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B12 Transport defects

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by Milford, Oct 14, 2013.

  1. Milford


    I am wanting to find out about B12 transport problems.... Am I right in thinking this is to do with Transcobalamin deficiencies ? What would make one consider this as an issue ? Which genes are responsible.... And can it be bypassed or corrected .
    Anyone have experience of this, or could point me in the right direction?
  2. taniaaust1

    taniaaust1 Senior Member

    Sth Australia
    Hi, some of my gene polymorphisms have defects which involve B12. I dont know if this will interest you or not, this is from my genetic gene report.

    MTR/MTRR Mutations
    MTRR (Methionine synthase reductase) helps recycle B12. The combination of MTR and MTRR mutations can deplete methyl B12. MTR A2756G, MTRR A66G, MTRR H595Y, MTRR K350A, MTRR R415T, MTRR S257T, and MTRR A664A all work together to convert homocysteine to methionine.

    MTR (5-methyltetrahydrofolate-homocysteine methyltransferase) provides instructions for making the enzyme methionine synthase. Methionine synthase helps convert the amino acid homocysteine to methionine. To work properly, methionine synthase requires B12 (specifically in the form of methylcobalamin). An MTR A2756G mutation increases the activity of the MTR gene causing a greater need for B12 since the enzyme causes B12 to deplete since it is using it up at a faster rate. Mutations in MTR have been identified as the underlying cause of methylcobalamin deficiency. Megaloblastic anemia can occur as a consequence of reduce methionine synthase activity."
  3. Freddd

    Freddd Senior Member

    Salt Lake City
    Hi Milford,

    The transport system for B12 is the most complicated of any vitamin. There is TC1 (haptocorrin) (HTC1 when CBL on board) in saliva and elsewhere that starts the process, is assisted by IF (Intrinsic factor), absorbed and handed of to TC2 (Transcobalamin 2) which becomes HTC2 (HoloTranscobalamin) when b12 is on board. This transports a limited amount of b12 to where it is needed according to the body's triage method. TC3 - HTC3 transports miscellaneous cobalamins, plant cobalamins, post use cobalamins, free cobalamins, back to the liver for disposal in the bile. I have no idea what genes are involved. Methylfolate helps one retain more b12 than folic acid. Glutathione flushes loads of free b12 out in the urine in hours. Taking sublingual AdoCbl and MeCbl (and there are brands that work much better than others) gets around all defects in transport and conversion by putting it directly into the blood by diffusion and rapidly distributed throughout the body by diffusion allowing widespread healing if other factors are present. The genetics of all of this is not known as far as I know.

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