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.
Saturday, January 26, 2008
Cholesterol Still Good For You
Via Half Sigma again: a New York Times editorial on cholesterol never having hurt a fly. Gary Taubes explains how cholesterol got its undeserved bad reputation:
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