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Home > Methylcobalamin (the active ingredient in Xobaline) is one of several forms of vitamin B12 known as ‘cobalamins’. Cobalamins
are unique vitamins in that they contain the mineral cobalt. Only two of the cobalamins actually play active roles in the body’s biochemistry, however — these are methylcobalamin and S-adenosylcobalamin. Since the methyl- and adenosyl- forms are interconvertable, a dietary source that contains methylcobalamin also serves as
a source of S-adenosylcobalamin.
Methylcobalamin serves as a co-enzyme for the enzyme methionine synthase — the enzyme that converts the substance homocysteine into the amino acid methionine.1 In this conversion a methyl fragment is, in effect, obtained from a molecule of folic acid (another vitamin), and attached to a molecule of homocysteine, converting the latter into methionine. This process of transferring methyl fragments from one biomolecule to another has been found to have far-reaching ramifications for health, some of which are only now coming to light. (Note: methylcobalamin and folic acid are both required for the conversion of homocysteine to methionine — LifeLink’s Xobaline therefore contains both of these vitamins.) Deficiencies of vitamin B12 result in harmful effects on the blood, nerves, vascular system, bone, and digestive tract:
The cobalamins are made only by microorganisms, not by plants or animals. This means that animals must obtain them either from their diet or from microorganisms living in their bodies. For example, cows get their vitamin B12 from gut-dwelling bacteria. Since the cobalamins are stored in animal cells, carnivores can get their vitamin B12 by eating meat, even though they don’t themselves have B12-producing gut-dwelling bacteria. Herbivores that lack B12-producing bacteria (such as human vegetarians or pet animals) will develop B12 deficiencies unless they use some kind of B12 supplement. Left untreated, such deficiencies will eventually do permanent damage to the body. What we can’t tell youIn the U.S. and some other industrialized countries, government agencies like the U.S. Food and Drug Administration have adopted censorship as a method for intensifying their control over the supplement industry and its customers. Thus, FDA regulations prohibit us from telling you that any of our products are effective as medical treatments, even if they are, in fact, effective. Accordingly, we will limit our discussion of methylcobalamin to a brief summary of relevant research, and let you draw your own conclusions about what medical conditions it may be effective in treating. Interest in methylcobalamin supplementation centers mainly on three applications:
Diabetic neuropathyDiabetic neuropathy is a decrease in nerve function typically affecting the lower limbs in people and animals with diabetes. The symptoms include muscle weakness, depressed reflexes, disturbances in gait or balance, numbness, tingling, burning, or shooting pains. Sensation can eventually become completely lost so that minor injuries may go unnoticed. Damage to the autonomic nervous system results in impaired circulation, so that wounds don’t heal properly. Thus, minor injuries can become major ones, greatly increasing the risk of gangrene and the need for amputation of affected body parts. Effective treatment of diabetic neuropathy has reportedly been achieved with methyl B12 in sufficiently large doses.10,11 The mechanism for these beneficial effects is not yet completely understood. It has been suggested that diabetics are deficient in B12 in their nerve tissue (not in the blood)15, and that B12 supplements correct this deficiency.12 Diabetes afflicts animals as well as humans, so it’s not surprising that pets can also suffer from diabetic neuropathy and that Xobaline is being used as a treatment. This subject is discussed in a separate article on this website. Neurodegenerative diseasesIn certain neurological conditions — such as Alzheimer’s, Parkinson’s, amyotrophic lateral sclerosis, and AIDS-related dementia — nerve cells are thought to be exposed to excessive amounts of the neurotransmitter glutamate, resulting in neurotoxicity.13 Recently high-dose methyl B12 has been shown to diminish glutamate-related neurotoxicity in animals14, suggesting that neurodegenerative diseases may be effectively treated with methyl B12. Several studies during the 1990s showed specific improvements