@neeche41 @LDLSkeptic @FatEmperor 1/ If only it were so simple. When statins are ingested, the liver absorbs most of it. Mevalonate synthesis in liver cells is blocked and liver cells are robbed of cholesterol and isoprenoids. The cells respond to the death threat and start making more reductase to try to turn
@neeche41 @LDLSkeptic @FatEmperor 2/ the mevalonate pathway back on. Because reductase is elevated, the nucleus wrongly thinks more LDL receptors are needed. What cells really need is more mevalonate. More LDL receptors are made anyway that snatch up cholesterol from the blood and pull it back into the liver
@neeche41 @LDLSkeptic @FatEmperor 3/ cells. Reductase is then decreased, so LDL receptor synthesis is decreased. BUT the liver detecting that cholesterol has been increased through LDLr's wants Isoprenoids. It turned on the mevalonate pathway and didn't get any. All it got was cholesterol. What the ?
@neeche41 @LDLSkeptic @FatEmperor 4/ Cells respond appropriately as wired. Reductase is turned back on again to try and make isoprenoids. LDL receptor synthesis is also turned up again (hard wired). More blood cholesterol is lowered as it is shoved into liver cells via LDL'rs.
@neeche41 @LDLSkeptic @FatEmperor 5/ What's really happening in humans is undetected cells throughout the rest of the body choking to death from isoprenoid deprivation. So basically take statins, choke off the lifecycle of liver cells so reductase kicks into overdrive to "trick" liver cells into mass producing
