality or total mortality have been improved with drugs the effect of which is cholesterol-lowering only. On the contrary, these drugs are dangerous to your health and may shorten your life.
6. The new cholesterol-lowering drugs, the statins, do prevent cardio-vascular disease, but this is due to other mechanisms than cholesterol-lowering. Unfortunately, they also stimulate cancer in rodents, disturb the functions of the muscles, the heart and the brain and pregnant women taking statins may give birth to children with malformations more severe than those seen after thalidomide.
7. Many of these facts have been presented in scientific journals and books for decades but are rarely told to the public by the proponents of the diet-heart idea.
8. The reason why laymen, doctors and most scientists have been misled is because opposing and disagreeing results are systematically ignored or misquoted in the scientific press.
9. The Benefits Of High Cholesterol
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1. Your cholesterol tells very little about your future health
An excerpt from my previous book The Cholesterol Myths
Cholesterol is a peculiar molecule. It is often called a lipid or a fat. However, the chemical term for a molecule such as cholesterol is alcohol, although it doesn't behave like alcohol. Its numerous carbon and hydrogen atoms are put together in an intricate three dimensional network, impossible to dissolve in water. All living creatures use this indissolvability cleverly, incorporating cholesterol into their cell walls to make cells waterproof. This means that cells of living creatures can regulate their internal environment undisturbed by changes in their surroundings, a mechanism vital for proper function. The fact that cells are waterproof is especially critical for the normal functioning of nerves and nerve cells. Thus, the highest concentration of cholesterol in the body is found in the brain and other parts of the nervous system. Because cholesterol is insoluble in water and thus also in blood, it is transported in our blood inside spheric particles composed of fats (lipids) and proteins, the so-called lipoproteins. Lipoproteins are easily dissolved in water because their outside is composed mainly of water-soluble proteins. The inside of the lipoproteins is composed of lipids, and here are room for water-insoluble molecules such as cholesterol. Like submarines, lipoproteins carry cholesterol from one place in the body to another.
The submarines, or lipoproteins, have various names according to their density. The best known are HDL (High Density Lipoprotein), and LDL (Low Density Lipoprotein). The main task of HDL is to carry cholesterol from the peripheral tissues, including the artery walls, to the liver. Here it is excreted with the bile, or used for other purposes, for instance as a starting point for the manufacture of important hormones. The LDL submarines mainly transport cholesterol in the opposite direction. They carry it from the liver, where most of our body's cholesterol is produced, to the peripheral tissues, including the vascular walls. When cells need cholesterol, they call for the LDL submarines, which then deliver cholesterol into the interior of the cells. Most of the cholesterol in the blood, between 60 and 80 per cent, is transported by LDL and is called ”bad” cholesterol, for reasons that I shall explain soon. Only 15-20 percent is transported by HDL and called ”good” cholesterol. A small part of the circulating cholesterol is transported by other lipoproteins.
You may ask why a natural substance in our blood, with important biologic functions, is called ”bad” when it is transported from the liver to the peripheral tissues by LDL, but ”good” when it is transported the other way by HDL. The reason is that a number of follow-up studies have shown that a lower-than-normal level of HDL-cholesterol and a higher than-normal level of LDL-cholesterol are associated with a greater risk of having a heart attack, and conversely, that a higher-than-normal level of HDL-cholesterol and a lower-than normal LDL-cholesterol are associated with a smaller risk. Or, said in another way, a low HDL/LDL ratio is a risk factor for coronary heart disease.
However, a risk factor is not necessarily the same as the cause. Something may provoke a heart attack and at the same time lower the HDL/LDL ratio. Many factors are known to influence this ratio.
What is good and what is bad? People who reduce their body weight also reduce their cholesterol. In a review of 70 studies Dr. Anne Dattilo and Dr. P.M. Kris-Etherton concluded that, on average, weight reduction lowers cholesterol by about 10 per cent, depending on the degree of the reduction. Interestingly, it is only cholesterol transported by LDL that goes down; the small part transported by HDL goes up. In other words, weight reduction increases the ratio between HDL- and LDL-cholesterol (1). An increase of the HDL/LDL ratio is called ”favorable” by the diet-heart supporters; cholesterol is changed from ”bad” to ”good”. But is it the ratio or the weight reduction that is favorable? When we become fat, other harmful things occur to us. One is that our cells become less sensitive to insulin, so that some of us develop diabetes. And people with diabetes are much more likely to have a heart attack than people without diabetes, because atherosclerosis and other vascular damage occur very early in diabetics, even in those without lipid abnormalities. In other words, overweight may increase the risk of a heart attack by mechanisms other than an unfavorable lipid pattern, while at the same time overweight lowers the HDL/LDL ratio. Also smoking increases cholesterol a little. Again, it is LDL-cholesterol that increases, while HDL-cholesterol goes down, resulting in an ”unfavorable” HDL/LDL ratio (2). What is certainly unfavorable is the chronic exposure to the fumes from burning paper and tobacco leaves. Instead of considering the low HDL/LDL ratio as bad it could simply be smoking itself that is bad. Smoking may provoke a heart attack and, at the same time, lower the HDL/LDL ratio.
Exercise decreases the bad LDL-cholesterol and increases the ”good” HDL-cholesterol (3). In well-trained individuals the ”good” HDL is increased considerably. In a comparison between distance runners and sedentary individuals, Dr. Paul D. Thompson and his colleagues found that the athletes on average had a 41 per cent higher HDL-cholesterol level (4). Most population studies have shown that physical exercise is associated with a lower risk of coronary heart disease, and a sedentary life with a higher risk. It also seems plausible that a well-trained heart is better guarded against obstruction of the coronary vessels than a heart always working at low speed. A sedentary life may predispose people to a heart attack and, at the same time, lower the HDL/LDL ratio.
A low ratio is also associated with high blood pressure (5). Most probably, the hypertensive effect is created by the sympathetic nerve system, which is often overstimulated in hypertensive patients. Hypertension (or too much adrenalin) may provoke a heart attack, for instance by inducing spasm of the coronary arteries or by stimulating the arterial muscle cells to proliferate, and, at the same time, lower the HDL/LDL ratio.
Univariate and multivariate As you see, it is not easy to know what is bad. Is it bad to be fat, to smoke, to be inactive, to have high blood pressure, or to be stressed? Or is it bad to have a lot of bad cholesterol? Or both? Is it good to be slim, to stop smoking, to exercise, to have normal blood pressure, to be emotionally calm? Or is it good to have much ”good” cholesterol? Or both? Thus, the risk of having a heart attack is greater than normal for people with high LDL-cholesterol, but so is the risk for fat, sedentary, smoking, hypertensive and mentally stressed individuals. And since such individuals usually have elevated levels of LDL-cholesterol, it is, of course impossible to know whether the increased risk is due to the previously mentioned risk factors (or to risk factors we do not yet know) or to the high LDL-cholesterol. A calculation of the risk of high LDL-cholesterol that ignores other risk factors is called a univariate analysis and is, of course, meaningless. To prove that high LDL-cholesterol is an independent risk factor, we should ask if fat, sedentary, smoking, hypertensive and mentally stressed individuals with a high LDL-cholesterol level are at greater risk for coronary disease than fat, sedentary, smoking, hypertensive and mentally stressed individuals with low or normal LDL cholesterol.
Using complicated statistical formulas, it is possible to do such comparisons in a population of individuals with varying degrees of the risk factors and varying levels of LDL-cholesterol, a so-called multivariate analysis. If a multivariate analysis of the prognostic value of LDL cholesterol also takes body weight into consideration, it is said to be ”adjusted for body weight”. A major problem with such calculations is that the data generated by these and other complicated statistical methods are almost impossible for most readers, including most physicians, to comprehend. For many years researchers in this area have not presented primary data, simple means, or simple correlations. Instead, their papers have been salted with meaningless ratios, relative risks, p-values, not to mention obscure concepts such as the standardized logistic regression coefficient, or the pooled hazard rate ratio. Instead of being an aid to science, statistics are used to impress the reader and cover the fact that the scientific findings are trivial and without practical importance.
2. Blood cholesterol has nothing to do with atherosclerosis
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.
The pathologist Dr. Kurt Landé and the biochemist Dr. Warren Sperry at the Department of Forensic Medicine of New York University were the first to study that question (25). 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 number of individuals who had died violently. In age group after age group their diagrams looked like the starry sky.
Drs. Landé and Sperry are never mentioned by the proponents of the diet-heart idea, or they misquote them and claim that they found a connection (26), or they ignore their results by arguing that cholesterol values in the dead are not identical with those in living people.
That problem was solved by Dr. J. C. Paterson from London, Canada and his team (27). For many years they followed about 800 war veterans. Over the years, Dr. Paterson and his coworkers regularly analyzed blood samples from these veterans. Because they restricted their study to veterans who had died between the ages of sixty and seventy, the scientists were informed about the cholesterol level over a large part of the time when atherosclerosis normally develops.
Dr. Paterson and his colleagues did not find any connection either between the degree of atherosclerosis and the blood cholesterol level; those who had had a low cholesterol were just as atherosclerotic when they died as those who had had a high cholesterol.
Similar studies have been performed in India (28), Poland (29), Guatemala (30), and in the USA (31), all with the same result: no correlation between the level of cholesterol in the blood stream and the amount of atherosclerosis in the vessels.
The question about blood cholesterol and atherosclerosis has been studied by coronary angiography also. It seems as if every specialist in coronary angiography in America has performed his own study, funded with federal tax money 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 (33).
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 between degree of atherosclerosis and level of blood cholesterol.
Studies based on coronary angiography are fundamentally flawed 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 relatively large number of patients with familial hypercholesterolemia must have been included. Again, there is an obvious risk for the kind of bias that I described above. The fact that this objection is justified was demonstrated in a Swedish study performed by Dr. Kim Cramér and his group in Gothenburg, Sweden (34). As in most other angiographic studies the patients with the highest cholesterol values had on average the most arteriosclerotic 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 hypercholesterolemia, the correlation between blood cholesterol and degree of atherosclerosis disappeared.
3. The diet has little to do with your blood cholesterol level
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.
Studies of African tribes have shown that intakes of enormous amounts of animal fat not necessarily raises blood cholesterol; on the contrary it may be very low. Samburu people, for instance, eat about a pound of meat and drink almost two gallons of raw milk each day during most of the year. Milk from the African Zebu cattle is much fatter than cow's milk, which means that the Samburus consume more than twice the amount of animal fat than the average American, and yet their cholesterol is much lower, about 170 mg/dl (38).
According to the view of the Masai people in Kenya, vegetables and fibers are food for cows. They themselves drink half a gallon of Zebu milk each day and their parties are sheer orgies of meat. On such occasions several pounds of meat per person is not unusual. In spite of that the cholesterol of the Masai tribesmen is among the lowest ever measured in the world, about fifty percent of the value of the average American (39).
Shepherds in Somalia eat almost nothing but milk from their camels. About a gallon and a half a day is normal, which amounts to almost one pound of butter fat, because camel's milk is much fatter than cow's milk. But although more than sixty percent of their energy consumption comes from animal fat, their mean cholesterol is only about 150 mg/dl, far lower than in most Western people (40).
Proponents of the diet-heart idea say that these African tribesmen are accustomed to their diet and that their organisms have inherited a cleverness to metabolize cholesterol. However, a study of Masai people who had lived for a long time in the Nairobi metropolis showed this to be wrong (41). If the low cholesterol of the Masai tribesmen was inherited it should have been even lower in Nairobi, because here their diet with all certainty included less animal fat than the diet of the Masai tribesmen. But the mean cholesterol level in twenty six males in Nairobi was twenty-five percent higher than that of their cattle-breeding colleagues in the countryside.
And there is more evidence. Although it is possible to change blood cholesterol a little in laboratory experiments and clinical trials by dieting, it is impossible to find any relationship between the make up of the diet and the blood cholesterol of individuals who are not participating in a medical experiment. In other words, individuals who live as usual and eat their food without listening to doctors or dieticians show no connection between what they eat and the level of their blood cholesterol.
If the diet-heart idea were correct individuals who eat great amounts of animal fat would have higher cholesterol than those who eat small amounts; and individuals who eat small amounts of vegetable fat should have higher cholesterol than those who eat great amounts. If not, there is no reason to meddle with people's diet.
In the early 1950's the Framingham study included dietary analyses. Almost one thousand individuals were questioned in detail about their eating habits. No connection was found between the composition of the food and the cholesterol level of the blood. Wrote Drs. William Kannel and Tavia Gordon, authors of the report: ”These findings suggest a cautionary note with respect to hypotheses relating diet to serum cholesterol levels. There is a considerable range of serum cholesterol levels within the Framingham Study Group. Something explains this inter-individual variation, but it is not diet.” For unknown reasons, their results were never published. The manuscript is still lying in a basement in Washington.
In a small American town called Tecumseh, Michigan a similar study was performed by a team of researchers from the University of Michigan headed by Dr. Allen Nichols (42). Experienced dieticians asked in great detail more than two thousand individuals what they had eaten during a twenty-four hour period. The dieticians also asked about the ingredients of the food, analysed the recipies of home-cooked dishes, and exerted great care to find out what kind of fat was used in the kitchen. Calculations were then performed using an elaborate list of the composition of almost 3000 American food items. Finally the participants were divided into three groups, a high, a middle, and a low level group, according to their blood cholesterol.
No difference was found between the amounts of any food item in the three groups; of special interest was that those with a low blood cholesterol ate just as much saturated fat as did those with a high cholesterol.
These studies concerned adults, but no association has been found in children either. At the famous Mayo Clinic in Rochester, Minnesota, for instance, Dr. William Weidman and his team analyzed the diet of about one hundred school children (43). Great differences were found between the amount of various food items eaten by these children, and also great differences between their blood cholesterol values, but there wasn´t the slightest connection between the two. The children who ate lots of animal fat had just as much or just as little cholesterol in their blood as the children who ate very little animal fat . A similar investigation of 185 children was performed in New Orleans with the same result (44).
Is it really wise to meddle with people's dietary habits if their food has no influence on their cholesterol? And how do those who believe that fat food is dangerous explain all these negative results?
The most common objection says that information about dietary habits is inaccurate, and it is. But even if it is uncertain what people say they ate yesterday, a crude relationship should appear if a sufficiently large number of individuals were questioned meticulously. If not, the influence of the diet, if any, is so minute that it cannot possibly have any importance.
