Cyanocobalamin is a vitamin commonly known as Vitamin B12. Vitamin B12 cannot be made by plants or by animals, as the only type of organisms that have the enzymes required for the synthesis of B12 are bacteria and archaea. The total synthesis of B12 was reported in 1973 by Robert Burns Woodward, and remains one of the classic feats of total synthesis.

B12 is the most chemically complex of all the vitamins. The structure of B12 is based on a corrin ring, which is similar to the porphyrin ring found in heme, chlorophyll, and cytochrome. The central metal ion is Co (cobalt). Four of the six coordination sites are provided by the corrin ring, and a fifth by a dimethylbenzimidazole group. The sixth coordination site, the center of reactivity, is variable, being a cyano group (-CN), a hydroxyl group (-OH), a methyl group (-CH3) or a 5'-deoxyadenosyl group (here the C5' atom of the deoxyribose forms the covalent bond with Co), respectively, to yield the four B12 forms mentioned above. The covalent C-Co bond is one of only two carbon-metal bonds known in biology. The other is a C-Ni bond in carbon monozide dehydrogenase, a bacterial enzyme.

Vitamin B12 deficiencies are the cause of several forms of anemia. The treatment for this disease was first devised by William Murphy who bled dogs to make them anemic and then fed them various substances to see what (if anything) would make them healthy again. He discovered that ingesting large amounts of liver seemed to cure the disease. George Minot and George Whipple then set about to chemically isolate the curative substance and ultimately were able to isolate Vitamin B12 from the liver.

The usual daily intake in the Western diet is 5–7 µg (Food and Drug Administration (FDA) Daily Value); the daily requirement is 1–2 µg. B12 is mostly absorbed in the terminal ileum. The production of intrinsic factor in the stomach is vital to absorption of this vitamin. Megaloblastic anemia can result from inadequate intake of Vitamin B12 inadequate production of intrinsic factor (pernicious anemia), disorders of the terminal ileum resulting in malabsorption, or by competition for available B12 (such as fish tapeworms or bacteria present in blind loop syndrome).

Hematological deficiency is manifested primarily by anemia and macrocytosis; other cell lines such as white blood cells and platelets are often also low. Bone marrow examination may show megaloblastic hemopoiesis. Serum homocysteine and methylmalonic acid levels are also high in B12 deficiency and can be helpful if the diagnosis is unclear.

Neurological signs of B12 deficiency, which can occur without accompanying hematologic abnormalities, include demyelination and irreversible nerve cell death. Symptoms include numbness or tingling of the extremities and an ataxic gait, a syndrome known as subacute combined degeneration of the cord.

The American Psychiatric Association's American Journal of Psychiatry has published studies showing a relationship between depression levels and deficient B12 blood levels in elderly people in 2000 and 2002.

Traditionally, treatment for B12 deficiency was through intramuscular injections of cyanocobalamin. However, it has recently been appreciated that deficiency can be treated with oral B12 supplements when given in sufficient doses. When given in oral doses ranging from 0.1–2 mg daily, B12 can be absorbed in a pathway that does not require an intact ileum or intrinsic factor. The Schilling test can determine whether symptoms of B12 deficiency are caused by lack of intrinsic factor, though this is being performed less often due to the lack of availability of reagent for the test.

Interestingly, certain insects such as termites have been found to contain B12.

Cyanocobalamin is also found in many energy drinks.

Vitamin B12 supplements should be avoided in people sensitive or allergic to cobalamin, cobalt or any other product ingredients

Side effects

Cardiovascular:
Caution should be used in patients undergoing angioplasty since an intravenous loading dose of folic acid, Vitamin B6 and Vitamin B12 followed by oral administration of folic acid 1.2mg plus Vitamin B6 48mg and Vitamin B12 60mcg taken daily after coronary stenting might actually increase restenosis rates. Due to the potential for harm this combination of vitamins should not be recommended for patients receiving coronary stents.

Dermatological:
Itching, rash, transitory exanthema, and urticaria have been reported. Vitamin B12 (20 micrograms/day) and pyridoxine (80mg/day) has been associated with cases of rosacea fulminans, characterized by intense erythema with nodules, papules, and pustules. Symptoms may persist for up to 4 months after the supplement is stopped, and may require treatment with systemic corticosteroids and topical therapy.

Gastrointestinal:
Diarrhea has been reported.

Hematologic:
Peripheral vascular thrombosis has been reported. Treatment of Vitamin B12 deficiency can unmask polycythemia vera, which is characterized by an increase in blood volume and the number of red blood cells. The correction of megaloblastic anemia with Vitamin B12 can result in fatal hypokalemia and gout in susceptible individuals, and it can obscure folate deficiency in megaloblastic anemia. Caution is warranted.

Leber's disease:
Vitamin B12 is contraindicated in early Leber's disease, which is hereditary optic nerve atrophy. Vitamin B12 can cause severe and swift optic atrophy.

Pregnancy and breastfeeding:
Vitamin B12 is likely safe when used orally in amounts that do not exceed the recommended dietary allowance (RDA). The RDA for Vitamin B12 in pregnant women is 2.6mcg per day and 2.8mcg during lactation periods.

There is insufficient reliable information available about the safety of consuming greater amounts of Vitamin B12 during pregnancy