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http://www.authintmail.com/index.php?q= ... lerosis-ms&

another misleading headline. What else is new, right?
The real study showed:
Calcitrol, aministered to mice with EAE, lead to a longer remission period from EAE disabilities (nine days) compared to steroids (six days.)

While she is excited about the prospect of her research helping MS patients someday, Hayes is quick to point out that it's based on a mouse model of disease, not the real thing. Also, while rodents are genetically homogeneous, people are genetically diverse.

"So it's not certain we'll be able to translate (this discovery to humans)," says Hayes. "But I think the chances are good because we have such a broad foundation of data showing protective effects of vitamin D in humans."

The next step is human clinical trials, a step that must be taken by a medical doctor, a neurologist. If the treatment works in people, patients with early symptoms of MS may never need to receive an official diagnosis.

http://www.news.wisc.edu/22163

Calcitrol is a man-made active form of vitamin D and a steroid hormone, prescribed to people with kidney disease or hypoparathyroidism who cannot make enough vitamin D, and do not have the ability of healthy kidneys to help in this process.
http://www.medicinenet.com/calcitriol-oral/article.htm

So--calcitrol did not halt MS in humans. It lead to a bit longer remission in mice with EAE. And vitamin D is most certainly implicated in MS, but we really don't know why yet.
But the headline sure made me click to check it out!
cheer

so what's going on in those kidneys then..

Site of 1,25(OH)2 vitamin D3 synthesis in the kidney (1978)
http://www.nature.com/nature/journal/v2 ... 287a0.html
"FRASER AND KODICEK1 have reported, and others have confirmed2–4, that the kidney is the exclusive site of synthesis of 1,25-dihydroxycholecalciferol (1,25(OH)2D3). "

1alpha-Hydroxylase and the action of vitamin D (2000)
http://jme.endocrinology-journals.org/c ... /141.short
"Synthesis of 1, 25(OH)(2)D(3) from the major circulating metabolite, 25-hydroxyvitamin D(3) (25(OH)D(3)), is catalysed by a mitochondrial cytochrome P450 enzyme, 25-hydroxyvitamin D-1alpha-hydroxylase (1alpha-OHase). Although 1alpha-OHase is expressed predominantly in the kidney, extra-renal production of 1,25(OH)(2)D(3) has also been demonstrated in tissues such as lymph nodes and skin."

HYDROXYLASE ENZYMES OF THE VITAMIN D PATHWAY: Expression, Function, and Regulation (2002)
http://www.annualreviews.org/doi/abs/10 ... 501.150216
Vitamin D is a secosteroid that is metabolically activated and degraded through the actions of three cytochrome P450 hydroxylase enzymes. Bioactivation occurs through the sequential actions of cytochromes P450C25 [aka CYP27A1] and P450C1, resulting in synthesis of the pleiotropic hormone 1,25-dihydroxyvitamin D (1,25VD), which regulates over 60 genes whose actions include those associated with calcium homeostasis and immune responses as well as cellular growth, differentiation, and apoptosis.

hepatic context not renal in this next bit, but i do believe this may be the first study i've found that specifically link zinc supplementation to P450 status. the abstract is not the clearest thing in the world and unfortunately i don't seem to have access to this particular journal. however, i'm taking the last two sentences to mean, possibly, that zinc supplementation did mitigate P450 depletion during induced cirrhosis:

The Antioxidant and Hepato-Protective Effects of Zinc are Related to Hepatic Cytochrome P450 Depression and Metallothionein Induction in Rats with Experimental Cirrhosis
http://medcontent.metapress.com/content ... 1rmj16286/
The aim of the present study was to investigate the time-course of changes in hepatic lipid peroxidation, cytochrome P450 and metallothionein concentrations, and superoxide dismutase and catalase activities in relation to the onset and development of cirrhosis in CCl4-treated rats. Further, the effects of oral zinc administration on these parameters were assessed. Cirrhosis was induced in 120 rats by intraperitoneal injections of CCl4 twice weekly over 9 weeks. Controls were 120 additional animals. Both groups were further subdivided to receive either a standard diet or one supplemented with zinc. Subsets of 10 animals each were euthanized at weeks 1, 2, 3, 5, 7 and 9 from the start of the study. Results indicated that zinc administration delayed the cirrhotic process and the increase in lipid peroxidation. These changes, consistently maintained during the first 5 weeks of the study, were associated with a significant decrease in the hepatic concentration of cytochrome P450 and an increase in the hepatic concentration of metallothioneins. Zinc supplementation did not produce any significant change in superoxide dismutase and catalase activities. [but did it affect P450 then? does the final sentence of the abstract answer this question?] These results suggest that cytochrome P450 and metallothioneins may play an important role in the hepato-protective effects of zinc against lipid peroxidation in experimental cirrhosis.

interesting stuff

Have a look at my post under Regimens called "Beyond Avonex and Valtrex" under the section called "Megalin and Cubilin". The latter is required for Vitamin D synthesis but it is only a very small (important) part of the road to MS.

Regards