SUBJECT: THE CHOLESTEROL MYTH
THE CHOLESTEROL MYTH
Part 1: Introduction
"The tragedy of science is the slaying of a beautiful hypothesis by an ugly fact." --T H Huxley
Over the past couple of decades there has been a growing concern about fats and cholesterol. Dieticians, nutritionists and doctors have been telling us that fat is a killer. Governments have introduced national policies based around its reduction. Eat less cholesterol, saturated fat and salt, eat more fibre-rich foods we are all told. The evidence is incontrovertible that if we do not, we are doomed to the West's greatest killer - heart disease.
But is the evidence so clear? Despite the certainty implied by the propaganda, the debate continues in the medical journals, behind the scenes. Is diet a killer? Apart from those with a very rare disease, has cholesterol got anything to do with heart disease - or any other disease? And even if it has, will a change of diet be beneficial?
Like all debates, this one about cholesterol has two sides. The Cholesterol Myth explores the evidence on which present healthy eating' dietary recommendations are based.
Much of the evidence used in the cholesterol debate is complex. Nevertheless, with so much of only one side of the debate having been published and your having been subjected to so much that is misleading, I will try to explain the other side in as much detail as this paper allows.
* * * * * *
THE B. M. A. AND THE GOVERNMENT RECOMMEND THAT THE BRITISH PEOPLE SHOULD DRINK EIGHTY PERCENT MORE MILK, EAT FIFTY-FIVE PERCENT MORE EGGS, FORTY PERCENT MORE BUTTER AND THIRTY PERCENT MORE MEAT.
On the basis of research in the 1920s and 1930s by Sir John Boyd Orr and others, that was the advice given to the British people in 1938. The Government introduced free school milk - full cream, that is - and later we 'went to work on an egg'. As a consequence, child deaths from diphtheria, measles, scarlet fever and whooping cough fell dramatically - well before the introduction of antibiotics and widespread immunisation. Rickets, called 'the English Disease' because it was so wide-spread, and other deficiency diseases were relegated to the past. Other factors helped, but most important of all was the better nutrition that gave children a higher resistance. The recommendations above shaped our diet for nearly fifty years and helped to give us a mean life expectancy that is now among the highest in the world. Sixty years in 1930, our mean life expectancy had climbed to seventy years by 1960 and to seventy-five years by 1990. Now we are told they are shortening our lives - killing us with coronary heart disease. Why the sudden change? To discover that, we need to know something of the history of coronary heart disease and how the strategy to combat it evolved.
Coronary heart disease
Cholesterol may be ingested in animal products, but less than twenty percent of your body's cholesterol needs will be supplied in this way. Your body then makes up the difference. If you eat less cholesterol, your body merely compensates by making more. Although the media and food companies still warn against cholesterol in diet, it has been repeatedly demonstrated that the level of cholesterol in your blood is affected very little by the amount of cholesterol you eat.
Cholesterol and CHD
In 1950 an American doctor, John Gofman, hypothesised that blood cholesterol was to blame. This was supported in 1951 when pathologists were sent to Korea to learn about war wounds by dissecting the bodies of dead soldiers. To their surprise they discovered unexpected evidence of coronary heart disease: unexpected for they knew that death from heart disease was extremely rare under middle age and these men averaged only twenty-two years of age. So the pathologists performed detailed dissections on the hearts of the next 300 corpses. In thirty-five percent they found deposits of fibrous, fatty material sticking to the artery walls. A further forty-one percent had fully formed lesions, and in three percent of the soldiers these lesions were sufficiently large that they blocked at least one coronary artery. Thus, over three-quarters of all the men examined showed evidence of serious coronary heart disease - and they were barely out of their teens.
Doctors now had a problem. As there are no symptoms with the partial blockage of the coronary arteries, how could they tell, without resorting to surgery, who was in danger? They had to find what was different in those with the disease and those free of it.
To cut a long story short, they found cholesterol in the material that builds up on artery walls and causes them to become blocked; people who died of heart disease often had high levels of cholesterol in their blood; and those who suffered the rare hereditary disease, familial hypercholesterolaemia (hereditary high blood cholesterol), also suffered a higher incidence of CHD. And so, not unnaturally perhaps, cholesterol and heart disease became linked.
But there are a number of significant points that the cholesterol theory overlooks. For example, there is a marked difference between the build-up found in those with familial hypercholesterolaemia and those with coronary heart disease: hypercholesterolaemia causes large deposits at the mouths of the coronary arteries, often leaving the arteries themselves unblocked, and so does not reproduce the type of obstruction found in coronary heart disease. People with myxoedema or nephrosis also have high blood cholesterol levels - yet in them, there is no increase in the incidence of CHD. Neither is raised blood cholesterol a predictor of CHD in people over sixty. It has also long been known that simple events, such as putting a cuff around the arm prior to taking a blood sample, or fear of the needle, can result in raised cholesterol values. And, even where these are avoided, large fluctuations are known with peak to nadir variations of as much as twenty-three percent. Lastly, cholesterol is only one of the constituents of an atheroma and, if you think about it, cholesterol is so necessary and so widespread in the body, it would have been surprising if it had not been found. Nevertheless the lowering of blood cholesterol became the sole objective in the fight against CHD; and the two principal methods used to achieve this are with diet and drugs.
J P Strong, H C McGill jr. The natural history of coronary atherosclerosis. Am J Pathol . 1962; 40: 37.
W F Enos, R H Holmes, J Beyer. Coronary disease among United States soldiers killed in action in Korea. Preliminary report. JAMA 1953; 152: 1090.Part 2: Dietary Fats and Heart Disease
For what a man would like to be true, that he more readily believes. Francis Bacon
That diet might play a part as a cause of CHD was hypothesised by another American doctor, Ancel Keys, in 1953. Using data from seven countries in his 'Seven Countries Study', Keys compared the death rates from CHD and the amounts of fats eaten in those countries to demonstrate that heart disease mortality was higher in the countries that consumed more fat than it was in those countries that consumed less. (At that time, data from many more countries were available. It seems that Keys ignored the data from those that did not support his hypothesis.) And so the 'diet/heart' hypothesis was born.
But how do we know it is true? It is all very well having a theory, what you have to do then is prove it. In medicine, the usual way is to select two groups of people, as identical for sex, age, and lifestyle as possible. One group called the control group , carries on as normal while the other, called the intervention group , tries the new diet, drug or whatever. After a suitable time, the two groups are compared and differences noted.
