In last week’s article about the ineffectiveness of statin drugs in reducing mortality in most populations I promised I would follow-up with an article on drug-free prevention of heart disease. I will do that this week, but it occurred to me that the first article in this series should have been one that dispels the myth that cholesterol causes heart disease. Understanding that is the key to the prevention strategies that will follow in the next article. So without further ado…
You are all no doubt acquainted with the popular hypothesis on cholesterol and heart disease. It has two parts: first, that eating cholesterol in the diet raises cholesterol levels in the blood; and two, that high cholesterol levels in the blood cause heart disease.
You might be surprised to learn that neither of these statements is true. The first one is relatively easy to dispatch. In the Framingham Heart Study, which is the longest-running and perhaps most significant study on heart disease done to date, it was demonstrated that intake of cholesterol in the diet had absolutely no correlation with heart disease. If you look at the graph below, you’ll see that both men and women with above average intake of cholesterol had nearly identical rates of heart disease as men and women with below average intake of cholesterol.
In fact, the “diet-heart hypothesis”, which is the scientific name for the idea that eating cholesterol causes heart disease, has even been discounted by the researchers who were responsible for its genesis. Ancel Keys, who in many ways can be considered the “father” of the cholesterol-heart disease hypothesis, had this to say in 1997:
“There’s no connection whatsoever between the cholesterol in food and cholesterol in the blood. And we’ve known that all along. Cholesterol in the diet doesn’t matter at all unless you happen to be a chicken or a rabbit.”
This is a reference to early studies performed on chickens and rabbits where they force-fed these animals high-levels of cholesterol. Since rabbits and chickens are mostly vegetarian, their physiology is not adapted for processing such large amounts of dietary cholesterol, so it’s no surprise they developed atherosclerosis. The mistake was assuming that the results of this experiment could be extrapolated to humans, who are omnivores with significant differences in physiology.
The second tenet of the cholesterol-heart disease hypothesis, the notion that high cholesterol levels in the blood cause heart disease, is referred to as the “lipid hypothesis” in the scientific community. Though it still accepted as gospel truth by the general public and many medical professionals, most researchers now believe the primary causes of heart disease are inflammation and oxidative stress. Unfortunately, the rest of us haven’t gotten the memo, so to speak, that cholesterol isn’t the cause of heart disease.
It would take several articles to explain this in complete detail, but I’d like to give at least a brief summary here.
If cholesterol caused heart disease, it should be a risk factor in 1) all ages, 2) both sexes and 3) all populations around the world (barring any protective factor, of course). Also, if cholesterol caused heart disease we would expect that lowering cholesterol would reduce heart disease. But none of these assumptions turn out to be true.
The rate of heart disease in 65-year old men is ten times that of 45-year old men. Yet a recent study in the Journal of American Medical Association indicated that high LDL cholesterol is not a risk factor for from coronary heart disease (CHD) mortality or total mortality (death from any cause). It is extremely unlikely that a risk factor for a disease would stop being a risk factor at a time when that disease kills the greatest number of people. That is akin to suggesting that smoking causes lung cancer in young men, but somehow stops doing so in older men!
Another consistent thorn in the side of supporters of the “lipid hypothesis” is that women suffer 300% less heart disease than men, in spite of having higher average cholesterol levels. At the recent Conference on Low Blood Cholesterol, which reviewed 11 major studies including 125,000 women, it was determined that there was absolutely no relationship between total cholesterol levels and mortality from cardiovascular or any other causes.
Nor is cholesterol a risk factor in all populations around the world. In fact, some of the populations with the highest levels of blood cholesterol have among the lowest rates of heart disease, and vice versa. Dr. Malcom Kendrick, a well-known skeptic of the lipid-hypothesis, explains this very well in the video below:
Finally, more than 40 trials have been performed to determine whether lowering cholesterol levels can prevent heart disease. In some trials heart disease rates went down, in others they went up. But when the results of all of the trials were taken together, just as many people died in the treatment groups (who had their cholesterol levels lowered by drugs) as in the control groups (who had no treatment).
If you’re still skeptical after reading all of this, perhaps William Castelli, the director of the famed Framingham Heart Study mentioned above can convince you:
“Serum cholesterol is not a strong risk factor for CHD, in the sense that blood pressure is a strong risk factor for stroke or cigarette smoking is a risk factor for lung cancer.”
Or how about Frederick Stare, a long-time American Heart Association member and (former) proponent of the lipid hypothesis:
“The cholesterol factor is of minor importance as a risk factor in CVD. Of far more importance are smoking, hypertension, obesity, diabetes, insufficient physical activity, and stress.”
