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Cholesterol Myths by Uffe Ravnskov MD, PhD: Myth 1: High-Fat Foods Cause Heart Disease
Wednesday, November 12, 2014 10:44 am Email this article
“Some circumstantial evidence is very strong, as when you find a trout in the milk.”
—Henry David Thoreau (1817-1862)
In 1953 Ancel Keys, director of the Laboratory of Physiological Hygiene at the University of Minnesota published a paper, which, looking back seems to have been an early kick-off for the cholesterol campaign.
The horizon for the US Public Health Service is too limited, he wrote; any major disease should be prevented, not only those of infectious or occupational origin.
It doesn’t matter that the necessary measures are not yet known. The mere hope that the incidence of a disease may be altered is sufficient reason to invest money and manpower.
What Dr. Keys had in mind was coronary heart disease. This disease is a threat, he continued. While all other diseases are decreasing in the United States, there has been a steady upward trend in the death rate from coronary heart disease. On this particular point the Americans are inferior to other countries; in the US, for instance, four to five times more die from a heart attack than in Italy.
Dr. Keys’s reservations regarding the preventive measures were mere rhetoric; he already knew what to do. He considered a defeatist attitude about coronary heart disease despicable. According to Dr. Keys it was “abundantly clear” that heart attacks could be prevented. And he knew the preventive measures. What was possible for the Italians should be possible for Americans also, he added, “These figures are a challenge.”
Remember that Dr. Keys was directing these words to Americans, a proud people for whom the word aggressive is a word of honor, in health care as in other matters. In the US more diagnostic tests are made than in any other country; surgery is preferred over drugs, and when drugs are chosen high doses and strong preparations are used. Ancel Keys’s words did not go unheeded either.
According to Dr. Keys, fat food was the culprit. His proof was a diagram, which showed that the intake of fat food and the death rates from coronary heart disease followed each other closely in six countries (fig. 1A). The points of the diagram lay as on a string, so that the curve he had drawn looked more like the result of a physical experiment than a biologic relationship. If you prolong the curve at the left it intersects the origin (= the intersection of the axes), thus suggesting that if you avoid fat food completely you will never have a coronary. Wrote a commentator in The Lancet the following year, “The curve shows an almost convincing relationship between the fat content of the food and the risk of dying from coronary heart disease.”
But why did Dr. Keys use the figures from six countries only? At that time information was available from 22 countries and if all of them were included the association was in fact rather weak. For instance, the death rate from coronary heart disease in some countries was 3-4 times higher than in countries where the consumption of fat was the same (fig. 1B).
Fig. 1A. Correlation between the consumption of animal fat in percent of the total calorie consumption, and mortality from coronary heart disease in six countries. Data from Keys.
Fig. 1B. Same as fig. 1A, but including all countries where data were available when Dr. Keys published his paper Data from Yerushalmy and Hilleboe.
Are consumption data accurate?
Let us have another look at the figures 1A and !B because we need to understand the data there. Similar figures are presented again and again by upholders of the diet-heart idea. What do the figures really mean?
Firstly, “Calories from fat” does not mean the amount of fat eaten in each country, only the amount available for consumption. By that is meant the sum of what is produced in the country and what is imported minus food used for purposes other than human nutrition. From this figure, which is the one used in figures 1A and 1B, should be subtracted the amount of fat that is never delivered to the consumers because it is lost, stolen, eaten by rats or mice, or disturbed because of bad storage. Further, some of it is eaten by dogs, cats and other pet animals; and some is thrown away in the kitchen or left on the plate. In the US where eating fat is considered almost as a sin much fat certainly disappears that way. In poor countries, however, where famine is a greater threat than overweight or heart disease, it is not so. Here, the diet includes even brain and bone marrow, both of which are crammed with animal fat and cholesterol.
Thus, the figures for fat consumption in various countries are most unreliable, to put it mildly. But the figures for heart mortality, those on the vertical axis are even more erroneous.
Are death certificates true?
When statisticians write their reports about numbers and causes of death in a population they consult the death certificates. Do you think that what is written on this piece of paper is the truth and nothing but the truth?
Certainly not. Again and again great differences have been found between the diagnosis set by the doctor while the patient was alive and the findings at the post-mortem. Even doctors with access to modern diagnostic equipment name the wrong diagnosis on the death certificate in one out of three cases. For instance, most doctors consider sudden, unexpected death to be caused by a heart attack due to coronary heart disease. Dr. George Lundberg from University of California and Professor Gerhard Voigt from University of Lund, Sweden showed this to be wrong. In 51 of one hundred such cases, the cause of death was due to something else.
