Post
by Dottore » Wed Aug 15, 2007 4:25 am
Just in case there is some confusion about the various players such as LDL, HDL. VLDL etc., here is a brief summary that I wrote for and posted in another forum:
Total normal cholesterol (TC) level is 260 mg/dl (6.7 mmol/L) worldwide but, here again, there really is no cholesterol level in the blood at all! Think about it.
Briefly, cholesterol is water soluble and needs to be carried inside submarines called lipoproteins.
There are two types of submarines, LDL and HDL. They keep the powder (chol.) dry on the journeys throughout the body.
And there are barges.
The LDL subs are made of low density materials for the purpose of taking up less space (they are in the majority) and for agility and manoeuvrability. Their task is to transport goods including cholesterol from the factory (liver) to those tissues that have placed an order. Orders can be standing or as needed (sporadic). All cells need regular cholesterol replenishment to survive.
HDL submarines are of high density materials, they are slow boats that pick up worn, depleted cholesterol and take it back to the factory (liver) for either re-processing or removal.
Calling LDL bad and HDL good is akin to calling the grocery delivery guys good and the undertaker's hearse bad.
Neither LDL nor HDL subs are normally capable of penetrating the canal banks called the endothelium, which is the inside of the arteries.
Thus , the theory that LDL will form fatty plaque leading to clots etc is simplistic. The number of LDL subs ought to correlate with prevalence of atherosclerosis, right? The more LDL subs the more athero.????
This is not the case, in fact the higher the LDL (recent research has proven) the better protected and supplied the tissues and the endothelial walls are.
Atherosclerosis is not caused by excess LDL or TC or HDL - ever.
Factors that weaken the banks of the canals (arteries only, not veins) like elevated homocysteine, smoking effects, microbial infection, glycemic problems (blood sugar), carb excess and, above all, lack of essential micronutrients damage the endothelium. As this happens, the liver will receive emergency orders to supply cholesterol for repair work. Again, LDL subs are dispatched en masse. Bad guys?????????
When something drastic happens to where the LDL subs are not able to pick up cholesterol from the factory due to inability to manufacture it or being sold out due to unexpected oversupply to needy areas of damaged structures the time soon comes where the moment of truth can be seen in TC blood levels. Drastically lowered cholesterol numbers that do NOT recover spell DEATH. The liver's ability to supply is overwhelmed and the patient is doomed.
Without cholesterol you die.
Now there is oxydized cholesterol, a different animal altogether. It's a rancid substance like a subload of rotten fish but that is not normal and a subject for another time.
And then there is VLDL. Sounds mysterious does it not?
When VLDL barges leave the liver, HDL uploads apolipoproteins to it. VLDL barges are mostly made of fats (triglycerides) with a bit of protein to strengthen the shell. When VLDL reduces in size enough, shrinks, it (as if by magic) becomes LDL, most of which is shuttled back into the liver. During this process the apolipoproteins are transferred back to HDL, ready to be stuck back onto the VLDL that emerges from the liver. I think this may be caused by trade union (wharf workers) activities.
Various factors such as insulin resistance and lack of Vitamin C interfere with the mobilisation (metabolisation) of VLDL's; hence there are fewer LDL subs, less apolips to be transferred back to HDL subs and thus a lesser need for HDL subs to ship goods.
So, the fewer the number of VLDL "blubber-barges" spotted in the system the smaller the number of (needed) HDL subs. Meaning low HDL equals reduced VLDL activity. High HDL is when plenty of VLDL barges are in the harbour and en route.
Does this explain things?
Dottore