Vitamin B12, specifically in its active coenzyme form 5-deoxyadenosylcobalamin, plays a well-established and scientifically validated role in supporting mitochondrial function. This form of B12 acts as a critical cofactor for the mitochondrial enzyme methylmalonyl-CoA mutase, which is essential in the catabolism of certain amino acids and fatty acids. Proper functioning of this enzyme ensures that methylmalonyl-CoA is converted to succinyl-CoA, an important intermediate in the Krebs (tricarboxylic acid) cycle—a central pathway for cellular energy production within the mitochondria.

Deficiency of B12 impairs this metabolic pathway, leading to accumulation of methylmalonic acid and disruption of energy metabolism, which can result in neurological and systemic symptoms. Clinical and biochemical research has long established that B12 deficiency is linked to mitochondrial dysfunction and that supplementation restores mitochondrial metabolic activity. This is further substantiated by studies on inherited disorders of B12 metabolism, where impaired mitochondrial function is a hallmark.

In summary, the use of B12 (5-deoxyadenosylcobalamin) to support the mitochondrial body system is strongly supported by biochemical, clinical, and physiological evidence, making its role in mitochondrial health one of the most well-characterized among vitamins.