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22/05/2010

Understanding cholesterol

As in his previous book, Dr. Ravnskov describes what cholesterol actually is and takes us on a tour of the “science” that identified it as the villain in heart disease. Using two of my favorite tools — logic and math — he simply shreds the Lipid Hypothesis, often using the proponents’ own data against them. In fact, that was one of the major revelations for me when I read The Cholesterol Myths: not just that the Lipid Hypothesis is wrong, but how much manipulation and flat-out dishonesty have gone into supporting it, from Ancel Keys on down. The lipophobes fell in love with their theory and simply aren’t willing to let it go. How else do you explain the theory’s longevity when Dr. Ravnskov — and anyone else who cares to look — can dig up the facts he cites in this book:

Thirty years after the start of the Framingham project, the researchers again asked themselves what had happened. This time, a few more of those with high cholesterol had died. I use the word “few” for a reason: On average, one percent of all men with high cholesterol had died during the 30 follow-up years.

Now to the interesting point. For men above age 47, their cholesterol made no difference. Those who had high cholesterol at age 48 lived just as long or longer as those with low cholesterol … I have never met any supporter of the cholesterol campaign who has ever raised an eyebrow when confronted with this astounding fact.

[Marmot] demonstrated that is was not the food that raised the cholesterol of the Japanese immigrants, nor high cholesterol that increased their risk of heart disease. He found that if they maintained their cultural traditions, they were proteted against heart attacks, even though their cholesterol increased as much as in Japanese immigrants who adoped a Western Lifestyle and died from heart attacks almost as often as native-born Americans … immigrants who became accustomed to the American way of life but preferred lean Japanese food had coronary disease twice as often at those who maintained Japanese traditions but preferred high-fat American food. Thus, instead of supporting the diet-heart hypothesis, the Japanese study in fact showed that high-fat food is better than low-fat.

In the elderly, high cholesterol even seems to be protective. This was the surprising finding of Dr. Harlan Krumholz and his co-workers at Yale. They followed about 1000 elderly men and women living in the Bronx, NY. During a four year period, about twice as many of those with low cholesterol had a heart attack or died from one, compared to those with the highest cholesterol.

At a workshop held at the National Heart, Lung and Blood Institute, researchers looked at every single study about the risk of having high or low cholesterol and came to the same conclusion: Mortality was higher for women with low cholesterol than for women with high cholesterol.

[In Finland] one-half of about 1200 more or less overweight male business executives with high cholesterol and high blood pressure were advised about smoking, exercise, weight reduction and diet; the other half were used as a control group. If cholesterol or blood pressure in the control group did not become normal, they were also treated with various blood pressure and cholesterol-lowering drugs. The experimenters were quite happy with the effects of their efforts on risk factors. But the improved risk factors did not lead to better end results: In the group that exercised, reduced their weight, ate less animal fat and more vegetable oil and quit smoking, there were twice as many heart attacks as in the control group.

Another finding that should cause some discomfort among proponents is that whereas high cholesterol is a risk factor in American men, it is not for men living in Canada. This conclusion was reached by Dr. Gilles Dagenais and his team in Quebec after having followed almost 5000 healthy middle-aged for 12 years. They explained away their results by assuming that more than 12 years were needed to see the harmful effects of high cholesterol.


Ah yes, explaining away the results we don’t like. As I learned from Dr. Ravnskov’s first book, it’s taken a lot “explaining” to keep this bogus theory alive. It’s also taken a lot of badly designed studies: comparing cholesterol levels and heart-disease rates without adjusting the data for smokers versus non-smokers (smoking raises your cholesterol), or without adjusting for age differences (cholesterol tends to go up as we age, and most heart attacks occur among the elderly). As Dr. Ravnskov explains, when you properly adjust the data, the only conclusion you can reach from some of these studies is that smoking is a bad idea … but we already knew that.