Keys' fat-diet/heart disease hypothesis was persuasive so, to test it, several large-scale, long-term, human intervention studies were set up in many parts of the world. These involved hundreds of thousands of subjects and hundreds of doctors and scientists and cost billions of dollars in an attempt to prove that a fatty diet caused heart disease.
Framingham Heart Study
Next, the scientists studied intakes of saturated fats but again they could find no relation. There was still no relation when they studied total calorie intake. They then considered the possibility that something was masking the effects of diet, but no other factor made the slightest difference.
After twenty-two years of research, the researchers concluded:
"There is, in short, no suggestion of any relation between diet and the subsequent development of CHD in the study group."
On Christmas Eve, 1997, after a further twenty-seven years, the Journal of the American Medical Association (JAMA) carried a follow-up report that showed that dietary saturated fat reduced strokes. As these tend to affect older men than CHD, they wondered if a fatty diet was causing those in the trial to die of CHD before they had a stroke. But the researchers discount this, saying:
"This hypothesis, however, depends on the presence of a strong direct association of fat intake with coronary heart disease. Since we found no such association, competing mortality from coronary heart disease is very unlikely to explain our results."
In other words, after forty-nine years of research, they are still saying that they can find no relation between a fatty diet and heart disease.
Multiple Risk Factor
"The overall results do not show a beneficial effect on Coronary Heart Disease or total mortality from this multifactor intervention."
The Tecumseh Study
WHO European Coronary
The North Karelia Project
These figures suggest that adopting a 'healthy' lifestyle may actually have inhibited the decline in heart disease. They certainly give it no support.
This paper does not allow me to go through the more minor studies but they all show little convincing correlation between either the amount of fat eaten and heart disease or the type of fat eaten and heart disease. A review of twenty-six studies published in 1992 concluded that:
"Lowering serum cholesterol concentrations does not reduce mortality and is unlikely to prevent coronary heart disease. Claims of the opposite are based on preferential citation of supportive trials."
One that seemed to support the 'healthy' recommendations was a Finnish trial published in 1975. In the five years that the trial ran, cholesterol levels were lowered significantly, and the study was hailed as a success. But in December 1991 the results of a 10-year follow-up to that trial found that those people who continued to follow the carefully controlled, cholesterol-lowering diet were twice as likely to die of heart disease as those who didn't - some success! Professor Michael Oliver, writing in the British Medical Journal commenting on the results, writes
"As multiple intervention against risk factors for coronary heart disease in middle aged men at only moderate risk seem to have failed to reduce both morbidity and mortality such interventions become increasingly difficult to justify. This runs counter to the recommendations of many national and international advisory bodies which must now take the recent findings from Finland into consideration. Not to do so may be ethically unacceptable."
Despite this wealth of evidence, nutritionists and the media continue to mislead us. They tell us, for example, that the recent fall in the numbers of heart deaths in the USA is because Americans are eating less fat. The graph below, however, shows clearly that while CHD in the USA peaked in the 1950s and has fallen consistently since, this is against a background of rising fat intake.
I find difficulty understanding how the fat hypothesis gained such credibility in the USA as its history more than most does not support it. The North American continent had been opened up by explorers and trappers who lived, very healthily, as did the Amerindians, almost entirely on fresh meat and pemmican. As real pemmican is half dried lean meat and half rendered animal fat, and as fat has over twice the calorific value of protein, more than seventy percent of the energy in their diet came from fat.
Dieticians also say that the British had less CHD in the 1940s when fat was rationed. However, the decade of rationing went on into the early 1950s with fat being the last food to come off ration in 1954. Again the graph shows clearly that the most rapid rise in CHD occurred during that period.
Also, during the period of rationing, British farmers had a very low incidence of heart disease when one would have expected their intake of fats, particularly animal fats, to have been higher than most.
Experience in other
1. In Japan, intakes of animal
fat have more than doubled since the end of the Second World War. Over
the same period their incidence of coronary heart disease has fallen consistently.
In Israel too an increased consumption of saturated fats was followed
by a fall in coronary deaths.
From as early as 1971, an excess of cancer deaths has been reported in trials using diets that were high in polyunsaturated fats. Polyunsaturated fats are also blamed for a doubling in the incidence of gallstones in the general public.
One of the pioneers of the polyunsaturated-fat-prevents-CHD hypothesis was the American cardiologist E. H. Ahrens Jr.. After twenty-five years of further research, however, he concluded that it was "irresponsible" to continue to press the polyunsaturated fat recommendations on the general public. He went on:
"If the public's diet is going to be decided by popularity polls and with diminishing regard for the scientific evidence, I fear that future generations will be left in ignorance of the real merits, as well as the possible faults in any dietary regimen aimed at prevention of coronary heart disease."
Another of the original proponents of the low-fat, low-cholesterol hypothesis, and a member of the Norwegian Council for Diseases of the Heart and Arteries, Professor Jens Dedichen of Oslo, also changed his mind. In the 1950s Norway launched a cholesterol-lowering regimen in which soy margarine, that is high in polyunsaturated fatty acids, replaced butter, and soy oil was used extensively. During the subsequent 20 years the increase in the use of soy-based products was accompanied by a steep and continuing rise in deaths from coronary thrombosis. Professor Dedichen drew attention to the failure of the programme - and received a very hostile reaction from his colleagues.
Also castigated were members
of the National Academy of Sciences and the National Research Council
of America when in a report of May 1980, they stated that prevention of
heart disease could not be achieved by reducing blood cholesterol using
either diet or drugs, and said that such measures should be abandoned.
In 1989, the petroleum-based solvent, benzene, that is known to cause cancer, was found in Perrier mineral water at a mean concentration of fourteen parts per billion. This was enough to cause Perrier to be removed from supermarket shelves. The first process in the manufacture of margarine is the extraction of the oils from the seeds, and this is usually done using similar petroleum-based solvents. Although these are then boiled off, this stage of the process still leaves about ten parts per million of the solvents in the product. That is 700 times as much as fourteen parts per billion.
