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    Cholesterol Myths by Uffe Ravnskov MD PhD: Myth 8: Polyunsaturated Oils are Good for You


    Posted by .(JavaScript must be enabled to view this email address)
    Wednesday, November 12, 2014 10:10 am Email this article

    Intervening is a way of causing trouble.
    —Lewis Thomas

    Risk at both ends of the scale

    The smaller number of heart deaths in the soybean trial of Dr. Dayton and his team, mentioned in chapter 6, was offset by a larger number of cancer deaths. Does it mean that soybean oil causes cancer?

    Diet-heart proponents would argue that Dr. Dayton’s soybean trial was an anomaly, and that other trials with polyunsaturated fat have not resulted in more cancer. However, never before had such huge amounts of polyunsaturated fat been eaten over such a long period of time. Dr. Dayton’s patients were also much older than in the other trials, and thus more susceptible to cancer, which means that a possible cancer-provoking effect could be detected more easily.

    Another disquieting fact is that many studies have reported a low cholesterol to be a risk factor for cancer. The purpose of these studies was to follow a great number of individuals for many years to see if the Framingham researchers were right when they claimed that high cholesterol means a high risk of a heart attack. Surprisingly, these more recent studies revealed that it was just as dangerous to have a very low cholesterol level, as it was to have a very high one. Those who had very low cholesterol levels had a greater incidence of cancer while those with very high cholesterol suffered more heart attacks.

    Most investigators thought that low cholesterol levels were not the cause but the result of the cancer since cancer cells need cholesterol, just as any other cells do. Perhaps their rapid growth and greater need for cholesterol reduced the cholesterol levels in the blood?

    It is interesting that the diet-heart proponents immediately relegate low cholesterol to a secondary and thus an innocent phenomenon in the etiology of cancer, but never admit that high cholesterol might be a secondary and thus innocent phenomenon in the etiology of heart disease. No, say the diet-heart proponents, high cholesterol is always dangerous and should be lowered by any means.

    A great number of studies also found that cholesterol was low many years before the cancer was discovered. [246] If the low cholesterol was a consequence of rapid cancer growth, then the level should decrease when the cancer started to grow. But in some patients cholesterol was low eighteen years before the cancer appeared.

    Of course, this fact was a serious drawback for those who planned cholesterol-lowering measures of most of the population, and the diet-heart proponents therefore met in 1981 to discuss the problem.[247]

    The meeting was of sufficient importance to attract most of the leading American cholesterol researchers, including Jeremiah Stamler, director of two major cholesterol-lowering trials and author of a large number of papers that expanded on the dangers of high cholesterol; Basil Rifkind, head of the Lipid Metabolism Branch at the National Heart, Lung and Blood Institute, and later head of the LRC trial; Robert Levy from Columbia University, chairman of the meeting and previously director of The National Heart, Lung, and Blood Institute; Antonio Gotto, director of the American Heart Association; Ancel Keys, and many more of those who made up the anti-cholesterol army.

    Predictably, the participants concluded that low cholesterol did not cause cancer, but they were unable to explain the phenomenon. It was a subject for future research, they noted, but not a threat to public health.

    The published report from the meeting stated: “It was an unanimous opinion of the panelists that the data did not preclude, countermand, or contradict the current public health message which recommends that those with elevated cholesterol levels seek to lower them. There is evidence of a possible increase in cancer risk at very low cholesterol levels (but) the risk is generally modest.”[248]

    These were their words. By “very low levels” the panel meant less than 4.7 mmol/l (183 mg/dl). But diet-heart proponents do not consider 4.7 mmol/l (183 mg/dl) too low when it comes to treatment of high cholesterol. A couple of years later for instance members of the National Heart, Lung, and Blood Institute and the American Heart Association (many of whom participated in the meeting) recommended that people should bring their cholesterol levels down to at least 4.85 mmol/l (188 mg/dl).

