Anonymoose wrote:[1]In your post before this, are you trying to say calcitriol is essential to all cell death and/or inflammation? It seems to me like there could still be cell death and inflammation without its involvement...but maybe it is essential for the death of certain cells. [2]If plain old 25OH is parking in the vdr receptors on those cells, preventing the active form from doing its job, would that not interfere with the body's efforts to fight off the disease?
I don't know and I certainly haven't delved into this nearly as much as or in the same manner you have. I'm a Monet style learner...with Picasso-like ideas.
You are more da Vinci. I'm not sure our minds will ever meet. Lol
[3]I do know I don't hurt today and I won't be taking any wicked vitamin d for quite some time!
The answer to question one, as far as I know, is yes. I have specifically looked at this in the context of skin cells. The Cell Replacement Cycle is initiated by calcitriol in response to senescence, infection or injury. In the case of immune cells, calcitriol is the only thing that activates the local adaptive immune response and also deactivates it through Programmed Cell Death or apoptosis. I have also looked at it in the context of endothelial, epithelial and neuroendocrine tissue and it is the only thing initiating the process. But I am FAR from having any expertise in this so I could be completely wrong and there could be other ways these things happen. There is a lot of redundancy in body systems so that if one pathway fails, there is an alternative. I just have not run into one as far as cell replacement or apoptosis.
In answer to your second question, I think the answer is IF plain old 25D is blocking VDRs. I don't that this has been proven. I have spent hours looking through what I think could loosely be described as the Marshall Group's papers on this and find an awful lot of "would, could, may, and might's" with very limited clinical data to back up these assertions. Very frustratingly, when you start tracing citations, they tend to be to papers by others in the same group and the cited source also phrases things as being conditional. None of that is to say that this may not be true, its just that to me, it is unconvincing at this point and I think there may be alternative explanations that are as plausible, if not more plausible.
Based on Hayes' study, it seemed to be fairly widely accepted that something was blocking the VDRs to explain the immortality of pro-inflammatory immune activity in EAE and MS, yet her tests of calcitriol + D3 shows clearly that this is not the case in EAE since if the VDRs weren't functioning, calcitriol would have no effect.
As far as Number 3, this has to be very rare that anyone has a negative reaction to Vit D3, particularly at the relatively low doses you are taking. I wish there were a way to demonstrate for certain that what you are feeling is clearly linked to vitamin D and not something else and thought from some of your earlier posts that your iron deficiency made more sense as the source of the problem. What changed that?
Hopefully we've stumbled upon the cure for my mysterious reaction to d3.