Saturday, July 19, 2008


I have been hearing a lot of controversy about the connection between Cholesterol and heart disease. So, I decided to take a look at a review paper on the field from last April, a paper "The Cholesterol Controversy Continues"

My current understanding of the debate is this.

Statins lower the risk of heart attack. They however do so by so little that it is arguable whether they make sense from a cost benefit standpoint. It is also arguable if their connection to Cholesterol levels has much to do with their lowering of heart disease rates. Reduced inflammation, or an unknown mechanism may be at work.

the rate of adverse events was 1.9% in the group of patients taking the drug and 3.0% in the placebo group (1.9 is about 36% less than 3.0). So, the difference in deaths was only 1.1%. Another calculation can be used to determine the number needed to treat (NNT), which is an epidemiological gauge to indicate how many patients would need to be treated with a drug in order for one patient to get the expected benefit (i.e., to be "saved" from a coronary event). It is simply calculated by taking the inverse of the absolute risk reduction (as a percent). Based on the ASCOT results, for every 91 people who took the drug for 3.3 years, only one person would realize a benefit, roughly two would still suffer a coronary event, and 88 would see no advantage (yet, be at risk of potential side effects). The NNT appears to be universally poor for many of the statin drugs, with results that average from about 50 to greater than 100.

Dietary Cholesterol is likely to be an insignificant source of Cholesterol.

Even though all cells have the ability to manufacture cholesterol, the liver synthesizes most of what is present in our bodies, and humans only derive about one-fourth of their cholesterol from dietary sources. Therefore, a reduction in dietary cholesterol would not appear to have a substantial impact on reducing plasma concentrations of cholesterol, and there are only a paucity of studies to suggest that reducing cholesterol intake has an impact on CVD risk reduction.

Cholesterol testing probably is a reasonable thing to do however. It does seem to correlate with heart disease rates. There are other biomarkers that may be significantly better however.

There is little argument concerning the utility of LDL-C as a key risk factor for CVD. Also, lowering LDL-C and raising HDL-C is clearly beneficial for lowering that risk. There is, however, much more to the multifactorial cardiovascular diseases. The literature is replete with markers other than LDL-C that have shown significant ties to risk and the development of CVD

Heart disease is an ancient disease, not something that was created entirely by poor life style in modern humans.

Today, there are many who would suggest that atherosclerosis is a man-made disease, viz., a product of the modern lifestyle. This does not appear, however, to be the case. About a century ago, the mummified remains of persons who lived thousands of years ago were unearthed from the Nile Valley and examined. Remarkably, due to the Egyptian embalming processes and ideal environmental factors, the integrity of the tissue was such that it still rendered acceptable histological studies to be performed on the aorta and other major arterial vessels. Reports of those investigations clearly indicate that atherosclerosis has been a common condition throughout antiquity, and that the histopathology of disease is independent of "race, diet, and the stresses of survival" with the arterial lesions in mummified remains being "no different from those we see today."

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