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I have not been able to find any discussion on ThisISMS with regards to multiple sclerosis and vitamin B (that's B as in Bromley come back). I did find a few references through Google scholar and they seem to be somewhat contradictory. I was wondering if anyone has looked into this, particularly vitamin B12. The articles I found were:
Reynolds EH, 'Multiple sclerosis and vitamin B12 metabolism' J Neuroimmunol 1992 Oct; 40(2-3):225-30.
Kira J, et al. 'Vitamin B12 metabolism and massive-dose methyl vitamin B12 therapy in Japanese patients with multiple sclerosis' Intern Med 1994 Feb; 33(2):82-6.
Vrethem M, et al. 'Increased plasma homocysteine levels without signs of vitamin B12 deficiency in patients with multiple sclerosis assessed by blood and cerebrospinal fluid homocysteine and methylmalonic acid' Multiple Sclerosis 2003; vol 9 no 3, p:239-245.

Any thoughts on vitamin B?

Wesley

Have a look at this page for information about B12:

http://www.davidwheldon.co.uk/ms-treatment.html

High-dose sublingual Vitamin B12 (methylcobalamin) should be taken; initially 4000 - 5000 micrograms several times a day, reducing to once daily after three months. This is to flood the system with methylcobalamin as there is often a functional B12 deficit, as evidenced by raised serum methylmalonate or homocysteine. Vitamin B12 (together with B6 and folate) counteracts the hyperhomocysteinaemia which frequently accompanies chronic Chl pneumoniae infection and which is thought to cause connective tissue damage. Excess homocysteine is a potent neurotoxin with activity against cortical and hippocampal neurones. [1. Kruman II, Culmsee C, Chan SL, et al., Homocysteine elicits a DNA damage response in neurons that promotes apoptosis and hypersensitivity to excitotoxicity. J Neurosci 2000;20:6920-6:] [2. Den Heijer T, Vermeer SE, Clarke R, Oudkerk M, Koudstaal PJ, Hofman A, et al. Homocysteine and brain atrophy on MRI of non-demented elderly. Brain 2002;126:170-5:] [3. Leblhuber F, Walli J, Artner-Dworzak E, Vrecko K, Widner B, Reibnegger G, et al. Hyperhomocysteinemia in dementia. J Neural Tansm 2000;107:1469-74.] An excellent review of Vitamin B12 and multiple sclerosis can be recommended here: [Miller A, Korem M, Almog R, Galboiz Y. Vitamin B12, demyelination, remyelination and repair in multiple sclerosis. J Neurol Sci 2005 Jun 15;233(1-2):93-7.]


As for the other sort of vitamin B, he won't be able to keep away for long!

Sarah

hi yea i read that there does seem to be low b12 and elevated homocysteine in your typical ms patient.

i have had chronically low b12 due to dietary negligence but typically i think in ms sufferers there is a b12 absorption problem which drives up the homocysteine coz ur bod is not processing it properly. i don't match because my homocysteine is lower than your average non-ms study participant. confusing.

neway i think the low b12 is common to ms patients whether ur in the subset w c. pneumoniae infection or not. so apparently, you want to avoid cyanocobalamin and take methylcobalamin - my doc has me on 1000mcg q 3 weekly, and my serum b12 is up to 640 while my homocysteine is 6. b12 is neuroprotective so it's good stuff for us ms-ers. also i believe you need calcium to properly absorb b12.

here's an abstract linking calcium and cobalamin absorption (in this case the gut's prob with absorbing b12 was caused by a medication):

Diabetes Care. 2000 Sep;23(9):1227-31. Related Articles, Links

Increased intake of calcium reverses vitamin B12 malabsorption induced by metformin.

Bauman WA, Shaw S, Jayatilleke E, Spungen AM, Herbert V.

Department of Medicine, Mount Sinai School of Medicine, New York, USA. bauman.william@bronx.va.gov

OBJECTIVE: Of patients who are prescribed metformin, 10-30% have evidence of reduced vitamin B12 absorption. B12-intrinsic factor complex uptake by ileal cell surface receptors is known to be a process dependent on calcium availability Metformin affects calcium-dependent membrane action. The objective of this study was to determine the magnitude and mechanism of the reduction in serum vitamin B12 after metformin administration. RESEARCH DESIGN AND METHODS: A comparative study design was employed using 2 groups (metformin and control). A total of 21 patients with type 2 diabetes received sulfonylurea therapy; 14 of these 21 patients were switched to metformin. Monthly serum total vitamin B12 measurements and holotranscobalamin (holoTCII) (B12-TCII) were performed. After 3 months of metformin therapy, oral calcium supplementation was administered. RESULTS: Serial serum vitamin B12 determinations revealed a similar decline in vitamin B12 and holoTCII. Oral calcium supplementation reversed the metformin-induced serum holoTCII depression. CONCLUSIONS: Patients receiving metformin have diminished B12 absorption and low serum total vitamin B12 and TCII-B12 levels because of a calcium-dependent ileal membrane antagonism, an effect reversed with supplemental calcium.

hi all,

know how they don't have as much ms in japan? and it's an anomaly in the otherwise temperate zone distribution of the disease?

guess what the bottom end of their normal range for b12 is? FIVE HUNDRED.

pass it on to everyone you know who doesn't have ms yet! or alzheimer's (another illness associated with low b12) for that matter - i hear they don't get that in japan either.

d

ps. in the abstract below it says supplementing w b12 doesn't help, but it's helping me. a lot.

Int J Neurosci. 1993 Jul-Aug;71(1-4):93-9.
Vitamin B12 and its relationship to age of onset of multiple sclerosis.
Sandyk R, Awerbuch GI.
NeuroCommunication Research Laboratories, Danbury, CT 06811.

Attention has been focused recently on the association between vitamin B12 metabolism and the pathogenesis of multiple sclerosis (MS). Several recent reports have documented vitamin B12 deficiency in patients with MS. The etiology of this deficiency in MS is unknown. The majority of these patients do not have pernicious anemia and serum levels of the vitamin are unrelated to the course or chronicity of the disease. Moreover, vitamin B12 does not reverse the associated macrocytic anemia nor are the neurological deficits of MS improved following supplementation with vitamin B12. It has been suggested that vitamin B12 deficiency may render the patient more vulnerable to the putative viral and/or immunologic mechanisms widely suspected in MS. In the present communication, we report that serum vitamin B12 levels in MS patients are related to the age of onset of the disease. Specifically, we found in 45 MS patients that vitamin B12 levels were significantly lower in those who experienced the onset of first neurological symptoms prior to age 18 years (N = 10) compared to patients in whom the disease first manifested after age 18 (N = 35). In contrast, serum folate levels were unrelated to age of onset of the disease. As vitamin B12 levels were statistically unrelated to chronicity of illness, these findings suggest a specific association between the timing of onset of first neurological symptoms of MS and vitamin B12 metabolism. In addition, since vitamin B12 is required for the formation of myelin and for immune mechanisms, we propose that its deficiency in MS is of critical pathogenetic significance.