Bioclinic Naturals, B12 Methylcobalamin 5000 mcg 60 lozenges

Benefits

• Methylcobalamin is the active form of vitamin B12 for maximum benefit
• Superior bioavailability to the more common form, cyanocobalamin, which does not convert to enough methylcobalamin to correct some forms of anemia, neurological defects, and aging1
• Lowers homocysteine levels for protective cardiovascular benefits
• Sublingual tablets allow for fast acting delivery system directly into the bloodstream

Feature Summary

Vitamin B12 is the cofactor in enzymatic reactions with diverse physiological functions. It is required for the conversion of methylmalonyl CoA to succinyl CoA, as well as for the conversion of homocysteine to methionine by methionine synthase, which is then converted into S-adenosylmethionine.2 A B12 deficiency causes impairments in both of these pathways, disrupting neurological function, including poor formation of myelin nerve sheaths, production of toxic levels of homocysteine, and inefficient energy production in all cells.3,4

Methylcobalamin, the principal circulating form of B12 and the one transported into peripheral tissues, has been shown to not only reduce homocysteine, but also to reduce inflammatory factors and the volume of carotid artery plaques among stroke patients, as well as pain, and neuropathy among diabetics.5-8 Because of its relationship to myelin production and neurological function, high-dose B12 has been used in a variety of neurodegenerative diseases, including Parkinson’s disease, amyotrophic lateral sclerosis, and multiple sclerosis.9–12

Some individuals, especially those with malabsorption or low dietary intake, are at higher risk for a B12 deficiency. Individuals with impaired absorption of B12 rely on passive absorption, which is typically 1% of the ingested amount. Thus, high doses may be required for those with greater B12 needs, such as elderly individuals and those with neurodegenerative disorders.13,14

Non-Medicinal Ingredients

Lactose monohydrate, microcrystalline cellulose, croscarmellose sodium, vegetable grade magnesium stearate (lubricant).

Dosage

Recommended Adult Dose: 1 tablet per day or as directed by a health care professional. Dissolve under the tongue. Consult a health care practitioner for use beyond 4 months.

Warnings

Consult a health care practitioner prior to use if you are pregnant or breastfeeding. Keep out of reach of children.

Allergens

Contains no artificial colours, preservatives, or sweeteners; no starch, sugar, wheat, gluten, yeast soy, corn, egg, fish, shellfish, salt, tree nuts, or GMOs. Suitable for vegetarians. It is sealed for your protection. Only use it if the seal is fixed. For freshness, store in a cool, dry place.

Contraindications

Consult a health care practitioner prior to use if you are pregnant or breastfeeding. High doses in oncology patients may be cautioned against because of their role in DNA synthesis. Supplemental folic acid may mask a B12 deficiency, which should be ruled out. Folic acid, as well as increased potassium intake, is recommended with B12 therapy. Keep out of reach of children.

Drug Interactions

Although several classes of drugs, such as aminoglycosides, anticonvulsants, bile acid sequestrants, and proton pump inhibitors are known to interfere with B12 absorption or function, there are no known negative interactions caused by B12 supplementation with any medications.16-22 B12 may enhance the function or reduce the adverse effects of several medication classes, such as SSRIs and oral contraceptives.23

