You Can Stop MS
If you're looking for ways to reverse MS, or MS prevention methods, then you've come to the right place. High dose vitamin D3 therapy (14,000 IU/day) can significantly inhibit the progression of multiple sclerosis, with no adverse side effects because it is a natural treatment for MS. Vitamin D (25(OH)D) blood levels between 80-120 ng/mL are safe and effective, and even occur naturally in many individuals. Other research also strongly suggests that if children maintain an adequate 25(OH)D level through puberty, they will not develop MS.
 I am neither a Physician nor a microbiologist and I am not offering medical advice of any kind. The information I found is available for everyone to read. If you want to institute high dose Vitamin D therapy, only do so with the guidance of your physician. Never abandon any treatment your physician recommended. What I offer on this website is a summary of research I found, and my own personal experience. I am an attorney, and I suffer from Primary Progressive Multiple Sclerosis. I have been able to stop the radiographic progression of my MS (for the past 6 years) through high dose vitamin D therapy.
 Based on the literature I reviewed it seems pretty clear that health care practitioners treating children ought to be recommending that their young patients maintain a 25(OH)D level of at least 50 ng/mL (and more likely around 80 mg/mL) through puberty to prevent MS (and a host of other conditions) from developing. Neurologists and other health care professionals treating patients with MS should probably be recommending that their MS patients maintain a 25(OH)D level between 80-100 ng/mL (within the range of normal according to the testing used today). I try to keep my own 25(OH)D level right around 120 ng/mL.

The Research
Mouse studies conducted over 10 years ago by Colleen Hayes, PhD at the University of Wisconsin-Madison revealed that vitamin D can stop immunodemyelinating disease. Since that time, multiple meta-analyses and clinical studies have shown that vitamin D decreases the incidence, and inhibits the progression, of Multiple Sclerosis. Let’s discuss the existing research, and how it fits together, starting with the mouse studies.

​The Research

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Dr. Hayes was inducing EAE (experimental autoimmune encephalomyelitis- the mouse model of MS) and discovered that pretreatment with calcitriol (the hormonal form of vitamin D) had astounding effects. Dr. Hayes reported that: “Moreover, 1a,25-(OH)2D3 pretreatment completely blocked EAE induction in MBP primed B10.PL mice (39). Further,1a25-(OH)2D3 treatment rapidly reversed the paralytic symptoms of mice with severe acute EAE (178)” (footnote 1).

Vitamin D has an obvious immunomodulating effect that stops white blood cells from attacking native tissue (nerve cells). Vitamin D not only completely stopped EAE (mouse MS) from developing, but vitamin D also reversed the effects of EAE when utilized during the acute phase of the disease (i.e. early). Dr. Hayes explained, “Our laboratory has also studied the process by which 1a,25-(OH)2D3 reversed EAE(178). Mice with severe acute EAE (complete hind limb paralysis) were randomized to receive 1a,25-(OH)2D3 or placebo treatment. The hormone-treated animals began walking with a wobbly gate [sic] at 3 days post treatment, whereas placebo treated mice remained paralyzed. A histolopathological examination at 3 days post treatment showed the hormone-treated mice had a 50% decrease in white matter and meningeal inflammation” (footnote 2).

Another study by Dr. Hayes and her group found that female mice responded far more than male mice to oral vitamin D supplements. Women in particular should pay attention to this finding, as women may benefit more than men from high dose vitamin D therapy where the source of the vitamin D3 is over the counter supplements.

The immunomodulating activity of vitamin D demonstrated in the mouse studies is also demonstrated in studies analyzing human populations. Two studies from the Harvard School of Public Health show that higher vitamin D levels decrease the incidence of MS in humans.
The first study involved analysis of data gathered between 1980 and 1999 from dietary assessments of 238,000 nurses involved in the Nurses’ Health Study and Nurses’ Health Study II. The results were stunning:

“We found a 40% reduction in risk of MS among women who use supplemental vitamin D, primarily in the form of multivitamins, compared with women who do not use supplements” (Footnote 3, emphasis added).

