Vitamin B12

Vitamin B12 (cobalamin) is a water-soluble vitamin first isolated in 1948 and later identified as the anti-pernicious anemia factor. It exists in several forms, including methylcobalamin and cyanocobalamin, which serve as cofactors for methionine synthase and methylmalonyl-CoA mutase. These enzymes are crucial for DNA methylation, red blood cell production, and neurotransmitter synthesis. Vitamin B12 is naturally obtained from animal products such as meat, fish, dairy, and eggs, as well as fortified foods. In the stomach, gastric parietal cells secrete intrinsic factor, which binds B12 and facilitates its absorption in the terminal ileum. Deficiency arises from inadequate dietary intake (common in strict vegans), malabsorption syndromes, pernicious anemia, or chronic use of proton pump inhibitors and metformin. Clinical manifestations range from macrocytic anemia, marked by fatigue and pallor, to neurological symptoms, including numbness, tingling, gait disturbances, and cognitive impairment. Early detection and treatment, often via high-dose oral supplementation or intramuscular injections, can reverse hematologic abnormalities and mitigate neurologic damage. Monitoring levels of serum methylmalonic acid and homocysteine aids in diagnosis. Pregnant and lactating women have higher requirements to support fetal development and neonatal stores. Regular screening in high-risk populations—elderly individuals, vegetarians, and those with gastrointestinal disorders—is recommended. Overall, vitamin B12 is vital for cellular metabolism, and maintaining adequate status prevents serious hematologic and neurologic complications. (Sources: https://ods.od.nih.gov/factsheets/VitaminB12-HealthProfessional/, https://www.nutritionaloutlook.com/view/clinical-benefits-b12-supplementation)

Vitamin B12 functions as a cofactor for two key enzymes: methionine synthase and methylmalonyl-CoA mutase. Methionine synthase catalyzes the remethylation of homocysteine to methionine, which is vital for DNA methylation and neurotransmitter synthesis. Methylmalonyl-CoA mutase converts methylmalonyl-CoA to succinyl-CoA, a critical step in fatty acid and amino acid metabolism. Deficiency impairs these reactions, leading to elevated homocysteine and methylmalonic acid levels. Additionally, B12 is required for the maturation of erythroid cells in bone marrow; inadequate B12 results in megaloblastic erythropoiesis. Absorption begins with release of protein-bound B12 in the stomach, binding to intrinsic factor, and uptake in the ileum. After absorption, B12 binds to transcobalamin II for transport to tissues. (Sources: https://ods.od.nih.gov/factsheets/VitaminB12-HealthProfessional/, DOI:10.1002/biof.552)

Vitamin B12 is naturally present in animal-based foods and fortified products. Major dietary sources include meat, fish, dairy, eggs, and vitamin-fortified cereals and plant-based milks.

Deficiency of vitamin B12 leads to megaloblastic anemia, causing fatigue, weakness, and pallor. Neurological symptoms include numbness, tingling in extremities, balance disturbances, and cognitive impairment such as memory loss and depression. Long-standing deficiency can result in irreversible neurologic damage.

Recommended daily intake values for vitamin B12 are established by NIH (USA) and vary by age, sex, and life stage. Adequate intake ensures proper hematopoietic and neurologic function.

Vitamin B12 is available as oral tablets, sublingual tablets, intramuscular injections, and nasal sprays. Bioavailability varies by form and requires intrinsic factor for proper absorption.