Diet-heart supporters also argue that most people in Western communities already eat great amounts of fat and cholesterol. This argument declares that we have already crossed a threshold of too much animal fat in the diet so that more fat does not make any impact on our blood cholesterol.
The argument is in conflict with the studies I have mentioned above. For instance, astonished by their negative results Dr. Nichols and his team from Michigan (42) tried to find explanations. But they did not find that all individuals ate much fat. Wrote the authors: ”The distribution of daily intake of total fat, saturated fat, and cholesterol by the individuals in this study was quite broad”.
Consider now that it is the goal of the National Cholesterol Education Program to lower the intake of animal fat of all Americans to about ten per cent of their caloric intake. Almost fifteen per cent of the Tecumseh participants (42) already ate that little animal fat, and yet it was impossible to see a difference between the cholesterol of those who ate that little and of those who ate much more. Does it make sense to recommend this drastic reduction of animal fat intake if the cholesterol of those who already eat that little is just as high as the cholesterol of the others?
In the study from the Mayo Clinic (43) there was also a wide range of fat intake. The lowest intake of animal fat was 15 grams per day (less than 10 per cent of the caloric intake); the highest was 60 grams per day. In the Bogalusa study, the range was still broader. The lowest intake of all fats (no information was given about the range of intake of animal fat) was 17 grams per day, the highest 325 grams per day.
In Jerusalem a team of researchers, led by Dr. Harold Kahn studied the diet and blood cholesterol of ten thousand male Israeli civil servants. The dietary habits varied considerably between people coming from Israel, Eastern Europe, Central Europe, Southern Europe, Asia and Africa. The intake of animal fat varied from ten grams up to two hundred grams daily, and there were also considerable differences between their cholesterol values (47).
If the intake of animal fat were of major importance for the cholesterol level in the blood it should be possible to find some kind of relationship from a study of so many individuals with such great variations in blood cholesterol and dietary habits. But there was no relation in this Israeli study either. Extremely low cholesterol values were seen both in those who ate little and in those who ate the most animal fat, and high cholesterol values were seen at all levels of animal fat intake.
The scientists from Israel also studied the value of various ways of dietary questioning. Many studies have recorded the diet of a 24 hour period only. Even if this information were accurate it may not be representative of the diet for the rest of the year, far less for a whole life time. The Israeli scientists found that the best information came from a questioning over several days in different seasons of the year, the method used in the study of the bank staff members. Using this expensive and time-consuming method in a smaller study of sixty-two individuals they could not find a correlation either; the correlation coefficient between animal fat intake and blood cholesterol was zero point zero (48).
4. Atherosclerosis and coronary heart disease have nothing to do with the diet
National consensus committees in many countries have declared that atherosclerosis and coronary heart disease can be prevented by an appropriate diet. Although the scientific evidence for this message is surprisingly meager, if present at all, it has gained status as established wisdom.
The definition of the ”prudent” diet has changed considerably with time. Initially, it was considered important to reduce dietary fat of all kinds. This advice was based on a review paper by Ancel Keys (49), the main designer of the so-called diet-heart idea. In his review Keys presented a perfect curvilinear correlation between the mortality from coronary heart disease and the consumption of fat in six countries, but his curve was based on a selection of countries that fit his hypothesis and it has not been confirmed in studies including many more countries (50).
The prudent diet was redefined a few years later based on a new study by Ancel Keys, ”Seven Countries” (51). According to that study the total fat intake was unimportant; heart mortality in these seven countries was best predicted by the intake of saturated fat . But within each country no association was seen. In Finland and Greece for instance, heart mortality in two districts varied with a factor five and seven, respectively, despite similar diets and other risk factors. Furthermore, no correlation was found between the diet and the major electrocardiographic findings. Considering that all electrocardiograms were analysed in the American study center this finding should carry more weight than the correlation with the clinical diagnosis, settled as it was by local doctors with varying competence and diagnostic habits.
The seven countries were admittedly selected by Keys. Such selection may be helpful to illustrate an idea at a preliminary stage, but a proof of causality demands random data. In more recent studies, including many more countries, the association was weak, absent, or inverse (52).
Conclusions from associations between national food consumption data and disease should be drawn with care. Most important, assumed intake of animal fat may be falsely high in prosperous countries, because available fat is not the same as fat eaten, but includes fat consumed by pet animals, fat discarded in the kitchen or on the plate, and fat which has never reached the consumer. With all certainty, these amounts are larger in prosperous countries.
The finding that an increased intake of polyunsaturated fatty acids, also called PUFA, can lower the serum cholesterol concentration in laboratory experiments has led to the belief that they would lower the risk of coronary heart disease also. Consequently, an increased intake of PUFA has been advised as an important part of the prudent diet. Initially, no limit was put to such intake, but by the years the limit has been lowered successively. Most recently, an upper limit of only 7 cal% was recommended because a high intake of PUFA promotes cancer, infections and testicular damage in rats (53). The average food intake in most western countries includes that amount of PUFA.
There is little evidence that an increased intake of PUFA protects against heart attacks. In ”Seven Countries” intake of PUFA was not associated with heart mortality, and studies of patients with coronary heart disease have shown that if anything, they eat more PUFA than do healthy individuals, see below.
If heart attacks are caused by eating too much animal fat or saturated fat, a rising intake in a population should of course be followed by more heart attacks and a decreasing intake by fewer attacks. No consistent pattern has been found, however. In a few countries the changes have followed each other and the data from these countries have been used eagerly to support national diet counceling. But in many countries fat consumption has changed whereas heart mortality has not, or vice versa; in many countries they have even changed at opposite directions (54).
In Switzerland, for instance, coronary mortality decreased after World War II. During the same period intake of animal fat increased by 20 per cent (55).
In England, the intake of animal fat has been relatively stable since at least 1910 while the number of heart attacks increased ten times between 1930 and 1970 (56).
In the US coronary mortality increased about ten times between 1930 and 1960, leveled off during the sixties and has since decreased. During the decline of mortality from coronary heart disease the consumption of animal fat declined, but so it did during the previous thirty years of sharply rising mortality (57). In Framingham the decline of coronary mortality was balanced by an increased number of non-fatal heart attacks (58) suggesting an effect of better treatment rather than an effect of dietary changes.
In Japan coronary heart disease is uncommon, allegedly due to the lean Japanese diet. A large study of Japanese emigrants (59) is often used as evidence because after migration to the United States these emigrants died from heart attacks almost as often as did Americans. The increased heart mortality after migration was not associated with the diet or the serum cholesterol, however, but with the cultural upbringing; those who lived according to Japanese traditions were protected. Most surprising, emigrants who stuck to the Japanese tradition, but ate the fat American food ran a smaller risk than those who were accustomed to the American way of life but ate the lean Japanese food (60).
If dietary fats were important this should obviously be reflected in the diet of patients who have had a heart attack. The following table gives the results from 13 studies, where the diet of patients with coronary heart disease was compared with the diet of healthy control individuals of the same age and sex. The amounts of dietary fats are given in percent of total calories. Asterisks means that the difference found was statistically significant. NS means that no absolute figures were given in the report, but that the difference was not statistically significant.
5. Cholesterol-lowering may shorten your life
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). Before the introduction of the new cholesterol lowering drugs, the statins, more than 40 trials have been performed to test if cholesterol-lowering can prevent a heart attack. In some of the trials the number of fatal heart attacks were lowered a little, in other trials the number of fatal heart attacks increased. Overviews of the trials have shown that when all results were taken together, just as many died in the treatment groups (e.g. those whose cholesterol was lowered) as in the untreated control group (78,79). The following table gives the accumulated results. None of the differences were statistically significant. Nor were they by more sophisticated analyses.
Some overviews have shown a positive result after cholesterol-lowering is because they had ignored or excluded one or more trials with a negative outcome (79).
The mentioned overviews included mostly diet and/or the older cholesterol-lowering drugs. But a new type of drugs, the socalled statins (for instance Zocord®, Mevacor®, Lescol®, Lipitor® and Pravachol®) have been succesful. However, their effect isn´t exerted through cholesterol-lowering, they have other and more useful properties Unfortunately they also stimulate cancer growth
6. The effect of the statins is not due to cholesterol-lowering
As mentioned in section 4 cholesterol-lowering by itself does not prolong your life. In the experiments, that have shown this fact beyond all doubt, cholesterol-lowering was performed by diet or by use of various older drugs such as clofibrate (Atromidin), gemfibrozil (Lopid), cholestyramine (Questran), colestipol (Lestid), and nicotinic acid (Nicangin). But a new type of cholesterol-lowering drugs, the so-called statins (for instance Zocor, Lipitor and Pravachol) have been succesful. For the first time cholesterol-lowering have shown significant improvement of mortality, both coronary mortality, stroke mortality and total mortality. These trials are therefore considered as strong arguments for the idea, that a high cholesterol is dangerous.
Have these trials really demonstrated that raised LDL cholesterol has importance for coronary heart disease, as the trial directors concluded in the reports?
There is reason to question that, because some of the results are not consistent with what we have learned about cholesterol.
First, old patients were protected from cardiovascular disease just as much (or as little) as young ones, although most studies have shown that a high cholesterol is a weak risk factor, or no risk factor at all, for old people. (Unfortunately, in the only trial that included old people only, the PROSPER trial, the lowering of heart mortality was smaller thanm the increse of cancer mortality).
Second, also the number of strokes was reduced after statin treatment, although no studies have shown that a high cholesterol is a risk factor for stroke.
Third, patients who had had a coronary were protected although most studies have shown that a high cholesterol is a weak risk factor, if any at all, for those who already have had a coronary. (In fact, this finding should have stopped all the previous, secondary preventive trials).
And finally, the statins protected against coronary heart disease whether the cholesterol was high or low although most studies have shown that a normal or low cholesterol is no risk factor for coronary disease.
How come that the statins are effective for old people, for patients who already have had a coronary, and even for those whose cholesterol is normal? If the cholesterol level for these people is no risk factor for coronary disease, how could a lowering of that cholesterol improve their chances to avoid a coronary? The only reasonable explanation is that the statins do more than just lower cholesterol. There is much evidence for that.
The protective effects of simvastatin has been demonstrated in animal experiments. In one of them, performed by Dr. B.M. Meiser and colleagues from Munich, Germany, hearts were transplanted into rats. Normally, the function of such grafts gradually deteriorates because the coronary vessels are narrowed by an increased growth of smooth muscle cells in the vascular walls, a condition called graft vessel disease. In Dr. Meiser's experiment, however, rats that were given simvastatin had considerably less graft vessel disease than control rats not given simvastatin, and this was not due to cholesterol lowering because simvastatin does not lower cholesterol in rats. In fact, LDL cholesterol was highest in the rats treated with simvastatin (84).
In another experiment, Dr. Maurizio Soma and his colleagues from Milan, Italy placed a flexible collar around one of the carotic arteries in rabbits. After two weeks arteries with collars became narrow but less so if the rabbit had been given simvastatin. Again, the effect was unrelated to the rabbits´ cholesterol level (85).
Thus, the statins in some way protect against cardiovascular disease, but their effect is not due to cholesterol-lowering.
But why bother about pharmacological mechanisms? Isn´t it wonderful that the statins work? Shouldn´t we all take statins?
The costs To answer that question it is necessary to look at the figures from the trials. To be short I have chosen the figures for coronary death. According to the results from the 4S trial (86) there was a 41% reduction in the risk of coronary death. According to the results from the CARE trial (87) the reduction was 24%, and according to the WOSCOP (88) trial the reduction was 28%. These figures seem impressive, but let us look at the absolute figures also. In the treatment group of the 4S trial five percent, or 111 individuals, died from a heart attack; in the control group 8.5 percent, or 189 individuals, died, a difference, or a risk reduction of 3.5%. To prevent these 3.5% of the patients (8.5% - 5%) or 78 individuals, from dying it was necessary to treat 2221 individuals during five years. You could also say that to prevent one death it was necessary to treat 25 individuals for five years. Or said in another way, if you have had a heart attack the chance to avoid death from a new one during five years is 91.5%. If you eat simvastatin this chance increases to 95%.
In the CARE trial 5.7%, or 119 individuals died from a heart attack in the control group and 4.6%, or 96 individuals in the treatment group. Thus, to prevent 23 coronary deaths (1.1%) it had been necessary to treat 2081 individuals for five years, which means that 90 patients were treated for each life saved.
In the WOSCOP trial, which concerned healthy individuals with a high cholesterol, the result was even less impressive. Here, 61 died in the placebo group, 41 in the treatment group, a risk reduction of 0.6%. To save these 20 lives it had been necessary to treat 3302 healthy individuals for five years, or 165 individuals for each life.
Said in another way, the risk of dying from a heart attack during five years if you are about 55 years old and if your cholesterol is around 272 mg per dl is 1.8%. With pravastatin treatment the risk is reduced to 1.2%. You could also say that the chance to avoid death from a heart attack for five years is 98.2%; with pravastatin the chance is 98.8%.
The reason why trial results should be given in absolute figures and not in relative is because the side effects are given in absolute figures. Let us assume that a mortal side effect occurs in 0.5 percent of the patients. You may belittle that if you compare this figure for instance with a relative risk reduction of 28%. But as the absolute risk reduction was 0.6% the effect of treatment has almost disappeared.
To be fair it should be mentioned that the number of non-fatal heart attacks was reduced also. In the WOSCOP trial for instance, 248 individuals in the control group had a fatal or non-fatal coronary, in the pravastatin group the number was 174. This means that to prevent a heart attack in a healthy 55 year old man with a high cholesterol it is necessary to treat about 45 men for five years. To prevent a new heart attack it is necessary to treat 34 patients for five years according to the CARE trial and 28 patients according to the 4S trial.
A few years ago Drs. Thomas Newman and Stephen Hulley published the results from a meticulous review of what we know about cancer and lipid-lowering drugs. They found that clofibrate, gemfibrozil and all the statins stimulate cancer growth in rodents (89).
Newman and Hulley asked themselves why these drugs had been approved by the Food and Drug Administration at all. The answer was that the doses used in the animal experiments were much higher than those recommended for clinical use. But as Drs. Newman and Hulley commented, it is more relevant to compare blood levels, and the levels achieved in rodents were very close to those seen in patients.
