Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by Gondwanaland, Aug 5, 2017.
Very good find!
Yes very interesting find.
Damn I do better in B6 than in P5p .....what's the threshold for inhibiting those other enzymes?
From the introduction to the study it appears that they are trying to imply that the neurological pain that was suffered was due to high pyroxidine buildup due to pyroxidine in effect lowering P5P the active form of B6.
This test was an in vitro study, In practice(not a lab test) high serum pyridoxine and low P5P levels are quite often due to the MTHFR gene mutations. Increasing folate and B12 will increase methylation and conversion of pyridoxine to P5P to solve the problem.
Would anybody have a view as to whether 50 mg daily of this vitamin could play a part in causing severe migraines? I have been trying to work out what could be causing my problems and hadn't realised I was taking such a high dose?
Yes, I had that with P5P. I assume it is serotonin build up (= B2 deficiency)
Thanks for that. This explains why the in vitro study perfectly matches my experience. When I first started taking B vits I would always get symptoms of B6 deficiency no matter how high or low my B6 intake was. It was only when I took P5P that I felt how a healthy B6 metabolism feels. B12 and folate cause me B1 deficiency.
I suppose your body will tell you.
I read the article you linked. It is nonsense. The MTHFR gene does NOT
The gene codes for an enzyme which converts 5,10 methylene THF to methyl THF - so yes it does create ONE of the active forms of folate, but it does not act on folic acid.
MethylTHF does in turn replenish the methyl group on methylB12 used in the methionine synthase reaction, so indirectly, yes, MTHFR is important for B12 function.
Activation of B6, however, involves phosphorylation (addition of a phosphate group), not methylation. It has nothing to do with MTHFR.
I do not question that, but I suppose that the methylation cycle gears in the urea cycle, so could it be an indirect activation?
Choline is a methyl donor ("system input") and it increases the need for B2 ("system output").
Thanks for the extra information. I just take folate and B12 when I get a build up of pyroxidine which for me seems to go hand in hand with low B12 symptoms.
Sorry - I don't follow the links. What is the connection between methylation and the urea cycle and what in turn does the urea cycle have to do with B6 activation?
Sorry again I don't follow the connection. Do you mean that anything which stimulates methylation will increase need for B2 and that this in turn might affect B6 activation (adversely) since B2 is required in this process?
Even if this were the case, and I'm not sure that it is, the article is saying the opposite - it claims increasing methylation will increase activation of B6.
Acetaldehyde is detoxified by B1, is it not? Subsequently inducing Thiamine Deficiency.
Maybe this is how taking a lot of thiamine has boosted my B6 levels (seen by increased dreaming).
Nice to start the day with a puzzle solved!
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