Chemical structure of Vitamin B12
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Vitamin B12 Deficiency

The term vitamin B12 (or B12 for short) is used in two different ways. In a broader sense it refers to a group of Co-containing compounds known as cobalamins - cyanocobalamin (an artefact formed as a result of the use of cyanide in the purification procedures), hydroxocobalamin and the two coenzyme forms of B12, methylcobalamin (MeB12) and 5-deoxyadenosylcobalamin (adenosylcobalamin - AdoB12). more...

VACTERL association
Van der Woude syndrome
Van Goethem syndrome
Varicella Zoster
Variegate porphyria
Vasovagal syncope
VATER association
Velocardiofacial syndrome
Ventricular septal defect
Viral hemorrhagic fever
Vitamin B12 Deficiency
VLCAD deficiency
Von Gierke disease
Von Hippel-Lindau disease
Von Recklinghausen disease
Von Willebrand disease

In a more specific way, the term B12 is used to refer to only one of these forms, cyanocobalamin, which is the principal B12 form used for foods and in nutritional supplements.

Pseudo-B12 refers to B12-like substances which are found in certain organisms, such as Spirulina spp. (blue-green algae, cyanobacteria). However, these substances do not have B12 biological activity for humans.


B12 is the most chemically complex of all the vitamins. B12's structure is based on a corrin ring, which, although similar to the porphyrin ring found in haem, chlorophyll, and cytochrome, has two of the pyrrole rings directly bonded. The central metal ion is Co (cobalt). Four of the six coordinations are provided by the corrin ring nitrogens, and a fifth by a dimethylbenzimidazole group. The sixth coordination partner varies, 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 the only carbon-metal bond known in biology. (p.32)


B12 cannot be made by plants or by animals, as the only type of organism that have the enzymes required for the synthesis of B12 are bacteria (eubacteria, archaebacteria).


Coenzyme B12's reactive C-Co bond participates in two types of enzyme-catalyzed reactions: (p.675)

  1. Rearrangements in which a hydrogen atom is directly transferred between two adjacent atoms with concomitant exchange of the second substituent, X, which may be a carbon atom with substituents, an oxygen atom of an alcochol, or an amine.
  2. Methyl (-CH₃) group transfers between two molecules.

In humans there are only two coenzyme B12-dependent enzymes:

  1. MUT which uses the AdoB12 form and reaction type 1 to catalyze a carbon skeleton rearrangement (the X group is -COSCoA). MUT's reaction converts MMl-CoA to Su-CoA, an important step in the extraction of energy from proteins and fats (for more see MUT's reaction mechanism)
  2. MTR, a methyl transfer enzyme, which uses the MeB12 and reaction type 2 to catalyzes the conversion of the amino acid Hcy into Met (for more see MTR's reaction mechanism).


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Folic acid and vitamin B12 prevent hip fractures
From Townsend Letter for Doctors and Patients, 7/1/05 by Alan R. Gaby

Six hundred twenty-eight Japanese patients (mean age, 71 years) with residual hemiplegia at least one year after their first ischemic stroke were randomly assigned to receive, in double-blind fashion, 5 mg/day of folic acid and 1,500 mcg/day of vitamin B12 (methylcobalamin) for two years. At baseline, the mean plasma homocysteine concentration was above the reference range, and the mean serum vitamin B12 concentration was below the reference range for the healthy Japanese elderly population. After two years, the mean plasma homocysteine concentration decreased by 38% in the treatment group and increased by 31% in the placebo group (p < 0.001). In intent-to-treat analysis, after 2 years, hip fractures had occurred in 6 patients in the treatment group and in 27 in the placebo group (1.9% vs. 8.6%; 78% reduction; p < 0.001). The mean number of falls per patient did not differ between groups, and the mean reduction in metacarpal BMD on both the hemiplegic and intact sides did not differ significantly between groups. Based on these results, it was calculated that 1 hip fracture would be prevented for every 15 patients treated. No significant adverse effects were reported.

Comment: Stroke increases the risk of subsequent hip fracture by 2- to 4-fold. Hip fractures usually occur relatively late after stroke onset and almost always on the paretic side of the body, apparently because bone mineral density (BMD) declines on that side as a result of inactivity. Hyperhomocysteinemia, which is a risk factor for both ischemic stroke and osteoporotic fractures in elderly men and women, may result in part from a deficiency of folic acid or vitamin B12.

The results of the present study indicate that treatment with folic acid and vitamin B12 reduced the incidence of hip fractures in hyperhomocysteinemic patients following a stroke. Since treatment did not influence BMD, the beneficial effect may have been due to an improvement in bone quality. Homocysteine has been shown to interfere with the formation of collagen cross-links, an effect that may lead to abnormalities of bone matrix, potentially resulting in increased bone fragility.

Other people with high homocysteine levels might also benefit from taking these vitamins. In addition to folic acid and vitamin B12, several other nutrients play a role in lowering homocysteine levels; these include vitamin B6, choline, and betaine.

Sato Y, et al. Effect of folate and mecobalamin on hip fractures in patients with stroke: a randomized controlled trial. JAMA 2005;293:1082-1088.

COPYRIGHT 2005 The Townsend Letter Group
COPYRIGHT 2005 Gale Group

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