Because the latent period between exposure to a cancer-stimulating chemical and the incidence of clinical cancer in humans may be 20 years or more, the absence of any controlled trials of this duration means that we do not know whether statin treament will lead to an increased rate of cancer in coming decades. There is reason to believe that it will, because as mentioned above, treatment of old people already has resulted in an increased number of cancer. The reason is probably that many old people already have cellular changes that rapidly may develop to clinical cancer if stimulated by a cancer-provoking drug..
Other nasty effects have been reported on human beings, side effects that have been reported after the end of the trials. They include peripheral neuropathy, a painful and invalidating disease mainly located to the legs (90a), memory loss (90b), short temper (90c), aggressive behavior (90d) and muscle problem that in rare cases have led to kidney failure and death. Most scary, considering that people with very high cholesterol, so-called familial hypercholesterolemia, automatically are prescribed statin treatment already from early childhood, is the recent report in prestigious New England Journal of Medicine (90e). Here the authors reported that almost 50 % of pregnant women who took a statin drug during early pregnancy gave birth to a child with malformations, some of them more severe than those seen after thalidomide treatment.
Those who argue for statin treatment say that these side effects are very rare. They will most certainly become much more common considering that the new cholesterol guidelines recommend that cholesterol should be lowered as much as possible, even if it may demand an eight times higher dose than used hitherto.
Thus, millions of asymptomatic people are being treated with medications, the ultimate effects of which are not yet known. Drs. Newman and Hulley therefore recommended that the new statins should be used for patients at very high risk for coronary disease only, whereas such treatment should be avoided for individuals with life expectancies of more than 10 to 20 years. And healthy people with a high cholesterol as the only risk marker belong to that category.
7. The many critical scientists
Those who propagate for a low-fat diet and cholesterol-lowering drugs claim that there is general agreement about the diet-heart idea. Nothing could be more wrong. Here follows, in alphabetic order, a selection of critical scientists. Mary Enig is an international expert in the field of lipid biochemistry, a nutritionist and a Consulting Editor to a number of scientific publications, among others the Journal of the American College of Nutrition. She is also the President of the Maryland Nutritionists Association. She has published many scientific papers on the subject of food, nutrition topics, food fats and oils, several chapters on nutrition for books and a book about dietary fats, oils and cholesterol (90a). Her main research has concerned the hazards associated with eating too much trans fatty acids. In an interview she was asked if saturated fats cause heart disease: 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. Read also hers and Sally Fallons paper The Oiling of America
Michael Gurr is an associate professor of biochemistry at the School of Biological & Molecular Sciences in Oxford, editor-in-chief of Nutrition Research Reviews and editor of three other scientific journals.Wrote Professor Gurr in his conclusion of a large review on the diet-heart idea (91): The arguments and discussion of the scientific evidence presented in this review will not convince those "experts" who have already made up their minds, for whatever reason, be it truly scientific or political, that a fatty diet is the cause of CHD [coronary heart disease]. However, I hope that some readers, who were, perhaps, unaware that the lipid hypothesis had any shortcomings, will have been persuaded that the relationships between the fats we eat and the likelihood that we may die from a heart attack is by no means as simple as these simplistic statements imply.
George Mann, 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).
After the start of the cholesterol campaign eight years later Mann summarized his criticism of the diet-heart idea in Nutrition Today (93). According to Mann, the diet-heart idea is the greatest scientific deception of our times. Mann is especially critical of the cholesterol-lowering trials. Never in the history of science have so many costly experiments failed so consistently, he declared.
Professor Mann also criticized the directors of the Lipid Research Clinics trial (LRC), the fundament of the cholesterol campaign. The unsupportive results from the LRC trial have not prevented them from bragging about this cataclysmic break-through, he wrote. And, he continued: The managers at the National Institutes of Health have used Madison Avenue hype to sell this failed trial in the way the media people sell an underarm deodorant. The Bethesda Consensus Panel ... has failed to acknowledge that the LRC trial, like so many before it, is saying firmly and loudly 'No, the diet you used is not an effective way to manage cholesterolemia or prevent coronary heart disease and the drug you so generously tested for a pharmaceutical house does not work either.
People who are faced with the many distorted facts about diet, cholesterol and heart disease often ask me why so many scientists unquestioningly accept the diet-heart idea. Here is Professor Mann's comment: Fearing to lose their soft money funding, the academicians who should speak up and stop this wasteful anti science are strangely quiet. Their silence has delayed a solution for coronary heart disease by a generation.
Professor Mann offers a little glimpse of hope at the end of his article in Nutrition Today (93): Those who manipulate data do not appreciate that understanding the nature of things cannot be permanently distorted - the true explanations cannot be permanently ignored. Inexorably, truth is revealed and deception is exposed. ...In due time truth will come out. This is the relieving grace in this sorry sequence.
Michael F. Oliver, a former professor and director of the Wynn Institute for Metabolic Research, London was one of the first to demonstrate that, on average, patients with coronary heart disease more often had abnomal levels of various fats in the blood than control individuals did. Professor Oliver still thinks that those with inherited diseases of cholesterol metabolism, or 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: Doubts about the promotional nature of these campaigns are not popular. Doubters are scorned, although this does not matter. But the issue is a very serious one if vast sums are spent and widespread changes are made in the lifestyle of normal people when the accumulated evidence is that total mortality is unchanged or possibly even increased (94).
Again and again, Professor Oliver has criticized those who think that the increased mortality from non-medical causes seen in many trials is an effect of chance. Rather, he thinks, the very lowering of blood cholesterol may be dangerous: Very little is known about the long-term effects of lowering cholesterol concentrations on the composition of cell membranes (95).
According to Oliver our bodies may regulate attempts to lower blood cholesterol in most cases, but ...would such homoeostatic [regulatory] mechanisms be effective in all patients, at all times, and in all cells--particular cells in which biologic function is impaired for other reasons? These doubts will not go away for several more years? (95) Other critical papers by Professor Oliver
Edward R. Pinckney is an editor of four medical journals and former co-editor of JAMA, the Journal of the American Medical Association. In 1973, together with his wife, he published a book, called ”The Cholesterol Controversy” (97) which summarized all the inconsistencies of the cholesterol idea. Dr. Pinckney describes all the factors that influence blood cholesterol in healthy people and how difficult it is to get a reliable measure of the cholesterol level because of the uncertainties of the analysis: The level of one's blood cholesterol is, at best, nothing more than an extremely rough indication of a great many different disease conditions. At worst, it can be more the cause of stress and the diseases that stress brings on. To alter one's life style as a consequence of this particular laboratory test may well cause more trouble than it could relieve.
The start of chapter 1 in Pinckney´s book is worth citing: Your fear of dying--if you happen to be one of the great many people who suffer from this morbid preoccupation- may well have made you a victim of the cholesterol controversy. For, if 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. 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.
Raymond Reiser is a former professor of biochemistry at Texas A&M university. In 1973 he criticized the recommendations for dietary treatment of high cholesterol by declaring: The authority quoted by these authors for the recommendation is not a primary source but another review similar to their own. It is this practice of referring to secondary or tertiary sources, each taking the last on faith, which has led to the matter-of-fact acceptance of a phenomenon that may not exist. (98)
Here is another citation from Professor Reiser´s papers (99): One must be bold indeed to attempt to persuade large segments of the populations of the world to change their accustomed diets and to threaten important branches of agriculture and agribusiness with the results of such uncontrolled, primitive, trial and error type explorations. Certainly modern science is capable of better research when so much is at stake.
Paul Rosch is President of The American Institute of Stress, Clinical Professor of Medicine and Psychiatry at New York Medical College, Honorary Vice President of the International Stress Management Association and Chairman of its U.S. branch. He is the editor or subeditor of three well-known medical journals, he has been a member of the board of several other journals, and has served as President of the New York State Society of Internal Medicine, as Chairman of the International Foundation for Biopsychosocial Development and Human Health, and has been an Expert Consultant on Stress to the United States Center for Disease Control. He has written extensively over the past forty-five years on the role of stress in health and illness, with particular reference to cardiovascular disease and cancer. He has appeared on numerous national and international television programs such as The Today Show, Good Morning America, 60 Minutes, Nova, CBS, NBC, PBS, BBC and CBC network presentations. His editorials and comments have been published in every major medical journal. Professor Rosch has also been interviewed and widely quoted in numerous major American newspapers and magazines.
As the author of the Newsletter of the American Institute of Stress Professor Rosch has published several articles about the cholesterol hypothesis and the diet-heart idea. His conclusions are close to those presented in this book: A massive crusade has been conceived to “lower your cholesterol count” by rigidly restricting dietary fat, coupled with aggressive drug treatment. Much of the impetus for this comes from speculation, rather than any solid scientific proof."
The result is well-known, says Professor Rosch: The public is so brainwashed, that many people believe that the lower your cholesterol, the healthier you will be or the longer you will live. Nothing could be further from the truth.
How can this go on year after year? Professor Rosch has several explanations: The cholesterol cartel of drug companies, manufacturers of low fat foods, blood testing devices, and others with huge vested financial interests have waged a highly successful promotional campaign. Their power is so great that they have infiltrated medical and governmental regulatory agencies that would normally protect us from such unsubstantiated dogma.
Professor Rosch reminds us that practicing physicians get most of their information from the drug companies. But compared to their peers a half century ago, most doctors don’t have the time or skills to critically evaluate reports, very few know anything about research, nor did the generation that taught them.
Ray Rosenman is the retired Director of Cardiovascular Research in the Health Sciences Program at SRI International in Menlo Park, California, and associate chief of medicine, Mt Zion Hospital and Medical Center in San Francisco. Since 1950 he has been a cardiologist and a researcher. He has published four books and many text chapters and journal articles about cardiovascular diseases. His main interest has been the influence of neurogenic and psychological factors on the blood lipids (100), but he has also written reviews critical of the diet-heart idea.
Here is the conclusion from his most recent review: These data lead to a conclusion that neither diet, serum lipids, or their changes can explain wide national and regional differences of IHD [coronary heart disease] rates, or the variable 20th century rises and declines of CHD mortality. This conclusion is supported by the results of many clinical trials which fail to provide adequate evidence that lowering serum cholesterol, particularly by dietary changes, is associated with a significant reduction of IHD mortality or improved longevity. It is variously stated that the preventive effects of dietary and drug treatments have been exaggerated by a tendency in trial reports, reviews, and other papers to cite and inflate supportive results, while suppressing discordant data, and many such examples are cited (101).
Russell Smith was an American experimental psychologist with a strong background in physiology, mathematics and engineering. No review written by the proponents of the diet-heart idea are remotely comparable with Smith's books and papers (102) when it comes to scientific depth and completeness. Smith's summation is devastating for the diet-heart proponents: Although the public generally perceives medical research as the highest order of precision, much of the epidemiologic research is, in fact, rather imprecise and understandably so because it has been conducted principally by individuals with no formal education and little on-the-job training in the scientific method. Consequently, studies are often poorly designed and data are often imappropriately analyzed and interpreted. Moreover, biases are so commonplace, they appear to be the rule, rather than the exception. It is virtually impossible not to recognize that many researchers routinely manipulate and/or interpret their data to fit preconceived hypotheses, rather than manipulate hypotheses to fit their data. Much of the literature, therefore, is nothing less than an affront to the discipline of science.
Dr. Smith concludes: The current campaign to convince every American to change his or her diet and, in many cases, to initiate drug "therapy" for life is based on fabrications, erroneous interpretations and/or gross exaggerations of findings and, very importantly, the ignoring of massive amounts of unsupportive data...It does not seem possible that objective scientists without vested interests could ever interpret the literature as supportive.
Dr. Smith is aware that he is up against some extremely powerful institutions: The political and financial power of the NHLBI and AHA team...is enormous and without equal. And because the alliance has substantial credibility in the eyes of the public and most practicing physicians, it has become a juggernaut, able to use its power and prestige to suppress a great body of unsupportive evidence and even defy the most fundamental tool of scientists, logic.
The scientists who have produced the misleading papers and reviews are, of course, the first whom Smith faults. But he adds: Equally culpable are the editors of the many journals who publish articles without regard to their quality or scientific import. It is depressing to know that billions of dollars and a highly sophisticated medical research system are being wasted chasing windmills.
William E. Stehbens is a professor at the Department of Pathology, Wellington School of Medicine, and director of the Malaghan Institute of Medical Research in Wellington, New Zealand. Based on his own studies and on extensive reviews of the literature he has effectively demonstrated the many fallacies of the diet heart-idea. In a thorough review of the experimental studies he concluded: Upon examination of this evidence and consideration of the specific criteria for the experimental production of atherosclerosis, any pathologist of independent mind and free from preconceived ideas would conclude that human atherosclerosis and the lesions induced by the dietary overload of cholesterol and fats are not one and the same disease (103).
Professor Stehbens has also pointed out the weaknesses of the epidemiologic studies that have used mortality statistics as proof for causality: Continued, unquestioned use of unreliable data has led to premature conclusions and the sacrifice of truth. The degree of inaccuracy of vital statistics for CHD is of such uncertain magnitude that, when superimposed on other deficiencies already indicated, the concept of an epidemic rise and decline of CHD in many countries must be regarded as unproven, and governmental or health policies based on unreliable data become untenable (104).
According to Professor Stehbens atherosclerosis is due to wear and tear of the arteries, not to too much cholesterol in the blood, and he has many good arguments for this idea. The following words from a 1988 paper (105) summarize Stehbens' view on the diet-heart idea: The perpetuation of the cholesterol myth and the alleged preventive measures are doing the dairy and meat industries of this and other countries much harm quite apart from their potential to endanger optimum nutrition levels and the health of the populace at large...It is essential to adhere to hard scientific facts and logic. Scientific evidence for the role of dietary fat and hypercholesterolemia in the causation of atherosclerosis is seriously lacking...The lipid hypothesis has enjoyed undeserved longevity and respectability. Readers should be aware of the unscientific nature of claims used to support it and see it as little more than a pernicious bum steer.
Other critical papers by Professor Stehbens
Lars Werkö was a professor of medicine at Sahlgren's Hospital, Gothenburg, Sweden, when he moved to become scientific director at the Astra Compagny. Later on he became head of the Swedish Council on Technology Assessment in Health Care, a governmental agency. Professor Werkö has been an opponent of diet-heart for many years. In 1976 he criticized the design in the large epidemiologic studies aimed at preventing coronary heart disease, most of all the Framingham study.
