- Vitamin D is a type of hormone and a powerful
mediator of immune function. The data documenting
an association between low Vitamin D
and high MS risk, relapses, disability, and CNS
inflammation now appear to be strong, consistent,
and reproducible. Data from a number of areas of
investigation suggests that Vitamin D may be one
underlying common factor that begins to make
sense of the large amount of data on the geographic
distribution of susceptibility to MS.
- Genetically, a link appears to exist between
changes in the genes involved in the synthesis of
the Vitamin D hormone and the Vitamin D
hormone receptor, and the risk of developingMS.
The strongest genetic risk factor for MS is a
specific gene (HLA DRB1*1501), whose activity
appears to be influenced by Vitamin D.
- Following a review published in 2010, cumulative
evidence led to a number of new clinical trials,
mostly using Vitamin D as an add-on to existing
therapies in Phase IV studies.
- Published in August 2011, an importantMS
breakthrough has found that Vitamin D directly
terminates production of disease-causing proteins.
When Vitamin D is given tomice with EAE (an
animalmodel ofMS), it blocks the gene that
encodes IL-17, stopping its production. IL-17
appears to be amajor inflammatory component in
MS. This breakthrough also demonstrates that
Vitamin D increases suppressive T cells that
- A Phase II study that is currently recruiting
participants is investigating whether Vigantol® oil,
a form of Vitamin D hormone supplement
(cholecalciferol), provides any added benefit when
given in conjunction with Rebif. The study will
have 348 participants; it began in February 2011
and is scheduled for completion inMarch 2014.
Primary outcome measures are the mean change
from baseline in the total volume of T2 lesions at
week 48 and the proportion of relapse-free
subjects at week 96. Secondary outcome
measures include sustained disability progression,
MRI measures of disease progression, the
proportion of subjects free from disease activity at
96 weeks, and changes in cognitive function.
- The French CHOLINE Phase II study of 250
individuals with RRMS who are receiving ongoing
treatment with Rebif began in January 2010 and is
scheduled for completion in December 2013.
Its primary outcome measure is a reduction in
relapse rate; secondary outcome measures
include the time to a first documented relapse,
the mean number of relapses per subject per year,
the number of relapse-free patients after two
years of treatment,MRI measures of progression
and lesion load, and change in quality of life.
- A Finnish Phase IV study with 70 participants is
investigating cholecalciferol (Vitamin D3) as an
add-on treatment to Betaseron in RRMS. It began
inMarch 2008 and was scheduled to end in June
2011. Its primary outcome measure is
biochemical; a secondary measure is the number
of gadolinium-enhancing lesions and/or new
- A small Phase IV study of 100 individuals with
RRMS being treated with beta interferon has as its primary outcome measure whether Vitamin D
supplementation may reduce or eliminate flu-like
symptoms and injection-site reactions from the
interferon. It will also determine any effects on
EDSS progression, relapse rate, and quality of life.
The study began in October 2010 and is
scheduled for completion in October 2011.
- A small Phase I study in 40 individuals with
MS, designed to determine the safety and
immunologic effects of supplementation with
low- (400 mg) and high-dose (10,000 mg)
cholecalciferol (Vitamin D3), is currently
recruiting participants whose serum levels of
Vitamin D indicate that they are good
candidates for supplementation. The study
began in March 2010 and is scheduled for
completion in December 2011. The primary
outcome measure is to determine the safety of
high-dose cholecalciferol and to assess the
effects of cholecalciferol supplementation on
serum immune markers; its clinical effects will
also be assessed.