The situation is no better when patients actually have died of heart attacks. Drs. Edwin Zarling, Harold Sexton and Pervis Milnor from Memphis, Tennessee, found that among one hundred patients who died from a heart attack according to the postmortem only fifty-three had a correct diagnosis before they died.
Consider that these studies were not performed in small local hospitals but at university hospitals with access to the finest diagnostic tools of modern medical science in the hands of experienced academic doctors.
Maybe you think that it is unimportant what the doctor diagnoses as cause of death because mistakes will be corrected by the coroner. But postmortems are performed only in a minority of cases; in the US in one out of five, in other countries much less often.
So, if the diagnostic accuracy is that bad in a modern, Western hospital, how do you think it is in poor countries where the cause of death is rarely written by doctors, much less by a coroner?
But even frequent postmortems are no guarantee of a correct diagnosis. This was amply demonstrated by the British professors D. D. Reid and Geoffrey Rose. They collected summaries from the hospital records of ten patients who had died from various heart, kidney and lung diseases. Except for the diagnoses, the summaries contained all information relevant to the cause of their death including results of the physical and laboratory examinations, statements from the X ray department and the post-mortem descriptions. Then, a number of experienced, academically trained doctors from university hospitals in Norway, England and the US were told: “Read the records and write the death certificates!”
Any scientist who considers statistics based on death certificates as a source of truth should look carefully at the fact that coronary heart disease was used as a diagnosis by the American doctors 33 percent more often than by the English doctors, and 50 percent more often than by the Norwegian doctors.
Someone who is not a physician may find it odd that doctors from countries with similar medical traditions and education systems act so differently when they put a diagnosis on the death certificate. The explanation is that there may be serious changes in many organs in a dying person, but on the death certificate and in the statistical tables there is room for only one diagnosis. Thus, in complicated cases American doctors, by unknown reason, are inclined to blame the death on changes of the vessels to the heart, whereas English and Norwegian doctors may instead hold lung or brain diseases responsible. Interestingly, the official death statistics from these three countries show the same tendency.
If death is labeled so differently in the US, England and Norway, where the medical education is similar, how is it labeled in countries such as Japan, Ceylon (Sri Lanka) or Mexico where the culture and medical traditions are fundamentally dissimilar?
Clearly, official death statistics are based on diagnoses which in at least half of the cases are plain wrong, and if they are not wrong, they do not tell the whole truth.
Television—a risk factor?
But let us assume that heart attacks are more common in countries where people eat much animal fat. What does it mean?
From Table 1 you can see that other factors than eating animal fat are associated with heart disease.
Table 1. Correlation coefficients between various consumption factors and mortality in coronary heart disease for men age 55-64 in 22 countries.
|Number of cigarettes sold per inhabitant||0.64|
|Number of cigarettes sold per inhabitant||0.64|
|Number of cars sold per 100 inhabitants||0.58|
|Total consumption of protein*||0.72|
|Consumption of animal protein*||0.73|
|Total consumption of fat*||0.56|
|Consumption of animal fat*||0.65|
|Consumption of cholesterol||0.69|
|Consumption of sugar*||0.68|
|*amount available for consumption|
The correlation coefficient in the right-hand column of the table tells how well various factors follow the number of deaths from heart attacks in the countries that were studied. The largest coefficient is 1, the weakest is zero. The table thus tells us that in countries where heart attacks are common (meaning where the diagnosis coronary heart disease is commonly used) people eat more protein, fat, cholesterol and sugar. They also smoke more cigarettes and buy more cars than in countries where heart attacks are less common.
What the statistics actually tell you is that the risk of having the diagnosis coronary heart disease written on one’s death certificate is greater for people in prosperous countries than for people in poor countries. Therefore, anything that follows with or from prosperity is automatically associated with mortality from coronary heart disease. Calories from animal fat, for instance, are more expensive than calories from other nutrients; people in prosperous countries therefore eat more animal fat than people in poor countries. And since the cause of death more often is called coronary heart disease in prosperous countries than in poor ones, intake of animal fat becomes statistically associated with the number of deaths from coronary heart disease.
Thus, population studies may point to factors that are associated with a certain diagnosis on the death certificates but they cannot tell us the cause of the disease; only experiments can. Factors which are statistically associated with a disease are called risk factors. A risk factor may be the cause of the disease, but most often it is not. Several hundred risk factors are known for coronary heart disease, for instance smoking, overweight, high blood pressure, lack of exercise, psychological stress, baldness, snoring, and eating too much or too little of a steadily increasing number of various food items, but the cause of the disease is still unknown. What the table demonstrates are just a few examples of risk factors for coronary heart disease.