According to Professor Werkö (107) the dogm is based on questionable "facts" rooted in hopes, wishful thinking and studies using selected materials: No studies have proved anything, but instead of formulating new hypotheses diet-heart supporters call the current one the most probable truth, and they have intervened in people's lives because they will not wait for the final proof.
8. How to create a false idea
In the numerous reviews written by upholders of the diet-heart idea it is often said that this idea is based on ”strong, scientific data”, the evidence is ”overwhelming” or ”extremely powerful” and ”controversy is unjustified”. If you have read the previous sections you will understand that nothing could be more advanced from the truth. To use such vocabulary it has been necessary to exaggerate trivial, apparently supportive findings, to belittle or ignore the wealth of controversial and disproving evidence and to quote unsupportive results as if they were supportive. How a ”fact” is created by misquoting unsupportive findings and exaggerating trivial findings is examplified in section 1, the story about the so-called ”good” and ”bad” cholesterol.
Observations that are totally devastating for the diet-heart idea are mostly ignored. A good example is the fact that if we exclude individuals with the rare disease familial hypercholesterolemia (less than 0.5 percent of mankind suffer from it) there is no association between the level of blood cholesterol and the degree of vascular atherosclerosis (section 2).
Another one. Before the statin-era overviews of all cholesterol-lowering trials have shown that mortality cannot be improved by lowering cholesterol. But diet-heart proponents usually mention the trials with a positive outcome only and ignore the trials with a negative outcome.
Thus, in 16 trial reports published between 1970 and 1992 a total of 40 citations were to (apparently) supportive or inconclusive trials, but with one exception, not a single citation was to unsupportive trials, although the number of supportive and unsupportive trials were equal (79). It is interesting to compare the number of citations of papers published in the same journal because few citiations of a paper may simply reflect that it has been published in a little-known or less reputable journal. In 1984 The Lipid Research Clinic´s coronary primary prevention trial was published in JAMA (110). In that trial 32 of the patients whose cholesterol was lowered died from a heart attack against 44 of the patients in the untreated control group. The total number of deaths (deaths from all causes) was 68 treated patients against 71 patients in the control group. These figures were not statistically significant by conventional statistics, but in spite of that the result was used as the main argument by the American cholesterol campaign.
In 1985 Dr. Miettinen and colleagues from Helsinki, Finland published another, but smaller cholesterol-lowering trial in the same journal (111). In that trial four patients whose cholesterol was lowered died from a heart attack, whereas only one died in the untreated control group, and the total number of deaths was ten in the treatment group against five in the control group.
Thus, both papers dealt with the same subject and were published in the same journal and no one has questioned the honesty of the experimenters or the quality of the studies. Reasonably, they should have been cited almost equally often. That the LRC trial, at least according to its directors, was supportive, and the Miettinen trial was not, is unimportant because the aim of research is to find the truth, whether it is happy or not. Here you can see how often the two papers have been cited by other scientists during the first four years after their publication:
An example of an unsupportive study which has been cited, many, many times, as if it was supportive is the Japanese migrant study. In Japan coronary heart disease is uncommon, allegedly due to the lean Japanese diet. A large study of Japanese emigrants (112) is often used as evidence because after migration to the United States, where the food generally is much fatter than in Japan, the serum cholesterol of these emigrants increased and they died from heart attacks almost as often as did Americans. The increased coronary mortality after migration was not associated with the diet or the serum cholesterol, however, but with the cultural upbringing: those who lived according to Japanese traditions were protected against heart attacks.
Especially striking was the finding that emigrants who stuck to the Japanese tradition, but ate American food ran a smaller risk of heart disease than emigrants who were accustomed to the American way of life but ate Japanese food (113). Here is another example. A common message from the American Heart Association and The National Heart, Lung, and Blood Institute to doctors is that there exist a close correspondence between degree of cholesterol lowering and degree of mortality reduction. Listen for example to the words from The Cholesterol Facts (114): ”The results of the Framingham study indicate that a 1% reduction of cholesterol corresponds to a 2% reduction in CHD (coronary heart disease) risk.” This statement was followed by a reference to a paper which reported the 30 years experience from Framingham (115).
9. The benefits of high cholesterol
ost people ‘know’ that high cholesterol is something to be afraid of and that the most important thing to do to avoid a heart attack is to lower one’s cholesterol as much as possible. But did you know that high cholesterol protects you against infectious diseases, which most probably explain that high cholesterol is associated with longevity? With these facts min mind, why should we care about high cholesterol?
Old people with high cholesterol live the longest. This statement seems so incredible that it takes a long time to clear one´s brainwashed mind, at least for those who haven’t read this book, to fully understand its importance. Yet the fact that people with high cholesterol live the longest emerges clearly from many scientific papers.1
Why High Cholesterol Is Good
In certain aspects low cholesterol is worse than high cholesterol. Already fifteen years ago American researchers found that low cholesterol predicts an increased risk of dying from diseases of the stomach, the intestines and the lungs.2
Most of such diseases are infectious. Therefore, a relevant question is whether it is the infection that lowers cholesterol or the low cholesterol that predisposes to infectious diseases You have probably already guessed what the directors of the cholesterol campaign have said, but is it true?
To answer that question the same researchers followed more than 100,000 healthy individuals in the San Francisco area for fifteen years. At the end of the study they noted that those who had low cholesterol at the start of the study had been admitted more often to hospital because of an infectious disease.3,4 This finding cannot be explained away with the argument that the infection had caused cholesterol to go down, because how could low cholesterol, recorded when these people had no evidence of infection, be caused by a disease they had not yet encountered? Isn’t it much more likely that low cholesterol in some way made them more vulnerable to infection? Much evidence exists to support that interpretation.
Low Cholesterol Predisposes To HIV And AIDS
Young, unmarried men with a previous sexually transmitted disease or liver disease run a much greater risk of becoming infected with HIV virus than other people. This was what a group of Minnesota researchers found by following such people for several years. Those who had low cholesterol at the beginning of the study were twice as likely to test positive for HIV compared with those with the highest cholesterol.5
Similar results came from another study of more than 300,000 young and middle-aged men. After sixteen years four times more in the low-cholesterol group had died from AIDS compared with the high-cholesterol group.6
Smith-Lemli-Opitz Syndrome
The benefit of high cholesterol also appears from studies of children with the Smith-Lemli-Opitz syndrome. They are born with very low cholesterol because an enzyme that is necessary for the body’s synthesis of cholesterol does not function properly. Most children with this syndrome are either stillborn or they die early because of serious malformations of the brain. Those who survive are imbecile or autistic, they have extremely low cholesterol, and they suffer from frequent and severe infections. However, if they are given extra cholesterol or eggs in their diet, their cholesterol goes up, their infections become less serious and less frequent, and their autistic and aggressive behavior improves.7
The lipoproteins
One of the many reasons not to name LDL as bad is that the lipoproteins have other important functions. One of them is to take care of microorganisms and their toxic products.
Staphylococcus aureus α-toxin is the most toxic substance produced by strains of the disease-promoting bacteria called staphylococci. It is able to destroy all kinds of human cells, including red blood cells. For instance, if minute amounts of the toxin are added to a test tube with red blood cells dissolved in salt water, the blood is hemolyzed, that is, the membranes of the red blood cells burst and hemoglobin from the interior of the cells leaks out into the solvent. Dr. Bhakdi and his team mixed purified α-toxin with human serum (the fluid in which the blood cells reside) and now the toxic effect of α-toxin almost disappeared. By various complicated methods they identified the protective substance in human serum as LDL, the carrier of the “bad” cholesterol. In accordance, nothing happened when they mixed α-toxin with purified human LDL.
Dr. Willy Flegel and his co-workers at Heidelberg University in Germany studied bacterial toxins in another way. As mentioned above, one of the effects of bacterial toxins is that they stimulate white blood cells to produce cytokines, hormones that start the inflammatory processes. The German researchers found that this effect disappeared almost completely if the toxin was mixed with purified LDL before they added the white blood cells to the test tubes.8,9 Obviously, LDL was able to neutralize the bacterial toxins.
Animal Experiments
The immune systems in various mammals including human beings have many similarities. Therefore, it is interesting to see what experiments with rats and mice can tell us. Professor Kenneth Feingold and his group at the University of California have published some interesting studies. In one of them they lowered LDL-cholesterol in rats by drugs with the result that they died much easier after an injection of bacterial toxins. The high mortality was not due to the cholesterol-lowering drug because, if they gave the animals an injection of human lipoproteins just before the experiment, they survived10
In another experiment, researchers from the Netherlands injected bacteria or their toxins into normal mice, and into mice with high cholesterol. Whereas all normal mice died, most of the mice with high cholesterol survived.11
Many of the roles played by the lipoprotein LDL are shared by HDL as well. This should not be too surprising considering that high HDL-cholesterol is associated with cardiovascular health and longevity. But there is more.
Triglycerides, molecules consisting of three fatty acids linked to a molecule named glycerol, are insoluble in water and are therefore carried through the blood inside lipoproteins, just as cholesterol. All lipoproteins carry triglycerides, but most of them are carried by the VLDL, the largest lipoprotein in our blood.
For many years it has been known that patients suffering from sepsis, a life-threatening condition caused by bacterial growth in the blood, have high levels of triglycerides. The serious symptoms of sepsis are due to bacterial toxins, most often produced by gut bacteria. Now to the interesting point. Solutions rich in triglycerides are also able to protect experimental animals from the dangerous effects of bacterial toxins, which means that the high level of triglycerides seen in sepsis is not a bad thing, but a normal response to infection.12 Usually sepsis bacteria come from the guts. It is therefore fortunate that the blood draining the guts is especially rich in triglycerides.
High cholesterol protects against allergy
Children with allergic problems, such as asthma and hay fever, have lower cholesterol than healthy children. As allergic diseases have become more common and is still increasing in the Western world it is tempting to suggest that the cause is the increasing consumption of the polyunsaturated vegetable oils of the omega-6 type, because these oils are known to stimulate inflammatory processes, and allergy is a kind of inflammation. But there is room for another explanation.
At the Skin and Allergy Hospital in Helsinki, Finland Dr.Maria Pesonen and her co-workers followed 200 children from their birth to their 20 year anniversary.13 They found that the children with allergic disorders had lower total and LDL cholesterol than the others. The difference was obvious already at a time where all the children were breastfed. Thus, the difference could not be explained by their dietary habits. The researchers had no explanation for their observation, but if the lipoproteins are able to bind microbial products, it seems not too far-fetched to assume that they can bind other molecules as well, for instance allergens, those molecules that starts the allergic reactions.
Is familial hypercholesterolemia a disease?
“The more LDL there is in the blood, the more rapidly atherosclerosis develops.”
This was the main conclusion of the American Nobel Price-winners, Joseph Goldstein and Michael Brown.14 They discovered that the cells of people with familial hypercholesterolemia had difficulties taking in cholesterol from the blood because of a defect in the LDL-receptor, the mechanism that transports these vital molecules into the cells. This was the reason why cholesterol was much higher than normal in these people. People with familial hypercholesterolemia also have more atherosclerosis than normal and some of them do die early in life from heart disease. It was therefore not too far-fetched for Goldstein and Brown to draw the conclusion they did, and also to assume that it was applicable to the rest of mankind. They were awarded the Nobel Prize in 1985 for their discovery, and many other researchers share their view.
Their finding is certainly interesting, a result of careful scientific work. Unfortunately, the conclusion they drew was too hasty. In fact, there are benefits associated with this condition, which is why I deliberately refer to individuals with familial hypercholesterolemia as people, not as patients. What is even more surprising is that the reason why some of them die at a young age from heart disease is not their high cholesterol, but something else. I shall come back to that.
In England The Simon Broome Familial Hyperlipidaemia Register Group have followed almost 3000 people with familial hypercholesterolemia for many years. At the most recent control they found that 102 of them, or 3.6 % had died from a heart attack. By analyzing mortality of the same age group in the English population they calculated that the expected number should have been 40, or 1.4 %. On the other hand, fewer had died from other causes, 112 against the expected number 193, or 4 % against 6.8 %. For instance, only half as many had died from cancer.30 If you add the figures and compare them you will see that people with familial hypercholesterolemia live at least as long as other people, if not longer. A little more die from heart disease, but fewer die from cancer and other diseases.
The authors of the scientific report stressed that the participants in their study were admitted because all of them had close relatives who had died at a young age. Cholesterol screening often identifies old people with familial hypercholesterolemia who have no such relatives. The authors therefore suggested that if the participants had been representative for all people with familial hypercholesterolemia, their mortality would have been even lower.
In Finland, Professor Tatu Miettinen and Dr. Helena Gylling studied about one hundred individuals with familial hypercholesterolemia.16 Fourteen to seventeen years later, 30 had died, 26 because of a heart attack and four of other causes. On average, initial LDL cholesterol was the same among those who had died and those who still were alive. If high LDL cholesterol was the most important cause of atherosclerosis and heart disease, as postulated by Nobel Award winners Goldstein and Brown, then we should have expected higher cholesterol in those who died, but that wasn’t the case. Many other researchers have confirmed the Finnish findings.17-23
Another conflicting observation is the fact that people with familial hypercholesterolemia have normal cerebral arteries, even though the same cholesterol-rich blood flows through their brain as through the rest of their body.25
A missing link
The genetic aberrations in people with familial hypercholesterolemia are more complicated than Brown and Goldstein assumed. For instance, in a study of 2400 such individuals, Dr. Angelique Jansen at the University of Amsterdam found that variations of the prothrombin gene were associated with an increased risk of heart disease in these people.26 Prothrombin is a substance necessary for blood coagulation and an abnormal prothrombin gene may lead to the production of too much of this substance. The result is an increased tendency to coagulation and clot formation. Thus, some individuals with familial hypercholesterolemia may form arterial clots more easily than other people, not because of their high cholesterol, but because of an abnormal coagulation system.
