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Cholesterol Heart Disease HDL LDL Fat


This Cholesterol Nonsense


Michael Sellar

"Frankly, the recommendation of the American Heart Association, government health agencies, and the media, — that people switch from saturated fats to polyunsaturated vegetable oils — has probably killed and crippled more Americans than both World Wars.” Former brain surgeon Russell Blaylock MD

The cholesterol campaign is “the greatest scientific deception of this century, perhaps of any century.” Physician and scientist George Mann

“The public is so brainwashed, that many people believe that the lower your cholesterol, the healthier you will be or the longer you will live. Nothing could be further from the truth.” Paul Rosch MD FACP “

..if you have come to believe you can ward off death from heart disease by altering the amount of cholesterol in your blood, whether by diet or by drugs, you are following a regime that has no basis in fact.” Edward Pinckney MD former co-editor of the Journal of the American Medical Association

“The current campaign to convince every American to change his or her diet, and in many cases to initiate drug ‘therapy’ for life is based on fabrications, erroneous interpretations and/or gross exaggerations of findings and, very importantly, the ignoring of massive amounts of unsupportive data.” Russell Smith MD

“Scientific evidence for the role of dietary fat and hypercholesterolemia in the causation of atherosclerosis is seriously lacking.” Professor and scientist William Stehbens MD

This article is based on the book Fat and Cholesterol are GOOD for You! by Uffe Ravnskov MD, PhD (2009).

It’s remarkable when you come to think about it how a substance so vital to the body that it is produced in large amounts by the liver, should have gained such a poor reputation. Instead of extolling its virtues, it is regarded in a negative light. It is thought to be the cause of heart disease. If we can only keep blood levels down, all will be well.

Routine blood tests will always include cholesterol and if it is higher than is deemed normal then dietary recommendations will be made in order to lower it or drugs will be prescribed. The doctor will actually believe he or she is doing something of value for their patient, helping to prevent them from the biggest disease killer, coronary heart disease (CHD). How did this situation come about?

Ancel Keys’ Dodgy Graph

It was in 1953 that Ancel Keys wrote that “it is a fact that a major characteristic of the sclerotic artery is the presence of abnormal amounts of cholesterol in that artery.” He went on to say “This cholesterol is derived from the blood.” The proof for this, the science behind it, was not discussed. And the reason for this high blood cholesterol, according to Keys was because of the amount of fat in the diet. He believed at that time that all fat was unhealthy.

He demonstrated quite clearly that in countries that eat a lot of fat (calculated from domestic fat production figures), their blood cholesterol is high. Where they eat little fat, it is low. He did this with a graph showing 6 countries with different fat consumption. In Japan the death rate from heart disease was low. As fat consumption increased in the different countries so did the death rate, with the USA at the top of the fat consumption death rate curve. It was published in The Lancet who wrote “the curve shows an almost convincing relationship between the fat content of the food and the risk of dying from coronary heart disease.”

But why did Keys use data from only 6 countries when data was available from 22 countries? If you plot all 22 countries on the map, guess what happens? The association disappears. Some countries that eat a lot of fat have low levels of heart disease. There can be large differences in fat consumption with the same death rate. Or large differences in the death rate with the same fat consumption. For instance the death rate in Finland was seven times that of Mexico with the same fat consumption.

Data Collection Problems

There are also a number of problems with this kind of data. Firstly the sum of fat produced in each country is not a reliable indicator for how much is consumed. How much was never delivered to consumers? How much was thrown away? How much was eaten by vermin? How much eaten by animals and pets? Richer countries are likely to be more wasteful than poorer ones. Secondly, how do we know that these people died from heart disease? Studies show that one in three death certificates have the wrong diagnosis. Even post-mortems are not totally reliable.

The Strange Case of Crete & Corfu

Keys published another study in 1970 where he concluded that the factor most likely to predict heart attacks was the amount of animal fat eaten. What Keys failed to do was look at his own data from within each of these countries. In 2 very similar districts in Finland with the same fat consumption, heart mortality was three times greater than the other. Similarly for Crete and Corfu. With the same fat consumption Corfu had sixteen times the heart mortality of Crete. Keys barely alluded to this.

The Masai & Samburu

Research carried out by other scientists show a different picture. In the 1960’s professor George Mann and his team travelled to Kenya to study the Masai who eat nothing but milk, blood and meat. He found that they do not die of heart disease and have amongst the lowest levels of blood cholesterol ever measured in the world. Keys was not interested in this finding and thought it to be of no relevance, though he didn’t explain why.

