Here's a good reason not to do that
FROM HEREAssociation of vitamin D metabolite levels with relapse rate and disability in multiple sclerosis.Smolders J, Menheere P, Kessels A, Damoiseaux J, Hupperts R.
School for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands. firstname.lastname@example.org
BACKGROUND: Multiple Sclerosis is associated with low serum levels of 25-hydroxyvitamin D (25(OH)D). We investigated the association between serum levels of 25(OH)D and 1,25-dihydroxyvitamin D (1,25(OH)2D), the biologically active metabolite, and clinical MS severity as expressed by EDSS-score and relapse rate. STUDY-DESIGN: Cross-sectional study. PATIENTS AND METHODS: Serum samples from 267 MS patients were collected for 25(OH)D and 1,25(OH)2D measurement. Clinical MS parameters at the date of serum sampling were determined. Results: Both metabolite levels were significantly lower in the progressive forms compared to the relapsing remitting (RR)MS phenotype. In RRMS patients (disease course < or = 5 years), high 25(OH)D levels were associated with a high chance of remaining relapse-free. Low 25(OH)D levels were associated with high EDSS-scores. 1,25(OH)2D was not directly associated with relapse rate or EDSS-score, and was dependent of age and 25(OH)D level. CONCLUSION: Serum levels of 25(OH)D were associated with both relapse rate and disability in MS patients. These results are suggestive for a disease modulating effect of the serum concentrations of 25(OH)D on MS. The low circulating 1,25(OH)2D levels in progressive MS are due to older age and lower 25(OH)D levels. The potential consequences for vitamin D supplementation in MS will be discussed.
The MP claims the proof that MS is a "TH1" disease according to their vitamin d parameters is that they say MSers all have low 25D and high 1,25D. What is happening, according to their theory, is that the germs are making 1,25D directly in the body. 1,25d is the active metabolite and is actually a hormone, a well known fact.
The computer model comes into play here again because Marshall says that according to is computer simulation, 1,25D, is able to bind and activate the steroid receptors in the same way prednisone or something like that would.
Ergo, they claimthat all MSers are walking around as if on steroids all the time. They say that's why taking vitamin d seems to help MS, it is as if taking a steroid. They claim that this is why MSers have this theoretical germ rampant in our bodies that we canoot defeat, our immunity is severely hampered by this theoretical chronic steroid stimulation and we will never get better unless we get rid of the vitamin D.
But high 1,25D is not what is seen in studies on MS and vitamin D like the examples above and below, which checked both metabolites.
So the claim that the 25D is being converted into 1,25D by germs in your body thus leaving the 25D low and the 1,25D high is not supported.
ANOTHER PAPER HERE LOW 1,25d AND 25D
As an added element it is absurd to imagine that the body could function if it willy nilly could allow one hormone, 1,25d, to activate the receptors of another hormone, corticosteroids. How oculd yor body function at all it that were true?
There is not one peer reviewed medical paper anywhere that shows that 1,25D can bind and activate the steroid receptors.
Additionally, the molecular genomic shape of a hormone is not the only thing that allows it to bind and activate a particular receptor pocket, there are additional proteins involved:CLICK FOR PAGE ON RECEPTOR PROTEINS HERE
These threads live for a long time I wanted to add enough that some future person looking at this marshall protocol and coming to TIMS for material would have what they need. As I said I almost went for this once...scary
I know I saw a study last year that showed supplementing with vitamin D reduced lesions on MRI...can anyone add that to this thread as well? I can't find it