Posted by Larry Hoover on November 10, 2003, at 13:08:35
In reply to B12: Methylcobalamin vs. Cyanocobalamin » Larry Hoover, posted by DSCH on November 10, 2003, at 12:48:46
> > http://www.thorne.com/altmedrev/fulltext/meth1-4.html
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> "Methylcobalamin's only known biological function in humans is in the remethylation of homocysteine to methionine via the enzyme methionine synthetase, also known as 5-methyltetrahydrofolate-homocysteine methyltransferase. In order to originally form methylcobalamin from cyanocobalamin or other Cob(III)alamin or Cob(II)alamin precursors, S-adenosylmethionine (SAM) must be available to supply a methyl group. Once methylcobalamin is formed it functions in the regeneration of methionine by transferring its methyl group to homocysteine. Methylcobalamin can then be regenerated by 5-methyl-THF (see Figure 4). The cell's ability to methylate important compounds such as proteins, lipids and myelin will be compromised by a deficiency of either folate or vitamin B12.37 Shortages of active folic acid, SAM, or a dietary deficiency of cobalamin will lead to a decrease in the generation of methylcobalamin and a subsequent impairment in homocysteine metabolism. Since lack of methylcobalamin leads to depressed DNA synthesis, rapidly-dividing cells in the brain and elsewhere are affected.
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> At least 12 different inherited inborn errors of metabolism related to cobalamin are known. Abnormalities are detectable by urine and plasma assays of methylmalonic acid and homocysteine, and plasma and erythrocyte analysis of cobalamin coenzymes, which can reveal deficiencies of methylcobalamin or adenosylcobalamin.38
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> Low plasma vitamin B12 levels have been shown to be an independent risk factor for neural tube defect in one study.39 This was an original finding and needs to be confirmed still in further studies. If methionine synthetase is the critical enzyme, methylcobalamin might be able to stimulate the abnormal enzyme as folic acid does, since active folic acid acts to provide the methyl group to cobalamin. It is quite probable that a deficiency in Vitamin B12, folic acid, or any of the cofactors required for their activation may result in a similar dysfunction."
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> Seems to me you *might* have it the other way around on the subject of B12, Larry. Care to discuss? :-)What I said, in reference to the diagram, was:
"Note that cyanocobalamin *consumes* SAMe. That's why methylcobalamin is the preferred form of B-12."The article quote, above, says:
"In order to originally form methylcobalamin from cyanocobalamin or other Cob(III)alamin or Cob(II)alamin precursors, S-adenosylmethionine (SAM) must be available to supply a methyl group."These appear to be equivalent statements, to my eye.
Cyanocobalamin is not normally found in nature. The cobalt-porphyrin complex typically has a hydroxyl group or a methyl group on it. Cyanocobalamin was actually created by accident, via filtration through impure charcoal during the first attempts to isolate the complex. Cyanide, the CN- moiety, is toxic, and stresses the liver glutathione system. Moreover, in order to turn the B-12 into a methyl donor, it consumes a methyl donor. There *must* be more to the picture, as oral cyanocobalamin is helpful when used for proven B-12 deficiency, but why not just use methylcobalamin in the first place?
poster:Larry Hoover
thread:278139
URL: http://www.dr-bob.org/babble/alter/20031104/msgs/278230.html