Heart patients with familial hypercholesterolemia more often have high concentrations of fibrinogen and factor VIII in their blood than healthy people with familial hypercholesterolemia. Also these substances participate in the coagulation process, and too much of them may stimulate to clot formation. And again, whereas the heart patients had much higher concentrations of fibrinogen and factor VIII, their total and LDL cholesterol did not differ from those measured in healthy people with familial hypercholesterolemia.27
In earlier times, people with familial hypercholesterolemia lived longer than other people! Dutch researchers tracked the ancestors of people with familial hypercholesterolemia and identified 412 individuals with a 50 percent chance of having this genetic abnormality. They also searched official records of deaths and found that the longevity of those with a family history of this genetic aberration was not lower before the year 1900; in fact, on average they lived longer than other people. As the most common cause of death at that time was infectious disease, the authors suggested that high cholesterol protects against infection.28
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1. Your cholesterol tells very little about your future health
An excerpt from my previous book The Cholesterol Myths
Cholesterol is a peculiar molecule. It is often called a lipid or a fat. However, the chemical term for a molecule such as cholesterol is alcohol, although it doesn't behave like alcohol. Its numerous carbon and hydrogen atoms are put together in an intricate three dimensional network, impossible to dissolve in water. All living creatures use this indissolvability cleverly, incorporating cholesterol into their cell walls to make cells waterproof. This means that cells of living creatures can regulate their internal environment undisturbed by changes in their surroundings, a mechanism vital for proper function. The fact that cells are waterproof is especially critical for the normal functioning of nerves and nerve cells. Thus, the highest concentration of cholesterol in the body is found in the brain and other parts of the nervous system. Because cholesterol is insoluble in water and thus also in blood, it is transported in our blood inside spheric particles composed of fats (lipids) and proteins, the so-called lipoproteins. Lipoproteins are easily dissolved in water because their outside is composed mainly of water-soluble proteins. The inside of the lipoproteins is composed of lipids, and here are room for water-insoluble molecules such as cholesterol. Like submarines, lipoproteins carry cholesterol from one place in the body to another.
The submarines, or lipoproteins, have various names according to their density. The best known are HDL (High Density Lipoprotein), and LDL (Low Density Lipoprotein). The main task of HDL is to carry cholesterol from the peripheral tissues, including the artery walls, to the liver. Here it is excreted with the bile, or used for other purposes, for instance as a starting point for the manufacture of important hormones. The LDL submarines mainly transport cholesterol in the opposite direction. They carry it from the liver, where most of our body's cholesterol is produced, to the peripheral tissues, including the vascular walls. When cells need cholesterol, they call for the LDL submarines, which then deliver cholesterol into the interior of the cells. Most of the cholesterol in the blood, between 60 and 80 per cent, is transported by LDL and is called ”bad” cholesterol, for reasons that I shall explain soon. Only 15-20 percent is transported by HDL and called ”good” cholesterol. A small part of the circulating cholesterol is transported by other lipoproteins.
You may ask why a natural substance in our blood, with important biologic functions, is called ”bad” when it is transported from the liver to the peripheral tissues by LDL, but ”good” when it is transported the other way by HDL. The reason is that a number of follow-up studies have shown that a lower-than-normal level of HDL-cholesterol and a higher than-normal level of LDL-cholesterol are associated with a greater risk of having a heart attack, and conversely, that a higher-than-normal level of HDL-cholesterol and a lower-than normal LDL-cholesterol are associated with a smaller risk. Or, said in another way, a low HDL/LDL ratio is a risk factor for coronary heart disease.
However, a risk factor is not necessarily the same as the cause. Something may provoke a heart attack and at the same time lower the HDL/LDL ratio. Many factors are known to influence this ratio.
What is good and what is bad? People who reduce their body weight also reduce their cholesterol. In a review of 70 studies Dr. Anne Dattilo and Dr. P.M. Kris-Etherton concluded that, on average, weight reduction lowers cholesterol by about 10 per cent, depending on the degree of the reduction. Interestingly, it is only cholesterol transported by LDL that goes down; the small part transported by HDL goes up. In other words, weight reduction increases the ratio between HDL- and LDL-cholesterol (1). An increase of the HDL/LDL ratio is called ”favorable” by the diet-heart supporters; cholesterol is changed from ”bad” to ”good”. But is it the ratio or the weight reduction that is favorable? When we become fat, other harmful things occur to us. One is that our cells become less sensitive to insulin, so that some of us develop diabetes. And people with diabetes are much more likely to have a heart attack than people without diabetes, because atherosclerosis and other vascular damage occur very early in diabetics, even in those without lipid abnormalities. In other words, overweight may increase the risk of a heart attack by mechanisms other than an unfavorable lipid pattern, while at the same time overweight lowers the HDL/LDL ratio. Also smoking increases cholesterol a little. Again, it is LDL-cholesterol that increases, while HDL-cholesterol goes down, resulting in an ”unfavorable” HDL/LDL ratio (2). What is certainly unfavorable is the chronic exposure to the fumes from burning paper and tobacco leaves. Instead of considering the low HDL/LDL ratio as bad it could simply be smoking itself that is bad. Smoking may provoke a heart attack and, at the same time, lower the HDL/LDL ratio.
Exercise decreases the bad LDL-cholesterol and increases the ”good” HDL-cholesterol (3). In well-trained individuals the ”good” HDL is increased considerably. In a comparison between distance runners and sedentary individuals, Dr. Paul D. Thompson and his colleagues found that the athletes on average had a 41 per cent higher HDL-cholesterol level (4). Most population studies have shown that physical exercise is associated with a lower risk of coronary heart disease, and a sedentary life with a higher risk. It also seems plausible that a well-trained heart is better guarded against obstruction of the coronary vessels than a heart always working at low speed. A sedentary life may predispose people to a heart attack and, at the same time, lower the HDL/LDL ratio.
A low ratio is also associated with high blood pressure (5). Most probably, the hypertensive effect is created by the sympathetic nerve system, which is often overstimulated in hypertensive patients. Hypertension (or too much adrenalin) may provoke a heart attack, for instance by inducing spasm of the coronary arteries or by stimulating the arterial muscle cells to proliferate, and, at the same time, lower the HDL/LDL ratio.
Univariate and multivariate As you see, it is not easy to know what is bad. Is it bad to be fat, to smoke, to be inactive, to have high blood pressure, or to be stressed? Or is it bad to have a lot of bad cholesterol? Or both? Is it good to be slim, to stop smoking, to exercise, to have normal blood pressure, to be emotionally calm? Or is it good to have much ”good” cholesterol? Or both? Thus, the risk of having a heart attack is greater than normal for people with high LDL-cholesterol, but so is the risk for fat, sedentary, smoking, hypertensive and mentally stressed individuals. And since such individuals usually have elevated levels of LDL-cholesterol, it is, of course impossible to know whether the increased risk is due to the previously mentioned risk factors (or to risk factors we do not yet know) or to the high LDL-cholesterol. A calculation of the risk of high LDL-cholesterol that ignores other risk factors is called a univariate analysis and is, of course, meaningless. To prove that high LDL-cholesterol is an independent risk factor, we should ask if fat, sedentary, smoking, hypertensive and mentally stressed individuals with a high LDL-cholesterol level are at greater risk for coronary disease than fat, sedentary, smoking, hypertensive and mentally stressed individuals with low or normal LDL cholesterol.
Using complicated statistical formulas, it is possible to do such comparisons in a population of individuals with varying degrees of the risk factors and varying levels of LDL-cholesterol, a so-called multivariate analysis. If a multivariate analysis of the prognostic value of LDL cholesterol also takes body weight into consideration, it is said to be ”adjusted for body weight”. A major problem with such calculations is that the data generated by these and other complicated statistical methods are almost impossible for most readers, including most physicians, to comprehend. For many years researchers in this area have not presented primary data, simple means, or simple correlations. Instead, their papers have been salted with meaningless ratios, relative risks, p-values, not to mention obscure concepts such as the standardized logistic regression coefficient, or the pooled hazard rate ratio. Instead of being an aid to science, statistics are used to impress the reader and cover the fact that the scientific findings are trivial and without practical importance.
2. Blood cholesterol has nothing to do with atherosclerosis
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.
The pathologist Dr. Kurt Landé and the biochemist Dr. Warren Sperry at the Department of Forensic Medicine of New York University were the first to study that question (25). 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 number of individuals who had died violently. In age group after age group their diagrams looked like the starry sky.
Drs. Landé and Sperry are never mentioned by the proponents of the diet-heart idea, or they misquote them and claim that they found a connection (26), or they ignore their results by arguing that cholesterol values in the dead are not identical with those in living people.
That problem was solved by Dr. J. C. Paterson from London, Canada and his team (27). For many years they followed about 800 war veterans. Over the years, Dr. Paterson and his coworkers regularly analyzed blood samples from these veterans. Because they restricted their study to veterans who had died between the ages of sixty and seventy, the scientists were informed about the cholesterol level over a large part of the time when atherosclerosis normally develops.
Dr. Paterson and his colleagues did not find any connection either between the degree of atherosclerosis and the blood cholesterol level; those who had had a low cholesterol were just as atherosclerotic when they died as those who had had a high cholesterol.
Similar studies have been performed in India (28), Poland (29), Guatemala (30), and in the USA (31), all with the same result: no correlation between the level of cholesterol in the blood stream and the amount of atherosclerosis in the vessels.
The question about blood cholesterol and atherosclerosis has been studied by coronary angiography also. It seems as if every specialist in coronary angiography in America has performed his own study, funded with federal tax money 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 (33).
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 between degree of atherosclerosis and level of blood cholesterol.
Studies based on coronary angiography are fundamentally flawed 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 relatively large number of patients with familial hypercholesterolemia must have been included. Again, there is an obvious risk for the kind of bias that I described above. The fact that this objection is justified was demonstrated in a Swedish study performed by Dr. Kim Cramér and his group in Gothenburg, Sweden (34). As in most other angiographic studies the patients with the highest cholesterol values had on average the most arteriosclerotic 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 hypercholesterolemia, the correlation between blood cholesterol and degree of atherosclerosis disappeared.
3. The diet has little to do with your blood cholesterol level
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.
Studies of African tribes have shown that intakes of enormous amounts of animal fat not necessarily raises blood cholesterol; on the contrary it may be very low. Samburu people, for instance, eat about a pound of meat and drink almost two gallons of raw milk each day during most of the year. Milk from the African Zebu cattle is much fatter than cow's milk, which means that the Samburus consume more than twice the amount of animal fat than the average American, and yet their cholesterol is much lower, about 170 mg/dl (38).
According to the view of the Masai people in Kenya, vegetables and fibers are food for cows. They themselves drink half a gallon of Zebu milk each day and their parties are sheer orgies of meat. On such occasions several pounds of meat per person is not unusual. In spite of that the cholesterol of the Masai tribesmen is among the lowest ever measured in the world, about fifty percent of the value of the average American (39).
Shepherds in Somalia eat almost nothing but milk from their camels. About a gallon and a half a day is normal, which amounts to almost one pound of butter fat, because camel's milk is much fatter than cow's milk. But although more than sixty percent of their energy consumption comes from animal fat, their mean cholesterol is only about 150 mg/dl, far lower than in most Western people (40).
Proponents of the diet-heart idea say that these African tribesmen are accustomed to their diet and that their organisms have inherited a cleverness to metabolize cholesterol. However, a study of Masai people who had lived for a long time in the Nairobi metropolis showed this to be wrong (41). If the low cholesterol of the Masai tribesmen was inherited it should have been even lower in Nairobi, because here their diet with all certainty included less animal fat than the diet of the Masai tribesmen. But the mean cholesterol level in twenty six males in Nairobi was twenty-five percent higher than that of their cattle-breeding colleagues in the countryside.
And there is more evidence. Although it is possible to change blood cholesterol a little in laboratory experiments and clinical trials by dieting, it is impossible to find any relationship between the make up of the diet and the blood cholesterol of individuals who are not participating in a medical experiment. In other words, individuals who live as usual and eat their food without listening to doctors or dieticians show no connection between what they eat and the level of their blood cholesterol.
If the diet-heart idea were correct individuals who eat great amounts of animal fat would have higher cholesterol than those who eat small amounts; and individuals who eat small amounts of vegetable fat should have higher cholesterol than those who eat great amounts. If not, there is no reason to meddle with people's diet.
In the early 1950's the Framingham study included dietary analyses. Almost one thousand individuals were questioned in detail about their eating habits. No connection was found between the composition of the food and the cholesterol level of the blood. Wrote Drs. William Kannel and Tavia Gordon, authors of the report: ”These findings suggest a cautionary note with respect to hypotheses relating diet to serum cholesterol levels. There is a considerable range of serum cholesterol levels within the Framingham Study Group. Something explains this inter-individual variation, but it is not diet.” For unknown reasons, their results were never published. The manuscript is still lying in a basement in Washington.
In a small American town called Tecumseh, Michigan a similar study was performed by a team of researchers from the University of Michigan headed by Dr. Allen Nichols (42). Experienced dieticians asked in great detail more than two thousand individuals what they had eaten during a twenty-four hour period. The dieticians also asked about the ingredients of the food, analysed the recipies of home-cooked dishes, and exerted great care to find out what kind of fat was used in the kitchen. Calculations were then performed using an elaborate list of the composition of almost 3000 American food items. Finally the participants were divided into three groups, a high, a middle, and a low level group, according to their blood cholesterol.
No difference was found between the amounts of any food item in the three groups; of special interest was that those with a low blood cholesterol ate just as much saturated fat as did those with a high cholesterol.
These studies concerned adults, but no association has been found in children either. At the famous Mayo Clinic in Rochester, Minnesota, for instance, Dr. William Weidman and his team analyzed the diet of about one hundred school children (43). Great differences were found between the amount of various food items eaten by these children, and also great differences between their blood cholesterol values, but there wasn´t the slightest connection between the two. The children who ate lots of animal fat had just as much or just as little cholesterol in their blood as the children who ate very little animal fat . A similar investigation of 185 children was performed in New Orleans with the same result (44).
Is it really wise to meddle with people's dietary habits if their food has no influence on their cholesterol? And how do those who believe that fat food is dangerous explain all these negative results?
The most common objection says that information about dietary habits is inaccurate, and it is. But even if it is uncertain what people say they ate yesterday, a crude relationship should appear if a sufficiently large number of individuals were questioned meticulously. If not, the influence of the diet, if any, is so minute that it cannot possibly have any importance.
Diet-heart supporters also argue that most people in Western communities already eat great amounts of fat and cholesterol. This argument declares that we have already crossed a threshold of too much animal fat in the diet so that more fat does not make any impact on our blood cholesterol.
