I've been thinking about how vitamin D relates to MC and other IBDs, (and probably to celiac disease as well), and I have a theory about why our vitamin D levels decline so drastically as our body is forced to deal with the demands imposed on it by the GI issues. (Yep, yet another wild theory.
)You've already seen my theory about how these diseases may cause approximately a 10-fold increase in the demand for cholesterol/bile fatty acids, but if anyone wants to review it, here's a recap:
OK, to expand on that, note that vitamin D is synthesized in the skin, by the initiating action of the sun on cholesterol. IOW, the sun triggers a chemical reaction that synthesizes vitamin D from cholesterol in the skin. If the availability of cholesterol in the skin, is reduced, then obviously, vitamin D production is going to suffer.Normally, about 90% of excreted bile acids are reabsorbed from the intestinal system and recycled back to the liver and the gallbladder. The reabsorption takes place in the terminal ileum. Apparently, though, the reabsorption process becomes compromised when the ileum, (along with the rest of the intestinal tract), is inflamed. In addition, another limiting factor that can inhibit reabsorption may be introduced as a side effect of the inflammation associated with IBDs. I have a hunch that the reason why the bile fatty acids are not properly recycled when they get to the terminal ileum, (as they should be, if the digestive process were proceeding normally), is because they are still coating the fat colloids when they reach the ileum, and so they are in a state where they cannot be absorbed. IOW, if the pancreatic lipase does not hydrolyze the fats, then the bile salts cannot be reabsorbed. Since they cannot be absorbed and recycled, they pass on through, causing D. That doesn't mean that bile is the initiating cause of the D, though - the failure of the pancreatic enzymes to hydrolyze the fats, is almost surely the cause of the problem, and the ultimate cause of the compromised pancreas function, is, of course, inflammation.
Also, consider this: If most of the bile is lost, rather than recycled, then the demand for bile is roughly 10 times the normal amount. In the long run, losing all that recycled bile is bound to place abnormal demands on the liver and gallbladder, just to keep up with the body's needs. This may be why so many of us with MC have gallbladder problems.
Those bile fatty acids are feedstock material that the body uses to manufacture cholesterol to supply it's needs. If 90%, (or whatever amount), of the bile salts that would normally be recycled, are lost, instead, (due to malabsorption), then the body would have to produce much more cholesterol from "scratch". Since that could be as high as 10 times the normal production requirements, it would seem logical that serum cholesterol levels would go down, as a function of a long-term malabsorption issue.
Cholesterol is absolutely essential to the cellular membranes of every cell in our body. It protects the cells from ion leaks, and it also helps to prevent oxidation damage to vital membrane fats. Since the brain comprises only about 2% of the mass of the body, but uses about 25% of the cholesterol, it's likely that in order to supply the brain, (and other vital body organs), if the body is forced to ration cholesterol, then it's probably going to limit cholesterol where a deficiency is least likely to interfere with vital bodily functions, namely, the skin.
And that, IMO, is why IBDs lead to a vitamin D deficiency. Of course, this is just my theory, so keep that in mind.
Tex