The oils then go through more than ten other processes: degumming, bleaching, hydrogenation, neutralization, fractionation, deodorisation, emulsification, interesterification, . . . that include heat treatment at 140 o -160 o with a solution of caustic soda; the use of nickel, a metal that is known to cause cancer, as a catalyst, with up to fifty parts per million of the nickel left in the product; the addition of antioxidants such as butylated hydroxyanisol (E320). These antioxidants are again usually petroleum based and are widely believed to cause cancer.
The hydrogenation process, that solidifies the oils so that they are spreadable, produces trans -fatty acids that rarely occur in nature.
The heat treatment alone is enough to render these margarines nutritionally inadequate. When the massive chemical treatment and unnatural fats are added, the end product can hardly be called either natural or healthy.
Recent United States studies showed that heart disease worsened in those who switched from butter to polyunsaturate-rich margarine. Research published in March 1993, confirmed this. In a study that involved 85,000 nurses, women who ate just four teaspoons of polyunsaturated margarine a day had a sixty-six percent increased risk of CHD compared to those who ate none. A review of men's experience in the Framingham Study published in 1995 also found that 6 teaspoons a day (mean of lowest intake vs mean of highest), increased risk by nearly a third. The authors conclude:
"Intake of margarine may predispose to development of CHD in men".
- and CHD is the one disease eating this sort of margarine was supposed to reduce!
You may be interested in a
list of the ingredients that may be present in butter and margarine:
Margarine: Edible oils,
Dietary fat patterns
It is interesting to compare the growth of heart disease in this country with intakes of different fats. The next graph illustrates the birth of CHD in Britain together with the intake of animal fat since the beginning of the century. When compared with the CHD curve, it is clear that there is no obvious relationship
If we plot CHD together with intakes of margarines and vegetable shortenings, however, we find a different curve.
Margarine use began around the turn of the century. Butter was expensive. The poor bought margarine as a substitute for butter and sales were brisk. The rapid rise in margarine consumption was followed a couple of decades later by that dramatic rise in heart disease deaths.
If there is a causal relationship between fat intake and heart disease, these two graphs suggest to me that it is the margarines that are the more likely candidates for suspicion.
Polyunsaturated fats and Cancer
Many laboratories have shown that diets high in polyunsaturates promote tumours. It has been known since the early 1970s that it is linoleic acid that is the major culprit. As Professor Raymond Kearney of Sydney University put it in 1987:
"Vegetable oils (eg Corn oil and sunflower oil) which are rich in linoleic acid are potent promoters of tumour growth."
Carcinogens - background radiation, ultraviolet radiation from the sun, particles in the air we breathe and the food we eat - continually attack us all. Normally, the immune system deals with any small focus of cancer cells so formed and that is the end of it. But linoleic acid suppresses the immune system. Indeed it is so good at this that in the 1970s sunflower oil was given to kidney transplant patients to prevent kidneys being rejected - until an excess of cancer deaths was reported. With a high intake of margarine, therefore, a tumour may grow too rapidly for the weakened immune system to cope thus increasing our risk of a cancer.
Since 1974, the increase of polyunsaturated fats has been blamed for the alarming increase in malignant melanoma (skin cancer) in Australia. We are all told that the sun causes it. Are Australians going out in the sun any more now than they were fifty years ago? They are certainly eating more polyunsaturated oils: even milk has its cream removed and replaced with vegetable oil. Victims of the disease have been found to have polyunsaturated oils in their skin cells. Polyunsaturated oils are oxidised readily by ultra-violet radiation from the sun and form harmful 'free radicals'. These are known to damage the cell's DNA and this can lead to the deregulation we call cancer. Saturated fats are stable. They do not oxidise and form free radicals.
Malignant melanoma is also said to be increasing in this country. Does the sun cause this? In Britain the number of sufferers is so small as to be relatively insignificant. Even so, it is not likely that the sun is to blame since all the significant increase is in the over-seventy-five-year-olds. People in this age group tend to get very little sun.
Melanoma occurs ten times as often in Orkney and Shetland than it does on Mediterranean islands. It also occurs more frequently on areas that are not exposed to the sun. In Scotland, for example, there are five times as many melanomas on the feet as on the hands; and in Japan, forty per cent of pedal melanomas are on the soles of the feet.
In 1991, two studies, from USA and Canada, found that linoleic acid, the major polyunsaturated fatty acid found in vegetable oils, increased the risk of breast tumours. This, it seems, was responsible for the rise in the cancers noted in previous studies. Experiments with a variety of fats showed that saturated fats did not cause tumours but, when small amounts of polyunsaturated vegetable oil or linoleic acid itself was added, this greatly increased the promotion of breast cancer.
A study of 61,471 women aged forty to seventy-six, conducted in Sweden, looked into the relation of different fats and breast cancer. The results were published in January 1998. This study found an inverse association with monounsaturated fat and a positive association with polyunsaturated fat. In other words, monounsaturated fats protected against breast cancer and polyunsaturated fats increased the risk. Saturated fats were neutral.
All polyunsaturated margarines, from the brand leader to shops' 'own brands' are around thirty-nine percent linoleic acid. Of cooking oils, sunflower oil is fifty percent and safflower oil seventy-two percent linoleic acid. Butter, on the other hand, has only a mere two percent and lard is just nine percent linoleic acid. Linoleic acid is one of the essential fatty acids. We must eat some to live, but we do not need much. The amount found in animal fats is quite sufficient.
Because of the heart disease risk, in 1994 the manufacturers of Flora changed its formula to cut out the trans fats and other manufacturers have since followed. But that still leaves the linoleic acid.
The anti-cancer fat
Conjugated linoleic acid has one other difference from the usual form - it is not found in vegetables but in the fat of ruminant animals. The best sources are dairy products and the fat on red meat, principally beef. It is another good reason not to give up eating red meat or to cut the fat off.
Scientists at the University of Wisconsin also believe that CLA has a slimming action. They put the dramatic increase in obesity in the USA down to Americans not eating beef fat.
Although the supposed virtues of monounsaturated fats are being talked of in the press as possible saviours of Western man, the monounsaturated theory is not new. It was first demonstrated over thirty years ago that giving people more unsaturated fats could lower blood cholesterol. However, surveys of countries with different tastes in fats and oils have failed to show that this protects against heart disease. For example, Norwegians, who eat a lot of saturated fats, have lower rates of the disease than New Zealanders who eat a similar amount. But if, as has been suggested, the Norwegians are protected by the monounsaturated oils in the fish that they eat, then why is it that in Aberdeen, where a lot of fish is also consumed, the heart disease rate is double that of Oslo? Proponents also forget that many other people, such as the Maasai tribes of Africa, who don't eat either fish or olive oil, also have a low incidence of heart disease.