One person who did provide an explanation was Dr Bruce Taylor who carried out his own expedition to Kenya. According to Taylor, the Masai are an isolated tribe and so their low cholesterol is built into their genes. This however is not true. The Masai are not isolated and so their genes are renewed continuously. If it was present in the genes then the Masai that moved into a big city should still have had low blood cholesterol but in fact it was much higher than the Masai tribesmen.

And the Masai are not alone. Further north are the Samburu. The younger men only consume animal food. They may drink over a gallon of milk a day and occasionally orgy on up to 10 pounds of meat each per day. If the cholesterol heart disease idea was valid these too should be collapsing with heart attacks. But they don’t. Proponents of the cholesterol hypothesis could maintain that regardless of their diet, their low blood cholesterol is what protects them from heart disease. However even this is not true.

Autopsies were carried out on a large number of Masai of all ages. It was found that they had just as much if not more atherosclerosis than Americans, but with one major difference. Their atheroslerosis was seen inside the vessel walls. Raised lesions on the inner surface of the arteries were rare, they remained smooth. They didn’t experience the severe changes seen in Americans. So although the Masai technically had heart disease, it didn’t affect them. It was speculated that their incredible physical fitness and resulting much wider coronary arteries protected them.

Other Population Studies

Staying with Kenya, a comparison between high saturated fat eating Muslim Indian’s and low saturated fat eating non Muslim Indians who emigrated to Africa found that the mortality rate from coronary heart disease was the same.

Another interesting study was published in 1967. This involved a million male employees of the Indian railways. Over a 5 year period, seven times more died of a heart attack in Madras than in Punjab and were on average 12 years younger. Yet the men of Punjab ate almost 18 times more fat, mostly of animal origin.

There have been over two dozen case controlled and cohort studies that compare people with and without heart disease. In virtually every study there is no difference in the amount of saturated fat and cholesterol eaten between those that have or don’t have heart disease.

As long ago as 1936 a study of people who died violently found no association between blood cholesterol and the degree of atherosclerosis. A similar study was carried out in 1961 with the same result.

800 war veterans were followed for many years. Autopsy findings found those with low cholesterol were just as atherosclerotic as those with high cholesterol.

The Framingham Study

The medical profession are totally convinced that high cholesterol causes heart disease. This doesn’t just come from Ancel Keys’ work.

The Framingham study began in the 1950’s and followed the lives of many of the citizens of this small Boston town. One of the cornerstones of the cholesterol campaign was the finding after the first five years that high cholesterol predicted a greater risk of heart attack.

But after 30 years a different picture emerged. It was found that for men over 47, their cholesterol levels made no difference.

After this age, whatever the cholesterol level, it made no difference to life expectancy. Yet 95% of heart attacks occur in people over this age. Atherosclerosis and heart disease make their appearance usually in older age groups. How can cholesterol be a risk factor for the young when little or no cholesterol is present in the arteries but not in older groups where it is present and accelerating?

The Framingham results get even more interesting. It was found that over the 30 years, those people whose cholesterol had decreased by itself were at a greater risk of dying than those whose cholesterol had increased. To quote the study: “for each 1% mg/dl drop of cholesterol there was an 11% increase in coronary and total mortality.”

A reasonable person might have thought that finding would have put an end to this cholesterol nonsense. But of course that’s not how it is in the real world. Generally whenever Framingham gets a mention, it is done to support the cholesterol hypothesis. For instance the American Heart Association and National Heart Lung and Blood Institute put out a joint statement saying: “The results of the Framingham Study indicate that a 1% reduction...of cholesterol [corresponds to a] 2% reduction in CHD risk.”

The study authors themselves put out a statement saying: “The most important finding is the emergence of the total cholesterol concentration as a risk factor for CHD in the elderly.”

MRFIT - Not Fit For Purpose

The proponents of the cholesterol causes CHD belief have more than Keys and Framingham to ‘prove’ their case.

The Multiple Risk Factor Intervention Trial (MRFIT) measured cholesterol in more than 300,000 middle aged men over 6 years. It found that four times more men died of heart attack in the high cholesterol group compared to the low cholesterol group. Four times more. The risk of dying with a cholesterol level above 265 (6.8) was 413% greater than with a level below 170 (4.4). Surely that’s game set and match for the cholesterol proponents. 413%. You can’t argue with that.