    It is not certain that low cholesterol levels provoke cancer: the fact that cancer is seen more often in individuals with low cholesterol is no proof of cause and effect. Low cholesterol level is a risk factor for cancer, precisely as high cholesterol is a risk factor for heart disease.

    Again, a risk factor is not necessarily the cause. Something may produce cancer and at the same time lower blood cholesterol. Chemical compounds with such a potential do exist.

    Burglars among molecules

    “Somewhere, on some remote planet… on the other side of our galaxy, there is at this moment a committee nearing the end of a year-long study of our own tiny, provincial solar system. The intelligent beings of that place are putting their signatures… to a paper, which asserts, with finality, that life is out of the question here and the place is not worth an expedition. Their instruments have detected the presence of that most lethal of all gases, oxygen, and that is the end of that.”

    With these words Lewis Thomas, the famous essayist and professor of medicine opened one of his speeches to his new students. Thomas’s story is not pure fantasy—oxygen can be dangerous.

    A civil war rages inside us from the sweet second of fecundation until we end as dust or ashes. Atoms and molecules are fighting for the tiny elements that are surrounding them, the electrons. The haze of electrons gives identity and character to each atom and molecule; if the number of electrons is altered, a valuable molecular citizen may, in a split second, be turned into a useless and even destructive hoodlum.

    Electrons prefer to be present as couples. Paired electrons furnish the atom or molecule with stability and resistance against harassment, but some pairs are more stable than others.

    The main part of a fatty acids is composed of a core of carbon atoms to which hydrogen atoms are attached. When the number of hydrogen atoms is optimal their electrons form stable pairs with those of the carbon atoms. Examples of stable molecules are the saturated fatty acids, those said to be dangerous to the heart and the vessels. They are called saturated because they are saturated with hydrogen.

    Unsaturated fatty acids are short of hydrogen atoms. Monounsaturated fatty acids are missing two, polyunsaturated fatty acids are missing four or more. This means that instead of sharing one pair of electrons with each other, some of the carbon atoms are sharing two pairs of electrons with his neighbor carbon instead of one pair, forming the so-called double bond.

    A double bond is less stable than a single bond. The hydrogen sitting close to the double bond is easily snatched by a free radical, a process called oxidation. Free radicals snatch hydrogen atoms because one or more of their electrons lack their partner; they are unpaired.

    Combustion fumes, such as cigarette smoke and diesel exhaust, are especially rich in free radicals, but even the oxygen molecule is a free radical. It is especially active when heated. If the temperature is high enough, all its neighbors are oxidized—they burn. But what we are interested in here is oxidation at body temperature.

    Inside the cells of our body oxidation is vital to cell function and life as long as this process is controlled by hormones and enzymes. Step by step sugar and other fuel molecules are oxidized to water and carbon dioxide, a process that releases energy for the cell machinery. So far, so good.

    But if oxidation occurs without control, as it may do if we are exposed to free radicals, molecules other than sugar may be oxidized. Among these others are the unstable polyunsaturated fatty acids. Loss of hydrogen atoms is disastrous to a polyunsaturated fatty acid (as to other molecules as well), because its stability is ruined and it is split into lesser molecules with nasty qualities.

    Usually the human body is protected against oxidation thanks to many various antioxidants, kind molecules that donate hydrogen atoms to the free radicals thus protecting us against uncontrolled oxidation. Vitamin E, for example, is a well-known and important antioxidant that protects the polyunsaturated fatty aids in our cell membranes. There are many others.

    But if too many polyunsaturated fatty acids are present, or if too many free radicals are available, or if the amount of antioxidants is insufficient, then protection from the antioxidants may fail.

    Nobody knows the limit between harmless and harmful amounts of polyunsaturated fatty acids. Cholesterol campaigners now recommend no more than 10 percent of our calories from polyunsaturated oils, but give no reasons for the limit. They don’t tell us about the evidence that an excess of dietary polyunsaturated fatty acids may be dangerous.

    Does polyunsaturated oil produce cancer?