There is also no evidence that either mono- or polyunsaturated oils are of benefit to those who have already suffered a heart attack. As long ago as 1965 survival rates were studied in patients eating different oils. Splitting patients into three groups, who were given polyunsaturated corn oil, monounsaturated olive oil and saturated animal fats respectively, it was found that only the corn oil lowered blood cholesterol levels. At first sight, therefore, it seemed that men in the polyunsaturated group had the best chance of survival. However, at the end of the two-year trial only fifty-two percent of the polyunsaturated corn oil group were still alive and free of a fresh heart attack. Those on the monounsaturated olive oil fared little better: fifty-seven percent survived and had no further attack. Those eating the saturated animal fats, however, fared much better with seventy-five percent surviving and without a further attack.
Breast Cancer. The Swedish study by Alicia Wolk and colleagues mentioned above did find, however, that monounsaturated fats were protective against breast cancer.
Animal fats such as lard are around 43% Saturated, 47% Mono-unsaturated and 10% Polyunsaturated - which the evidence suggests is just about ideal.
J M McMichael. Fats and atheroma: an inquest. BMJ . 1979; 279: 890.
- Diet and coronary disease. Acta Med Scand . 1980; 207(3): 151.
E B Smith, R H Smith. Early changes in aortic intima. Atheroscler Rev. 1976; I: 119.
V J Wass, et al. Does the nephrotic syndrome increase the risk of cardiovascular disease? Lancet. 1979; ii: 664.
R A Moore. Variation in serum cholesterol. Lancet . 1988; ii: 682.
Editorial. Virus infections and atherosclerosis. Lancet. 1978; ii: 821.
J L Houghton, T W von Dohlen, M J Frank. Myocardial ischaemia without atherosclerosis. Postgrad Med . 1989; 86 (5): 121.
J M Woodhill, et al. Low fat, low cholesterol diet in secondary prevention of coronary heart disease . In: D Kritschevky, R Paoletti, W L Holmes Eds. Drugs, lipid metabolism and atherosclerosis. New York: Plenum Press, 1978: 317.
Diet and Cardiovascular Disease. Committee on Medical Aspects of Food. DHSS. 1984.
W B Kannel and T Gordon. The Framingham Diet Study: diet and the regulations of serum cholesterol (Sect 24 ). Washington DC, Dept of Health, Education and Welfare, 1970.
W B Kannel and W P Castelli. Is serum cholesterol an anachronism? Lancet . 1979; 2: 950.
M W Gillman, et al. Inverse association of dietary fat with development of ischemic stroke in men. JAMA 1997; 278: 2145.
Multiple Risk Factor Intervention Trial. J A M A . 1982; 248: 1465.
A B Nichols, et al. Daily nutritional intake and serum lipid levels: The Tecumseh Study. Am J Clin Nutr . 1976; 29: 1384.
World Health Organisation. European Collaborative Group. Multi-factorial trial in the prevention of coronary heart disease: 3. Incidence and mortality results. Eur Heart J . 1983; 4: 141
J T Salonen, et al. Changes in morbidity and mortality during comprehensive community programme to control cardiovascular diseases during 1972-1977 in North Karelia. BMJ. 1979; iv: 1178.
P Puska. The North Karelia Project: a community based programme for the prevention of heart and vascular disease. Duodecim (Helsinki). 1985; 101(23): 2281.
Lipid Research Clinic Programme. LRC-CPPT results. Reduction in incidence of coronary heart disease. J A M A. 1984; 251: 351.
V Ravnskov. Cholesterol lowering trials in coronary heart disease: frequency of citation and outcome. BMJ 1992; 305: 15.
W A Gortner. Nutrition in the United States, 1900 to 1974. Cancer Res. 1975; 35: 3246.
D J P Barker, C Osmond. Diet and coronary heart disease in England and Wales during and after the Second World War. J Epidemiol Com Hlth. 1986; 40: 37
P M McKeigne, G P Miller and M G Marmot. Coronary heart disease in South Asians overseas: A review. J Clin Epidemiol. 1989; 42(7): 597.
M G Marmot. Interpretation of Trends in Coronary Heart Disease Mortality. Acta Med Scand . 1985 (Suppl); 701: 58.
R Beaglehole, et al. Cholesterol and mortality in New Zealand Maoris. BMJ. 1980; 1: 285.
E H Ahrens. Dietary fats and coronary heart disease: unfinished business. Lancet . 1979; 2: 1345.
J Dedichen. Cholesterol and arteriosclerosis again. Are we on the wrong track? T Norske Laegeforen. 1976; 16: 915.
M L Pearce, S Dayton. Incidence of cancer in men on a diet high in polyunsaturated fat. Lancet . 1971; 1: 464.
A F Hofmann, T C Northfield, J L Thistle. Can a cholesterol-lowering diet cause gallstones? New Eng J Med . 1973; 288 (1): 46.
W C Willett, et al. Intake of trans fatty acids and risk of coronary heart disease among women. Lancet 1993; 341: 581.
K K Carroll. Dietary fats and cancer. Am J Clin Nutr 1991; 53: 1064S.
T France, P Brown. Test-tube cancers raise doubts over fats. New Scientist , 7 December 1991, p 12.
R Kearney. Promotion and prevention of tumour growth -effects of endotoxin, inflammation and dietary lipids. Int Clin Nutr Rev 1987; 7: 157.
P R Uldall, et al. Lancet 1974; ii: 514.
M Balter. Europe: as many cancers as cuisines. Science 1991; 254: 114
H K Koh. Cutaneous melanoma. N Eng J Med 1991; 325: 171.
R MacKie, J A A Hunter, et al. Cutaneous malignant melanoma, Scotland, 1979-89. Lancet 1992; 339: 971.
H Takematsu, et al. Melanoma in Japan: experience at Tohoku University Hospital Sendai . In: C M Balch, G W Milton, eds. Cutaneous Melanoma . Philadelphia: Lippincott, 1984: 499.
G A Rose, et al. Corn oil in treatment of ischaemic heart disease. BMJ 1965; 1: 1531-33.