in the condition of patients with amyotrophic lateral sclerosis, multiple sclerosis, or Alzheimer’s, when they were given large doses of methylcobalamin.5,6,7 Parkinson’s Disease is usually treated with the drug L-dopa, which has, as a side effect, the elevation of homocysteine levels. Parkinson’s patients are therefore at increased risk of cardiovascular damage. A study in 2005 reported that dual supplementation with cobalamin and folic acid effectively reduced these elevated homocysteine levels — as one would expect.8 Cardiovascular diseaseResearch into the effects of methylcobalamin and other vitamin B12 variants on cardiovascular disease has been focused entirely on the prevention of homocysteine excesses in the body. Since methylcobalamin is required for homocysteine metabolism, B12 deficiencies can cause the body to accumulate too much homocysteine and cause coronary artery disease.2 Methylcobalamin supplementation is a well-accepted treatment for such deficiency-caused cardiovascular problems, which may include ischemic heart disease, stroke, and peripheral vascular disease.9,4 Methylcobalamin supplementation may also be useful for lowering homocysteine levels that are elevated for reasons other than B12 deficiencies.4 Stroke and osteoporosisAn elevated homocysteine level is a risk factor for both ischemic stroke and osteoporotic fractures in elderly men and women.4 In a 2005 study it was shown that in stroke patients, a two-year treatment with methylcobalamin (1500 mcg/day) plus folic acid (5 mg/day) reduced plasma homocysteine levels by 38% and reduced the rate of hip fractures by about a factor of 4.4 ConclusionAre methylcobalamin supplements useful for the conditions and purposes mentioned above? We aren’t allowed to tell you, so you should take a look at some of the references cited here, and then decide for yourself. References[1] Vitamin B12: Are you getting it? [PDF, 406KB] Vegan Outreach website Jack Norris [2] Vitamin B12 PDR Health website [3] Vitamin B12 (Cobalamin) University of Maryland Medical Center website [4] Effect of folate and mecobalamin on hip fractures in patients with stroke: a randomized controlled trial. JAMA. 2005 Mar 2;293(9):1082-8 Sato Y, Honda Y, Iwamoto J, Kanoko T, Satoh K [5] Effect of ultrahigh-dose methylcobalamin on compound muscle action potentials in amyotrophic lateral sclerosis: a double-blind controlled study. Muscle Nerve. 1998 Dec;21(12):1775-8 Kaji R, Kodama M, Imamura A, Hashida T, Kohara N, Ishizu M, Inui K, Kimura J [6] Vitamin B12 metabolism and massive-dose methyl vitamin B12 therapy in Japanese patients with multiple sclerosis. Intern Med. 1994 Feb;33(2):82-6. Kira J, Tobimatsu S, Goto I [7] Treatment of Alzheimer-type dementia with intravenous mecobalamin. Clin Ther. 1992 May-Jun;14(3):426-37 Ikeda T, Yamamoto K, Takahashi K, Kaku Y, Uchiyama M, Sugiyama K, Yamada M [8] Hyperhomocysteinemia in L-dopa treated Parkinson's disease patients: effect of cobalamin and folate administration. Eur J Neurol. 2005 May;12(5):365-8 Lamberti P, Zoccolella S, Armenise E, Lamberti SV, Fraddosio A, de Mari M, Iliceto G, Livrea P [9] Role of hyperhomocysteinemia in endothelial dysfunction and atherothrombotic disease. Cell Death Differ. 2004 Jul;11 Suppl 1:S56-64 Austin RC, Lentz SR, Werstuck GH [10] Clinical usefulness of intrathecal injection of methylcobalamin in patients with diabetic neuropathy. Clin Ther. 1987;9(2):183-92 Ide H, Fujiya S, Asanuma Y, Tsuji M, Sakai H, Agishi Y [11] Effects of methylcobalamin on diabetic neuropathy. Clin Neurol Neurosurg. 1992;94(2):105-11 Yaqub BA, Siddique A, Sulimani R [12] Effectiveness of vitamin B12 on diabetic neuropathy: systematic review of clinical controlled trials. Acta Neurol Taiwan. 2005 Jun;14(2):48-54 Sun Y, Lai MS, Lu CJ [13] Role of glutamate and excitotoxicity in neurologic diseases [in French] Rev Neurol (Paris). 1996;152(4):239-48 Hugon J, Vallat JM, Dumas M [14] Methylcobalamin attenuates the hypoxia/hypoglycemia- or glutamate-induced reduction in hippocampal fiber spikes in vitro. Eur J Pharmacol. 1995 Aug 15;281(3):335-40 Yamamoto Y, Shibata S, Hara C, Watanabe S [15] Relation of partial deficiency of cobalamins to occurrence of diabetic neuropathy. Gato Y et al., eds., Diabetic Neuropathy, Excerpta Medica International Congress Series 581, Amsterdam. 1982:114-119. Tanaka N, Yamazaki Y, Sakato H, Maeno H et al. [not available online] |
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