The second study by the Harvard School of Public Health involved analysis of blood samples obtained from the Department of Defense. More than seven million blood samples were available, and from those samples and other records 257 cases of MS were identified. Those cases were then matched to 2 controls by age, sex, race/ethnicity, and dates of blood collection. The 25(OH)D blood levels were analyzed, and the individuals with the highest 25(OH)D levels had a 62% lower incidence of MS than individuals with the lowest 25(OH)D blood levels (Footnote 4, emphasis added).

In addition to the Harvard studies, other research has revealed a direct link between vitamin D and a gene suspected of causing MS, and Clinical trials have demonstrated that high dose vitamin D can reduce the frequency of MS attacks, and the number of active MS lesions, by 50% or more.

In a study funded by the MS Society of Canada, the UK MS Society, the Wellcome Trust and the Medical Research Council, Dr. Julian C. Knight (University of Oxford, UK) and collaborators at Oxford and the University of British Columbia have established a direct relationship between a gene believed to play a role in MS and vitamin D (footnote 5). According to a February 6, 2008 article entitled “Study Shows link Between vitamin D and an MS Gene”, appearing on the National Multiple Sclerosis Society website:”The researchers found that proteins activated by vitamin D in the body bind to a particular DNA sequence lying next to the DRB1*1501 variant, in effect switching the gene on. The authors believe that vitamin D deficiency may lead to lowered expression of this gene, in turn altering immune processes that ultimately trigger the immune attack on brain and spinal cord tissues in MS” (emphasis added).
The gene study again demonstrates the link between adequate levels of vitamin D and preventing MS. “Our study implies that taking vitamin D supplements during pregnancy and the early years may reduce the risk of child developing MS in later life," lead author Dr. Sreeram Ramagopalan said in the news release. "Vitamin D is a safe and relatively cheap supplement with substantial potential health benefits. There is accumulating evidence that it can reduce the risk of developing cancer and offer protection from other autoimmune diseases." (“Vitamin D Deficit May Trigger MS Risk Gene”, U.S. News and World Report (Health), February 5, 2009.)

In a presentation at the 2008 annual meeting of the American Academy of Neurology on April 28, 2008, a group of Canadian researchers presented the results of a study sponsored by the Canadian MS Society. The study involved a group of 25 MS patients who took an average of 14,000 IU of vitamin D3/day for 1 year (high dose group), and a group of 24 MS patients who took an average of 1000 IU/day for 1 year. The contrasting results were astounding. The group taking 14,000 IU/day suffered 41% fewer relapses that they did in the year before the study began, and only 16% suffered any relapses in the year of the study. By contrast, in the group taking 1000 IU/day, there were only 17% fewer relapses, and 40% suffered relapses during the year of the study. The high dose D3 group was also given 1200 mg/day of calcium. Even though the high dose group reached a maximum mean 25(OH)D level of 413 nmol/L (165 ng/mL), there were no adverse side effects reported, including calcium abnormalities. High dose vitamin D therapy cut the relapse rate by over 50% (Footnote 6).