    When too much polyunsaturated oil is given to laboratory animals their white blood cells are damaged so that the animals die more easily from infectious diseases and cancer. We do not know for sure whether the same is valid for human beings, but we do know that our immune system is sensitive to a surplus of polyunsaturated fatty acids. If a preparation of such oils is added to the diet of patients who have received a kidney graft the function of their white blood cells is hampered resulting in a better acceptance of foreign material, including the transplanted kidney.[249]

    But other foreign and less useful material, such as bacteria and virus, may be accepted also. One of the great problems with transplant patients is that their immunosuppressive treatment makes them more vulnerable to infection. It is a general rule that any substance which harms the white blood cells also stimulates infections. Some of these substances may even stimulate cancer.

    It has never been proved that polyunsaturated fatty acids stimulate cancer, but proof may come in time. By analogy, cigarette smoke may produce cancer, but only after many years of exposure.

    Do polyunsaturated oils make you age faster?

    It is commonly accepted that aging is partly a result of the eternal fight of free radicals for electrons. If laboratory animals are exposed to free radicals, or to substances highly sensitive to free radicals—if, for instance, these animals eat great amounts of polyunsaturated oils?—yellowish pigments are stored in many organs. The same pigments develop in most creatures including man, and accumulates with age.

    The fact that polyunsaturated oils may accelerate aging was demonstrated by Dr. Edward Pinckney. In collaboration with a plastic surgeon he asked a large number of patients how much polyunsaturated oil they usually consumed.

    Fifty-four percent of the patients said that they had increased their intake considerably. Of those patients 78 percent showed marked clinical signs of premature aging, and 60 percent had required the removal of one or more skin lesions because of suspected malignancy. Of the patients who had made no special efforts to consume polyunsaturated oils the figures were 18 and 8 percent respectively.[250]

    Today most deep-frying is done in vegetable oils. Very few know that if polyunsaturated oils are kept hot over many hours, its ability to produce cancer in laboratory animals increases.[251]

    Do polyunsaturated oils make you stupid?

    Polyunsaturates have other nasty effects. Premature children have only small amounts of vitamin E in their bodies. Dr. Joshua Ritchie and his team in San Francisco studied seven premature babies who were admitted to the hospital with widespread edema, anemia, disturbances of the blood cells and lack of vitamin E. The researchers found that the most plausible cause was the food; these children had all received commercial formulas composed of skim milk and vegetable oils with a high content of polyunsaturated fatty acids.[252]

    The brain has low levels of vitamin E. This fact may explain why chickens fed polyunsaturated fat develop brain damage very quickly.[253]

    Do polyunsaturated oils cause atherosclerosis?

    A new theory about the origin of atherosclerosis is that it is not normal cholesterol, but oxidized cholesterol that is dangerous.[254] And oxidized cholesterol means cholesterol that has been damaged by free radicals.

    Even in the fetus the walls of the arteries are speckled with fat. The microscope shows that these speckles or fatty streaks are composed of white blood cells filled with tiny bubbles. These cells are called foam cells. But the substance is not foam; it is cholesterol.

    Patients with homozygous familial hyper?cholesterolemia have foam cells also. This fact was a stumbling block to the Nobel prize winners Michael Brown and Joseph Goldstein. What they discovered was that in individuals with the rare genetic error called familial hypercholesterolemia, cholesterol molecules in the blood do not enter the cells as they do in normal individuals. The reason is that their key to the cell, the so-called LDL-receptor, is defective. Individuals who have inherited the disease from one parent (heterozygous form) have too few receptors; those who have inherited the disease from both parents (homozygous form) have no receptors at all. The lack of LDL-receptors explains why patients with familial hypercholesterolemia have a high blood cholesterol level.

    But how can cholesterol enter the foam cells in patients with the homozygous form of familial hypercholesterolemia if, as Brown and Goldstein suggested, the cholesterol door to the cell is closed? This is certainly a crucial question because diet-heart proponents consider these foam cells the forerunner of atherosclerosis.

