Holistic Health!

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Your cholesterol tells very little about your future health!

 

      What is cholesterol? 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 there is 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. Only 15-20 percent is transported by HDL and called ”good” cholesterol. A small part of the circulating cholesterol is transported by other lipoproteins.

 

Ø      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. 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. 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. 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. 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. 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.

 

Ø      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, inactivity, smoking, hypertension 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. To prove that high LDL-cholesterol is an independent risk factor, we should ask if fat, inactivity, smoking, hypertension and mentally stressed individuals with a high LDL-cholesterol level are at greater risk for coronary disease than fat, inactivity, smoking, hypertension and mentally stressed individuals with low or normal LDL cholesterol.

 

A word about science and statistics. 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. Nevertheless, let us have a look at some of the studies concerning cholesterol.

 

The ”good” one

 

      Publications almost beyond counting have studied the prognostic value of the ”good” HDL-cholesterol. The reason is, of course, that it is hard to find any prognostic value. If HDL-cholesterol had a heart-protecting effect of real importance, it would not be necessary to use the tax payers' money to demonstrate the effect again and again in expensive studies. In 1986 the medical statistician, Dr. Stuart Pocock and his coworkers published a report concerning more than 7000 middle-aged men in 24 British towns. The men had been followed for about four years after a detailed analysis of their blood lipids. During this period 193 of the men had had a heart attack. As in most previous studies, these men had on average a lower HDL-cholesterol at the beginning than the men who did not have a heart attack. The mean difference between the cases and the other men was 2.7 mg/dl, or about 6 per cent. This difference was small of course, but thanks to the large number of individuals studied it was statistically significant.

 

This difference, however, can be explained by many ways. A multivariate analysis adjusted for age, blood pressure, body weight, cigarette smoking and non-HDL-cholesterol reduced the difference to an insignificant 0.9 mg/dl, or 2 per cent. This means that those who had suffered a heart attack had a lower HDL-cholesterol mainly because they were older, fatter, had a higher blood pressure and smoked more than those who had not had a heart attack. Dr. Pocock and his colleagues concluded that a low HDL-cholesterol level is not a major risk factor for coronary heart disease. Their results were challenged in 1989 by nine American scientists headed by Dr. David Gordon. They had analysed the predictive value of HDL-cholesterol in four large American studies, a total of more than 15,000 men and women. They thought that the British scientists had used an incorrect way to adjust their figures. If another formula is used, the American researchers wrote, HDL-cholesterol is a much better predictor. But in one of the four studies, analyzed by Dr. Gordon and his colleagues, the number of fatal heart attacks was identical in the first and second HDL groups (individuals were classified into three groups, according to their HDL-cholesterol). In one of the studies the number of fatal cases was identical in the second and the third groups, and in one study more deaths were seen in the third group (those who had the largest amount of the ”good” cholesterol) than in the second group. And these figures were the unadjusted ones. After adjustment for age, cigarette smoking, blood pressure, body weight and LDL-cholesterol the differences were even smaller. In three of the four studies, the differences lost statistical significance. And remember that the figures were not adjusted for physical activity or mental stress, not to mention the risk factors we do not know yet.

 

The ”bad” one

 

      “LDL has the strongest and most consistent relationship to individual and population risk of CHD[coronary heart disease], and LDL-cholesterol is centrally and causally important in the pathogenetic chain leading to atherosclerosis and CHD”.

 

These words you will find in the large review Diet and Health. Reviews by distinguished scientific bodies are supposed to meet high standards. Therefore, you are probably wondering how the authors of Diet and Health, an official, most authoritative and supposedly reliable review from the National Research Council in Washington, had reached their conclusion about LDL-cholesterol. Four publications were mentioned, yet none of these publications supported the fact that LDL was a CAUSAL  factor of heart disease. In fact, the second paper claimed by the Diet and Health-authors was a 1977 report from the Framingham Study by Dr. Tavia Gordon and her colleagues. This study showed that women at that age ran a greater risk of having a heart attack if their LDL-cholesterol was low than if it was high. Thus, there was no support from this  paper that LDL was a CAUSAL  factor of heart disease, in fact the opposite, yet please note my friends that they used this study  to say the opposite of what the study revealed.

 

Ø      So, we see that the ”large body of evidence” was cooked down to one single study, which showed a predictive value for LDL-cholesterol but for a few age groups only. LDL-cholesterol is neither centrally nor causally important, it has not the strongest and most consistent relationship to risk of CHD, it has not a direct relationship to the rate of CHD, and it has not been studied in more than a dozen randomized trials.

 

But how then has the idea of the bad cholesterol emerged? As mentioned in the National Cholesterol Education Program, there are two main reasons:-

Ø      First, there was the discovery of a defective LDL-receptor in familial hypercholesterolemia and its consequence, the extremely high level of LDL-cholesterol in the blood of individuals with this disease. The discoverers, Nobel prize winners Michael Brown and Joseph Goldstein, suggested that the high LDL-cholesterol was the direct cause of the vascular changes seen in such individuals and also suggested that a similar mechanism was operating in the rest of us.