Because a risk factor and the cause of a disease may stem from a common factor, for instance a country’s prosperity, it is self-evident that the elimination of the risk factor does not automatically prevent the disease; the main cause is still there.
Let us assume that the real cause of coronary heart disease is car exhaust. (This is most likely totally wrong but that doesn’t matter; I have made this assumption only to demonstrate how factors that vary together may create false associations.) More people are exposed to car exhaust in prosperous countries because cars are more common in prosperous countries, and as we assumed that coronary heart disease was due to car exhaust, heart attacks should also be more common. Logically, death rates from coronary disease in various countries become associated with the number of cars sold. But people in prosperous countries buy many other things more often, for instance television sets, and thus the coronary death rates also become associated with the number of television sets sold. You may therefore call “possession of a television set” a risk factor although it was not the television set but the car exhaust which caused coronary heart disease. Clearly, it is a bad idea to throw the television set out the window to save the heart.
To carry our example one step further, see figure 1C, which shows the correlation between the tax rate and death from heart disease in the municipal tax districts of the county of Stockholm, Sweden. The graph implies that if the municipal tax rate is lowered to 9.95 percent, no one will die from a heart attack—a challenge to all politicians!
Figure 1C. Correlation between tax rate and heart mortality in the municipal tax districts of the county of Stockholm.
Vertical axis: Heart mortality per 100,000; Horizontal axis: Municipal tax rate 1976; percentage
Another example. People with yellow fingers die more often than others from a heart attack. “Yellow fingers” is therefore a risk factor for coronary heart disease. But it doesn’t help to scrub away the yellow color, because the discoloration is due to cigarette smoking. The cause of coronary heart disease is not the yellow color, but either the smoke from the tobacco or the paper, or the mental stress that starts the habit of smoking, or a factor associated with the habit of smoking or the feeling generated by nicotine.
Risk factors do not necessarily produce disease. But most diet-heart supporters rarely distinguish between risk factor and cause. They consider every new risk factor as something that should be reduced or eliminated.
Seven random countries
To prove his idea Dr. Keys organized a study of coronary heart disease in seven countries. To this end he selected sixteen local populations in the Netherlands, Yugoslavia, Finland, Japan, Greece, Italy and the US. Men between the age of 40 and 59 were studied. In cooperation with local doctors, scientists and health authorities anything which might conceivably cause coronary heart disease was investigated. The men were followed for about five years, and all heart symptoms and all deaths were recorded.
In each country two or three groups of people were studied. Among other things the investigators looked at the diet, they measured the blood pressure and weighed all participants, and asked how much they smoked and exercised.
The conclusion from this gigantic project was that what best could predict the number of heart attacks in a country was how much animal fat people ate in that country. In countries where people ate much animal fat, heart attacks were common; in countries where people ate little such fat, heart attacks were rare.
But within the countries the number of heart attacks did not follow the diet. Here I shall tell about the two Finnish populations; the one from East Karelia and that from Turku; in another chapter I shall tell about the people on two Greek Islands.
At the start, forty-two of 817 men from East Karelia had coronary heart disease, in the district of Turku only fifteen of 860. And during the next five years sixteen men died from a heart attack in Karelen, but only four in the district of Turku. Taking all factors in consideration heart attacks wee seen five times more often in Karelen than in the district of Turku.
If you think that the natives lived especially carelessly in Karelen you are wrong. The living conditions in the two areas were practically identical. These people lived isolated as farmers or lumberjacks, their body weight and height were identical, they smoked equally much, and they ate the same amount of polyunsaturated fat. The blood pressure was a few percent higher in Karelen, and here they also ate a few percent more animal fat than around Turku.
Dr. Keys declared that coronary heart disease was five times more common in Finland than in Japan because of the food, but he did not explain why coronary heart disease was five times more common in eastern than in western Finland although the difference between the common risk factors was only marginal. He mentioned it as a minor, abnormal finding which he (erroneously) stated would be explained by further studies.
This way of arguing is common among the proponents to the diet-heart idea. Observations that support this idea are trumpeted forth as positive proofs while unsupportive findings, if they are mentioned at all, are considered as “rare exceptions” or “something which cannot yet be explained.”
Up and down in statistics
To see if fat food causes heart attacks it should be of interest to study how the eating habits in a country have changed during a period of time and to ask if the number of heart attacks has changed in the same direction. If animal fat is an important cause of coronary heart disease the number of heart attacks should increase during periods of increasing intake of such fat; and it should decrease when less animal fat is eaten.
But even if these figures follow each other up and down, we have not proved that eating animal fat is the cause of the increasing mortality. Again an unknown factor could create parallel changes in fat intake and heart mortality. Let me give an example.