A Wolk, et al. A Prospective Study of Association of Monounsaturated Fat and Other Types of Fat With Risk of Breast Cancer. Arch Intern Med . 1998; 158: 41-45
C Ip, J A Scimeca, Thompson H. Effect of timing and duration of dietary conjugated linoleic acid on mammary cancer prevention. Nutr Cancer. 1995; 24: 241.
C desBordes, MA Lea. Effects of C18 fatty acid isomers on DNA synthesis in hepatoma and breast cancer cells. Anticancer-Res . 1995; 15: 2017-21Part 3: The Bran Wagon
The tragedy of science is the slaying of a beautiful hypothesis by an ugly fact. T H Huxley
The belief that regular bowel movement is important for health is very ancient. But the present theory is based on Dr. Dennis Burkitt's discovery that relatively few rural black Africans suffer from cancer of the colon. He attributed this to their relatively crude diet.
The theory was that, as fibre made food travel through the gut faster, it allowed less time for cancer-inducing agents to form. This, of course, presupposed that food became carcinogenic in the gut and there was no evidence that it did. Neither was there any evidence that moving food through the intestine at a faster rate decreased the risk of colon cancer. Moreover, the rural Africans' lifestyle was far from that of the Western city dweller: their diet is different, but also they were not exposed to so many pollutants, toxins or mental stresses. Indeed, there were many factors that could have been responsible for a difference in disease patterns. Other communities - the Mormons of Utah, for example - also enjoyed a low incidence of colon cancer yet they ate a low-fibre diet.
So the theory was unsubstantiated at the time and it was to be disproved in practice later as the rural Africans moved into towns and adopted a Western style low fibre diet. Their incidence of colon cancer has remained low and this has continued with the second generation. Nevertheless, these later findings were not publicised. Burkitt's theories caught the attention of the media. Always ready to exploit a good story, they expanded what was at best a very weak hypothesis into a treatment dogma that teaches that fibre is a panacea for all manner of illnesses.
Commercial interests were quick to see the potential in the recommendation and jump on the bran wagon. Burkitt's recommendation was based on vegetable fibre, but bran (cereal fibre) has a far higher fibre content and bran was a practically worthless by-product of the milling process that, until then, had been thrown away. Almost overnight, it became a highly priced profit maker. Although totally inedible, backed by Burkitt's fibre hypothesis, bran could now be promoted as a valuable food. But Dr. Hugh Trowell, Burkitt's partner and another strong advocate of dietary fibre, stated in 1974 that:
"A serious confusion of thought is produced by referring to the dietary fibre hypothesis as the bran hypothesis, for many Africans do not consume cereal or bran"
Fibre and coronary
Fibre and other diseases.
Moreover, there is no direct evidence that an increase of fibre by itself will prevent or cure the other diseases. With respect to colon cancer, Burkitt's theory was questioned with the suggestion that the low cancer rates in rural Africans may be due to their high early death rates from other causes, so that they do not reach the age at which cancer peaks in Europeans. As the Africans' life expectancy was only forty years at the time Burkitt did his research and Western cancers don't peak until the age of sixty-five, one wonders why this wasn't noticed before.
There is also a growing scepticism in the USA that lack of fibre causes cancer; some studies even suggesting that a fibre-enhanced diet increases the risk of colon cancer.
Other adverse effects
These findings are a cause for concern in several sections of the population who are at considerable risk from eating too much fibre - and bran fibre in particular:
1. The incidence of osteoporosis
(brittle bone disease) is increasing and now affects one in two post-menopausal
women, one in five of whom will die as a direct result. Osteoporosis is
also increasingly affecting men. Osteoporosis is caused by several factors,
but lack of calcium is the basic problem. Bran both inhibits the absorption
of calcium from food and depletes the body of the calcium it has. Moreover,
zinc, which bones need to heal, is another mineral whose absorption is
adversely affected by bran.
Because of the phytate, Professor David Southgate, arguably the world's leading authority on the effects of fibre, concludes that infants, children, young adolescents and pregnant women whose mineral needs are greater should be protected from excessive consumption of fibre.
Writing of the colon cancer risk, Drs. H. S. Wasan and R. A. Goodlad of the Imperial Cancer Research Fund stated in 1996:
"Until individual constituents of fibre have been shown to have, at the very least, a non-detrimental effect in prospective human trials, we urge that restraint should be shown in adding fibre supplements to foods, and that unsubstantiated health claims be restricted." . . . "Specific dietary fibre supplements, embraced as nutriceuticals or functional foods, are an unknown and potentially damaging way to influence modern dietary habits of the general population."
Until fibre can be shown not to be detrimental they suggest that
"restraint should be shown in adding fibre supplements to foods, and that unsubstantiated health claims should be restricted".
January 1999 saw the publication of the largest trial into the effects on fibre on colon cancer ever conducted. After studying 88,757 women for sixteen years, doctors at the Brigham and Women's Hospital and Harvard Medical School say that
"No significant association between fiber intake and the risk of colorectal adenoma was found." . . . "Our data do not support the existence of an important protective effect of dietary fiber against colorectal cancer or adenoma."
D P Burkitt, et al. Some geographical variations in disease patterns in East and Central Africa. E Afr Med J . 1963; 40: 1.
H C Trowell. Fibre and irritable bowels. BMJ. 1974; 3: 44.
- Dietary fibre, ischaemic heart disease and diabetes mellitus. Proc Nutr Soc. 1973; 32: 151.
C Y Francis, P J Whorwell. Bran and irritable bowel syndrome: time for reappraisal. Lancet 1994; 344: 39.
F Swain, et al. Comparison of the effects of oat bran and low-fiber wheat on serum lipoprotein levels and blood pressure. New Eng J Med. 1990; 322(3): 147.
W E Connor. Dietary fiber - nostrum or critical nutrient? New Eng J Med. 1990; 322 (3): 193.
E Marshall. Diet Advice, with a Grain of Salt and a Large Helping of Pepper. Science. 1986; 231: 537.
M J Lichtenstein, et al. Heart rate, employment status and prevalent ischaemic heart disease confound relationship between cereal fibre intake and blood pressure. J Epid Comm Hlth. 1986; 40(4): 330.
D Norman, et al. The impact of dietary fat and fibre on intestinal carcinogenesis. Prev Med. 1987; (4): 554.