Dosage/Side Effects
A 2007 study from the University of Wisconsin-Madison revealed that MS patients could take fairly large amounts of vitamin D3, with no side effects. The 28 week study involved only 12 patients with RRMS that were given increasing doses of vitamin D3, escalating from 28,000 t0 280,000 IU/week. The searchers found that “Patients’ serum 25(OH)D concentrations reached twice the top of the physiologic range without eliciting hypercalcemia or hypercalciuria. The data support the feasibility of pharmacologic doses of vitamin D3 for clinical research, and they provide objective evidence that vitamin D intake beyond the current upper limit is safe by a large margin.” Kimball, Ursell, O’Connor and Vieth; “Safety of Vitamin D3 In Adults With Multiple Sclerosis”; The American Journal of Clinical Nutrition; Vol. 86, pp.645-651, at 645 (2007) An ancillary finding was that over the short course of the study, the number of gadolinium enhancing lesions(by MRI) among the study participants decreased by 50%. (Footnote 7)
The Wisconsin Study and the Canadian Study (discussed above) both provide good evidence that high dose vitamin D therapy is safe. Since it has been reported that 14,000 IU/day is safe, and given the results of the Canadian Study, 14,000 IU/day of vitamin D3 appears to be a good therapeutic dose and, based on my own research and experience, should result in a 25(OH)D blood level between 80 and 120 ng/mL, depending on the patient’s weight. Dr. Hayes stresses the importance of 25(OH)D blood level over any oral dosage of vitamin D. Dr. Hayes noted; “Adults living or working in sunny environments easily generate >10,000 IU/day of vitamin D through sun exposure without adverse effects., so the safe upper limit for total vitamin D nutrition is at least 10,000 IU/day (Vieth 1999)”(footnote 7)., and that “Adults living or working in sunny environments, where MS prevalence is lowest, have circulating 25-hydroxyvitamin D3 levels between 105 and 163 nmol/L (or 42 to 65 ng/mL) (Vieth 1999). Thus a serum 25-hydroxyvitamin D > 100 nmol/L (40ng/mL) may be optimal to prevent MS.” (Footnote 8, parenthetical added).

Vitamin B3 also appears to restrict the development of PPMS and SPMS

In 2006 researchers at children's Hospital Boston conducted malice research where increasing the blood level of nicotinamide adenine dinucleotide (NAD) dramatically reduced the effects of progressive EAE in mice. The NAD levels were maintained by giving the mice daily injections of nicotinamide, the chemical precursor of NAD (footnote 9). The study seems to support the idea that nicotinamide may be helpful in all forms of MS.
 Nicotinamide tablets are available and health food stores and online for a reasonable price. Nicotinamide is actually a byproduct of niacin. Nicotinamide does not have the flushing effects associated with niacin, but it also does not have the cholesterol-lowering capability of niacin.

Nicotinamide has some toxicity, and it has been reported that doses exceeding 3 g day are associated with liver toxicity (footnote 10).

High dose of vitamin D3 therapy has proven effective in significantly decreasing the number of active MS lesions, and the frequency and severity of MS attacks.

There is a proven relationship between the amount of UVB light available from sunlight and the number of active MS lesion in an MS patient. The more UVB is available (summer or southern latitudes) the fewer active lesions are found (footnote 11). For all MS patients, fewer lesions mean less disability.

Recent studies have consistently shown that high dose vitamin D3 therapy reduces the number of active lesions, and the frequency and severity of attacks in RRMS patients. In fact, patients who took an average of 14,000 IU of vitamin D3 per day had TWO THIRDS FEWER ATTACKS than patients taking 1000 IU/day (footnote 6).
Personal and Anecdotal Experience
I was diagnosed with PPMS in February, 2004, and was advised that there was nothing available that could stop the progression of the disease. I had active MS lesions by gadolinium MRI at the time of my diagnosis. My research revealed the mouse studies by Dr. Hayes and the Harvard School of Public Health analysis of the Nurses Health Studies. I raised my 25(OH)D level to between 100 and 150 ng/mL, and have maintained that level for the past 6 years.

Ten months after my diagnosis I had a second gadolinium enhanced MRI, and there were no active MS lesions. I have obtained regular gadolinium enhanced MRIs, and have had no active MS lesions for 6 years (4 consecutive MRIs- most recent in May, 2011). High dose vitamin D3 therapy has stopped the radiographic progression of my MS, and reversed significant bowel symptoms I experienced prior to institution of the therapy (although I have not experienced any reversal of motor symptoms in arms, trunk and legs).