During World War II people in Finland, Norway, Sweden and Great Britain died less often from heart attacks than before the war. Said Haquin Malmroos, a professor of medicine in Lund, Sweden: “this is because people ate less animal fat.”
But other things of importance for heart disease occurred during the war. For instance, people’s body weight and blood pressure went down considerably, fewer people smoked, and the lack of gasoline for cars and other machinery should also have favored a healthier way of life. A common denominator of the war was lack of goods—lack of fat food for instance, but also lack of other nutrients and of gasoline and cigarettes. Nobody knows which of these factors, if any, caused the decrease in heart disease. The explanation that people ate less animal fat is unlikely because it has never been possible to lower the death rate from coronary heart disease with a low-fat diet in experiments of the same length as World War II. Furthermore, the mortality curves turned upwards again long before the increase of the consumption of animal fat took place.
Thus, although a risk factor changes parallel to the death rate it is not necessarily the cause. But if the risk factor is the cause, its rise and fall must be reflected in the death rate from the disease. If heart attacks are caused by eating too much animal fat, heart attacks should of course become more frequent if people started to eat more of such fat. Likewise, if people changed their diet and ate less animal fat, fewer heart attacks should occur. This is not so.
From World War I up to the 1980s, the number of deaths from heart attacks increased substantially in most countries while the intake of animal fat decreased or was unchanged. For instance, the death rate from cardiovascular diseases of middle aged Yugoslavians increased three to four times between 1955 and 1965, while the intake of fat decreased by 25 percent.
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.
In the US coronary mortality increased about ten times between 1930 and 1960, leveled off during the 1960s and has since decreased slowly. During the decline of heart mortality the consumption of animal fat declined also, but during the thirty years of sharply rising coronary mortality the consumption of animal fat decreased.
In Framingham the number of fatal heart attacks went down during the decline of animal fat consumption, but the number of non-fatal heart attacks increased with the same number. The authors of the Framingham report explained this discrepancy by saying that it takes much longer time to lower the number of non-fatal heart attacks than to lower the number of fatal cases. (A much better explanation is, that to-day more people survive a coronary because of improved treatment).
In Japan the number of fatal heart attacks between 1950 and 1970 increased as did the intake of animal fat appearing to confirm the diet-heart idea. But the increase in coronary mortality was seen only above the age of 70 and especially above 80. In the latter age group, the increase in coronary mortality more than counterbalanced the decrease in the other age groups. In other words, younger Japanese people died less often of coronary disease, although they ate more animal fat. During the same period mortality from most diseases decreased in Japan. Thus, the increasing death rate from coronary disease among old people in Japan could not be caused by an increased intake of animal fat; if it were, the number of coronary deaths should have increased in all age groups. The explanation is that the general health in Japan has improved steadily since the war, as has the people’s mean length of life. Many more have become old, and since coronary heart disease is a disease of old age, the death rate due to heart disease has of course increased.
This torpedo against the diet-heart idea was presented as the first paper at an international conference in 1981. Yet the paper created no intellectual explosions. The author of the paper, Dr. Kimura concluded: “… if this food supply and nutrient intake pattern continues the same evolution in Japan, incidence of ischemic heart disease will increase in the future.”
And the conference continued with paper after paper acknowledging the diet-heart idea. But in spite of a continuing increase in the intake of animal fat in Japan also after 1970, and a steady increase of the mean serum cholesterol level the number of fatal heart attacks decreased in all age groups, contrary to Dr. Kimuras prophecy.
While the death rate from coronary disease increased in most countries after World War II it decreased in Switzerland. If this decrease had been followed by a decline in the intake of animal fat, Switzerland would have been a model for health care in other countries. But Switzerland is never mentioned because parallel with the declining heart mortality, the Swiss intake of animal fat increased by twenty percent.
The shepherds of Kenya
The many exceptions to Ancel Keys’s hypothesis indicate that something in the Western life style other than fat food is the cause of coronary heart disease. To be absolutely sure it is necessary to study people who eat just as much animal fat as we do but who are not exposed to the menaces of Western civilization. If the diet were the most important factor people in such countries would have equally high cholesterol and die just as often from heart attacks as we do.
In the early 1960s, Professor George Mann and his team from the Vanderbilt University in Nashville, went to Kenya in Africa with a mobile laboratory to study the Masai people. The diet-heart idea had just started its triumphal progress. Professor Mann had heard that the Masai people did not eat anything but milk, blood and meat. Wouldn’t it be a good idea to test the diet-heart idea on the Kenyan plateau? Shortly before and with the same purpose Dr. Gerald Shaper from the Makerere University of Uganda had traveled a little further north to another tribe, the Samburus.