The argument is in conflict with the studies I have mentioned above. For instance, astonished by their negative results Dr. Nichols and his team from Michigan (42) tried to find explanations. But they did not find that all individuals ate much fat. Wrote the authors: ”The distribution of daily intake of total fat, saturated fat, and cholesterol by the individuals in this study was quite broad”.
Consider now that it is the goal of the National Cholesterol Education Program to lower the intake of animal fat of all Americans to about ten per cent of their caloric intake. Almost fifteen per cent of the Tecumseh participants (42) already ate that little animal fat, and yet it was impossible to see a difference between the cholesterol of those who ate that little and of those who ate much more. Does it make sense to recommend this drastic reduction of animal fat intake if the cholesterol of those who already eat that little is just as high as the cholesterol of the others?
In the study from the Mayo Clinic (43) there was also a wide range of fat intake. The lowest intake of animal fat was 15 grams per day (less than 10 per cent of the caloric intake); the highest was 60 grams per day. In the Bogalusa study, the range was still broader. The lowest intake of all fats (no information was given about the range of intake of animal fat) was 17 grams per day, the highest 325 grams per day.
In Jerusalem a team of researchers, led by Dr. Harold Kahn studied the diet and blood cholesterol of ten thousand male Israeli civil servants. The dietary habits varied considerably between people coming from Israel, Eastern Europe, Central Europe, Southern Europe, Asia and Africa. The intake of animal fat varied from ten grams up to two hundred grams daily, and there were also considerable differences between their cholesterol values (47).
If the intake of animal fat were of major importance for the cholesterol level in the blood it should be possible to find some kind of relationship from a study of so many individuals with such great variations in blood cholesterol and dietary habits. But there was no relation in this Israeli study either. Extremely low cholesterol values were seen both in those who ate little and in those who ate the most animal fat, and high cholesterol values were seen at all levels of animal fat intake.
The scientists from Israel also studied the value of various ways of dietary questioning. Many studies have recorded the diet of a 24 hour period only. Even if this information were accurate it may not be representative of the diet for the rest of the year, far less for a whole life time. The Israeli scientists found that the best information came from a questioning over several days in different seasons of the year, the method used in the study of the bank staff members. Using this expensive and time-consuming method in a smaller study of sixty-two individuals they could not find a correlation either; the correlation coefficient between animal fat intake and blood cholesterol was zero point zero (48).
4. Atherosclerosis and coronary heart disease have nothing to do with the diet
National consensus committees in many countries have declared that atherosclerosis and coronary heart disease can be prevented by an appropriate diet. Although the scientific evidence for this message is surprisingly meager, if present at all, it has gained status as established wisdom.
The definition of the ”prudent” diet has changed considerably with time. Initially, it was considered important to reduce dietary fat of all kinds. This advice was based on a review paper by Ancel Keys (49), the main designer of the so-called diet-heart idea. In his review Keys presented a perfect curvilinear correlation between the mortality from coronary heart disease and the consumption of fat in six countries, but his curve was based on a selection of countries that fit his hypothesis and it has not been confirmed in studies including many more countries (50).
The prudent diet was redefined a few years later based on a new study by Ancel Keys, ”Seven Countries” (51). According to that study the total fat intake was unimportant; heart mortality in these seven countries was best predicted by the intake of saturated fat . But within each country no association was seen. In Finland and Greece for instance, heart mortality in two districts varied with a factor five and seven, respectively, despite similar diets and other risk factors. Furthermore, no correlation was found between the diet and the major electrocardiographic findings. Considering that all electrocardiograms were analysed in the American study center this finding should carry more weight than the correlation with the clinical diagnosis, settled as it was by local doctors with varying competence and diagnostic habits.
The seven countries were admittedly selected by Keys. Such selection may be helpful to illustrate an idea at a preliminary stage, but a proof of causality demands random data. In more recent studies, including many more countries, the association was weak, absent, or inverse (52).
Conclusions from associations between national food consumption data and disease should be drawn with care. Most important, assumed intake of animal fat may be falsely high in prosperous countries, because available fat is not the same as fat eaten, but includes fat consumed by pet animals, fat discarded in the kitchen or on the plate, and fat which has never reached the consumer. With all certainty, these amounts are larger in prosperous countries.
The finding that an increased intake of polyunsaturated fatty acids, also called PUFA, can lower the serum cholesterol concentration in laboratory experiments has led to the belief that they would lower the risk of coronary heart disease also. Consequently, an increased intake of PUFA has been advised as an important part of the prudent diet. Initially, no limit was put to such intake, but by the years the limit has been lowered successively. Most recently, an upper limit of only 7 cal% was recommended because a high intake of PUFA promotes cancer, infections and testicular damage in rats (53). The average food intake in most western countries includes that amount of PUFA.
There is little evidence that an increased intake of PUFA protects against heart attacks. In ”Seven Countries” intake of PUFA was not associated with heart mortality, and studies of patients with coronary heart disease have shown that if anything, they eat more PUFA than do healthy individuals, see below.
If heart attacks are caused by eating too much animal fat or saturated fat, a rising intake in a population should of course be followed by more heart attacks and a decreasing intake by fewer attacks. No consistent pattern has been found, however. In a few countries the changes have followed each other and the data from these countries have been used eagerly to support national diet counceling. But in many countries fat consumption has changed whereas heart mortality has not, or vice versa; in many countries they have even changed at opposite directions (54).
In Switzerland, for instance, coronary mortality decreased after World War II. During the same period intake of animal fat increased by 20 per cent (55).
In England, the intake of animal fat has been relatively stable since at least 1910 while the number of heart attacks increased ten times between 1930 and 1970 (56).
In the US coronary mortality increased about ten times between 1930 and 1960, leveled off during the sixties and has since decreased. During the decline of mortality from coronary heart disease the consumption of animal fat declined, but so it did during the previous thirty years of sharply rising mortality (57). In Framingham the decline of coronary mortality was balanced by an increased number of non-fatal heart attacks (58) suggesting an effect of better treatment rather than an effect of dietary changes.
In Japan coronary heart disease is uncommon, allegedly due to the lean Japanese diet. A large study of Japanese emigrants (59) is often used as evidence because after migration to the United States these emigrants died from heart attacks almost as often as did Americans. The increased heart mortality after migration was not associated with the diet or the serum cholesterol, however, but with the cultural upbringing; those who lived according to Japanese traditions were protected. Most surprising, emigrants who stuck to the Japanese tradition, but ate the fat American food ran a smaller risk than those who were accustomed to the American way of life but ate the lean Japanese food (60).
If dietary fats were important this should obviously be reflected in the diet of patients who have had a heart attack. The following table gives the results from 13 studies, where the diet of patients with coronary heart disease was compared with the diet of healthy control individuals of the same age and sex. The amounts of dietary fats are given in percent of total calories. Asterisks means that the difference found was statistically significant. NS means that no absolute figures were given in the report, but that the difference was not statistically significant.
5. Cholesterol-lowering may shorten your life
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). Before the introduction of the new cholesterol lowering drugs, the statins, more than 40 trials have been performed to test if cholesterol-lowering can prevent a heart attack. In some of the trials the number of fatal heart attacks were lowered a little, in other trials the number of fatal heart attacks increased. Overviews of the trials have shown that when all results were taken together, just as many died in the treatment groups (e.g. those whose cholesterol was lowered) as in the untreated control group (78,79). The following table gives the accumulated results. None of the differences were statistically significant. Nor were they by more sophisticated analyses.
Some overviews have shown a positive result after cholesterol-lowering is because they had ignored or excluded one or more trials with a negative outcome (79).
The mentioned overviews included mostly diet and/or the older cholesterol-lowering drugs. But a new type of drugs, the socalled statins (for instance Zocord®, Mevacor®, Lescol®, Lipitor® and Pravachol®) have been succesful. However, their effect isn´t exerted through cholesterol-lowering, they have other and more useful properties Unfortunately they also stimulate cancer growth
6. The effect of the statins is not due to cholesterol-lowering
As mentioned in section 4 cholesterol-lowering by itself does not prolong your life. In the experiments, that have shown this fact beyond all doubt, cholesterol-lowering was performed by diet or by use of various older drugs such as clofibrate (Atromidin), gemfibrozil (Lopid), cholestyramine (Questran), colestipol (Lestid), and nicotinic acid (Nicangin). But a new type of cholesterol-lowering drugs, the so-called statins (for instance Zocor, Lipitor and Pravachol) have been succesful. For the first time cholesterol-lowering have shown significant improvement of mortality, both coronary mortality, stroke mortality and total mortality. These trials are therefore considered as strong arguments for the idea, that a high cholesterol is dangerous.
Have these trials really demonstrated that raised LDL cholesterol has importance for coronary heart disease, as the trial directors concluded in the reports?
There is reason to question that, because some of the results are not consistent with what we have learned about cholesterol.
First, old patients were protected from cardiovascular disease just as much (or as little) as young ones, although most studies have shown that a high cholesterol is a weak risk factor, or no risk factor at all, for old people. (Unfortunately, in the only trial that included old people only, the PROSPER trial, the lowering of heart mortality was smaller thanm the increse of cancer mortality).
Second, also the number of strokes was reduced after statin treatment, although no studies have shown that a high cholesterol is a risk factor for stroke.
Third, patients who had had a coronary were protected although most studies have shown that a high cholesterol is a weak risk factor, if any at all, for those who already have had a coronary. (In fact, this finding should have stopped all the previous, secondary preventive trials).
And finally, the statins protected against coronary heart disease whether the cholesterol was high or low although most studies have shown that a normal or low cholesterol is no risk factor for coronary disease.
How come that the statins are effective for old people, for patients who already have had a coronary, and even for those whose cholesterol is normal? If the cholesterol level for these people is no risk factor for coronary disease, how could a lowering of that cholesterol improve their chances to avoid a coronary? The only reasonable explanation is that the statins do more than just lower cholesterol. There is much evidence for that.
The protective effects of simvastatin has been demonstrated in animal experiments. In one of them, performed by Dr. B.M. Meiser and colleagues from Munich, Germany, hearts were transplanted into rats. Normally, the function of such grafts gradually deteriorates because the coronary vessels are narrowed by an increased growth of smooth muscle cells in the vascular walls, a condition called graft vessel disease. In Dr. Meiser's experiment, however, rats that were given simvastatin had considerably less graft vessel disease than control rats not given simvastatin, and this was not due to cholesterol lowering because simvastatin does not lower cholesterol in rats. In fact, LDL cholesterol was highest in the rats treated with simvastatin (84).
In another experiment, Dr. Maurizio Soma and his colleagues from Milan, Italy placed a flexible collar around one of the carotic arteries in rabbits. After two weeks arteries with collars became narrow but less so if the rabbit had been given simvastatin. Again, the effect was unrelated to the rabbits´ cholesterol level (85).
Thus, the statins in some way protect against cardiovascular disease, but their effect is not due to cholesterol-lowering.
But why bother about pharmacological mechanisms? Isn´t it wonderful that the statins work? Shouldn´t we all take statins?
The costs To answer that question it is necessary to look at the figures from the trials. To be short I have chosen the figures for coronary death. According to the results from the 4S trial (86) there was a 41% reduction in the risk of coronary death. According to the results from the CARE trial (87) the reduction was 24%, and according to the WOSCOP (88) trial the reduction was 28%. These figures seem impressive, but let us look at the absolute figures also. In the treatment group of the 4S trial five percent, or 111 individuals, died from a heart attack; in the control group 8.5 percent, or 189 individuals, died, a difference, or a risk reduction of 3.5%. To prevent these 3.5% of the patients (8.5% - 5%) or 78 individuals, from dying it was necessary to treat 2221 individuals during five years. You could also say that to prevent one death it was necessary to treat 25 individuals for five years. Or said in another way, if you have had a heart attack the chance to avoid death from a new one during five years is 91.5%. If you eat simvastatin this chance increases to 95%.
In the CARE trial 5.7%, or 119 individuals died from a heart attack in the control group and 4.6%, or 96 individuals in the treatment group. Thus, to prevent 23 coronary deaths (1.1%) it had been necessary to treat 2081 individuals for five years, which means that 90 patients were treated for each life saved.
In the WOSCOP trial, which concerned healthy individuals with a high cholesterol, the result was even less impressive. Here, 61 died in the placebo group, 41 in the treatment group, a risk reduction of 0.6%. To save these 20 lives it had been necessary to treat 3302 healthy individuals for five years, or 165 individuals for each life.
Said in another way, the risk of dying from a heart attack during five years if you are about 55 years old and if your cholesterol is around 272 mg per dl is 1.8%. With pravastatin treatment the risk is reduced to 1.2%. You could also say that the chance to avoid death from a heart attack for five years is 98.2%; with pravastatin the chance is 98.8%.
The reason why trial results should be given in absolute figures and not in relative is because the side effects are given in absolute figures. Let us assume that a mortal side effect occurs in 0.5 percent of the patients. You may belittle that if you compare this figure for instance with a relative risk reduction of 28%. But as the absolute risk reduction was 0.6% the effect of treatment has almost disappeared.
To be fair it should be mentioned that the number of non-fatal heart attacks was reduced also. In the WOSCOP trial for instance, 248 individuals in the control group had a fatal or non-fatal coronary, in the pravastatin group the number was 174. This means that to prevent a heart attack in a healthy 55 year old man with a high cholesterol it is necessary to treat about 45 men for five years. To prevent a new heart attack it is necessary to treat 34 patients for five years according to the CARE trial and 28 patients according to the 4S trial.
A few years ago Drs. Thomas Newman and Stephen Hulley published the results from a meticulous review of what we know about cancer and lipid-lowering drugs. They found that clofibrate, gemfibrozil and all the statins stimulate cancer growth in rodents (89).
Newman and Hulley asked themselves why these drugs had been approved by the Food and Drug Administration at all. The answer was that the doses used in the animal experiments were much higher than those recommended for clinical use. But as Drs. Newman and Hulley commented, it is more relevant to compare blood levels, and the levels achieved in rodents were very close to those seen in patients.
Because the latent period between exposure to a cancer-stimulating chemical and the incidence of clinical cancer in humans may be 20 years or more, the absence of any controlled trials of this duration means that we do not know whether statin treament will lead to an increased rate of cancer in coming decades. There is reason to believe that it will, because as mentioned above, treatment of old people already has resulted in an increased number of cancer. The reason is probably that many old people already have cellular changes that rapidly may develop to clinical cancer if stimulated by a cancer-provoking drug..