1. References:
2. [No authors listed]. (1998). Methylcobalamin. Altern Med Rev, 3(6), 461-3.
3. Guéant, J.L., Caillerez-Fofou, M., Battaglia-Hsu, S., et al. (2013). Molecular and cellular effects of vitamin B12 in the brain, myocardium, and liver through its role as a co-factor of methionine synthase. Biochimie, 95(5), 1033-40.
4. Calderón-Ospina, C.A., Nava-Mesa, M.O. (2020). B Vitamins in the nervous system: Current knowledge of the biochemical modes of action and synergies of thiamine, pyridoxine, and cobalamin. CNS Neurosci Ther, 26(1), 5-13.
5. Austin, R.C., Lentz, S.R., Werstuck, G.H. (2004). Role of hyperhomocysteinemia in endothelial dysfunction and atherothrombotic disease. Cell Death Differ, 11(Suppl 1), S56-64.
6. Miranda-Massari, J.R., Gonzalez, M.J., Jimenez, F.J., et al. (2011). Metabolic correction in the management of diabetic peripheral neuropathy: improving clinical results beyond symptom control. Curr Clin Pharmacol, 6(4), 260-73.
7. Yuan, M., Wang, B., Tan, S. (2018). Methylcobalamin and early functional outcomes of ischemic stroke patients with H-type hypertension. Rev Assoc Med Bras (1992), 64(5), 428-432.
8. Jiang, D.Q., Zhao, S.H., Li, M.X., et al. (2018). Prostaglandin E1 plus methylcobalamin combination therapy versus prostaglandin E1 monotherapy for patients with diabetic peripheral neuropathy: A meta-analysis of randomized controlled trials. Medicine (Baltimore), 97(44), e13020.
9. Buesing, S., Costa, M., Schilling, J.M., et al. (2019). Vitamin B12 as a Treatment for Pain. Pain Physician, 22(1), E45-E52.
10. Sun, Y., Lai, M.S., Lu, C.J. (2005). Effectiveness of vitamin B12 on diabetic neuropathy: systematic review of clinical controlled trials. Acta Neurol Taiwan, 14(2), 48-54.
11. Kumar, N. (2014). Neurologic aspects of cobalamin (B12) deficiency. Handb Clin Neurol, 120, 915-26.
12. McCaddon, A. (2013). Vitamin B12 in neurology and aging; clinical and genetic aspects. Biochimie, 95(5), 1066-76
13. Kaji, R., Imai, T., Iwasaki, Y., et al. (2019). Ultra-high-dose methylcobalamin in amyotrophic lateral sclerosis: a long-term phase II/III randomized controlled study. J Neurol Neurosurg Psychiatry, 90(4), 451-457.
14. Delpre, G., Stark, P., Niv, Y. (1999). Sublingual therapy for cobalamin deficiency as an alternative to oral and parenteral cobalamin supplementation. Lancet, 354(9180), 740-1.
15. Gröber, U., Kisters, K., Schmidt, J. (2013). Neuroenhancement with vitamin B12-underestimated neurological significance. Nutrients, 5(12), 5031-45.
16. Paul, C., & Brady, D.M. (2017). Comparative Bioavailability and Utilization of Particular Forms of B12 Supplements With Potential to Mitigate B12-related Genetic Polymorphisms. Integr Med (Encinitas), 16(1), 42-49.
17. McColl, K.E. (2009). Effect of proton pump inhibitors on vitamins and iron. Am J Gastroenterol, 104(Suppl 2), S5-9.
18. Aslan, K., Bozdemir, H., Unsal, C., et al. (2008). The effect of antiepileptic drugs on vitamin B12 metabolism. Int J Lab Hematol, 30(1), 26-35.
19. Markkanen, T., Salmi, H.A., Sotaniemi, E. (1965). Effect of neomycin treatment on the vitamin B12 content of human serum and urine. Z Vitam Horm Fermentforsch, 14(1), 66-71.
20. Karadag, A.S., Tutal, E., Ertugrul, D.T., et al. (2011). Effect of isotretinoin treatment on plasma holotranscobalamin, vitamin B12, folic acid, and homocysteine levels: non-controlled study. Int J Dermatol, 50(12), 1564-9.
21. Aroda, V.R., Edelstein, S.L., Goldberg, R.B., et al. (2016). Long-term Metformin Use and Vitamin B12 Deficiency in the Diabetes Prevention Program Outcomes Study. J Clin Endocrinol Metab, 101(4), 1754-1761.
22. de Jager, J., Kooy, A., Lehert, P., et al. (2010). Long-term treatment with metformin in patients with type 2 diabetes and risk of vitamin B-12 deficiency: randomized placebo-controlled trial. BMJ, 340, c2181.
23. Dierkes, J., Westphal, S., Kunstmann, S., et al. (2001). Vitamin supplementation can markedly reduce the homocysteine elevation induced by fenofibrate. Atherosclerosis, 158(1), 161-4.
24. Syed, E.U., Wasay, M., Awan, S. (2013). Vitamin B12 supplementation in treating major depressive disorder: a randomized controlled trial. Open Neurol J, 7, 44-8.