Vitamin B12 is an essential nutrient with profound effects on human health. It is naturally present in animal derived foods such as meat, poultry, fish, eggs, milk and other dairy products. Since the body cannot manufacture B12, it must be consumed in the diet. An adequate supply of B12 is required to produce DNA, the genetic material in all cells, and for several vital body functions.
B12 is required for two essential biochemical reactions in most cells of the body. The products of these reactions are needed to make DNA, and many proteins, hormones, and fats. B12 works together with folate, another important B vitamin, in many biochemical pathways. B12 helps convert a substance called homocysteine into methionine, a major route for lowering homocysteine levels. This reaction also transforms folate into the active form needed to make DNA.
The two B12 reactions are crucial for rapidly growing cells and the key to understanding its major functions in the body. For example, the bone marrow, a sponge-like tissue inside bones, needs B12 to produce healthy red blood cells. B12 is also required to maintain the rapidly dividing cells lining the gastrointestinal tract. Since B12 is required for DNA production and cell division, adequate levels during pregnancy are necessary for normal fetal growth and development.
B12 also has a fundamental role in the development and function of the brain and nervous system. B12 is involved in the formation of myelin, the protective coating that surrounds nerve fibers. It is also need to produce neurotransmitters, the chemicals that carry nerve signals between cells.
The confirmed consequences of a deficiency shed light on B12's normal function in the body. B12 deficiency impairs DNA synthesis, which affects all proliferating cells. Without B12, developing cells in the bone marrow cannot divide normally to form mature red blood cells. Instead, they become unusually large and misshapen, and most never leave the bone marrow. This results in a specific type of anemia, a deficiency of red blood cells. A similar accumulation of large abnormal cells lining the digestive tract can cause a sore mouth and tongue, and interfere with absorption of nutrients.
B12 deficiency damages nerve cells in the brain and spinal cord. In a 2009 study in the "Journal of Neurology Neurosurgery and Psychiatry," magnetic resonance imaging or MRI, of the brain showed evidence of extensive loss of myelin in people with low B12 levels. A persistent deficiency causes irreversible nerve damage, reflected by symptoms such as numbness and tingling, balance problems, memory loss, and depression. These serious complications confirm the importance of B12 for normal neurological function.
Other consequences of B12 deficiency suggest the possibility B12 may contribute to bone health and normal immune function. Low B12 levels are linked to osteoporosis, a condition causing weak brittle bones and an increased risk of fractures. A study in the "Journal of Bone and Mineral Research" in 2005 found that low B12 levels were associated with a 3-fold increased risk of bone fractures due to osteoporosis.
B12 deficiency is also associated with abnormalities of the immune system. A study in the "Annals of Internal Medicine" in 1996 reported that people with low B12 levels have a poor response to the vaccine for pneumococcal pneumonia, a serious lung infection. Other abnormalities include defective function of infection fighting cells, and an increased susceptibility to tuberculosis.
One theory proposes that many benefits of B12 may result from its homocysteine-lowering effect. High homocysteine levels increase the risk of heart attacks, strokes, blood clots, and miscarriages. They may also accelerate bone loss, increasing the risk of osteoporosis and fractures. Some evidence suggests accumulation of homocysteine in the brain and nervous system contributes to nerve damage in B12 deficiency. However, the possible roles of homocysteine and B12 in these diseases and their prevention require further study
- "Blood Reviews"; Disorders of Cobalamin (Vitamin B12) Metabolism: Emerging Concepts in Pathophysiology, Diagnosis and Treatment; L. Solomon; Volume 21 pg 113-130; 2007
- "Journal of Neurology Neurosurgery Psychiatry"; Plasma Vitamin B12 Status and Cerebral White-Matter Lesions; L. de Lau, A. Smith, H. Refsum, C. Johnston and M. Breteler; Volume 80 pg 149-157; 2009
- "Journal of Bone and Mineral Research"; Homocysteine and Vitamin B12 Status Relate to Bone Turnover Markers, Broadband Ultrasound Attenuation, and Fractures in Healthy Elderly People; R. Dhonukshe-Rutten, S. Pluijm, L. de Groot, P. Lips, J. Smit and W. van Staveren; Volume 20 pg 921-929; 2005
- "Annals of Internal Medicine"; Impaired Antibody Responses to Pneumococcal Polysaccharide in Elderly Patients with Low Serum Vitamin B12 Levels; F. Fata, B. Herzlich, G. Schiffman and A. Ast; Volume 124 pg 299-304; 1996