I learn a few things from this presentation by Trevor Marshall:http://vimeo.com/32641708
1. (amended) Vitamin D and in particular the active form 1,25D may have effects on many other receptors
including the Thyroid receptor; the link with the the Vitamin D Receptor (VDR) might not even be so important .. see his video from 16:45 onwards.
What seems important is that active 1,25D binds to the same points on these receptors as the inactive form 25OH. The 1,25 then enables / activates these receptors to do what they must do e.g. to activate the oligodendrocytes essential for maintaining the myelin and remyelination..
Now, it could well be that in the early stages of the disease
, a high 25OH inactive form (through supplementation) could be useful to help raise 1,25D and thus to help activate receptors. For this reason vitamin D 25OH supplementation could help us ...
However, in the later stage of the disease
when many receptors are already knocked out, a high 25OH may get in the way as it binds to the same points on the receptors as the active form 1,25D. I have seen that my body regulated 25OH down as -I guess- the body seeks ways to make extra room for active 1,25D to bind. To that end, it is known that a high 1.25D is a market of MS (we know this) and also that there actually is not only the forward path (from 25OH to 1.25D) but also a path back from the 1,25D to the passive 25OH.
2. lipids may also activate receptors...
3. I learn that the Chlamydia bacteria, just like the Bar-Eppstein virus, knocks out the VDR receptor. Of the Bar-Eppstein virus, we knew, there is also published on PubMed referred to in a posting above. Of the Chlamydia bacteria, I did not know.
These bacteria can apparently keep quiet for many years to break out - then this may give rise to flares in the first benign form ..
The bacteria may infect the brains (compromised BBB) but it may also -and that is important here- besides affecting the VDR (impair micro cellular nutrition, glucose deficiency, ion pump failure), affect many other receptors that control very important processes for maintaining our myelin (the maintenance of oligodendrocytes / remyelination).
Where the outbreak of the bacteria directly affects our myelin, as we know best..