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. 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.

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. 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.

Some individuals, especially those with malabsorption or low dietary intake, are at higher risks 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.