Replies

The research, funded by the British Heart Foundation (BHF), found that 'ultrabad' cholesterol, called MGmin-low-density lipoprotein (LDL), which is more common in people with type 2 diabetes and the elderly, appears to be 'stickier' than normal LDL. This makes it more likely to attach to the walls of arteries. When LDL attaches to artery walls it helps form the dangerous 'fatty' plaques' that cause coronary heart disease (CHD).

Yet again we have the error of referring to the LDL as cholesterol. There is no good cholesterol or bad cholesterol. All cholesterol is cholesterol. The difference is the lipoprotein associated with it: VLDL, LDL, HDL1, 2, and 3. These are all involved in various phases of transport of cholesterol and fatty acids (VLDL, LDL) and reverse transport of cholesterol (the HDLs). The problem with LDL is that some people have defects in their LDL gene that produces an LDL that is not readily cleared, to one degree or other, by LDL receptors and, so, stays in the blood stream too long, becomes oxidized, scavenged by foam cells, and then deposited by these cells between the intimal lining of the arteries and the smooth muscle. These are the plaques that build up and can constrict blood flow. They can also rupture and in this event are highly thrombogenic and will produce blood clots that will cause a heart attack or stroke. People can also have defects in LDL receptors with the same results.