Uffe Ravnskov, a Swedish doctor, wrote a paper titled “Is atherosclerosis caused by high cholesterol?” (An admirably clear title.) His answer was no. He submitted it to a medical journal. One of his empirical points was that there was no relationship between cholesterol level and atherosclerosis growth. One reviewer commented:
Lack of relationship can be explained by more factors that only absence of it: small numbers, incorrect or indirect measurements of variables of interest, imprecision in measurement, confounding factors, etc.
To which Ravnskov replied:
If it is impossible to find exposure-response between changes of blood cholesterol and atherosclerosis growth in 22 studies including almost 2500 individuals a relationship between the two, if any, must be trivial.
Which sounds reasonable. But an even larger number of clinical trials failed to find clear evidence that omega-3 supplementation reduces heart disease. Yet I am sure that, with a large enough dose, it does.
Most people believe clinical trials, which are usually double-blind when possible and placebo-controlled. “The gold standard,” they are called. Science writer Gary Taubes, for example, believes them: When the results of a clinical trial contradicted a survey result, he believed the clinical trial. His recent NY Times magazine article was based on the assumption that clinical trials are trustworthy. This is such an article of faith that he gave no evidence for it.
That the heart disease clinical trials failed to clearly show benefits of omega-3 supplementation had large and unfortunate consequences. Not only because heart disease is the leading cause of death in many places, including America, but also because I am sure proper omega-3 supplementation would reduce many other problems, including falls, memory loss, gum disease, and other diseases of too much inflammation.
I don’t know why the big clinical trials failed to point clearly in the right direction. I can think of several possibilities:
1. Too large. Hard to control quality — verify data, for example. People near the bottom doing the work have little stake in accuracy of the outcome.
2. Poor compliance. If you are taking the placebo, why bother? And the odds are fifty-fifty you are. Lots of people have trouble following SLD, which obviously works.
3. Degradation. My belief that omega-3 is powerful comes from experiments (mine) and examples involving flaxseed oil. Flax grows at room temperature. The heart disease studies used fish oil; fish live in cold water. The omega-3 fats in fish oil may degrade at room temperature. The omega-3 fat in flaxseed oil may be far more stable at room temperature.
4. Wrong dose. Self-experimentation made it easy for me to figure out the correct dosage. People studying heart disease had no similar data to guide them. They could not realistically expect people to consume as much fish oil as the Eskimos whose rate of heart disease was so low.
5. Too sure. Self-experimentation encourages skepticism about one’s results because new experiments are easy to do. If I can think of reasons to doubt my results so far, that’s a good excuse for a new experiment. The more experiments the better. Each one is easy; I just need a good story line, a good reason for each one. Whereas if you are doing an experiment that cannot be repeated, any skepticism about it — e.g., about accuracy of measurements — is discouraged: It would cast doubt on the whole enterprise.
There’s lots of evidence for the link between cholesterol and heart attacks. For example, heart attacks are virtually unknown in those people with a cholesterol level of 150 or below. Epidemiological evidence is strong: Third World nations that eat a traditional diet have low cholesterol levels and no heart attacks. And I wouldn’t think that all of them necessarily have lots of omega-3 in their diets; the common factor is that they eat little fat, especially saturated fat.
Malcolm Kendrick reviews briefly some data from the WHO MONICA (Multinational MONItoring of trends and determinants in CArdiovascular disease) Project* here:
https://www.youtube.com/watch?v=i8SSCNaaDcE
These figures don’t seem to support the conclusion that high cholesterol is linked to cardiovascular disease.
