Here’s the link to a great article that i found for you about vitamin D and MS. The article goes into great detail about why ditamin D is important for MS sufferers and why MS sufferers should supplement their diet with this hormone to help prevent relapses.
DR. CARTWRIGHT’S COMMENT: REFERENCES & FIGURES AS WELL AS CERTAIN SUB-HEADINGS OF THIS ARTICLE, LISTED BELOW, HAVE BEEN EDITED OUT FOR PURPOSES OF LENGTH. THE FULL DOCUMENT CAN BE VIEWED AT: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2733195/
J Neurol. 2009 September; 256(9): 1468–1479 Published online 2009 April 28 © The Author(s) 2009
Clinical implications of a possible role of vitamin D in multiple sclerosis
Risk factors for MS are becoming clearer even if the mechanisms leading from these risk factors to the disease itself remain obscure. There are two main types of risk factors for MS, i.e. genetic and environmental, likely with complex interactions between them and effects which may be deleterious or protective, depending on the case. Genetic risk factors are numerous, but they are still relatively not well known and will not be dealt with here. Three environmental risk factors have recently emerged from the literature—i.e. hypovitaminosis D, past infection with Epstein-Barr virus (EBV) and smoking—with effects that could be cumulative. In this review, we shall confine our analysis to hypovitaminosis D, which is the risk factor currently the most promising in terms of immediate clinical implications.
Hypovitaminosis D has long been suspected of being a risk factor for MS but there has recently been a sharp increase of interest in this factor. The putative protective role of vitamin D in MS is based on a wide-ranging series of arguments. The first group of arguments exists outside, or indeed before, the disease, including physiological, metabolic, experimental and immunological factors, in addition to which there are epidemiological data on the effects of latitude, past exposure to sunlight and serum vitamin D levels on the risk of MS in the general population. The second group of arguments stems from data on MS patients derived from biological and therapeutic studies. We shall begin by looking at how these very diverse experimental and epidemiological arguments have progressively accumulated to strengthen the hypothesis that vitamin D plays a substantial protective role in MS. Then, even though there is no incontrovertible evidence from clinical studies to confirm that vitamin D can also have a curative effect, in the last chapter we shall propose the clinical applications that it would appear could be made available to MS patients without further delay. This paper is, to our knowledge, the first proposing such practical measures after the recent information reported on vitamin D in MS.
Effect of vitamin D treatment in MS
Studies on the use of vitamin D in MS are still rare and limited in scope. After a two-year course of treatment with vitamin D (5,000 IU/d in the form of cod liver oil), 10 patients with MS had a 60% reduction in the predicted number of relapses, but there was no control group. In another uncontrolled study, 15 patients who received 100 IU/d for 48 weeks experienced a 50% reduction in relapses. In a study on 39 patients with MS (17 treated with 1,000 IU/d of vitamin D3 (cholecalciferol) for 6 months and 22 control subjects), the treated patients had a significantly increased level of TGF-?1, an anti-inflammatory cytokine affected by vitamin D in EAE. Lastly, a Canadian team recently demonstrated that the use of high doses of vitamin D3 (cholecalciferol, 14,000 IU/d) during a long period (6 months–1 year) did not induce hypercalcaemia or notable side-effects, despite serum vitamin D levels of nearly 400 nmol/l. After 1 year of such treatment, a 41% reduction in the number of relapses and a significant improvement in EDSS was observed in the treated patients (n = 25 vs. 24 untreated patients). The results of these methodologically weak studies do not of course allow us to draw any definite conclusions. However, taking into account the full scientific context, they are encouraging and provide ample justification for much more extensive therapeutic trials (phase II or phase III). The appropriate vitamin D doses will, however, have to be determined, since the daily dosages in the aforementioned four studies were 100, 1000, 5,000 and 14,000 IU/d, a situation that raises the perplexing question of the useful therapeutic dosage.
Based on considerable physiological evidence, a large body of experimental findings, consistent epidemiological data and limited but promising clinical studies, the hypothesis that hypovitaminosis D is one of the environmental risk factors for MS has rapidly gained support and could soon be confirmed by more extensive clinical studies. Over and above its possible role in MS, hypovitaminosis D—due to its widespread distribution among the general population in countries with low levels of sunlight—now raises a crucial public health problem which must be solved if we are to achieve optimal prevention of a number of general affections that are common in these countries. Neurologists, like all medical practitioners, should be keenly aware of this problem, but those who are more particularly involved in caring for MS patients must be doubly receptive and rapidly preventive, since ‘time is brain’ is also applicable to MS.
Physiological and metabolic basis
Experimental and immunological studies
Effect of latitude on the prevalence of MS
Effect of latitude on serum vitamin D levels in the general population
Effect of exposure to sunlight on the risk of MS
Effect of the serum vitamin D level in the general population on the risk of MS
Biological studies related to vitamin D in MS
Effect of vitamin D treatment in MS
Questions and practical clinical approach to vitamin D in MS
To Your Health,
Dr. Rudy Cartwright
PS: As always, please leave your comments below.