Robert Baker, M.D. is an Internal Medicine Specialist in Cherry Hill New Jersey who treats patients with MS. Dr. Baker reported complete remission of one of his patients with PPMS using the type of vitamin D therapy that worked for me. You can find his article entitled “Case History - Complete Remission of 16 years of Progressive MS with Vitamin D” at

Prevention of Multiple Sclerosis
Both the Harvard School of Public Health, and Dr. Hayes, discuss the important findings of immigration studies that strongly suggest that if children maintain an adequate level of vitamin D through puberty, they do not develop MS (footnote 1 and footnote 4).


Studies to date have found that high dose vitamin D therapy will significantly reduce the frequency of MS attacks in individuals with RRMS. After extensive research, no contrary studies were located. Neurologists (or others) who treat patients with Multiple Sclerosis should be recommending to those patients that they increase their 25(OH)D blood levels to between 100-150 ng/mL. If Physicians are concerned about making recommendations outside the accepted “normal” range, then the recommendation should be to at least raise the 25(OH)D blood level to 80-100 ng/mL. Patients can safely take an average of 14,000 IU/day with no adverse side effects. No author has suggested any adverse side effects at this level, and the collateral benefits are significant.

Physicians who treat children ought to be recommending that their young patients maintain a 25(OH)D level of 50-100 ng/mL through puberty to prevent MS (and a variety of other chronic and debilitating conditions). Again, there are no known adverse side effects at these blood levels, and there are significant collateral benefits.
Epilogue: Guillian-Barre Syndrome
It appears that the induction of EAE in mice mimics the onset of Guillian-Barre syndrome. Perhaps high dose vitamin D3 should be administered, in addition to undertaking appropriate diagnostic procedures, at the first sign of unexplained neurologic symptoms. There are no reported side effects of high dose vitamin D therapy, and all of the studies, particularly the mouse studies, indicate that high dose vitamin D therapy (probably Calcitrol) is likely to stop the demyelinating process and rapidly reverse the symptoms, if instituted early in the diagnostic process.

1.” Hayes,, “The Immunological Functions of the Vitamin D Endocrine System”, Cellular and Molecular Biology, (at page 11) 49(2), 03-34 Mar, 2003, ISSN 0145-5680/03, citing

2. Id, at p. 12)

3. Munger,, “Vitamin D intake and the incidence of multiple sclerosis”, NEUROLOGY, pp.60-65, at 64,January (1 of 2) 2004.

4. “Serum 25-Hydroxyvitamin D Levels and Risk of Multiple Sclerosis”;

Kassandra L. Munger, Lynn I. Levin, Bruce W. Hollis, Noel S. Howard, and Alberto Ascherio; JAMA. Vol.296, No.23, pp.2832-2838 (December., 2006)

5. “Expression of the Multiple Sclerosis associated MHC class II allele HLA-DRB1*1501 is Regulated by Vitamin D” is published in PLoS Genetics.

6.” Immunological Analysis of a Phase I/II Dose-Escalation Trial of Oral Vitamin D3 with Calcium Supplementation in Patients with Multiple Sclerosis’ presented April 28, 2009 at the annual meeting of the American Academy of Neurology.

7. Hayes, “Vitamin D: a Natural Inhibitor of Multiple Sclerosis”, Proceedings of the Nutrition Society, 2000, v.59, p531-535, at p.533.

8. Ibid.

9. “Protecting Axonal Degeneration by Increasing Nicotinamide Adenine Dinucleotide

Levels in Experimental Autoimmune Encephalomyelitis Models”;

Shinjiro Kaneko, Jing Wang, Marie Kaneko, Glenn Yiu, Joanna M. Hurrell, Tanuja Chitnis, Samia J. Khoury, and Zhigang He; The Journal of Neuroscience, September 20, 2006

10. Knip M, Douek IF, Moore WP, et al. (2000). "Safety of high-dose nicotinamide: a review". Diabetologia 43 (11): 1337-45. doi:10.1007/s001250051536. PMID 11126400.

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