    Recent studies have shown that it is not normal cholesterol which accumulates in the foam cells. Instead, it is oxidized cholesterol. And oxidized cholesterol has no problem entering the cells; it takes another route. The problem seemed solved. But how has cholesterol been oxidized?

    There is much evidence that free radicals are the cause of the oxidation, and the source of free radicals is most probably the polyunsaturated fatty acids. For example, scientists can reduce the fatty streaks (called atherosclerosis by the proponents) in rabbits with familial hyper?cholesterolemia[255] (named Watanabe rabbits) with the drug probucol, without lowering blood cholesterol.[256] The explanation may be that probucol, just like vitamin E, is an antioxidant that hampers the attacks of free radicals.

    On the other hand, lowering cholesterol in Watanabe rabbits does not reduce the fatty streaks.[257]

    If polyunsaturated fatty acids promote oxidation of cholesterol and thus atherosclerosis we should avoid eating too much of them. But diet-heart proponents continue to insist that it is more important to lower cholesterol by avoiding saturated fat and continue to recommend polyunsaturates as a substitute.

    It is difficult to follow the proponents line of thought. The depositing of cholesterol in the artery walls of Watanabe rabbits was not reduced by lowering the blood cholesterol but by preventing its oxidation. Then, does it make sense to lower cholesterol with polyunsaturated oils if too much of it stimulates oxidation?

    One of the scientists introducing the new theory about oxidized cholesterol is Dr. Daniel Steinberg, from the University of California in La Jolla. He was the chairman of the consensus committee that started the American cholesterol campaign. This campaign has recommended that all Americans eat polyunsaturated vegetable oils instead of saturated fat. The committee recommended an upper limit of 10% for the consumption of polyunsaturated oil (now the reader know why). However, the committee did not call attention to the fact that the food they had previously called a protection against atherosclerosis was now seen as its cause.

    It has not been proved, however, that oxidized cholesterol is the forerunner of atherosclerosis. A link is missing.

    What has been demonstrated is that oxidized cholesterol is accumulated as fatty streaks, but the presence of fatty streaks is not the same as atherosclerosis. And the accumulation of cholesterol in fatty streaks has been shown in Watanabe rabbits, not in common rabbits. Because Watanabe rabbits inherit the same defect in cholesterol metabolism as people with familial hyper?cholesterolemia, the correct conclusion from the rabbit experiments is perhaps that fatty streaks in individuals with familial hypercholesterolemia may be induced by oxidized cholesterol.

    However, there are observations that do suggest an adverse effect of polyunsaturated oil. In the worldwide epidemiological study of atherosclerosis the investigators found a connection between the degree of atherosclerosis and the total intake of fat. As there was no association between the intake of saturated fat and degree of atherosclerosis, the association obviously concerned unsaturated fats.

    What we know for certain is that polyunsaturated fatty acids may produce a great many unfortunate things, none of them pleasant for human beings. We need polyunsaturated oils in small amounts to keep us healthy; some of them are even essential to life. Thanks to their lack of electrons, polyunsaturated fatty acids are soft and flexible. If our cell walls had only saturated fats, we would probably become as stiff as candles. But to have too many polyunsaturated fatty acids is undesirable. After all, who would like his home to be occupied by terrorists?[258]

    Trans fat

    The fact that polyunsaturated fats such as corn, soybean, and sunflower oils are liquid, even at cold temperatures, has been a problem for the oil manufacturers in countries where butter and lard, not oil, are used in the diet. However, early in this century, French and German food technologists invented a method for converting vegetable oil into solid fat. They heated the oil to 150-200º Celsius in large reactors, mixed the oil with nickel powder that acted as a catalyst, and then forced hydrogen through this unappetizing soup. This method, still used today, changes the chemical structure of the polyunsaturated fatty acids and creates something called trans fatty acids. Trans fatty acids are also unsaturated, but the hydrogen molecules in the double bonds have been arranged so that the resulting molecules behave like the more solid saturated fatty acids. The final product, which is a mixture of various polyunsaturated, saturated, and trans fatty acids, is called partially hydrogenated oil and is used as an ingredient in many food products including margarine, crackers, cookies, doughnuts, french fries, potato chips, pastries and sweets.