The Samburus and the Masai people are slender people who have survived as shepherds for thousands of years. Their life is free from the mental stress and competition of Western civilization, but you cannot call it comfortable. Every day they walk or run many miles with their cattle, searching for food and water.
Their own diet is extreme. According to their view, vegetables and fibers are food for cows; they themselves eat milk, meat and blood only, or at least the younger men do. A male Samburu may drink almost a gallon of milk each day. He has never heart about the cholesterol campaign, and therefore he drinks the creamy milk as it is, which means that his intake of animal fat is far above that of most Western people. Also, his intake of cholesterol is high, especially during periods when he adds 2-4 pounds of meat to his daily diet.
Masai people drink “only” half a gallon of milk each day. However, they eat more meat than the Samburus. Their parties are sheer orgies of meat; on such occasions 4-10 pounds of meat per person is not unusual, according to Professor Mann.
If the diet-heart idea was correct, coronary heart disease should be epidemic in Kenya. But Mann found that no Masai dies from a coronary. Rather, the Masai people would die of laughter if they heard about the cholesterol campaign.
But this was not the only surprise. The cholesterol of the Masai tribesmen was not sky-high as Mann had expected; it was very low. In fact, their cholesterol was among the lowest ever measured in healthy people, about fifty percent of the value of most Americans.
Another cholesterol safari
Now to Dr. Bruce Taylor from Chicago. He was the first to induce a coronary in an ape by cholesterol feeding (see Chapter 6). The papers about the Samburu and the Masai people were published shortly after Dr. Taylor’s successful experiment. Certainly he must have asked himself why the cholesterol of his laboratory animals skyrocketed on their fat diet, but not the cholesterol of the Masai and the Samburu people. To answer this question he was on his way to Kenya with his own expedition a few years later.
Like other mammals, we produce cholesterol ourselves, day and night. When we eat lots of cholesterol or animal fat, our own production of cholesterol decreases automatically. If we eat only a little, our production increases. This mechanism keeps the cholesterol level in the blood fairly constant and explains why it is so difficult to lower cholesterol with diet. After his investigations Dr. Taylor reached an unusual conclusion about this balancing mechanism in the Masai people.
According to Dr. Taylor the African tribes do not contradict the diet-heart idea because their ability to reduce their own cholesterol production is superior to other people. Because the Masai people have been isolated from other tribes for many thousands of years, they have developed this ability so well that it has been built into their genes, Taylor said. Taylor and his colleagues considered their results so important that they published them with minor variations in four different scientific journals.
In science there are often alternative explanations to a new observation, and most scientists therefore discuss which model or hypothesis the new piece of evidence fits into the best. But Taylor did not. He could have considered the possibility that it is not the Masai people who are superior to others in reducing their cholesterol production but instead, we who are inferior, perhaps because of environmental factors, perhaps because we are less active than the Masai people, or perhaps because of something we haven’t yet imagined. But he did not.
It would have been possible to get an answer to these questions if he had continued his expedition to the city of Nairobi and studied Masai people there to see if some factor associated with the more comfortable life style of a big city might have increased their cholesterol. This method is often used by the defenders of the diet-heart idea to demonstrate that low cholesterol goes up when people from poor, undeveloped countries with a low fat intake move to a more prosperous and technologically developed country where the fat intake is high.
But in this case, the study concerned human beings who already ate more fat than ever recorded. After migration to Nairobi their diet most probably became more diversified, and if the diet-heart idea was true their blood cholesterol should have become even lower.
What had happened with the cholesterol of the urbanized Masai people? Why did Taylor and his colleagues not proceed to Nairobi to get an answer to this simple question?
Taylor’s explanation that the low cholesterol of the Masai people is genetic is not a valid one. Acquired properties are not transferred to people’s descendants. This idea was abandoned as scientifically wrong many years ago. An inborn metabolic trait—in this case the ability to reduce the body’s own production of cholesterol when presented to large amounts of cholesterol in the diet — is either present in the genes, or it arises by mutation. If the property is important for survival, the number of individuals with this property increases over time, and eventually these people may outnumber those without it. But this will happen only if the inborn trait improves survival before sexual maturity. Individuals with a trait that protects them against a disease, which strikes after sexual maturity, such as coronary heart disease, do not outnumber individuals without this trait, because the latter transfer their defective genes to their children before they develop the disease.
And, contrary to Taylor’s statements, the Masai people are not an isolated tribe. They are warlike people who have taken cattle and women from the neighboring tribes for thousands of years. In this way they have achieved a steady genetic renewal in their cattle and in themselves.
