Ive been going through Dayspring's excellent lipid lectures for doctors. Not for the faint hearted. Im doing the hyperabsorption one now. I had forgotten most of this from my biochemistry three decades ago but luckily still have the context and the basic science to understand.http://www.lecturepad.org/index.php/201 ... ds-to-know
Take home points for those with a non science background or not yet up with the details:
Ive got half way and need to write down my thoughts.
Background: Dont confuse cholesterol with other fats. Hyperabsorption of this and related molecules such as the phyotosterols are a separate issue from "fat" in diet. Sterols are a subgroup of fats. There are a few. The mos famous is cholesterol which is of animal origin. The other sterol molecules are called campesterol sitosterol etc. and they are of plant origin.. Hyperabsorption only pertains to cholesterol and other sterol molecules.
The overwhelming bulk of the cholesterol in the gut comes from SYNTHESIS IN LiVER CELLS which is excreted into the bile and thru the bile duct into the intestine and reabsorbed. Food sources of cholesterol are a very small contributor to this pool available for absorption. We cannot change our LDL significantly by reducing our cholesterol intake (remember cholesterol is not synonymous with saturated fat for instance. We are only talking sterols here)
Then there is a balance between two membrane bound proteins on the guts cells and on the liver cells. One pulls sterols in and the other pushes them out. If the one that pushes them out doesnt work so well then we have the hyperabsorption state. Hyperabsorption doesnt mean the pulling in protein is stronger. It means the pushing out one is weaker. The pushing out protein might be absent or defective. E4s ***might*** be associated with weaker pushing out proteins in some of us. This is a very very new area of research so its not certain yet what the implications are and how big a problem it is. The study he cites had only 78 patients and 14 e4s ( mixedhetero and homo). And it was just a snapshot blood level. Nothing clinical, not correlated to any outcome. But we are unlikely to be able to increase our pushy out protein by diet. The plant sterols Dayspring was talking about in his answers to us are higher in the blood in hyoerabsorbers cos the pushy out protein ***might*** be weaker in us. Ezetimibe blocks the pulling in protein, thus makes both proteins equally weaker so they are balanced again.
Plant sterols are thought not to be good for humans. ie campesterol sitosterol etc. we need our pushy out protein to excrete them.
Ok. Onto second half.
But take home message so far is...
Like bowties, eggs are cool. (Dr Who allusion for the non-nerd)
Ezetimibe might be needed if this is the problem IN AN INDIVIDUAL cos there aint another option at this stage. But its individual. Some ppl havent got the pushy thing at all and some ppl have a weaker one. But its a separate gene to apoe4 completely