I’m not going to say this book is a simple read, because it isn’t. It’s not as scientifically dense as Good Calories, Bad Calories, but Dr. Ravnskov shreds the Lipid Hypothesis by applying critical thinking to the studies that claimed to support it, and he invites his readers to think critically as well. He explains — clearly — the scientific method that scientists are supposed to embrace, and walks us through clinical-research concepts such as randomizing a study population, limiting the variables, double-blinding, and distinguishing between an association and a cause.

(As you may recall, in a recent post I borrowed his chart showing an association between high tax rates and heart disease. Have any of the health authorities suggested lowering taxes to reduce heart disease? Should we oppose the new health-care taxes on the grounds that more people will suffer heart attacks?)

As a kid who liked science, I assumed scientific research was a wide-open quest for truth, with the best theories bubbling up to the top. I know better now, thanks in part to reading Dr. Ravnskov’s works. In addition to the manipulation of data he spells out, there’s a huge amount of selection bias in the health and nutrition field. Badly-designed studies that support the Lipid Hypothesis are 10 to 20 times more likely to cited in journals and academic papers than well-designed studies that dispute it.

Dr. Ravnskov’s letters and papers critical of the Lipid Hypothesis have been turned down by medical journals over and over, often with some ridiculous explanations. (I’m on the email list for THINCS, the International Network of Cholesterol Skeptics, and I’ve read quite a few other letters from members that were sent to medical journals but never published.)

Why the bias? I’m sure you can guess. Follow the money.

Large, well-controlled studies are expensive, so much of the funding comes from pharmaceutical companies that sell statins. They run the studies, they gather the results, and they crunch the numbers. If they don’t like the numbers, they crunch them again. As Dr. Ravnskov discovered, they’ll even divide subjects into “subgroups” after the fact to produce statistics they like. And of course, they also provide a lot of revenue for the major medical journals.

The other 800-pound gorillas of funding for heart-disease research are two organizations that fully support the Lipid Hypothesis: the National Heart, Lung and Blood Institute and the American Heart Association. As Dr. Ravnskov says, “Researchers critical of the diet-heart idea have little chance of obtaining financial support.” Or as Dr. Mary Eades put it to me: “They live by their grants. No grants, no work, no job.”

To give you an idea of just how militantly these organizations protect the Lipid Hypothesis, consider this fact from the Framingham Study: After 30 years, the data showed that those whose cholesterol dropped as they aged ran a greater risk of dying than those whose cholesterol increased. Specifically, for each 1% drop in cholesterol, there was an 11% increase in total and coronary mortality.

Still with me? Good. Now here’s how the NHLBI and AHA reported the findings:

The results of the Framingham study indicate that a 1% drop of cholesterol corresponds to a 2% reduction in CHD risk.

That must’ve been some very interesting number-crunching.

As you might expect, Dr. Ravnskov is highly critical of statins. He notes that they do appear to reduce heart disease (very slightly) in a small fraction of the population — middle-aged men who have existing heart disease — but cites some interesting statistics to suggest that they also produce cancer. And data from the pharmaceutical companies’ own research indicates that they don’t do diddly for people who don’t have heart disease but are merely “afflicted” with high cholesterol.

Think about that for a moment. Millions of people are prescribed statins simply because their cholesterol is above some magic threshold: 200, or 220. Doctors aren’t treating heart disease; they’re treating a cholesterol score. And in the process, they’re prescribing a drug that can also produce muscle weakness, memory problems, susceptibility to infections, sexual dysfunction and perhaps cancer.

It’s infections that Dr. Ravnskov covers in the last part of the book. Far from being the villain we’ve been led to believe, Dr. Ravnskov believes LDL fights infections. A century ago, when infections killed more people than heart disease, people with high cholesterol — even those with the genetic disorder that leads to very high cholesterol — lived the longest on average. In fact, Dr. Ravnskov proposes a new hypothesis (which he fully admits is just a hypothesis) for heart disease in this book: plaques begin as the result of microbial infections.