I MacDonald. Nonsense and non-science in nutrition.. Proc Nutr Soc. 1983; 42: 513
Anon. BMJ . 1986; 292: 494.
J L Kelsay. A review of research on effect of fibre intake on man. Am J of Clin Nutr. 1978; (31): 142.
K Kaneko, et al. Effect of fibre on protein, fat and calcium digestibilities and fecal cholesterol excretion. J Nutr Sci Vitaminol (Tokyo). 1986; 32(3): 317.
D Kritchevsky. Fibre and cancer. In Dietary Fibre: Basic and Clinical Aspects. (G V Vahouny and D Kritchevsky eds.) p427. Plenum, NY. 1986.
- Dietary studies of cancer of the large bowel in the animal model . Ibid p469.
H S Wasan, R A Goodlad. Fiber-supplemented foods may damage your health. Lancet 1996; 348: 319-20.
C S Fuchs, et al. Dietary Fiber and the Risk of Colorectal Cancer and Adenoma in Women. N Eng J Med 1999; 340: 169.
G Gerutti, et al. Phytic acid in bran and in 'natural' foods. Bolletino Chimico Farmaceutico, Milan.
J Stevens, et al. Effect of psyllium gum and wheat bran on spontaneous energy intake. Am J Clin Nutr. 1987; 46: 812.
Editorial. The Bran Wagon. Lancet. 1987; i: 782.
Y P Suri. The Bran Wagon. Lancet. 1987; ii: 42.
G S Bindra and R S Gibson. Iron status of predominantly lacto-ovo-vegetarian East Indian immigrants to Canada: a model approach. Am J Clin Nutr. 1986; 44: 643.
J R Turnlund, et al. A stable isotope study of zinc absorption in young men: effects of phytate and alpha-cellulose. Am J Clin Nutr. 1984; 40: 1071.
B Sandstrom, et al. The effects of vegetables and beet fibre on the absorption of zinc in humans from composite meals. Br J Nutr. 1987; 58 (1): 49.
L Hallberg, et al. Phytates and the inhibitory effect of bran on iron absorption in man. Am J Clin Nutr. 1987; 45(5): 988.
R Balasubraminian, et al. Effect of wheat bran on bowel function and fecal calcium in older adults. J Am Coll Nutr . 1987; 6(3): 199.
J Hallfisch, et al. Mineral balances of men and women consuming high fibre diets with complex or simple carbohydrate. J Nutr . 1987; 117(2): 403.
Fractured neck of femur: prevention and management. A report of the Royal College of Physicians, London. 1989.
Editorial: Why so many fractured hips? Lancet. 1989; 1: 57.
A M Fehily. Dietary determinants of bone mass and fracture risk: a review. J Hum Nutr and Diet . 1989; 2: 299.
M J Wargovich, A R Baer. Basic and Clinical Investigations of Dietary Calcium in the Prevention of Colorectal Cancer. Prev Med. 1989; 18: 672.
BBC. Horizon: The Poison That Waits . BBC2 broadcast 16 Jan 1989.
N Bishop, M McGraw and N Ward. Aluminium in infant formulas. Lancet. 1989; i: 490.
B E Golden, M H N Golden. Plasma zinc, rate of weight gain and the energy cost of tissue deposition in children recovering from malnutrition on cows' milk or a soya protein based diet. Am J Clin Nutr . 1981; 34: 892.
A Prasad. The role of zinc in gastrointestinal and liver disease. Clin Gastroenterol. 1983; 12: 713.
P Aggett, N Davies. Some nutritional aspects of trace elements. J Inter Metab Dis. 1983; 6(2): 22.
M Hambidge. The role of zinc and other trace metals in paediatric nutrition and health. Paediat Clin N Am. 1977; 24: 95.
D Bryce-Smith, R Simpson. Anorexia, depression and zinc deficiency. Lancet. 1984; ii: 1162.
V Fonesca, C Harvard. Electrolyte disturbances and cardiac failure with hypomagnesaemia in anorexia nervosa. BMJ. 1985; 291: 1680
N Meadows, et al. Zinc and small babies. Lancet . 1981; ii: 1135.
D Bryce-Smith. Environmental chemical influences on behaviour and mentation. John Jeyes lecture. Chem Soc Rev. 1986; 15: 93.
A McMichael, et al. A prospective study of serial maternal zinc levels and pregnancy outcome. Early Human Development. 1982 (Elsevier); 7: 59.
D Addy. Happiness is: iron. BMJ. 1986; 292: 969
E M Luk'ianova. Diagnosis of vitamin D deficiency rickets. Pediatriia. 1988;(3):15.
R Adelman. Nutritional rickets. Am J Dis Child. 1988; 142(4): 414.
M R Clements. The problem of rickets in UK Asians. J Hum Nutr Diet , 1989; 2: 105.
R E Hughes. A new look at dietary fibre. Hum Nutr Clin Nutr. 1986; 40c: 81.
R E Hughes, E Johns. Apparent relation between dietary fibre and reproductive function in the female. Ann Hum Biol. 1985; 12: 325.
T Lloyd, et al. Inter-relationships of diet, athletic activity, menstrual status and bone density in collegiate women. Am J Clin Nutr. 1987; 46: 681.
D A T Southgate. Minerals, trace elements and potential hazards. Am J Clin Nutr. 1987; 45: 1256.
H S Wasan, R A Goodlad. Fiber-supplemented foods may damage your health. Lancet 1996; 348: 319-20.
C S Fuchs, et al. Dietary Fiber and the Risk of Colorectal Cancer and Adenoma in Women. N Eng J Med 1999; 340: 169.Part 4: The Dangers of Low Blood Cholesterol
Nature has taken good care that theory should have little effect on practice. Samuel Johnson
Low blood cholesterol and cancer
Countries with diets high in saturated fats also tend to have high levels of colon cancer. In 1974 a review of the Framingham data and those from Keys' 'Seven Countries' study was carried out. It was expected to show that the cancer could also be blamed on high blood cholesterol. However, the baffled researchers found the opposite: those with the cancer had cholesterol levels that were lower than average.
Reports of more than twenty studies into the relation between blood cholesterol and cancer have been published since 1972. Most have reported an association between low blood cholesterol and cancer. The authors of the Renfrew and Paisley Study conclude:
"it may be a mistake to assume that dietary advice given to the general population to reduce the intake of saturated fat will necessarily reduce overall mortality."
