Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by Anne P, Jan 24, 2011.
What is the name of your hydration drink, AnneLR? My potassium orotate is only 90mg.
If you have a methyl-trap in progress caused by glutathione precursors I found that it was absolutely impossible to overpower the methyltrap with more b12 or folate while taking the glutathione precursors. The reason apparently being is that there was about 1000 times more glutathione than needed to disable 100% of the active b12s and thereby flush the folates out of the cell where they are used into the serum where they are useless but tested.
Sorry I missed this until now Lala.
I make the drink myself. The store bought versions often have undesirable ingredients.
Link to post with recipe: http://forums.aboutmecfs.org/showth...ation-Recipes-Ingredients&p=153591#post153591
Klinghardt recommends adding liquid trace minerals to the solution, but that's not necessary I guess if you're covered with other supplements.
Thank to you both. Unfortunately NAC made me physically better together with further medcs, so I can not stop it.
I think we can clear up a misunderstanding here. What makes you think that you have a "methyl-trap" going on. Are you having the specific symptoms of the methyl-trap? Are you taking the other half of the glutathione precursor pair, glutamine in some form or another?
I don't know what NAC all by itself does but it probably isn't the same as when taken as part of a pair of precursors producing glutathione. Even in taking that pair, some people have some degree of relief before enough glutathione accumulates in their body to cause the methyl-trap. Then they usually call it "glutathione detox reaction", which has nothong to do with detox and everything to do with acute mfolate deficiency plus b12 deficiencies.
You might start with the first post on this link that lists the symptoms we are talking about.
Following an adrenal crisis (due to secondary addisons disease) which caused low pottassium I had to take a replacement supplement but once the levels came up I was told told not to continue to take pottassium supplements (because it could be dangerous)unless my blood tests showed that it was necessary.
I think the daily fludrocortisone I take is supposed to help prevent loss of sodium and pottassium. (Not completely sure about the pottassium). Having blood tests right now is not possible as too sick to get them done.I am having some mild muscle spasms in feet and hands but then I often do. In the past I have used soluble calcium which stopped the cramps.
I tried to up the actifolate to 1/4 tab but got increased pain so I am back to 1/8th tab plus 1/2 b12 1000mcg.
I suppose I won't know if I have a methylation trap until I get into much higher doses of B12 and folate. I will order some adb12one day soon. I may not have problems with a methyltrap as It was many years ago now that I supplemented with glutathione and precursers.
Hi Anne P,
The replacement potassium you were likely taking was a much larger dose than what is sold as a supplement. The supplements are usually about 3% of MDR, 99mg. That makes titration for removal of early symptoms easy without a lot of overshoot.
Methyl-trap and methyl-block are two entirely separate things. If you have been on glutathione for years and never had a glutathione free period with Methylfolate and MB12 you would never notice the symptoms as they would be part of your "normal" symptomology with mb12. adb12 and mfolate deficiencies. The methyl-trap is only obvious by comparison to a relatively symptom free period.
Thanks Fredd for the explanations. I will get the pottassium supplement. Even though you and Rich have explained it all I am embarrassed and have to confess that after reading and reading about the methylation trap as apart from the methylation block, my poor old foggy brain simply will not co-operate and make me understand what the difference is. So I will just continue with the protocol and deal with symptoms as they arise.
Hi Anne P, so sorry to hear your experience. Didn't see you mention it so I wanted to give a shout out for magnesium. I've done both B12 protocols, and a good absorbable magnesium made a huge difference.
Methyl-block presents as primarily mb12 deficiency symptoms. Methyl-trap presents first as a severe folate deficiency and then adds in over time both mb12 and adb12 deficiency symptoms.
Hi, Anne P.
Since I think I'm the one who introduced the partial methylation cycle block and the methyl trap to the discussion here, I will try to describe what they are.
I invented the term "partial methylation cycle block." What I mean by it is that the methionine synthase reaction that links the methylation cycle to the folate metabolism is chronically operating more slowly than is normal. This is usually caused by an insufficiency of methylcobalamin (methyl B12), which serves as a coenzyme for this reaction, but it can also be caused by an insufficiency of methylfolate (Metafolin, FolaPro, MethylMate B or Deplin), which is one of the reactants in this reaction, and which leaks out of the cells via the "methyl trap" mechanism (see below). That's why both a B12 and a folate are necessary to lift this partial block. In my hypothesis for ME/CFS, the reason for the insufficiency of methyl B12 is that B12 is lost to reactions with toxins because there is insufficient glutathione in the cells to protect the B12 from this hijacking by toxins. The reason such a high B12 dosage is needed, compared to the usual RDA requirement for B12, is this hijacking. Enough B12 needs to be put in so that some is left over to do its normal jobs, and it can require large dosages to do this.
The "methyl trap," on the other hand, is not something I invented. It is discussed in the published research on folate metabolism. What it means is that when the methionine synthase reaction is running more slowly than normal (i.e. a partial methylation cycle block is present), the cells will produce more methylfolate than is being used in this reaction, which is essentially the only reaction that makes use of methylfolate (except that it has been found to react with peroxynitrite). Methylfolate, unlike other folate forms in the cells, does not have a glutamate tail (which is negatively charged because glutamate ionizes under the pH condition in the cells). The absence of this charge enables methylfolate to diffuse through the cell membrane into the blood. As this process continues, other forms of folate in the cells decrease, and methylfolate rises in the blood serum. Because of the methyl trap mechanism, it is necessary to take a folate supplement as part of the treatment to lift the partial methylation cycle block. Once the methionine synthase reaction gets going at a normal rate again, the requirement for B12 should drop back down, and probably the folate requirement will come down some, too.
Rich. Thanks for the explanation.
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