A friend of a friend recently went on dialysis due to kidney failure, and it got me to thinking. As I understand it, the threat from cholesterol is that if the blood contains too much it can start to form deposits on artery walls, eventually getting to the point where it will restrict blood flow. Shouldn’t it be possible to utilize a dialysis-like procedure to filter excess cholesterol from the blood? Even if it proved impractical for most people, maybe certain high-risk patients would benefit from such an approach?
I would imagine it might be possible, but there wouldn’t be a market for it. Dialysis is not something you want to be on. And why be hooked up to a machine for a few hours, unable to go anywhere, when instead you can just take some Lipitor and eat healthier?
And in the case of severe cholosterol needed immediate action, an angioplasty procedure is not that hard or life threatening. Just slide the ol’ catheter up the vein and squeeze away. Hell, I can’t imagine it takes that much more time that being hooked to a (theoretical) lipid dialysis machine would take.
It can be done. But it’s not without risk. And cholesterol levels rise back up after anyway. And since the process involves removing, filtering, then replacing one’s plasma volume you see it’s not a small procedure.
Easier to diet, exercise, and if need be, take meds to lower cholesterol.
It tends to be reserved for the most severe cases of high cholesterol, which usually arise on a genetic basis (lack of LDL receptors ==> nothing to upregulate as a result of statin interference with cholesterol synthesis).
For more info, search under “LDL apheresis” or “cholesterol apheresis”.
I actually had a patient who underwent that procedure back when I was a med student working at the Lipid Research Center at the Hop. She had a cholesterol level of 1200 and xanthomas all over, under her skin. She was 9.
Back then, those folks (the ones without cholesterol receptors in their liver cells) tended to have heart disease by their teens and die in their twenties. Even with the aphereisis.
What do they do now? What causes these ridiculous cholesterol levels? You say they lack cholesterol receptors - does that mean that the feedback mechanism designed to control it doesn’t work because there aren’t any receptors?
Yes, that’s exactly the problem - the cholesterol regulation mechanisms are broken.
My mother has a “mild” form of this condition - fortunately, I did not inherit it.
Liver cells need cholesterol in order to make bile (as well as to form their cell membranes). Normally, liver cells have two ways of getting cholesterol:
- by synthesizing it themselves
- by expressing LDL receptors which then pull cholesterol (i.e. LDL cholesterol) into the cell from the bloodstream.
Statins work by interfering with the liver cells’ cholesterol synthesis. Hence, in order to meet their cholesterol needs, the liver cells upregulate their LDL receptors. The net result is that they get the needed cholesterol at the expense of lowering the level of circulating LDL (a good thing).
In the absence of LDL receptors (or in the presence of non-functional LDL receptors), the administration of a statin is pointless since even if it inhibits liver cell cholesterol synthesis, there are no LDL receptos to be upregulated.
Further, in the absence of LDL receptors, the only way to get LDL out of the plasma is via the so-called scavenger receptor (found on macrophages). You may already know that a cholesterol filled macrophage is the prototypical “foam cell”, i.e. a key cell in the development of atherosclerosis. Interestingly, in order for LDL to be taken up by the macrophages, the LDL must first be ‘modified’. Oxidized LDL and glycated LDL are two examples of such. Thus, the interest in antioxidants to prevent atherosclerosis with respect to the former, and the high frequency of atherosclerosis in diabetes with respect to the latter.
KarlGauss - thanks! Extremely interesting post!