Ø      Second, feeding experiments in animals raised the animals' LDL-cholesterol and produced vascular changes that have been called atherosclerosis by the experimenters.

 

      These arguments are weak, however. If LDL-cholesterol were the devil himself LDL-cholesterol would clearly be a better predictor than total cholesterol, because the latter includes also the ”good” HDL-cholesterol. And experiments on animals can only be suggestive and cannot prove anything about human diseases. Besides, the vascular findings in laboratory animals do not look like human atherosclerosis at all, and it is impossible to induce a heart attack in animals by diet alone. And finally, findings pertaining to people with a rare genetic error in cholesterol metabolism are not necessarily valid for the rest of us. Thus, the experimenters claim support from unsupportive epidemiological and clinical studies, and the epidemiologists and the clinicians claim support from inconclusive experimental evidence. The victims of this miscarriage of justice are an innocent and useful molecular construction in our blood, producers and manufacturers of animal fat all over the world, and millions of healthy people who are frightened and badgered into eating a tedious and flavorless diet that is said to lower their bad cholesterol.

 

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. 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, 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. 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 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, Poland, Guatemala, and in the USA, all with the same result: no correlation between the level of cholesterol in the blood stream and the amount of atherosclerosis in the vessels.

 

Ø      In Japan the food is meager, blood cholesterol is low and the risk of getting a heart attack is much smaller than in any other country. Given these facts you will most probably say that in Japan atherosclerosis must be rare. The condition of the arteries of American and Japanese people was studied in the fifties by Professors Ira Gore and A. E. Hirst at Harvard Medical School and Professor Yahei Koseki from Sapporo, Japan. At that time US people on average had a blood cholesterol of 220 whereas Japanese had about 170. The aorta, the main artery of the body, from 659 American and 260 Japanese people were studied after death. Meticulously all signs of atherosclerosis were recorded and graded. As expected, atherosclerosis increased from age 40 and upwards, both in Americans and in Japanese. Now to the surprising fact. When degree of atherosclerosis was compared in each age group there was hardly any difference between American and Japanese people. Between age forty and sixty Americans were a little more arteriosclerotic than Japanese; between sixty and eighty there was practically no difference, and above eighty Japanese were a little more arteriosclerotic than Americans.  A similar study was conducted by Dr J.A. Resch from Minneapolis and Dr.s N. Okabe and K. Kimoto from Kyushu, Japan. They studied the arteries of the brain in 1408 Japanese and in more than 5000 American people and found that in all age groups Japanese people were more arteriosclerotic than were Americans.

 

Ø      The conclusion from these studies is of course that the level of cholesterol in the blood has little importance for the development of atherosclerosis, if any at all.

 

Our diet has little to do with our 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 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 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 do not necessarily raise 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. Please explain that to me. 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. 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. 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. 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.  What does this mean my friends? How can this be so? I’ll tell you. The Masai tribesmen were eating unpolluted food from nature, whereas the Masai who lived in the city had switched to eating poisonous chemicalized food bought from modern supermarkets!!! That is what made them sick and not the healthy, natural, high-fat diet!!!

 

      There is more evidence. Dr Uffe Ravnskov, a world authority on cholesterol, is quoted as saying:

“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.”  This, my friends is startling information! My poor father who believed the lie that he must avoid all the foods he enjoyed and eat only boiled foods with very little or no fat in them for 25 yrs so as to void high cholesterol, did so in vain. Why? I repeat, Dr Uffe Ravnskov, a world authority on cholesterol, is quoted as saying:

“…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.” 

 

 

Ø      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 lower 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. 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 recipes 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. 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.   Even if no pains are spared to investigate the diet of people the information gathered, is of course, uncertain. Who can recall everything that he has eaten in the last twenty four hours? And the diet of one 24-hour period may not be representative of the usual diet of the individual. A better result can be achieved by studying the diet over several days, preferably during various seasons of the year. In London professor Jeremy Morris and his team used this method and asked ninety-nine middle-aged male bank staff members to weigh and record what they ate over two weeks. Have you ever bargained in a bank? Maybe you will succeed in the director's office, but certainly not at the teller's counter. If anyone is scrupulous with nickels and dimes, it is those sitting behind the glass of the bank. Ninety-nine of these honorable men were asked to sit at home with a letter balance and weigh every morsel they ate for a whole week. But again, this meticulous method revealed no connection either between the food and the blood cholesterol level.  To be certain, seventy-six of the bank men repeated the procedure for another week at another time of the year: no connection was found, once again. To be absolutely certain the researchers selected those whose records were especially detailed and accurate. Once more, no connection was found.

 

Ø      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.

 

      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 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? 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 the many studies, involving so many individuals with such great variations in blood cholesterol and dietary habits. But there is no relation in the studies. Instead we see no correlation of cholesterol values between those who eat little animal fat and those who eat a lot of animal fat.

 

      Vegetarians usually have lower cholesterol than other people and they eat little animal fat. But vegetarians differ from the rest of the human population in more than their diet. They usually smoke less, they are usually thinner, and they usually exercise more often than other people. Whether it is their diet, or their other living habits, or perhaps something else that lowers their blood cholesterol is unknown.