Well it’s not quite that simple. 98.7% of those with the highest cholesterol levels were still alive compared with 99.7% of those with the lowest levels. So the difference is 1%. To get the 413% figure, you take the percentage dying in the high cholesterol group - 1.3% and divide it by the percentage dying in the low cholesterol group - 0.3%. That’s how statisticians get a big scary figure. However 1% is 1%. That is significant.

Well not exactly. Once you take out smokers from the calculations the difference becomes too trivial to mention. All the study showed was that smoking is a risk factor for heart disease. Isn’t that a surprise? So what was considered to be one of the greatest medical experiments in history doesn’t add up to very much at all.

Fat Consumption Over Time

Since cholesterol containing animal fat is supposed to play such an important role in heart disease, how does one explain the fact that consumption was stable or decreased throughout most to the twentieth century, yet heart disease exploded?

For instance the CHD death rate nearly quadrupled in Yugoslavia between 1955 - 1965 while their fat intake decreased by 25%. In England fat intake has been stable while heart attacks increased ten fold between 1930 - 1970.

Let’s Examine The Fat Cells Themselves

The trouble with many population studies is that they rely on questionnaires about peoples’ eating habits. These can never be totally reliable. One way of overcoming this is to look at the fat cells themselves. The more saturated fat is eaten the more short chain fatty acids are found in the cells. This analysis of the cells themselves is very reliable in determining our eating habits. Six such studies have looked to see if heart patients have more of these short chain fatty acids. In half the studies no difference was found. In the other half, there was a definite relationship. The heart patients had less of these fatty acids. Could it be that a high intake of fat protects against heart disease?

Let’s Look At The Arteries

Another type of study is to look at autopsies of people whose diet is known as with the Masai study. Three such studies have taken place. In each case the amount of saturated fat eaten was compared with the degree of atherosclerosis. No difference was found between those that avoided animal foods and those that gorged on it.

The International Atherosclerosis Project meticulously examined the arteries of 20,000 dead people from a number of countries. Again no association could be found.

Familial Hypercholesterolemia

Some people are born with this inborn error that gives them a high blood cholesterol and there is a very rare and more serious form called homozygous familial hypercholesterolemia. Such people are interesting to study.

3000 FH patients have been followed for many years. It was found that they live as long, if not longer than those without FH. It is true that more died from heart disease, but much less died from other diseases particularly cancer. The figures are actually even better than recorded because for the study, subjects were chosen who had a close relative who died at a young age, so their risk of a heart attack was quite high. The report authors suggested that if the subjects had been more representative of people with FH, the mortality rate would have been lower.

A Finnish study looked at 100 people with FH over a 17 year period, none of whom were taking cholesterol lowering drugs. 26 out of 30 died from heart attack. However two thirds of these were smokers.

Nobel prizes were given to Goldstein and Brown who studied those with FH. They stated that “the more LDL there is in the blood, the more rapidly atherosclerosis develops.” The very interesting finding of the Finnish study was that the initial LDL cholesterol was no different between those who had died and those that were still living. Research groups from 3 different countries came up with similar findings to the Finnish study. One of these found that those without heart disease had a higher LDL cholesterol.

Many with FH have circulatory problems in the legs. Yet a Dutch study found these problems were independent of their cholesterol levels.

An Italian study looked at ten people with the homozygous form. They wanted to see if they had signs of atherosclerosis in brain arteries. Even though half of them had heart disease, the brain arteries were normal. Not the finding one would expect if cholesterol is the cause of atherosclerosis.

An interesting aside from this study was that those with heart disease had a cholesterol level of 562 (14.5), those with no heart disease had a level of 694 (17.9). [Under 200 (5.2) is considered desirable]

Cholesterol or Clotting Factors?

There is no question that those with FH do have a higher rate of heart disease. So it seems reasonable to conclude that it is the high blood cholesterol that causes it. But these studies suggest that it isn’t. Also autopsies on young FH people found that though lesions could be seen in the arteries, they were not the same as seen in early atherosclerosis. So if cholesterol isn’t the problem, what can it be?

Genetic aberrations are more complex in those with FH than Goldstein and Brown had thought. Studies of people with FH have found they had problems with another gene that controls coagulation, so they have a tendency to produce too much prothrombin, fibrinogen and factor VIII. They form arterial clots more easily. The heart patients had more of these clotting factors but their total and LDL cholesterol did not differ from those with no heart disease. Other studies that lowered LDL cholesterol and raised HDL in those with FH either through surgical procedure or drugs found that it either made no difference or they were worse off. It’s quite clear from the research on those with FH that they have a higher susceptibility to clot formation. This is why they are more likely to have heart disease and to have it at an earlier age.

