The potential cocarcinogenic effect of vitamin B12 deficiency

Abstract

Since vitamin B12 serves as a cofactor in the synthesis of methyl precursors for biological methylation and enables methylfolate to be recycled for nucleotide synthesis, B12 deficiency has been known to induce hyperhomocysteinemia and inadequate DNA synthesis, along with "methylfolate trap". Even though depletion of B12, a common B-vitamin deficiency in the elderly, has not often been invoked as a causative factor in carcinogenesis, a recent animal study demonstrated that a B12-deficient diet, which was of insufficient severity to cause anemia or illness, disturbed normal homeostasis of one-carbon metabolism in the colonic mucosa and resulted in diminished genomic DNA methylation and increased uracil misincorporation in DNA, both of which are purported mechanisms for one-carbon metabolism-related colonic carcinogenesis.