ccording to proponents of the cholesterol theory of cardiovascular disease, dietary cholesterol raises plasma levels of certain lipoproteins, which leads to the development of atherosclerosis and cardiovascular disease. The treatment for this problem is claimed to be the administration of cholesterol lowering drugs, which reduce circulating levels of low density lipoprotein (LDL) and total cholesterol. However, this theory is so fanciful, unscientific and embellished, that it would not appear out of place in a fairy tale. In fact, the theory that cholesterol is placed in the arteries at night during sleep by the magic cholesterol fairy has just as much credibility to anyone who has an understanding of the scientific literature. The cholesterol theory of cardiovascular disease has in fact become so convoluted and distorted due to the continual need to explain unwanted scientific findings, that it no longer even represents rational thought.
The main problem with the cholesterol theory of cardiovascular disease is that dietary cholesterol does not cause modification to the plasma cholesterol levels of healthy humans. However, many other dietary components do, and to a much greater extent that is claimed for dietary cholesterol. For example, dietary fibre is known to favourably modify plasma cholesterol as has been documented in considerable detail by the nutritional sciences. Proponents of the cholesterol theory of cardiovascular disease also claim that dietary saturated fat increases fasting plasma triglycerides and thus increases the risk of cardiovascular disease. However, this theory is flawed and appears to be based on such a misunderstanding of nutritional biochemistry that is calls into question the intellect of those who prescribe to such an idea. Saturated fat does not cause increases to the fasting serum triglyceride concentration of healthy human subjects, however, low intakes of essential fatty acids do.
So why then are raised plasma cholesterol and triglycerides not seen as a fibre and essential fatty acid deficiency when scientific evidence supports this contention? This is a good question, the answer to which has more to do with politics and money than it does with science and understanding. In fact the history of the cholesterol theory of cardiovascular disease has been steeped in skulduggery, spin, obfuscation, lies and outright fraud since it was first conceptualised in the 1950’s by a series of flawed and questionably fraudulent scientific papers that have since been discredited as pseudoscience. This hidden agenda behind the cholesterol theory of cardiovascular disease is illustrated by the total mainstream ignorance of scientific data showing the efficacy of the cholesterol lowering effects of niacin, the generic name for the two components, nicotinamide and nicotinic acid, that comprise B3 group of vitamins.
Niacin favourably modulates plasma lipoprotein concentrations, yet has been almost totally ignored by mainstream medicine. The effects of niacin on plasma levels of cholesterol have been known since the 1950’s and yet despite the knowledge about this cheap vitamin, huge resources were spent designing, testing and marketing the statin drugs which have been shown to be less effective that niacin (here). Niacin in doses of 1-3 g/d can favourably affect plasma cholesterol concentrations because it alters a number of steps in the metabolism of lipoproteins which results in decreases in plasma levels of triglycerides and apolipoprotein B100 containing lipoproteins. The apolipoprotein B100 containing lipoproteins include LDL, independent density lipoprotein (IDL), very low density lipoprotein (VLDL) and the often ignored lipoprotein(a). Raised plasma levels of these lipoproteins indicate the presence of metabolic syndrome, the presence of which increases the risk of cardiovascular disease considerably.
Niacin is effective at lowering plasma levels of the triglycerides because it can inhibit the lipolysis of triglycerides from adipose tissue through inhibition of adenylate cyclise activity (cAMP). Reduced concentrations of cAMP then cause a decrease in hormone sensitive lipase and decreased levels of plasma free fatty acids. The decreased levels of free fatty acids causes a decrease in triglyceride synthesis in the liver, which is enhanced because niacin can also inhibit hepatic activity of diacylglycerol acyltransferase. The decrease in the synthesis of triglycerides from the liver causes an increase degradation of Apo B100 particles because fewer are required for the production of VLDL due to decreased synthesis of triglycerides. The lower production of VLDL causes a decrease in all the degradation products of VLDL, which include LDL and apolipoprotein(a). A reduction in large triglyceride rich VLDL1 particles may also cause a reduction in small dense LDL production, which are produced via the action of hepatic and lipoprotein lipase.
Niacin then can decrease circulating levels of the apolipoprotein B100 containing lipoproteins and this favourably affects plasma levels of cholesterol. However, niacin can also increase circulating levels of high density lipoprotein (HDL), something it does better than any other pharmacological agent. This may occur because niacin can inhibit the HDL catabolism receptor which prevents removal the Apo A1 containing HDL particles thus increasing the half life of the HDL particles in circulation. This increased plasma half life also allows the size of the particles to increase from HDL2 to HDL3 through increased cholesterol uptake from peripheral tissues thus lowering concentrations over time. Therefore niacin can favourably affect the LDL to HDL ratio and lower plasma fasting triglycerides. Also of particular interest is the ability of niacin to lower levels of the lipoprotein(a) particle, something statins are not able to do.
RdB