In a study from the USA published in 1990, changes in blood cholesterol over time were studied in patients with colon cancer. The doctors found that there had been an average thirteen percent decline in blood cholesterol levels in the ten years prior to diagnosis of the cancer compared with an average increase of two percent in the control group. Both those with the cancer and those free from it had similar blood cholesterol levels initially. It is possible that the decline in blood cholesterol levels was a result of the cancer, not the cause of it, but this is ruled out by the investigators. They compare cholesterol studies with apparently contrary findings and show that in reality they are consistent. Comparing those that reported normal or high cholesterol readings several years prior to diagnosis with others where, at the time of diagnosis, levels were low, they conclude that it was a long term lowering of blood cholesterol levels that gave rise to the cancers. Interestingly, the average blood cholesterol level of those who developed the cancers declined to an average 5.56 mmol/l and yet the British government's Health of the Nation strategy still aims to reduce everyone's levels to below 5.2 mmol/l.
Low cholesterol means
Over the past few decades, Japan has experienced a rapid change in its living and eating patterns. The Japanese are eating more total fat, saturated fatty acids and cholesterol, animal fats and protein, and less rice and vegetables. This has provided a unique opportunity for a large-scale, natural experiment into the effects of those changes.
Investigators have shown that this change to Western and urban eating patterns, departing as it does from centuries old traditions, has been accompanied by a general lowering of blood pressure and a large decline in the incidence of stroke deaths and cerebral haemorrhage between the 1960s and the 1980s. They attribute this decline to an increase in blood cholesterol levels over the period. Supporting their findings were the results of a follow-up of 350,000 men screened for the MRFIT in the United States that showed that the risk of death from cerebral haemorrhage in middle-aged men was six times greater if they had low blood cholesterol levels.
On Christmas Eve, 1997, yet one more study's results were headlined in the press. The Framingham researchers said that "Serum cholesterol level is not related to incidence of stroke . . ." and showed that for every three percent more energy from fat eaten, strokes would be cut by fifteen percent. They conclude:
"Intakes of fat and type of fat were not related to the incidence of the combined outcome of all cardiovascular diseases or to total or cardiovascular mortality."
So, after forty-nine years of research, they are still saying that there is no relation between a fatty diet and heart disease. The evidence now is clear and unequivocal: animal fats are not harmful.
Two more studies, which considered total blood cholesterol levels and mortality in the elderly, were published in the Lancet almost simultaneously in 1997. In the first, scientists working at the Leiden University Medical Centre found that
"each 1 mmol/l increase in total cholesterol corresponded to a 15% decrease in mortality".
Similarly, doctors at Reykjavik Hospital and Heart Preventive Clinic in Iceland noted that the major epidemiological studies had not included the elderly. They too studied total mortality and blood cholesterol in the over 80s to show that men with blood cholesterol levels over 6.5 had less than half the mortality of those whose cholesterol level was around the 5.2 we are told is "healthy".
Low cholesterol and
And at the other end
Low blood cholesterol,
aggressive behaviour and suicide
In institutions, aggressive people and those with antisocial personality have been found to have lower blood cholesterol levels than normal: Typically 5.04mmol/l vs 6.02mmol/l. Mental patients with high blood cholesterol (7.55mmol/l) were less regressed and withdrawn than those with lower (4.80mmol/l).
Dr Matthew G Dunnigan of Stobhill General Hospital, Glasgow, concludes that:
"Without definite data on all-cause mortality and with current unresolved concerns about excess deaths from non-cardiac causes in RCTs, decisions to embark on lifelong lipid lowering drug treatment in most patients with primary hypercholesterolaemia depend on the doctor's interpretation of available evidence. As in other situations in which certainty is illusory, this varies from evangelical enthusiasm for lowering lipid concentrations to therapeutic nihilism."
F Cambien, et al. Total serum cholesterol and cancer mortality in a middle aged male population. Am J Epid . 1980; 112: 388.
M R Garcia-Palmieri, et al. An apparent inverse relation- ship between serum cholesterol and cancer mortality in Puerto Rico. Am J Epid. 1981; 114: 29.
D Kozarevic, et al. Serum cholesterol and mortality: the Yugoslavian cardiovascular diseases study. Am J Epid . 1981; 114: 21.
R A Hiatt, B H Fireman. Serum cholesterol and the incidence of cancer in a large cohort. J Chronic Dis . 1986; 39: 861.
A Schatzkin, et al. Serum cholesterol and cancer in the NHANES I epidemiologic follow up study. Lancet. 1987; ii: 298.
A Kagan, et al. Serum cholesterol and mortality in a Japanese-American population: the Honolulu heart program. Am J Epid. 1981; 114: 11.
C G Isles, et al. Plasma cholesterol, coronary heart disease and cancer in the Renfrew and Paisley survey. BMJ. 1989; 298: 920.
S J Winawer, et al. Declining Serum Cholesterol Levels Prior to Diagnosis of Colon Cancer. JAMA . 1990; 263 (15): 2083.
Takashi Shimamoto, et al. Trends for Coronary Heart Disease and Stroke and Their Risk Factors in Japan. Circulation . 1989; 3: 503.
M W Gillman, et al. Inverse association of dietary fat with development of ischemic stroke in men. JAMA 1997; 278: 2145.
AWE Weverling-Rijnsburger, et al. Total cholesterol and risk of mortality in the oldest old. Lancet 1997; 350: 1119-23.
A Jonsson, H Sigvaldason, N Sigfusson. Total cholesterol and mortality after age 80 years. Lancet . 1997; 350: 1778-9.
J Foreman. Cholesterol curb urged for children over 2. The Boston Globe 9 April 1991: 1, 4.
Child mortality under age 5 per 1,000. 1992 Britannia Book of the Year. Encyclopaedia Britannica, Chicago.
F M Corrigan, et al. Dietary supplementation with zinc sulphate, sodium selenite and fatty acids in early dementia of Alzheimer’s Type II: Effects on lipids. J Nutr Med 1991; 2: 265-71.