But what finally proved that Taylor was wrong was a study of Masai people living in the big city of Nairobi performed by Dr. José Day at St. Mary’s Hospital in London. Again, if the low cholesterol of the Masai was inherited it should have been even lower in Nairobi, because here their diet should most likely include 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.
Taylor’s genetic explanation has been popular among upholders of the diet-heart idea, such as Dr. Keys. He wrote: “… the fact is that the peculiarities of those primitive nomads have no relevance to diet-cholesterol-coronary heart disease relationships in other populations.”
Taylor studied not only blood cholesterol but also atherosclerosis in the Masai. It was important to show that their low cholesterol level protected the Masai people from atherosclerosis. Ten aortas from deceased Masais were sent to New York where the pathologists said that atherosclerosis was almost absent.
But Professor Mann studied a much greater number of hearts and aortas from Masai people of all ages and found that the coronary vessels of Masai people were just as atherosclerotic as those from US citizens, perhaps even more. But severe sclerotic changes, so-called plaques or raised lesions, were rare; the sclerotic changes were situated inside the vessel walls whereas the inner surface of the vessels was smooth. And in the fifty hearts he studied there was no evidence of myocardial infarctions in any.
Professor Mann thought that the Masai were protected from coronary heart disease by the size of their coronary arteries. These were much wider than those of most Western people, probably because the hearts of the Masai have worked hard while the men were running after the cattle. Many of the Masai people Mann examined were splendidly fit, as good as, or better than, superior sportsmen. It is no coincidence that the world’s best runners tend to come from Kenya.
Thus, it is possible to gorge on cholesterol and animal fat and still keep the blood cholesterol very low. The diet-heart idea should be smashed after such evidence, and the message about the Masai and Samburu people should challenge any defender of the diet-heart idea. But the idea is still flourishing, and nobody seem challenged. In fact, the Masai and the Samburu people are not mentioned at all in the official reviews of the diet-heart idea.
It is worth mentioning another interesting observation from Kenya. In that country there are many Indian emigrants. Although they all come from India their diet are not similar. Non-Muslim Indians from Gujarat live on a lactovegetarian diet while Muslim Indians from Punjab eat eggs and meat and drink twice the amount of milk as their compatriots from Gujarat, and they never use vegetable oil. The non-Muslim Indians thus live as if they had been listening to the cholesterol campaign to avoid coronary heart disease, while the Muslims act as if they’re doing what they can to get it. But the mortality rate from coronary heart disease is equal in both populations.
However, this aberration from the diet-heart idea seems petty compared with the next one. Curiously, Dr. S. L. Malhotra from Bombay, India is never cited in the many reviews advocating for the prudent diet. He studied coronary heart disease among more than one million male employees of the Indian railways. During a five-year period he recorded 679 deaths from that disease. Most cases, 135 per 100.000 employees, were noted in Madras in southern India; fewest cases, 20 per 100.000 employees, were noted in Punjab in northern India.
Thus, death from coronary heart disease was seen about seven times more frequently in Madras, and those who died were on average twelve years younger than in Punjab. But in Punjab, people ate 10-20 times more fat, and they smoked eight times more cigarettes. And while the small amount of fat that people ate in the weak-hearted province of Madras was mainly of vegetable origin, the fat they gorged on in the strong-hearted Punjab was mainly of animal origin.
Have coronary patients eaten more fat?
A way of searching for the cause of a disease is by using the so-called case-control study. In a case-control study scientists question randomly selected control persons of the same age and sex and from the same geographic area as the patients with the disease under investigation. In which way do the patients differ from the controls? What do they do for a living? How much do they smoke and drink? What do they eat? Are they fatter or slimmer than the controls? How is their blood composed? Are they exposed more than the controls to environmental pollutants? Only your imagination and your money put a limit to your questions.
In North Dakota in the USA, Dr. William Zukel and his team performed a case-control study. They studied all the men who had had heart symptoms during one year; for each case they chose two healthy men of the same age as the controls. Dr. Zukel was especially interested in the diet of the participants during the month before the first symptoms or before the interview. If the interviewee had died, his wife or nearest relatives were questioned.
Altogether 228 men had had symptoms of coronary disease. A detailed description of the diet was gained from 162 of them. The conclusion of the study was that control individuals were more often manual workers, and patients were more often smokers. But the diet did not differ between patients and control individuals; they ate the same amount of saturated and polyunsaturated fat, and their caloric consumption did not differ either.
In Ireland another group of researchers under the guidance of Dr. Aileen Finegan performed a similar investigation. For a whole year they studied the diet of one hundred men who had suffered from a heart attack. Their diet was compared with that of fifty healthy men of the same age.