So there you have it. Contrary to popular belief, cholesterol is not a dangerous poison that causes heart disease. Rather, it is an essential nutrient present in the cell membranes of all tissues of all mammals, and has some very important functions in the body. In fact, in many studies low cholesterol has been associated with an increase in total mortality!
Again, the Framingham Study which followed 15,000 participants over three generations:
“There is a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years.”
In other words, as cholesterol fell death rates went up.
The Honolulu Heart Program study, with 8,000 participants, published in 2001:
“Long-term persistence of low cholesterol concentration actually increases the risk of death. Thus, the earlier the patients start to have lower cholesterol concentrations, the greater the risk of death.”
And finally, the huge Japanese Lipid Intervention Trial with over 47,000 participants:
“The highest death rate observed was among those with lowest cholesterol (under 160mg/dl); lowest death rate observed was with those whose cholesterol was between 200-259mg/dl”
In other words, those with the lowest cholesterol had the highest death rate, and those with cholesterol levels that would today be called “dangerous” had the lowest death rate.
As you can see, not only does high cholesterol not cause heart disease, low cholesterol can actually be dangerous to your health. So toss out your vegetable oil and start eating butter and eggs again! But more on that next week…
- Handouts from my recent public talk on cholesterol
- Dr. Uffe Ravnskov’s “The Cholesterol Myths”
- The International Network of Cholesterol Skeptics
Tags: attack, cardiovascular, cholesterol, coronary, featured
Also, the animal studies used oxidized cholesterol and they fed the animals vegetable oils high in PUFAs. They used fractionated processed cholesterol and PUFA vegetable oils. All of their conclusions should have been suspect, from the beginning. None of them have been proven in human studies with real food prepared in natural ways. Even animals don’t get atherosclerosis when fed non-oxidized cholesterol and saturated animal fats. Most studies feed animals refined sugar/grain and casein powder and assume the same thing will happen on a diet with natural foods.
T. Colin Campbell is the biggest proponent of this brand of junk science. He says that animal protein causes cancer, but his studies actually show that casein powder causes cancer, in the context of a diet of refined sugar, corn starch, and PUFA oils (like corn oil). That doesn’t show that a diet of natural foods causes cancer. It only shows that the diet he fed the animals caused cancer and it could be related to the other foods.
Campbell’s studies and conclusions are the most outrageous. Here is one of his studies, claiming that a high (animal) protein diet causes liver cancer. When you look at table 1 on page 2 of the pdf, you see that the animals got diets of powdered casein, fractionated methionine, table sugar, corn starch, and corn oil. He also exposed them to large doses of aflatoxin to initiate the cancers.
As Michael Eades would say, ‘the data shows what it shows,’ but it doesn’t show that natural animal protein would cause cancer (except in the context of sucrose, corn starch, corn oil, protein powders, and aflatoxin). Campbell and other vegan activists confuse correlation with causality when they look at epidemiological studies. They also tend to confuse ‘whole animal protein’ with fractionated powders and isolated amino acids, even though evidence clearly shows these two things are not the same.
I don’t think we can ignore all of the confounding variables in his study, like refined sugar, corn starch, corn oil, DL-methionine, cellulose, etc. Maybe the results would be different if the animals were fed natural animal foods, and saturated fats like butter, tallow, coconut oil, etc. We have to consider the interaction of variables in a study, nad how the results might be different if one food (sugar) was changed for another (comb honey).
I had a nutrition teacher in chiropractic school who told us that when the early animal studies on high cholesterol diets were conducted high concentrations of pufas were added to the animal feeds. He asserted that it was the high level of these and especially the trans fats that resulted in the higher levels of disease and the cholesterol.
corection: He asserted that it was the high level of these and especially the trans fats that resulted in the higher levels of disease and the cholesterol.
He asserted that it was the high level of these and especially the trans fats that resulted in the higher levels of disease and NOT the cholesterol.
You can probably correlate trans fat with sugar and HFCS and flour and other junk carbs. Most people nowadays also eat a lot of PUFAs. On CNN’s special “Fed Up: America’s Killer Diet”, they said the average Americans eat 10% of their calories calories from soybean oil alone. So, the question is whether the trans fats are really as bad as we are led to believe, or is it the refined carbs and PUFA oils that are the problem? Most of the studies on trans fat seem to be epidemiological and I have yet to find long-term controlled studies which prove the assertion that trans fats are bad. Partially hydrogenated oils still contain PUFAs and MUFAs (double bonds). It would be good to test a fully hydrogenated coconut oil (100% saturated) to see if it caused problems. It’s hard to isolate the trans fat from rancid unsaturated fat, you see.
The “Average Serum Cholesterol Levels” graph lacks both a y-axis and error bars. It’s difficult for the reader to grasp the true significance of such an image.
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Hi! I was surfing and found your blog post… nice! I love your blog. Cheers! Sandra. R.
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