Other nasty effects have been reported on human beings, side effects that have been reported after the end of the trials. They include peripheral neuropathy, a painful and invalidating disease mainly located to the legs (90a), memory loss (90b), short temper (90c), aggressive behavior (90d) and muscle problem that in rare cases have led to kidney failure and death. Most scary, considering that people with very high cholesterol, so-called familial hypercholesterolemia, automatically are prescribed statin treatment already from early childhood, is the recent report in prestigious New England Journal of Medicine (90e). Here the authors reported that almost 50 % of pregnant women who took a statin drug during early pregnancy gave birth to a child with malformations, some of them more severe than those seen after thalidomide treatment.
Those who argue for statin treatment say that these side effects are very rare. They will most certainly become much more common considering that the new cholesterol guidelines recommend that cholesterol should be lowered as much as possible, even if it may demand an eight times higher dose than used hitherto.
Thus, millions of asymptomatic people are being treated with medications, the ultimate effects of which are not yet known. Drs. Newman and Hulley therefore recommended that the new statins should be used for patients at very high risk for coronary disease only, whereas such treatment should be avoided for individuals with life expectancies of more than 10 to 20 years. And healthy people with a high cholesterol as the only risk marker belong to that category.
7. The many critical scientists
Those who propagate for a low-fat diet and cholesterol-lowering drugs claim that there is general agreement about the diet-heart idea. Nothing could be more wrong. Here follows, in alphabetic order, a selection of critical scientists. Mary Enig is an international expert in the field of lipid biochemistry, a nutritionist and a Consulting Editor to a number of scientific publications, among others the Journal of the American College of Nutrition. She is also the President of the Maryland Nutritionists Association. She has published many scientific papers on the subject of food, nutrition topics, food fats and oils, several chapters on nutrition for books and a book about dietary fats, oils and cholesterol (90a). Her main research has concerned the hazards associated with eating too much trans fatty acids. In an interview she was asked if saturated fats cause heart disease: 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. Read also hers and Sally Fallons paper The Oiling of America
Michael Gurr is an associate professor of biochemistry at the School of Biological & Molecular Sciences in Oxford, editor-in-chief of Nutrition Research Reviews and editor of three other scientific journals.Wrote Professor Gurr in his conclusion of a large review on the diet-heart idea (91): The arguments and discussion of the scientific evidence presented in this review will not convince those "experts" who have already made up their minds, for whatever reason, be it truly scientific or political, that a fatty diet is the cause of CHD [coronary heart disease]. However, I hope that some readers, who were, perhaps, unaware that the lipid hypothesis had any shortcomings, will have been persuaded that the relationships between the fats we eat and the likelihood that we may die from a heart attack is by no means as simple as these simplistic statements imply.
George Mann, 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).
After the start of the cholesterol campaign eight years later Mann summarized his criticism of the diet-heart idea in Nutrition Today (93). According to Mann, the diet-heart idea is the greatest scientific deception of our times. Mann is especially critical of the cholesterol-lowering trials. Never in the history of science have so many costly experiments failed so consistently, he declared.
Professor Mann also criticized the directors of the Lipid Research Clinics trial (LRC), the fundament of the cholesterol campaign. The unsupportive results from the LRC trial have not prevented them from bragging about this cataclysmic break-through, he wrote. And, he continued: The managers at the National Institutes of Health have used Madison Avenue hype to sell this failed trial in the way the media people sell an underarm deodorant. The Bethesda Consensus Panel ... has failed to acknowledge that the LRC trial, like so many before it, is saying firmly and loudly 'No, the diet you used is not an effective way to manage cholesterolemia or prevent coronary heart disease and the drug you so generously tested for a pharmaceutical house does not work either.
People who are faced with the many distorted facts about diet, cholesterol and heart disease often ask me why so many scientists unquestioningly accept the diet-heart idea. Here is Professor Mann's comment: Fearing to lose their soft money funding, the academicians who should speak up and stop this wasteful anti science are strangely quiet. Their silence has delayed a solution for coronary heart disease by a generation.
Professor Mann offers a little glimpse of hope at the end of his article in Nutrition Today (93): Those who manipulate data do not appreciate that understanding the nature of things cannot be permanently distorted - the true explanations cannot be permanently ignored. Inexorably, truth is revealed and deception is exposed. ...In due time truth will come out. This is the relieving grace in this sorry sequence.
Michael F. Oliver, a former professor and director of the Wynn Institute for Metabolic Research, London was one of the first to demonstrate that, on average, patients with coronary heart disease more often had abnomal levels of various fats in the blood than control individuals did. Professor Oliver still thinks that those with inherited diseases of cholesterol metabolism, or 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: Doubts about the promotional nature of these campaigns are not popular. Doubters are scorned, although this does not matter. But the issue is a very serious one if vast sums are spent and widespread changes are made in the lifestyle of normal people when the accumulated evidence is that total mortality is unchanged or possibly even increased (94).
Again and again, Professor Oliver has criticized those who think that the increased mortality from non-medical causes seen in many trials is an effect of chance. Rather, he thinks, the very lowering of blood cholesterol may be dangerous: Very little is known about the long-term effects of lowering cholesterol concentrations on the composition of cell membranes (95).
According to Oliver our bodies may regulate attempts to lower blood cholesterol in most cases, but ...would such homoeostatic [regulatory] mechanisms be effective in all patients, at all times, and in all cells--particular cells in which biologic function is impaired for other reasons? These doubts will not go away for several more years? (95) Other critical papers by Professor Oliver
Edward R. Pinckney is an editor of four medical journals and former co-editor of JAMA, the Journal of the American Medical Association. In 1973, together with his wife, he published a book, called ”The Cholesterol Controversy” (97) which summarized all the inconsistencies of the cholesterol idea. Dr. Pinckney describes all the factors that influence blood cholesterol in healthy people and how difficult it is to get a reliable measure of the cholesterol level because of the uncertainties of the analysis: The level of one's blood cholesterol is, at best, nothing more than an extremely rough indication of a great many different disease conditions. At worst, it can be more the cause of stress and the diseases that stress brings on. To alter one's life style as a consequence of this particular laboratory test may well cause more trouble than it could relieve.
The start of chapter 1 in Pinckney´s book is worth citing: Your fear of dying--if you happen to be one of the great many people who suffer from this morbid preoccupation- may well have made you a victim of the cholesterol controversy. For, if 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. 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.
Raymond Reiser is a former professor of biochemistry at Texas A&M university. In 1973 he criticized the recommendations for dietary treatment of high cholesterol by declaring: The authority quoted by these authors for the recommendation is not a primary source but another review similar to their own. It is this practice of referring to secondary or tertiary sources, each taking the last on faith, which has led to the matter-of-fact acceptance of a phenomenon that may not exist. (98)
Here is another citation from Professor Reiser´s papers (99): One must be bold indeed to attempt to persuade large segments of the populations of the world to change their accustomed diets and to threaten important branches of agriculture and agribusiness with the results of such uncontrolled, primitive, trial and error type explorations. Certainly modern science is capable of better research when so much is at stake.
Paul Rosch is President of The American Institute of Stress, Clinical Professor of Medicine and Psychiatry at New York Medical College, Honorary Vice President of the International Stress Management Association and Chairman of its U.S. branch. He is the editor or subeditor of three well-known medical journals, he has been a member of the board of several other journals, and has served as President of the New York State Society of Internal Medicine, as Chairman of the International Foundation for Biopsychosocial Development and Human Health, and has been an Expert Consultant on Stress to the United States Center for Disease Control. He has written extensively over the past forty-five years on the role of stress in health and illness, with particular reference to cardiovascular disease and cancer. He has appeared on numerous national and international television programs such as The Today Show, Good Morning America, 60 Minutes, Nova, CBS, NBC, PBS, BBC and CBC network presentations. His editorials and comments have been published in every major medical journal. Professor Rosch has also been interviewed and widely quoted in numerous major American newspapers and magazines.
As the author of the Newsletter of the American Institute of Stress Professor Rosch has published several articles about the cholesterol hypothesis and the diet-heart idea. His conclusions are close to those presented in this book: A massive crusade has been conceived to “lower your cholesterol count” by rigidly restricting dietary fat, coupled with aggressive drug treatment. Much of the impetus for this comes from speculation, rather than any solid scientific proof."
The result is well-known, says Professor Rosch: The public is so brainwashed, that many people believe that the lower your cholesterol, the healthier you will be or the longer you will live. Nothing could be further from the truth.
How can this go on year after year? Professor Rosch has several explanations: The cholesterol cartel of drug companies, manufacturers of low fat foods, blood testing devices, and others with huge vested financial interests have waged a highly successful promotional campaign. Their power is so great that they have infiltrated medical and governmental regulatory agencies that would normally protect us from such unsubstantiated dogma.
Professor Rosch reminds us that practicing physicians get most of their information from the drug companies. But compared to their peers a half century ago, most doctors don’t have the time or skills to critically evaluate reports, very few know anything about research, nor did the generation that taught them.
Ray Rosenman is the retired Director of Cardiovascular Research in the Health Sciences Program at SRI International in Menlo Park, California, and associate chief of medicine, Mt Zion Hospital and Medical Center in San Francisco. Since 1950 he has been a cardiologist and a researcher. He has published four books and many text chapters and journal articles about cardiovascular diseases. His main interest has been the influence of neurogenic and psychological factors on the blood lipids (100), but he has also written reviews critical of the diet-heart idea.
Here is the conclusion from his most recent review: These data lead to a conclusion that neither diet, serum lipids, or their changes can explain wide national and regional differences of IHD [coronary heart disease] rates, or the variable 20th century rises and declines of CHD mortality. This conclusion is supported by the results of many clinical trials which fail to provide adequate evidence that lowering serum cholesterol, particularly by dietary changes, is associated with a significant reduction of IHD mortality or improved longevity. It is variously stated that the preventive effects of dietary and drug treatments have been exaggerated by a tendency in trial reports, reviews, and other papers to cite and inflate supportive results, while suppressing discordant data, and many such examples are cited (101).
Russell Smith was an American experimental psychologist with a strong background in physiology, mathematics and engineering. No review written by the proponents of the diet-heart idea are remotely comparable with Smith's books and papers (102) when it comes to scientific depth and completeness. Smith's summation is devastating for the diet-heart proponents: Although the public generally perceives medical research as the highest order of precision, much of the epidemiologic research is, in fact, rather imprecise and understandably so because it has been conducted principally by individuals with no formal education and little on-the-job training in the scientific method. Consequently, studies are often poorly designed and data are often imappropriately analyzed and interpreted. Moreover, biases are so commonplace, they appear to be the rule, rather than the exception. It is virtually impossible not to recognize that many researchers routinely manipulate and/or interpret their data to fit preconceived hypotheses, rather than manipulate hypotheses to fit their data. Much of the literature, therefore, is nothing less than an affront to the discipline of science.
Dr. Smith concludes: The current campaign to convince every American to change his or her diet and, in many cases, to initiate drug "therapy" for life is based on fabrications, erroneous interpretations and/or gross exaggerations of findings and, very importantly, the ignoring of massive amounts of unsupportive data...It does not seem possible that objective scientists without vested interests could ever interpret the literature as supportive.
Dr. Smith is aware that he is up against some extremely powerful institutions: The political and financial power of the NHLBI and AHA team...is enormous and without equal. And because the alliance has substantial credibility in the eyes of the public and most practicing physicians, it has become a juggernaut, able to use its power and prestige to suppress a great body of unsupportive evidence and even defy the most fundamental tool of scientists, logic.
The scientists who have produced the misleading papers and reviews are, of course, the first whom Smith faults. But he adds: Equally culpable are the editors of the many journals who publish articles without regard to their quality or scientific import. It is depressing to know that billions of dollars and a highly sophisticated medical research system are being wasted chasing windmills.
William E. Stehbens is a professor at the Department of Pathology, Wellington School of Medicine, and director of the Malaghan Institute of Medical Research in Wellington, New Zealand. Based on his own studies and on extensive reviews of the literature he has effectively demonstrated the many fallacies of the diet heart-idea. In a thorough review of the experimental studies he concluded: Upon examination of this evidence and consideration of the specific criteria for the experimental production of atherosclerosis, any pathologist of independent mind and free from preconceived ideas would conclude that human atherosclerosis and the lesions induced by the dietary overload of cholesterol and fats are not one and the same disease (103).
Professor Stehbens has also pointed out the weaknesses of the epidemiologic studies that have used mortality statistics as proof for causality: Continued, unquestioned use of unreliable data has led to premature conclusions and the sacrifice of truth. The degree of inaccuracy of vital statistics for CHD is of such uncertain magnitude that, when superimposed on other deficiencies already indicated, the concept of an epidemic rise and decline of CHD in many countries must be regarded as unproven, and governmental or health policies based on unreliable data become untenable (104).
According to Professor Stehbens atherosclerosis is due to wear and tear of the arteries, not to too much cholesterol in the blood, and he has many good arguments for this idea. The following words from a 1988 paper (105) summarize Stehbens' view on the diet-heart idea: The perpetuation of the cholesterol myth and the alleged preventive measures are doing the dairy and meat industries of this and other countries much harm quite apart from their potential to endanger optimum nutrition levels and the health of the populace at large...It is essential to adhere to hard scientific facts and logic. Scientific evidence for the role of dietary fat and hypercholesterolemia in the causation of atherosclerosis is seriously lacking...The lipid hypothesis has enjoyed undeserved longevity and respectability. Readers should be aware of the unscientific nature of claims used to support it and see it as little more than a pernicious bum steer.
Other critical papers by Professor Stehbens
Lars Werkö was a professor of medicine at Sahlgren's Hospital, Gothenburg, Sweden, when he moved to become scientific director at the Astra Compagny. Later on he became head of the Swedish Council on Technology Assessment in Health Care, a governmental agency. Professor Werkö has been an opponent of diet-heart for many years. In 1976 he criticized the design in the large epidemiologic studies aimed at preventing coronary heart disease, most of all the Framingham study.
According to Professor Werkö (107) the dogm is based on questionable "facts" rooted in hopes, wishful thinking and studies using selected materials: No studies have proved anything, but instead of formulating new hypotheses diet-heart supporters call the current one the most probable truth, and they have intervened in people's lives because they will not wait for the final proof.