Briefly as I can summarize it, the theory goes like this: LDL is part of the immune system and attacks infections. If the structure of the LDL is changed after attacking a microbe, it will in turn be treated as a foreign substance and swallowed up and oxidized by macrophages — white blood cells within tissues — producing the inflammation that’s common in heart disease. If the immune system works well, the infection is destroyed and HDL carries away the oxidized LDL.

However, if the immune system is weak, too many of the oxidized LDL particles clump together and become stuck in the capillaries that feed the coronary arteries. Part of the arterial wall dies, and something like a boil is formed — what Dr. Ravnskov calls a vulnerable plaque. If the plaque bursts, a clot can obstruct the artery. Now you’ve got a heart attack on your hands.

Again, it’s just a theory, although Ravnskov cites a lot of evidence to support it. Up to half of all heart-attack victims, for example, have recently had an infection of some kind. Either way, it makes a lot more sense than the notion that our bodies are stupid and produce so much cholesterol, it ends up clogging our arteries.

If you’re interested in the science — good and bad — behind fats, cholesterol and heart disease, I urge you to get a copy of this book. (No, I’m not getting a commission.) Better yet, buy a copy for yourself and another one for your doctor. Perhaps you can prevent a few needless prescriptions for Lipitor.


Why Clogged Arteries
Arteriosclerosis

Arteriosclerosis may be caused by excessive levels of homocysteine, which is the normal breakdown product of the amino acid methionine. High levels of homocysteine can damage artery walls. The walls become hardened containing calcium deposits called plaque. Arteries containing plague are more disposed to become atherosclerotic.

The normal metabolic breakdown of homocysteine is disrupted when amounts of vitamins B6, B12, and folic acid are inadequate. Some say high homocysteine levels are better correlated with atherosclerosis and heart disease than cholesterol.

The cholesterol page (URL http://www.modern-diets-and-nutritional-di...holesterol.html )can contribute to a better understanding of the importance of cholesterol.

Linus Pauling, a two time Nobel prize winner, showed that cholesterol is the bodies answer to atherosclerosis in the absence of adequate amounts of ascorbic acid (vitamin C). Sixty milligrams , the current MDR, is not enough vitamin C. The body needs 8-12 grams a day. This, of course,is disputed by mainstream medicine and the pharmaceutical industry.

Malcolm Kendrick M.D., a Scottish physician, obtained data from the WHO MONICA study of many nations that did not show cholesterol as a cause of heart disease. From the same study he showed that saturated fat actually protected against death from heart disease. Eight countries that ate the lowest amount of saturated fat had higher death from coronary heart disease than all eight countries that ate the most saturated fat.

Atherosclerosis

Atherosclerosis is an advanced form of arteriosclerosis characterized by deposits of cholesterol, fats, and blood clots that form within the plaque. This results in roughened raised areas in arteries that can disrupt blood flow. Atherosclerosis and high blood pressure increase with age.

Atherosclerosis is said to be the cause of coronary heart disease (CHD). Anything that obstructs the flow of blood in coronary arteries may produce heart disease.

Studies of the hearts of people who have died of coronary heart disease reveal that about a fifth of those who died did not have obstructed coronary arteries. The arrested blood flow in such cases may have been due to a spasm of a coronary artery that obstructed the blood flow.

Another possibility is a clot formation that dissolved before death. Dr. Ravnskov says the cause of death may not be known in such cases.

A coronary artery may become completely clogged and yet never give any symptoms such as angina, or pain. The reason is that fine branches of the main coronary arteries have branches that communicate with each other.

If the arterial occlusion occurs slowly enough the communicating branches slowly widen enough to take care of adequate blood flow. That is collateral, or alternative, circulation may develop.

A heart attack may occur even though the coronary arteries are perfectly normal, and coronary heart disease may be absent even when coronary arteries are completely blocked.

Dr. Ravnskov maintains that arteriosclerosis, and subsequently atherosclerosis, and coronary heart disease are separate conditions. Problem is many researchers have confused our thinking by regarding them as the same thing.

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