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* https://www.ktl.fi/monica/index.html
Interesting video. However, “The Framingham Heart Study established that high blood cholesterol is a risk factor for coronary heart disease (CHD). Results of the Framingham study showed that the higher the cholesterol level, the greater the CHD risk. On the other end of the spectrum, CHD is uncommon at total cholesterol levels below 150 milligrams per deciliter (mg/dL). A direct link between high blood cholesterol and CHD has been confirmed by the Lipid Research Clinics-Coronary Primary Prevention Trial (1984) which showed that lowering total and LDL (“bad”) cholesterol levels significantly reduces CHD. A series of more recent trials of cholesterol lowering using statin drugs have demonstrated conclusively that lowering total cholesterol and LDL-cholesterol reduces the chance of having a heart attack, needing bypass surgery or angioplasty, and dying of CHD-related causes.” https://www.nhlbisupport.com/chd1/why.htm
Dennis, thanks for the additional info. I don’t have an opinion on this. However, the cross-country epidemiology certainly doesn’t support the idea that high cholesterol causes heart attacks. In the MONICA study, two countries — China and Japan — had very low values of both heart disease and cholesterol. The other countries had higher values of both measures; but within this group there appears to be no correlation. So essentially you have a two-point scatter plot. Such plots of course tell you nothing about strength of correlation.
Dennis, the Framingham study proves nothing of the kind. Here is an ACTUAL QUOTEfrom the study:
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There is no indication of a relationship between dietary cholesterol and serum cholesterol level. If the intake on animal fat is held constant there is still no relation of cholesterol intake to serum cholesterol level. If (further) a multiple regression is calculated [using animal fat and dietary cholesterol] there is also little suggestion of an association between this pair of variables and serum cholesterol level.
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In the period between the taking of the diet interviews and the end of the 16-year follow-up, 47 cases of de novo CHD developed in the Diet Study group. The means for all the diet variables measured were practically the same for these cases as for the original cohort at risk. There is, in short, no suggestion of any relation between diet and the subsequent development of CHD in the study group…
Very interesting, Tom.
Tom: You could at least provide a link. Anyway, your first post says that dietary cholesterol doesn’t correlate with serum cholesterol, and that animal fat doesn’t either, which I have a hard time believing. In any case, it’s serum cholesterol (and other things too) that causes heart disease. Your second post says that diet wasn’t a factor in the development of heart disease. However, all the study participants were very likely eating very similar diets, with none of them eating an actual low-fat (10% of calories), high-fiber diet. People who eat these latter type of diet, whether here or in Third World countries, don’t get heart disease.
Here are a few items from the Framingham Heart Study homepage. https://www.nhlbi.nih.gov/about/framingham/timeline.htm
“1961 Cholesterol level, blood pressure, and electrocardiogram abnormalities found to increase the risk of heart disease
1987 High blood cholesterol levels found to correlate directly with risk of death in young men
1988 High levels of HDL cholesterol found to reduce risk of death
1990 Homocysteine (an amino acid) found as possible risk factor for heart disease [The significance of this is that homocysteine levels are diet-related; specifically, eating meat raises serum homocysteine.]
1997 Report on the cumulative effects of smoking and high cholesterol on the risk for atherosclerosis”
Obviously, research is ongoing. But to dismiss diet and cholesterol as causes of heart disease goes against everything we know.
Well, the MONICA data I described show that cholesterol levels — at the population level — predict nothing. China and Japan are obviously different from European countries in dozens of ways; that they havelower heart disease AND lower cholesterol means almost nothing. Then there are all the other countries where there is no correlation. As I said I haven’t studied the matter enough to have an opinion. But the data I do know about imply that the answer is not obvious and that the effect, if any, must be small relative to other causes. One view is that high cholesterol is caused by inflammation, which also causes heart disease.
The Framingham Heart Study originally showed a strong but non-significant trend. I can’t speak to any results after the early 1960′s, but I remember being struck by the graphs showing lowest overall mortality for women with cholesterol between 220 and 260.
But to dismiss diet and cholesterol as causes of heart disease goes against everything we know.
Exactly. Paul Ewald, for one, has been challenging the medical status quo as to the root causes of various diseases and ailments. I strongly recommend his book Plague Time: The New Germ Theory of Disease.
Something to think about – infection as a root cause of heart disease, not cholesterol:
Infection is a key source of inflammation, hence the association between heart and periodontal disease.
Another important reason to keep drinking your flax oil!
Also the omega-3 studies didn’t lower omega-6 consumption, which is important since omega-6 competes with omega-3 in the body. Too much 6 will drown the three out. The letters following the omega-3 studies have a lot of interesting info about this problem.
here is a Framingham link:
Castelli; Archives of Internal Medicine; July 1992: 152;1371-1372
no correlation of CHD and cholesterol