    Tiny amounts of certain trans fatty acids are also found in animal fats. However, the kinds of trans fatty acids that are produced by industrial hydrogenation have another chemical structure and are rarely found in natural food. By mistaking them for naturally occurring fatty acids, the human body may place them in the cell walls and other parts of human cells and because these trans fatty acids differ chemically there is a risk that we may suffer disturbances in cellular function if we eat too much of them.[259]

    Some fatty acids are vital just as vitamins are. This means that we cannot synthesize them ourselves, but need a small amount of them in our food. Normally, the risk is very small that we should suffer from lack of these fatty acids, because they are found naturally in most fats. However, when experimental animals are fed with trans fatty acids from hydrogenation, they develop symptoms similar to those that occur after a shortage of the vital fatty acids, either because the trans fatty acids are toxic by themselves or because they in some way inhibit the usage of the vital fatty acids. The most serious effects concern reproduction. The testicles of rats are damaged, and the rats become sterile;[260] in mice, the fat content of the milk decreases.[261]

    In human beings, trans fatty acids in the mother’s blood pass over to the fetus. Whether it has any importance is uncertain, but a study by Dr. B. Koletzko at the Pediatric Department at Ludwig-Maximilians University in Munich on premature infants is suggestive. He found that a low birth weight in these children was associated with a higher proportion of trans fatty acids in the blood.[262] Of course, this is no proof that the low birth weight of these children was due to the excess of trans fatty acids, but the finding certainly gives rise to concern, because there is experimental evidence that trans fatty acids may inhibit growth, for instance from a study by Dr. Atal and his coworkers at various institutions at the University of Maryland and at the National Institutes of Health.[263] They gave young mice two different diets. The only difference between the diets was that a tiny amount of normal fatty acids (not of the vital ones) was substituted with the same amount of trans fatty acids. After two years the body weight of the mice fed with trans fatty acids was 20-25% lower than the weight of the control mice. Thus, although the mice had been given exactly the same amount of calories, those which ate trans fatty acids instead of other fatty acids did not grow as they should have done.

    Too much dietary trans fat makes the blood cholesterol level rise.[264] Not that this effect matters in itself; if you haven’t skipped Chapter 4 you may recall that atherosclerosis has nothing to do with the blood cholesterol level, and from Chapter 2 you may remember that most heart attacks are seen in people with normal cholesterol levels. But people who think that the cholesterol level is important should know, that by following the official recommendations and eating margarine rather than animal fats, they might raise their cholesterol instead of lowering it.

    Trans fat is present in considerable amounts in solid margarine and in bakery shortenings. The consumption of trans fat has increased substantially in most Western countries during the last century. In the United States, it has increased from 12 grams per day and person before World War I to about 40 grams in 1985. This is the average figure; some people may eat more, especially if they have followed the recommendations of the National Cholesterol Education Program, because very often fat that is called polyunsaturated on the food labels may be trans fat. Even the few people who prefer butter over margarine consume trans fat if they eat processed food products such as those mentioned above.

    Many researchers, in particular those who advocate for the diet-heart idea, argue that the evidence is weak that trans fat is harmful to human beings. However, the mere suspicion that reproduction and growth may be hampered by an artificial nutrient, or that the same component may stimulate cancer growth, demands careful studies before it is distributed as food to most of mankind.

    ———

    Here are links to the other chapters in the book.

    ———

    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.

    Several versions of the ebook can downloaded from Dropbox here or from SmashWords here.

    Uffe Ravnskov, MD, PhD is the founder of The International Network of Cholesterol Skeptics (THINCS.org) which can be found here.

    Articles on the same subject can be found here:


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