AbstractThe high circulating LDL‐cholesterol levels seen in the inherited disease familial hypercholesterolaemia cause high rates of cardiovascular disease whereas the low circulating LDL‐cholesterol levels following statin treatment cause low rates of cardiovascular disease. This is why LDL‐cholesterol is referred to as bad cholesterol by the media. Atherosclerosis is caused not by native circulating LDL particles but rather by oxidized LDL particles in the arterial wall. Oxidized LDL particles unlike native particles are taken up by macrophages via scavenger receptors to form foam cells and are treated as autoantigens by the immune system provoking inflammation. Hence many of the characteristics of the atherosclerotic plaque including its tendency to rupture and cause thrombosis and heart attacks can be explained in molecular detail by the effects of oxidized LDL particles.