Synopsis

Source of validity: Scientific
Rating (out of 5): 4

Vitamin B12, particularly in its active coenzyme form deoxyadenosylcobalamin, is scientifically validated as essential for mitochondrial function. Deoxyadenosylcobalamin acts as a critical cofactor for the mitochondrial enzyme methylmalonyl-CoA mutase, which is required for the conversion of methylmalonyl-CoA to succinyl-CoA, a key step in the metabolism of certain amino acids and odd-chain fatty acids. This metabolic process feeds into the citric acid (Krebs) cycle, directly supporting mitochondrial energy production. Individuals with vitamin B12 deficiency can develop elevated methylmalonic acid levels, a biomarker of mitochondrial dysfunction, and may experience neurological and hematological symptoms due to impaired mitochondrial metabolism. Clinical evidence demonstrates that B12 supplementation corrects these abnormalities and restores normal mitochondrial function, particularly in cases of inherited defects (e.g., methylmalonic acidemia) or acquired deficiency. While most clinical attention focuses on B12’s role in red blood cell production and nervous system maintenance, its mitochondrial role is well-characterized in biochemistry and metabolic medicine literature. Therefore, the use of vitamin B12 (as deoxyadenosylcobalamin) to support mitochondrial function is justified by robust scientific evidence.

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