Cholesterol & Infections

Interestingly it was found that before 1900 those with FH lived longer than those without. Since people usually died of infectious diseases at that time, it was suggested that high cholesterol protects against infection.

15 years ago researchers found that low cholesterol predicted an increased risk of dying from diseases of the stomach, the guts and the lungs; diseases mostly caused by bacteria or viruses.

A fifteen year study of 100,000 healthy people found those who had low cholesterol at the start of the study were admitted more often to hospital because of an infectious disease.

Young men with a previous sexually transmitted diseases were twice as likely to test positive for HIV if they had low cholesterol compared to those with high cholesterol.

A study of 300,000 men over 16 years found that four times as many people died of AIDS in the low cholesterol group compared to the high cholesterol group.

An infectious process is believed to play a part in chronic heart failure. Several research groups have noted that patients with this condition live longer if their cholesterol is high.

The Wonder of LDL

Cholesterol LDL has been labelled ‘bad’ cholesterol as distinct from HDL, the ‘good’ type. The reality however is that LDL is an important member of our immune system. Laboratory experiments have shown that LDL is able to neutralise bacterial toxins. It was found that white blood cells were lower in those with low LDL cholesterol, so it may have a directly beneficial effect on the immune system, which is what the researchers suggested. Animals that had their LDL artificially lowered died much easier after being injected with bacterial toxins. But if they were injected with human LDL just before the bacterial assault, they survived. In a similar animal experiment, all the normal cholesterol group died, but most of the high cholesterol group survived.

High Cholesterol, The Elderly & Women

Old people with high cholesterol levels live longer. A 1994 study showed that old people with low cholesterol died twice as often from a heart attack as did those with high cholesterol.

Eleven studies of the elderly show that high cholesterol is not a risk factor for heart disease. A 1989 study found that women with an average age of 82 who had high cholesterol lived the longest. The optimum reading was 7.0. Those with very low cholesterol had five times the death rate. A 1997 study found “In people older than 85 years, high total cholesterol concentrations are associated with longevity owing to lower mortality from cancer and infection.” In fact women don’t have to worry about their cholesterol levels at all. Almost all studies found that cholesterol is not a risk factor for them.

A 1992 review of all the literature concluded that mortality was higher for women with low cholesterol than for women with high cholesterol.

Saturated Fat & The Risk Of ...

Since the narrowing of arteries also increases the risk of stroke, one would expect, under the cholesterol hypothesis, to see a relationship between saturated fat intake and stroke. At least ten studies have looked at this. Not a single study found stroke patients ate more saturated fat. In fact 7 of the 10 found they had eaten less. Could it be that a high intake of fat protects against stroke?

At least 14 studies have shown that high cholesterol is not a risk factor for those with diabetes. It is not a risk factor for those with kidney failure. It is not a risk factor for those with arterial disease of the legs. It is not important for those that have already had a heart attack.

Food Cholesterol & Blood Cholesterol

Even if one is convinced by the cholesterol propaganda to lower animal fat consumption, this won’t necessarily have any effect on blood cholesterol levels. Our cholesterol production is regulated internally according to our needs. A 2003 study put subjects on a low cholesterol diet for 2 weeks followed by a high cholesterol diet for two weeks. For some, cholesterol levels rose by 42%. For others it fell by 11%. Another study was carried out on the same people. They were put on a high cholesterol diet only for two weeks. This time there was little change in blood cholesterol across the whole group. The authors commented: “Quite a number of subjects who appeared hyper-responsive in one experiment proved to be hypo-responsive in another experiment.”

A Risky Future

Many decades of research have demonstrated that the cholesterol levels in the blood have little relationship to heart and circulatory health. If anything, high cholesterol is protective. The failure of lowering cholesterol with diet to bring about improvements in health have led to drug based therapies that lower cholesterol very effectively. Statins have become the new wonder drug. They certainly have a role, but only in a small percentage of heart patients. Their benefits have nothing to do with cholesterol lowering. These drugs have anti-inflammatory and blood thinning properties. To roll out these drugs to healthy people who happen to have high cholesterol is insane and will only lead to a great deal of misery in the years to come.

This article was first published in Enzyme Digest No 86, 2010

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