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FAQs About Methylcobalamin B12

Methylcobalamin B12


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The Most Potent Form of Vitamin B12 Available

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High-Potency Sublingual Vitamin B12 in its Active Form


Preferred Sublingual Methyl-B12 is a high-potency dietary supplement providing 5,000 mcg (5 mg) of vitamin B12 as Methylcobalamin. This convenient, sublingual tablet formulation is intended to be dissolved in the mouth or under the tongue to facilitate more direct absorption into the bloodstream through sublingual tissues. Methylcobalamin tablets contain mannitol and xylitol as natural sweetening and dispersing agents. Natural cherry flavor is added.


Methylcobalamin, one of two active coenzyme forms of vitamin B12 (cobalamin), plays an important role in red blood cell formation, methylation reactions, brain and nervous system function, and immune system regulation.

Cobalamin deficiency may manifest as megaloblastic anemia, peripheral neuropathy, irritability, dementia, depression, psychosis, and increased risk of myocardial infarction and stroke.

With early diagnosis and prompt treatment, progressive and irreversible neurologic and cognitive impairment can be avoided. However, circulating levels of cobalamin are not always a reflection of tissue levels. In fact, even if an adequate supply of cobalamin is present in the circulation, a functional deficiency of the coenzyme forms might exist in tissues or other body fluids.

Evidence indicates methylcobalamin has metabolic benefits and potential therapeutic applications not offered by other forms of vitamin B12. Although cyanocobalamin is the most commonly used form of vitamin B12 in dietary supplements, it must be enzymatically converted into one of two metabolically active coenzyme forms, i.e. S-adenosylcobalamin or methylcobalamin. Nutritional inadequacies, enzyme defects, and tissue abnormalities can reduce the body’s ability to synthesize these active forms.

Methylcobalamin participates in the transfer of methyl groups as an essential cofactor for methionine synthase, a critical enzyme required for synthesis of methionine from homocysteine. This contributes to lowering of homocysteine levels, which is recognized as a risk factor for cardiovascular disease. Methylcobalamin also participates in synthesis of S-adenosylmethionine (SAM), important for formation of the neurotransmitters dopamine and serotonin involved in mood regulation.

The biologically active, methylcobalamin form of vitamin B12 is a crucial donor of methyl groups to the myelin sheath that insulates nerve fibers and regenerates damaged neurons. Recent data suggests that methylcobalamin may be beneficial for patients with neuropathies.

Patients with non-insulin dependent mellitus treated with 500 mcg methylcobalamin intramuscularly three times a week for four weeks then followed by 500 mcg orally three times a day for an additional eight weeks responded favorably with improvements in sensation and other symptoms. Patients with uremia and uremic-diabetic polyneuropathies receiving 500 mcg methylcobalamin injections experienced lessening of pain or parasthesia (numbness or tingling) and improved sensory nerve conduction velocities.

Administration of methylcobalamin along with folic acid has also been shown to reduce total plasma homocysteine levels in hemodialysis patients whereas administration of cyanocobalamin was less effective. Both folic acid and vitamin B12 are required for the remethylation pathway to regain and maintain normal activity.

Deterioration of this pathway is related to an inhibition of folate enzymes as well as deficiency of methylcobalamin. Cyanocobalamin may not be as effective in lowering homocysteine levels when the body’s ability to metabolize and transmethylate it into methylcobalamin is impaired.

Of all the forms of vitamin B12, methylcobalamin appears to have greater application in the unique metabolic biochemistry seen in children with regressive autism. A growing body of evidence indicates that children on the autism spectrum have complex biochemical abnormalities including impaired methylation chemistry with increased oxidative stress, alterations in detoxification pathways, significant gastrointestinal pathology resulting in nutritional deficits, neurotoxicity associated with additional compromised metabolic issues, and immune dysregulation, all leading to impaired CNS or neurological function.

Researchers and clinicians are finding that nutritional support of methylation biochemistry with nutrients such as methylcobalamin shows promise in supporting the complex immune, metabolic, and neurological impairments seen in regressive autism.

Use of oral methylcobalamin may thus offer biochemical and therapeutic advantages over traditional forms of oral vitamin B12.


Methylcobalamin can be administered whenever a need for supplemental vitamin B12 exists. It may be particularly useful for individuals with impaired methylation capacity, including those with elevated homocysteine or neurological impairments.


Dissolve 1 tablet daily in the mouth or under the tongue or as directed by a physician.


Oral forms of cobalamin have been shown to be safe and well tolerated. Current research suggests oral cobalamin is often as equally effective, more cost-effective, and better tolerated than intramuscular cobalamin injections.


None Reported.


None Reported.


Vitamin B12 should be taken at different times of the day from tetracycline. Use of metformin for diabetes, acid-reducing medications for ulcers, and long-term treatment with phenobarbital or phenytoin for seizure disorders may interfere with the body's ability to use vitamin B12.


60 sublingual tablets per bottle with full-bottle shrink-wrap. Packaged 12 bottles per case. 

You can learn more about the importance of methylcobalamin and how to order by clicking here.


Store in a cool, dry place (59°F-85°F) away from direct light or keep refrigerated. Keep out of reach of children.


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Elia M. Oral or parenteral therapy for B12 deficiency. Lancet 1998;352:1721-1722.

James SJ, Cutler P, Melnyk S, Jernigan S, Janak L, Gaylor DW, Neubrander JA. Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism. Am J Clin Nutr. 2004 Dec;80(6):1611-7.

Kelly G. The coenzyme forms of vitamin B12: toward an understanding of their therapeutic potential. Alt Med Rev 1997;2(5):459-471.

Koyama K, Usami T, Takeuchi O, et al. Efficacy of methylcobalamin on lowering total homocysteine plasma concentrations in haemodialysis patients receiving high-dose folic acid supplementation.

Kuwabara S, Nakazawa R, Azuma N, et al. Intravenous methylcobalamin treatment for uremic and diabetic neuropathy in chronic hemodialysis patients. Intern Med 1999;38(6):472-475.

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Leal N, Olteanu H, Banerjee R, et al. Human ATP:Cob(I)alamin adenosyltransferase and its interaction with methionine synthase reductase. J Biol Chem 2004;279(46):47536-47542.

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Oh R, Brown D. Vitamin B12 deficiency. Am Fam Physician 2003;67:979-986.

Okuda K, Yashima K, Kitazaki T, et al. Intestinal absorption and concurrent chemical changes of methylcobalamin. J Lab Clin Med 1973;81:557-567.

Solomon L. Cobalamin-responsive disorders in the ambulatory care setting: unreliability of cobalamin, methylmalonic acid, and homocysteine testing. Blood 2005;105:978-985.

Suormala T, Baumgartner M, Takasaki Y, Moriuchi Y, Tsushima H, et al. Effectiveness of oral B12 therapy for pernicious anemia and vitamin B12 deficiency anemia. Rinsho Ketsueki 2002;43(3):165-169.

Tsukerman E, Pomerantseva T, Poznanskaia A, et al. Effect of methylcobalamin and adenosylcobalamin on the process of hematopoiesis and vitamin B12 exchange in experimental phenylhydrazine-induced anemia in rabbits. Vopr Med Khim 1989;35(1):106-111.

Weir D, Scott J. Vitamin B12 “Cobalamin.” In: Maurice E. Shils, ed. Modern nutrition in health and disease, 9th edition, Lippincott Williams & Wilkins, 1999:447-458.




The Most Potent Form of Vitamin B12 Available

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