8. How to create a false idea
In the numerous reviews written by upholders of the diet-heart idea it is often said that this idea is based on ”strong, scientific data”, the evidence is ”overwhelming” or ”extremely powerful” and ”controversy is unjustified”. If you have read the previous sections you will understand that nothing could be more advanced from the truth. To use such vocabulary it has been necessary to exaggerate trivial, apparently supportive findings, to belittle or ignore the wealth of controversial and disproving evidence and to quote unsupportive results as if they were supportive. How a ”fact” is created by misquoting unsupportive findings and exaggerating trivial findings is examplified in section 1, the story about the so-called ”good” and ”bad” cholesterol.
Observations that are totally devastating for the diet-heart idea are mostly ignored. A good example is the fact that if we exclude individuals with the rare disease familial hypercholesterolemia (less than 0.5 percent of mankind suffer from it) there is no association between the level of blood cholesterol and the degree of vascular atherosclerosis (section 2).
Another one. Before the statin-era overviews of all cholesterol-lowering trials have shown that mortality cannot be improved by lowering cholesterol. But diet-heart proponents usually mention the trials with a positive outcome only and ignore the trials with a negative outcome.
Thus, in 16 trial reports published between 1970 and 1992 a total of 40 citations were to (apparently) supportive or inconclusive trials, but with one exception, not a single citation was to unsupportive trials, although the number of supportive and unsupportive trials were equal (79). It is interesting to compare the number of citations of papers published in the same journal because few citiations of a paper may simply reflect that it has been published in a little-known or less reputable journal. In 1984 The Lipid Research Clinic´s coronary primary prevention trial was published in JAMA (110). In that trial 32 of the patients whose cholesterol was lowered died from a heart attack against 44 of the patients in the untreated control group. The total number of deaths (deaths from all causes) was 68 treated patients against 71 patients in the control group. These figures were not statistically significant by conventional statistics, but in spite of that the result was used as the main argument by the American cholesterol campaign.
In 1985 Dr. Miettinen and colleagues from Helsinki, Finland published another, but smaller cholesterol-lowering trial in the same journal (111). In that trial four patients whose cholesterol was lowered died from a heart attack, whereas only one died in the untreated control group, and the total number of deaths was ten in the treatment group against five in the control group.
Thus, both papers dealt with the same subject and were published in the same journal and no one has questioned the honesty of the experimenters or the quality of the studies. Reasonably, they should have been cited almost equally often. That the LRC trial, at least according to its directors, was supportive, and the Miettinen trial was not, is unimportant because the aim of research is to find the truth, whether it is happy or not. Here you can see how often the two papers have been cited by other scientists during the first four years after their publication:
An example of an unsupportive study which has been cited, many, many times, as if it was supportive is the Japanese migrant study. In Japan coronary heart disease is uncommon, allegedly due to the lean Japanese diet. A large study of Japanese emigrants (112) is often used as evidence because after migration to the United States, where the food generally is much fatter than in Japan, the serum cholesterol of these emigrants increased and they died from heart attacks almost as often as did Americans. The increased coronary mortality after migration was not associated with the diet or the serum cholesterol, however, but with the cultural upbringing: those who lived according to Japanese traditions were protected against heart attacks.
Especially striking was the finding that emigrants who stuck to the Japanese tradition, but ate American food ran a smaller risk of heart disease than emigrants who were accustomed to the American way of life but ate Japanese food (113). Here is another example. A common message from the American Heart Association and The National Heart, Lung, and Blood Institute to doctors is that there exist a close correspondence between degree of cholesterol lowering and degree of mortality reduction. Listen for example to the words from The Cholesterol Facts (114): ”The results of the Framingham study indicate that a 1% reduction of cholesterol corresponds to a 2% reduction in CHD (coronary heart disease) risk.” This statement was followed by a reference to a paper which reported the 30 years experience from Framingham (115).
9. The benefits of high cholesterol
ost people ‘know’ that high cholesterol is something to be afraid of and that the most important thing to do to avoid a heart attack is to lower one’s cholesterol as much as possible. But did you know that high cholesterol protects you against infectious diseases, which most probably explain that high cholesterol is associated with longevity? With these facts min mind, why should we care about high cholesterol?
Old people with high cholesterol live the longest. This statement seems so incredible that it takes a long time to clear one´s brainwashed mind, at least for those who haven’t read this book, to fully understand its importance. Yet the fact that people with high cholesterol live the longest emerges clearly from many scientific papers.1
Why High Cholesterol Is Good
In certain aspects low cholesterol is worse than high cholesterol. Already fifteen years ago American researchers found that low cholesterol predicts an increased risk of dying from diseases of the stomach, the intestines and the lungs.2
Most of such diseases are infectious. Therefore, a relevant question is whether it is the infection that lowers cholesterol or the low cholesterol that predisposes to infectious diseases You have probably already guessed what the directors of the cholesterol campaign have said, but is it true?
To answer that question the same researchers followed more than 100,000 healthy individuals in the San Francisco area for fifteen years. At the end of the study they noted that those who had low cholesterol at the start of the study had been admitted more often to hospital because of an infectious disease.3,4 This finding cannot be explained away with the argument that the infection had caused cholesterol to go down, because how could low cholesterol, recorded when these people had no evidence of infection, be caused by a disease they had not yet encountered? Isn’t it much more likely that low cholesterol in some way made them more vulnerable to infection? Much evidence exists to support that interpretation.
Low Cholesterol Predisposes To HIV And AIDS
Young, unmarried men with a previous sexually transmitted disease or liver disease run a much greater risk of becoming infected with HIV virus than other people. This was what a group of Minnesota researchers found by following such people for several years. Those who had low cholesterol at the beginning of the study were twice as likely to test positive for HIV compared with those with the highest cholesterol.5
Similar results came from another study of more than 300,000 young and middle-aged men. After sixteen years four times more in the low-cholesterol group had died from AIDS compared with the high-cholesterol group.6
Smith-Lemli-Opitz Syndrome
The benefit of high cholesterol also appears from studies of children with the Smith-Lemli-Opitz syndrome. They are born with very low cholesterol because an enzyme that is necessary for the body’s synthesis of cholesterol does not function properly. Most children with this syndrome are either stillborn or they die early because of serious malformations of the brain. Those who survive are imbecile or autistic, they have extremely low cholesterol, and they suffer from frequent and severe infections. However, if they are given extra cholesterol or eggs in their diet, their cholesterol goes up, their infections become less serious and less frequent, and their autistic and aggressive behavior improves.7
The lipoproteins
One of the many reasons not to name LDL as bad is that the lipoproteins have other important functions. One of them is to take care of microorganisms and their toxic products.
Staphylococcus aureus α-toxin is the most toxic substance produced by strains of the disease-promoting bacteria called staphylococci. It is able to destroy all kinds of human cells, including red blood cells. For instance, if minute amounts of the toxin are added to a test tube with red blood cells dissolved in salt water, the blood is hemolyzed, that is, the membranes of the red blood cells burst and hemoglobin from the interior of the cells leaks out into the solvent. Dr. Bhakdi and his team mixed purified α-toxin with human serum (the fluid in which the blood cells reside) and now the toxic effect of α-toxin almost disappeared. By various complicated methods they identified the protective substance in human serum as LDL, the carrier of the “bad” cholesterol. In accordance, nothing happened when they mixed α-toxin with purified human LDL.
Dr. Willy Flegel and his co-workers at Heidelberg University in Germany studied bacterial toxins in another way. As mentioned above, one of the effects of bacterial toxins is that they stimulate white blood cells to produce cytokines, hormones that start the inflammatory processes. The German researchers found that this effect disappeared almost completely if the toxin was mixed with purified LDL before they added the white blood cells to the test tubes.8,9 Obviously, LDL was able to neutralize the bacterial toxins.
Animal Experiments
The immune systems in various mammals including human beings have many similarities. Therefore, it is interesting to see what experiments with rats and mice can tell us. Professor Kenneth Feingold and his group at the University of California have published some interesting studies. In one of them they lowered LDL-cholesterol in rats by drugs with the result that they died much easier after an injection of bacterial toxins. The high mortality was not due to the cholesterol-lowering drug because, if they gave the animals an injection of human lipoproteins just before the experiment, they survived10
In another experiment, researchers from the Netherlands injected bacteria or their toxins into normal mice, and into mice with high cholesterol. Whereas all normal mice died, most of the mice with high cholesterol survived.11
Many of the roles played by the lipoprotein LDL are shared by HDL as well. This should not be too surprising considering that high HDL-cholesterol is associated with cardiovascular health and longevity. But there is more.
Triglycerides, molecules consisting of three fatty acids linked to a molecule named glycerol, are insoluble in water and are therefore carried through the blood inside lipoproteins, just as cholesterol. All lipoproteins carry triglycerides, but most of them are carried by the VLDL, the largest lipoprotein in our blood.
For many years it has been known that patients suffering from sepsis, a life-threatening condition caused by bacterial growth in the blood, have high levels of triglycerides. The serious symptoms of sepsis are due to bacterial toxins, most often produced by gut bacteria. Now to the interesting point. Solutions rich in triglycerides are also able to protect experimental animals from the dangerous effects of bacterial toxins, which means that the high level of triglycerides seen in sepsis is not a bad thing, but a normal response to infection.12 Usually sepsis bacteria come from the guts. It is therefore fortunate that the blood draining the guts is especially rich in triglycerides.
High cholesterol protects against allergy
Children with allergic problems, such as asthma and hay fever, have lower cholesterol than healthy children. As allergic diseases have become more common and is still increasing in the Western world it is tempting to suggest that the cause is the increasing consumption of the polyunsaturated vegetable oils of the omega-6 type, because these oils are known to stimulate inflammatory processes, and allergy is a kind of inflammation. But there is room for another explanation.
At the Skin and Allergy Hospital in Helsinki, Finland Dr.Maria Pesonen and her co-workers followed 200 children from their birth to their 20 year anniversary.13 They found that the children with allergic disorders had lower total and LDL cholesterol than the others. The difference was obvious already at a time where all the children were breastfed. Thus, the difference could not be explained by their dietary habits. The researchers had no explanation for their observation, but if the lipoproteins are able to bind microbial products, it seems not too far-fetched to assume that they can bind other molecules as well, for instance allergens, those molecules that starts the allergic reactions.
Is familial hypercholesterolemia a disease?
“The more LDL there is in the blood, the more rapidly atherosclerosis develops.”
This was the main conclusion of the American Nobel Price-winners, Joseph Goldstein and Michael Brown.14 They discovered that the cells of people with familial hypercholesterolemia had difficulties taking in cholesterol from the blood because of a defect in the LDL-receptor, the mechanism that transports these vital molecules into the cells. This was the reason why cholesterol was much higher than normal in these people. People with familial hypercholesterolemia also have more atherosclerosis than normal and some of them do die early in life from heart disease. It was therefore not too far-fetched for Goldstein and Brown to draw the conclusion they did, and also to assume that it was applicable to the rest of mankind. They were awarded the Nobel Prize in 1985 for their discovery, and many other researchers share their view.
Their finding is certainly interesting, a result of careful scientific work. Unfortunately, the conclusion they drew was too hasty. In fact, there are benefits associated with this condition, which is why I deliberately refer to individuals with familial hypercholesterolemia as people, not as patients. What is even more surprising is that the reason why some of them die at a young age from heart disease is not their high cholesterol, but something else. I shall come back to that.
In England The Simon Broome Familial Hyperlipidaemia Register Group have followed almost 3000 people with familial hypercholesterolemia for many years. At the most recent control they found that 102 of them, or 3.6 % had died from a heart attack. By analyzing mortality of the same age group in the English population they calculated that the expected number should have been 40, or 1.4 %. On the other hand, fewer had died from other causes, 112 against the expected number 193, or 4 % against 6.8 %. For instance, only half as many had died from cancer.30 If you add the figures and compare them you will see that people with familial hypercholesterolemia live at least as long as other people, if not longer. A little more die from heart disease, but fewer die from cancer and other diseases.
The authors of the scientific report stressed that the participants in their study were admitted because all of them had close relatives who had died at a young age. Cholesterol screening often identifies old people with familial hypercholesterolemia who have no such relatives. The authors therefore suggested that if the participants had been representative for all people with familial hypercholesterolemia, their mortality would have been even lower.
In Finland, Professor Tatu Miettinen and Dr. Helena Gylling studied about one hundred individuals with familial hypercholesterolemia.16 Fourteen to seventeen years later, 30 had died, 26 because of a heart attack and four of other causes. On average, initial LDL cholesterol was the same among those who had died and those who still were alive. If high LDL cholesterol was the most important cause of atherosclerosis and heart disease, as postulated by Nobel Award winners Goldstein and Brown, then we should have expected higher cholesterol in those who died, but that wasn’t the case. Many other researchers have confirmed the Finnish findings.17-23
Another conflicting observation is the fact that people with familial hypercholesterolemia have normal cerebral arteries, even though the same cholesterol-rich blood flows through their brain as through the rest of their body.25
A missing link
The genetic aberrations in people with familial hypercholesterolemia are more complicated than Brown and Goldstein assumed. For instance, in a study of 2400 such individuals, Dr. Angelique Jansen at the University of Amsterdam found that variations of the prothrombin gene were associated with an increased risk of heart disease in these people.26 Prothrombin is a substance necessary for blood coagulation and an abnormal prothrombin gene may lead to the production of too much of this substance. The result is an increased tendency to coagulation and clot formation. Thus, some individuals with familial hypercholesterolemia may form arterial clots more easily than other people, not because of their high cholesterol, but because of an abnormal coagulation system.
Heart patients with familial hypercholesterolemia more often have high concentrations of fibrinogen and factor VIII in their blood than healthy people with familial hypercholesterolemia. Also these substances participate in the coagulation process, and too much of them may stimulate to clot formation. And again, whereas the heart patients had much higher concentrations of fibrinogen and factor VIII, their total and LDL cholesterol did not differ from those measured in healthy people with familial hypercholesterolemia.27
In earlier times, people with familial hypercholesterolemia lived longer than other people! Dutch researchers tracked the ancestors of people with familial hypercholesterolemia and identified 412 individuals with a 50 percent chance of having this genetic abnormality. They also searched official records of deaths and found that the longevity of those with a family history of this genetic aberration was not lower before the year 1900; in fact, on average they lived longer than other people. As the most common cause of death at that time was infectious disease, the authors suggested that high cholesterol protects against infection.28
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