Expanding on this: Cholesterol is a key culprit in atherosclerosis, not just a marker. It accumulates in the walls of blood vessels in the form of fibro-fatty

Expanding on this: Cholesterol is a key culprit in atherosclerosis, not just a marker. It accumulates in the walls of blood vessels in the form of fibro-fatty plaques that are responsible for angina, infarctus, stroke etc. The reason why it accumulates has not been completely elucidated (related to endothelium stress, caused by toxins like tobacco and bacteria that break in into the blood because of gingivitis). The higher the level of cholesterol (especially LDL [†]) in the blood, the more plaque forms and the more one is at risk of consequences (plaque formation is rate-limited by cholesterolemia (blood cholesterol levels)). Cholesterolemia in physiological conditions is independent of intake. If the body is in demand, the liver will synthetise cholesterol de novo in the absence of dieatary intake. I don't think we know at this point what drives the demand, but we've developed drugs that work well on the innner supply end, namely statins, that block the production of cholesterol by the liver. They are, however, ineffective if you eat boatloads of cholesterol. ---- † Recent findings seem to show that HDL is not in itself protective, and that high levels of HDL (that are correlated with fewer complications) may be a passive marker of another protective process.