What's Cholesterol Got To Do With It?
Gary Taubes, who wrote the terrific book, Good Calories, Bad Calories, that shows that much of what we believe to be dietary science is actually "science," has another debunker in The New York Times. An excerpt:
In the 1950s, two hypotheses competed for attention among heart disease researchers. It had been known for decades that cholesterol was a component of atherosclerotic plaques, and people who have a genetic disorder that causes extremely high cholesterol levels typically have clogged arteries and heart attacks. As new technology enabled them to look more closely at lipoproteins, however, researchers began to suspect that these carrier molecules might play a greater role in cardiovascular disease than the cholesterol inside them. The cholesterol hypothesis dominated, however, because analyzing lipoproteins was still expensive and difficult, while cholesterol tests were easily ordered up by any doctor.In the late 1960s, biochemists created a simple technique for measuring, more specifically, the cholesterol inside the different kinds of lipoproteins — high-density, low-density and very low-density. The National Institutes of Health financed a handful of studies to determine whether these “cholesterol fractions” could predict the risk of cardiovascular disease. In 1977, the researchers reported their results: total cholesterol turned out to be surprisingly useless as a predictor. Researchers involved with the Framingham Heart Study found that in men and women 50 and older, “total cholesterol per se is not a risk factor for coronary heart disease at all.”
The cholesterol in low-density lipoproteins was deemed a “marginal risk factor” for heart disease. Cholesterol in high-density lipoproteins was easily the best determinant of risk, but with the correlation reversed: the higher the amount, the lower the risk of heart disease.
These findings led directly to the notion that low-density lipoproteins carry “bad” cholesterol and high-density lipoproteins carry “good” cholesterol. And then the precise terminology was jettisoned in favor of the common shorthand. The lipoproteins LDL and HDL became “good cholesterol” and “bad cholesterol,” and the lipoprotein transport vehicle was now conflated with its cholesterol cargo. Lost in translation was the evidence that the causal agent in heart disease might be abnormalities in the lipoproteins themselves.
The truth is, we’ve always had reason to question the idea that cholesterol is an agent of disease. Indeed, what the Framingham researchers meant in 1977 when they described LDL cholesterol as a “marginal risk factor” is that a large proportion of people who suffer heart attacks have relatively low LDL cholesterol.
So how did we come to believe strongly that LDL cholesterol is so bad for us? It was partly due to the observation that eating saturated fat raises LDL cholesterol, and we’ve assumed that saturated fat is bad for us. This logic is circular, though: saturated fat is bad because it raises LDL cholesterol, and LDL cholesterol is bad because it is the thing that saturated fat raises. In clinical trials, researchers have been unable to generate compelling evidence that saturated fat in the diet causes heart disease.
The other important piece of evidence for the cholesterol hypothesis is that statin drugs like Zocor and Lipitor lower LDL cholesterol and also prevent heart attacks. The higher the potency of statins, the greater the cholesterol lowering and the fewer the heart attacks. This is perceived as implying cause and effect: statins reduce LDL cholesterol and prevent heart disease, so reducing LDL cholesterol prevents heart disease. This belief is held with such conviction that the Food and Drug Administration now approves drugs to prevent heart disease, as it did with Zetia, solely on the evidence that they lower LDL cholesterol.
But the logic is specious because most drugs have multiple actions. It’s like insisting that aspirin prevents heart disease by getting rid of headaches.
One obvious way to test the LDL cholesterol hypothesis is to find therapies that lower it by different means and see if they, too, prevent heart attacks. This is essentially what the Vytorin trial did and why its results argue against the hypothesis.
Other such tests have likewise failed to confirm it. A recent trial of torcetrapib, a drug that both raises HDL and lowers LDL cholesterol, was halted midstream because the drug seemed to cause heart attacks and strokes rather than prevent them. Estrogen replacement therapy also lowers LDL cholesterol, but it too has failed to prevent heart disease in clinical trials. The same goes for eating less saturated fat.
So it is reasonable, after the Vytorin trial, to question the role of LDL cholesterol in heart disease. Not whether statins help prevent heart disease, but whether they work exclusively, or at all, by this mechanism.
It doesn't take much research to find problems with the cholesterol myth. Given all the money that has been made and will be made, by what is arguably the greatest medical sham in history, I expect the myth to live on for some time.
Nice to see someone shining a light on the lie though. Check out "The Great Cholesterol Con"by Anthony Colpo. It is the best and most detailed refutation of the cholesterol myth I have ever seen.
Thanks for putting this out there Amy.
Richard at January 27, 2008 9:01 AM
One of four great books that I've picked up on Amy's recommendation (Amy, you need to get a kick back from Amazon.ca). I've been trying to share it with as many people as possible -- especially those of my friends with some extra pounds and warnings from their doctors about cholesterol. It's amazing how hard it is to convince people that popular opinion may not, in fact, be science. Here they are going through a slurpee a day, bread, crackers and so on, while cutting out "fat" and wondering why they continue to grow....
moreta at January 27, 2008 10:32 AM
Amy,
Once again, good job! You shine a light on very interesting and important anomalies in what we think we "know." Correlation is NOT causation. I did some research on the internet when my doctor wanted to prescribe a statin -- the more I looked into it, the less I liked it. I decided to lose 25 pounds instead. It worked like a charm!
Jay R at January 27, 2008 11:36 AM
Gee, Amy, didja have to post an article with so many big words? This is one of those times I envy the reclusive Mr. Sutton...
This is also a good time to talk to your doctor about this - because he or she graduated from medical school consisting of classes teaching the subject link. In that conversation, I intend to get mine to explain all the factors, as he has before when recommending treatment.
But don't forget one thing about this heart business: when the autopsy is done, and the cause was heart failure, something had to cause it. Read this article above carefully, and notice what it does and doesn't say. It admits that abnormalities in lipoproteins may cause heart disease; LDL contains those proteins; lower LDL means fewer abnormal lipoproteins; this actually supports the idea that lower LDL = lower disease rates. Casting doubt is not the provision of answers.
Amy, I remind you now of an article you posted long ago, which said that earlier detection of some cancers was not improving the "cure" or survival rate. Part of the reason there was that different people's immune systems respond in different ways to cancer cells. I suggest now that part of this issue is driven by an overweight public flocking to be tested. After all, the #1 indicator of breast cancer and heart disease risk is body fat percentage.
Radwaste at January 27, 2008 11:52 AM
Abject apologies to Mr. Sutter... I would have gotten the two g's right, though.
Radwaste at January 27, 2008 3:50 PM
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