Dr. Finegan and her team could not find any dietary differences; the patients had eaten practically the same amount and kind of fats as the control individuals.
A similar study was performed in collaboration between researchers from Harvard and the University of Dublin in Ireland under the guidance of Dr. Lawrence Kushi. Irish men and their brothers who had been living in Boston for at least ten years were selected. These two groups were compared with each other and with a third group of adult sons of Irish emigrants in Boston, a total of one thousand men. Now to the questions. How many would die from a coronary during the next twenty years? And did their way of living differ from that of the others?
The researchers did not get a simple answer. Relatively speaking, more Boston brothers had died from a heart attack than either of the other two groups, but the difference was so small that it could well have been due to chance. It could also have been because the Boston brothers smoked more often and because their blood pressure was higher. The notion that their diet played an important role is unlikely because, contrary to the diet-heart idea, the men in Boston had eaten less animal fat and less cholesterol than the Irish brothers, and more polyunsaturated fat than the emigrants’ sons. And there was no difference between the blood cholesterol values of the three groups. Yet, in spite of these negative findings this study is often cited as a strong support of the diet-heart idea.
Another “proof” of the diet-heart idea is a study performed in cooperation between the National Heart, Lung and Blood Institute and the University Hospital in Puerto Rico, conducted by Dr. Tavia Gordon. In Framingham, Puerto Rico and Honolulu more than sixteen thousand healthy, middle-aged men were questioned about their dietary habits. Six years later the dietary habits of those who had had a heart attack were compared with the habits of those who had not.
In Puerto Rico and Honolulu heart attack victims had eaten less starch than the others; in Framingham they had eaten smaller amounts of other carbohydrates. Eating starch or other carbohydrates should therefore protect against coronary heart disease according to the authors of the report.
But the percentage of calories from starch did not differ between the healthy individuals and the patients except in Framingham, where those who had suffered a heart attack had eaten more starch than the others.
In Puerto Rico and in Honolulu those who had had a heart attack had eaten more polyunsaturated fat than those who had not had an attack. Although this observation is contrary to what was expected and thus most discouraging for those who advise people to eat more of such fat it was not mentioned in the summary of the paper.
A similar study was performed by researchers from Framingham and Honolulu, led by Dr. Daniel McGee of the Framingham Heart Study. They asked 8000 Japanese migrants in Hawaii about their diet over a 24-hour period, and ten years later they compared the diet of those who had suffered a heart attack during the ten years with the diet of those who had not.
Those who had suffered a heart attack had eaten just as much animal fat and protein but less carbohydrates as the others. The authors therefore recommended either eating more carbohydrates or less animal fat; either way should have the same preventive effect. In the summary of the report from the study, the authors did not mention that the difference between the diets in the two groups was not greater than what could have been produced by chance.
Today (1998) a total of 27 similar studies have been published including 34 groups (cohorts) of patients and control individuals. Totally, the incredible number of more than 150,000 individuals have been investigated. In three of these 34 cohorts patients with coronary disease had eaten more saturated or animal fat than the control individuals, in one cohort they had eaten less, in the rest no difference was seen. In three cohorts the patients had eaten more vegetable or polyunsaturated fat than the control individuals, in only one they had eaten less.
In the studies mentioned above, the researchers try to press the figures down into the cholesterol shoe, but neither heels nor toes fit in. According to some authorities, we should eat less saturated fat; according to others we should eat more polyunsaturated fat. Still others recommend carbohydrates, if not starch, or fibers, or vegetables, depending on the haphazard results of the most recent investigation.
More critical diet-heart supporters object that information about the diet is unreliable; people simply cannot remember exactly what they have eaten. This objection is correct, of course. The point is, however, that these unsupportive results are used as support, even in the most prestigious reviews. Listen for instance to the words from the review “Diet and Health,” published by the National Research Council: “Percentage of calories from SFAs [saturated fatty acids] was positively associated with risk of CHD in the rural sample of the Puerto Rican and the Ireland-Boston studies.”
If you go to the library and look into the tables of these papers you will see that the differences found were not statistically significant, which means that the results were simply due to chance. And why did the authors of Diet and Health only cite these two studies? Why didn’t they mention that, if anything, coronary patients have eaten more polyunsaturated fatty acids?
Or listen to the joint statement by the American Heart Association and the National Heart, Lung, and Blood Institute: “… showing the link between diet and CHD particular impressive results [were produced in] the Western-Electric, the Honolulu Heart, the Zutphen, and the Ireland-Boston studies.”
Looking into the tables from these reports it appears that only in the Honolulu Heart study the patients had eaten significantly more saturated fat, but in that study they had eaten significantly more polyunsaturated fat also, opposite to what we should expect.