H Engleberg . Low serum cholesterol and suicide. Lancet 1992; 339: 727-9
Modai I, Valevski A, Dror S, Weizman A. Serum cholesterol levels and suicidal tendencies in psychiatric inpatients. J Clin Psychiatry 1994; 55:6; 252-4
Dursun SM, Burke JG, Reveley MA. Low serum cholesterol and depression. Br Med J 1994; 309: 273-4.
MG Dunnigan. The problem with cholesterol: No light at the end of this tunnel? Br Med J 1993; 306: 1355-6.
Part 5: Cholesterol-Lowering
Although it became clear that a change in diet had little effect on CHD, that did not end the scientists' efforts to demonstrate that CHD could be prevented. If diet couldn't do it, then intervention with drugs would provide the evidence. And since drugs could be controlled much more strictly, and used in conjunction with placebos, the findings would be more demonstrable. But the drugs used to reduce blood cholesterol have all proved to be something of a disaster.
Launched on the public in 1961, Triparanol causes the levels of blood cholesterol to fall by inhibiting the liver's ability to make cholesterol. Two years later it was with- drawn because of serious side effects. Luckily for triparanol's manufacturers, a public scandal was avoided as the media's attentions were focussed on another drug marketed at the same time and by the same company - thalidomide.
More recently, a number of other drugs have been the subject of extensive and expensive trials. First was Cholestyramine (Questran) which reduces cholesterol by interfering with digestion. The gall bladder manufactures bile acid from cholesterol, and the bile acid is used in the intestine to digest fats. But when the drug is present in the gut, it binds with the bile acid, removing it from its normal function. Because the drug is indigestible, it, together with the bile acid, is excreted and the gall bladder has to make more by drawing cholesterol from the bloodstream.
As the trial would be very expensive, the scientists examined 480,000 men over a period of three years to find suitable subjects. They had to be men in the coronary age group and with extremely high blood cholesterol levels. As such men are in the most vulnerable group, their chances of success were greatly increased.
The investigators confidently announced in advance that blood cholesterol levels would be lowered by an average of 28% and, after seven years, coronary heart disease would be reduced by 50% in the treatment group.
At the end of the trial, however, cholesterol levels had fallen by less than a quarter of that called for at the start and heart disease rates were hardly affected. The $142 million trial was a total flop. Even if it had proved a success, however, those participating were so unrepresentative of the population that the question of its efficacy for the typical adult would still have remained. Another flaw that became apparent was an increase in the incidence of oral-gastro-intestinal cancers which could not be dismissed as a random chance. In the Lipid Research Clinics trial there were 21 cases and 8 deaths from gastrointestinal cancer in those taking the drug, compared to 11 cases and just 1 death in the control group.
Other organisations tested other drugs. The World Health Organisation sponsored its own trial with Clofibrate (Atromid). This too was targeted against cholesterol and was confidently expected to lower blood cholesterol levels by 30%.
As with cholestyramine, the
levels were lowered by much less than the expected amount and at the end
of the trial it became clear that there had been many more deaths in the
group taking clofibrate than in the control group - notably from gallstones,
and cancer of the liver and digestive system. In the WHO clofibrate trial,
as Table IV demonstrates, the drug killed more than it saved.
Among other drugs to be tested were:
a. The female hormone Oestrogen on the theory that if premenopausal women did not get heart disease, perhaps oestrogen would protect men. But the hormone caused heart attacks rather than preventing them.
b. The hormone Dextrothyroxine , which lowers cholesterol levels, abandoned quickly when an increase in mortality was noticed in the treatment group.
c. The vitamin Niacin, which looked promising, but although there appeared to be a reduction in non-fatal heart attacks, there were marked side effects: skin disorders such as darkening, itches and rashes, as well as digestive problems and gout.
d. Gemfibrozil (Lopid) was tested and again an increase in deaths was noticed in the treatment group although this time the numbers did not reach statistical significance.
e. Compactin which worked in a similar way to triparanol was withdrawn hurriedly and in some secrecy. The reason this time appears to be connected with cancer in dogs.
f. Lastly, despite the previous experiences with triparanol and compactin, yet another inhibitor, Lovastatin, has been approved for lifetime use on the general public after tests of very short duration only. (Derivatives pravastatin and simvastatin are marketed as Lipostat and Zocor.)
A study of all trials into cholesterol lowering by drugs up to 1987 showed an increase in mortality in those treated with drugs of 13.6%.
In 1993 a meta-analysis of all randomised controlled trials of cholesterol-lowering treatments showed that only those with very high risk showed any evidence of benefit. In all others mortality was increased. Its authors conclude that:
"Currently evaluated cholesterol-lowering drugs seem to produce mortality benefits in only a small proportion of patients at very high risk of death from coronary heart disease . . . a cautious approach to the use of cholesterol lowering drugs should be advocated".
Despite this, nearly eight times as many prescriptions for cholesterol-lowering drugs were being issued just 6 years later!
Lipid Research Clinics Coronary Primary Prevention Trial: I. Reduction in incidence of coronary heart disease. II. The relationship of reduction in incidence of coronary heart disease to cholesterol lowering. J A M A. 1984; 251: 351.
Committee of Principle Investigators: World Health Organization co-operative trial on primary prevention of ischaemic heart disease using clofibrate to lower serum cholesterol: the final mortality follow up. Lancet. 1984; ii: 379.
M H Frick, et al. Helsinki Heart Study: primary prevention trial with gemfibrozil in middle aged men with dyslipidemia. New Eng J Med. 1987; 317: 1237.
Coronary Drug Project Research Group: Gall bladder disease as a side effect of drugs influencing lipid metabolism. New Eng J Med. 1977; 296: 1185.
M N G Dukes. Drugs affecting lipid metabolism. in: Meyler's Side Effects of Drugs , Ninth Edition. M N G Dukes ed. Excerpta Medica, Amsterdam, 1980.
S Yusuf, J Cutler. Single factor trials: drug studies. in A G Olsson, ed. Atherosclerosis. Edinburgh: Churchill-Livingstone, 1987: 389.
G Davey Smith, F Song, TA Sheldon. Cholesterol lowering and mortality: the importance of considering initial level of risk. BMJ 1993; 306: 1367.BACK TO BAD MEDICINE
Dianne Jacobs Thompson Est. 2003
Also http://legaljustice4john.com The Misdiagnosis of "Shaken Baby Syndrome" --an unproven theory without scientific support, now in disrepute and wreaking legal and medical havoc world-wide
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