uperficially the cholesterol theory of cardiovascular disease holds water as a valid scientific theory, but under closer scrutiny the hypothesis that dietary cholesterol is the cause of atherosclerosis becomes unscientific and even absurd. While proponents of the theory fight a rear guard action against the overwhelming and mounting contradictory scientific evidence, the pharmaceutical companies and its paid agents continue to create huge profits for themselves at the expense of others. It is true that diet is able to cause modifications to plasma cholesterol levels. It is however not cholesterol or saturated fat that are able to cause such modification. In fact, many components of the diet are known to modify the plasma lipid levels in humans to a much greater degree than is claimed for cholesterol. Of the possible plasma cholesterol modifying agents in the diet, alcohol has received much attention, since the discovery of the French paradox.
That the French eat large amounts of saturated fat and cholesterol, yet have low rates of cardiovascular disease argues against dietary lipids as the causative factor. The French drink wine, the ethanol within which has been shown to favourably affect plasma cholesterol concentrations. For example, researchers1 have investigated the effects of moderate alcohol consumption on plasma total cholesterol, low density lipoprotein (LDL) and high density lipoprotein (HDL) in healthy normal weight subjects aged 21 to 35 years. Subjects consumed 40 grams of ethanol per day as beer, or maintained their normal drinking habits for 6 weeks, and then abstained from alcohol for 3 weeks, whereas a control group drank no alcohol. During consumption of alcohol, both drinking groups experienced an increase in HDL, which decreased significantly during abstinence. The LDL and total cholesterol were also lower in the subjects who maintained their normal drinking habits.
Subjects who maintained their normal drinking habits and drank mainly over the weekend had a decrease of 0.18 mmol/L HDL upon abstinence of alcohol. Whereas those who were mainly weekend drinkers had a decrease of 0.31 mmol/L HDL following abstinence. This suggests that alcohol favourable affects the LDL to HDL ratio because while it has a negligible affect the plasma concentrations of LDL, it significantly raises the plasma concentration of HDL. Other data indicate that alcohol may also decrease levels of lipoprotein(a). This suggests that moderate alcohol consumption is beneficial to the health and reduces the risk of cardiovascular disease. Alcohol consumption is thought to affect a number of steps in the metabolism of lipoproteins including the synthesis of apolipoproteins, the activity of lipoprotein and hepatic lipase, as well as the function of the cholesterol transfer protein. Acetylaldehyde, a product of alcohol metabolism may also affect lipoprotein metabolism.
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