In conclusion, there is a weak association between the coronary mortality in various countries and the amount of fat available for them to eat, but no difference between the amount of fat eaten by coronary patients and by healthy individuals. This is no paradox, but typical of factors that follow each other roughly because they have a common cause. The mean income in various countries, for instance, parallels the number of heart attacks; coronary heart disease is common in rich countries and low in poor countries. But in rich countries poor people die more often from heart attacks than rich people.
Again, calories from animal food are more expensive than calories from vegetable food. The common denominator for countries where people eat lots of animal food is prosperity. In prosperous countries fat food is abundant, but so also are stress-provoking factors. Also more people smoke, fewer people perform manual labor, industrial pollution of the environment is most often worse, and the ability to diagnose coronary heart disease is better. People in prosperous countries also live longer; instead of dying from infectious diseases or malnutrition when they are young they die from diseases related to old age such as coronary heart disease. Any of these factors, or their combination, or something else that I have not thought about, may explain why people die more often from a heart attack in prosperous countries.
Prosperity, fat food, and coronary heart disease thus follow each other. Statistical correlations may therefore arise when different countries are compared, especially if countries that do not follow the usual pattern are excluded. But inside the countries there is no correlation because it is not prosperity or the fat food itself that cause coronary disease.
Here are links to the other chapters in the book.
- Cholesterol Myths by Uffe Ravnskov, MD, PhD: Forward to Book by Michael Gurr, PhD
- Cholesterol Myths by Uffe Ravnskov, MD, PhD: Author’s Foreword
- Cholesterol Myths by Uffe Ravnskov MD, PhD: Introduction: The Diet-Heart Idea: A Die-Hard Hypothesis
- Cholesterol Myths by Uffe Ravnskov MD, PhD: Myth 1: High-Fat Foods Cause Heart Disease
- Cholesterol Myths by Uffe Ravnskov MD, PhD: Triglycerides
- Cholesterol Myths by Uffe Ravnskov MD, PhD: Myth 2: High Cholesterol Causes Heart Disease
- Cholesterol Myths by Uffe Ravnskov MD: Familial hypercholesterolemia—not as risky as you may think
- Cholesterol Myths by Uffe Ravnskov MD, PhD: Myth 3: High-Fat Foods Raise Blood Cholesterol
- Cholesterol Myths by Uffe Ravnskov MD, PhD: Myth 4: High Cholesterol Blocks Arteries
- Cholesterol Myths by Uffe Ravnskov MD, PhD: Myth 5: Animal Studies Prove the Diet-Heart Idea
- Cholesterol Myths by Uffe Ravnskov MD, PhD: Cholesterol lowering in children
- Cholesterol Myths by Uffe Ravnskov MD: Myth 6: Lowering Cholesterol Will Lengthen Your Life (Part 1)
- Cholesterol Myths by Uffe Ravnskov MD: Myth 6: Lowering Cholesterol Will Lengthen Your Life (Part 2)
- Cholesterol Myths by Uffe Ravnskov MD PhD: Myth 7: The Statins — Gift to Mankind (Part 1)
- Cholesterol Myths by Uffe Ravnskov MD PhD: Myth 7: The Statins — Gift to Mankind (Part 2)
- Cholesterol Myths by Uffe Ravnskov MD PhD: “The most exact data base”—the screenee
- Cholesterol Myths by Uffe Ravnskov MD PhD: Myth 8: Polyunsaturated Oils are Good for You
- Cholesterol Myths by Uffe Ravnskov MD PhD: Dr. Ornish and The Lifestyle Heart trial
- Cholesterol Myths by Uffe Ravnskov MD PhD: Myth 9: The Cholesterol Campaign is Based on Good Science
- Cholesterol Myths by Uffe Ravnskov MD PhD: Insider Insight
- Cholesterol Myths by Uffe Ravnskov MD PhD: Myth 10: All Scientists Support the Diet-Heart Idea
- Cholesterol Myths by Uffe Ravnskov MD PhD: Epilogue
- Cholesterol Myths by Uffe Ravnskov MD PhD: References
This chapter is from the book
The Cholesterol Myths: Exposing the Fallacy that Saturated Fat and Cholesterol Cause Heart Disease
by Uffe Ravnskov, MD, PhD.
Dr. Ravnskov has given me the permission to share this version of his book to help educate the world about the cholesterol campaign.
Information about Uffe Ravnskov, MD, PhD is posted here.
More information about Cholesterol Myths is posted on his website here.
Dr. Ravnskov posted his book for free here.
Uffe Ravnskov, MD, PhD is the founder of The International Network of Cholesterol Skeptics (THINCS.org) which can be found here.
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