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Overmethylated, yet inspired! What next?

pemone

Senior Member
Messages
448
What happened:
  • I gradually worked up to 400mcg methylfolate w/ mB12.

  • With each step up I got big improvements in energy, mood, and my need for thyroid and ribose dropped off. But at the 400mcg mark I developed severe insomnia - COULD. NOT. SLEEP. :woot: Similar effect to taking 400mg SAMe.

  • I dropped back down to 267mcg methylfolate, but still had powerful insomnia.:wide-eyed:

  • I went off methylfolate for 4 days. Took Nicotionic acid as needed. The insomnia gradually decreased each night I was off. I could sleep again. :sleep:

  • On Monday I started over again with just 67mcg methylfolate, thinking that wold be more gentle. The insomnia came right back.:confused: But my energy / PEM threshold has risen.
What I surmise from my reactions:
  1. It appears that my methylation cycle was previously disrupted or broken.
  2. It appears that taking methylfolate with B12 restarted my methylation cycle successfully, keeping it going even after I stopped methylation supplements.
  3. It appears I am very sensitive to methylfolate. (I'm more like @Avalon or @caledonia, less like @Freddd )
  4. It appears I am mostly tolerant to mB12 - it feels good, doesn't seem to bother me.

I am impressed that you were able to correlate the insomnia with particular supplements and test that. Since starting both forms of B12 (MeCbl and AdCbl) and L5-MTHF and high dose B6 I have been having problems getting to sleep before 3am. Now you have me thinking.

At this point there is no dose of MTHF you can tolerate?
 

Sherpa

Ex-workaholic adrenaline junkie
Messages
699
Location
USA
@pone I went off methylfolate for a few weeks. Then I started it back slow. I could take 50mcg. Can take 100mcg, no problem. Jumped back up to 200mcg today and felt a huge rush of energy all day, mostly positive, but a touch of mania.

Now towards the evening I am feeling tension (inflammation?) and pain in my trapezus muscles, shoulders. :( Blah. It's methylfolate side effects.


I'm reading this article on Preventing Methylfolate Side effects has got me thinking. I have SOD detox SNPs and very probable zinc / copper imbalances.

If glutathione and electrolytes don’t cut it, then superoxide dismutase, known commonly as SOD, may be deficient for various reasons. If you have SOD snps, are low in zinc, copper and/or manganese, then the likelihood you will experience side effects from methylfolate is high.
 

pemone

Senior Member
Messages
448
@pone I went off methylfolate for a few weeks. Then I started it back slow. I could take 50mcg. Can take 100mcg, no problem. Jumped back up to 200mcg today and felt a huge rush of energy all day, mostly positive, but a touch of mania.

Now towards the evening I am feeling tension (inflammation?) and pain in my trapezus muscles, shoulders. :( Blah. It's methylfolate side effects.


I'm reading this article on Preventing Methylfolate Side effects has got me thinking. I have SOD detox SNPs and very probable zinc / copper imbalances.

If glutathione and electrolytes don’t cut it, then superoxide dismutase, known commonly as SOD, may be deficient for various reasons. If you have SOD snps, are low in zinc, copper and/or manganese, then the likelihood you will experience side effects from methylfolate is high.

So I ended up getting an oxidative stress panel done, and to my surprise my SOD levels are in the toilet. REALLY bad. You might want to get that done as well.

Since I have "pyluria", and one of the consequences of that is that I pee out my manganese, my osteopath had me start supplementing manganese. I have grave reservations about doing that given that a slight overdose of manganese can be neurotoxic.

All of that brings me to my latest discovery, which I think you will appreciate:

http://www.bodybio.com/BodyBio/docs/BodyBioBulletin-LiquidMinerals.pdf

The beauty of this product is that you can easily self-regulate the amounts of minerals you take, using just the fact that the body's taste perception of an isolated mineral will swing from sweet to bitter based on your physiological need. That's such a simple but clever observation, and I just ordered this product and will start to adjust my dosing according to ongoing testing.
 

Freddd

Senior Member
Messages
5,184
Location
Salt Lake City
@pone I went off methylfolate for a few weeks. Then I started it back slow. I could take 50mcg. Can take 100mcg, no problem. Jumped back up to 200mcg today and felt a huge rush of energy all day, mostly positive, but a touch of mania.

Now towards the evening I am feeling tension (inflammation?) and pain in my trapezus muscles, shoulders. :( Blah. It's methylfolate side effects.


I'm reading this article on Preventing Methylfolate Side effects has got me thinking. I have SOD detox SNPs and very probable zinc / copper imbalances.

If glutathione and electrolytes don’t cut it, then superoxide dismutase, known commonly as SOD, may be deficient for various reasons. If you have SOD snps, are low in zinc, copper and/or manganese, then the likelihood you will experience side effects from methylfolate is high.

Hi Sherpa,

I have no disagreement with having a good mineral/electrolyte balance. It is essential. Perhaps it is possible that I had only signs of healing type side effects (induced deficiencies causing increased paradoxical folate deficiency and hypoglycemia) because I has already been working on minerals for decades. Despite my agreement with minerals, glutathione destroys AdoCbl and MeCbl about as fast and thoroughly as cyanide or nitrous oxide abuse (or other cause of daily use) and can cause demyelination of nerves starting in less than two weeks in some cases. It can be dangerous. I don't think anybody knows what the minimum dose of glutathione causes methyltrap. I do know that from personal experience does that. I was just following the directions on the packaging, nothing extreme or unusual. I was very hopeful of benefit, not additional damage that 5-6 years later has only partly corrected.

Increased pain in muscles with methylfolate are often because of induced deficiencies. Have you looked at the 10 (if I'm remembering correctly) different muscle pains described as well as people could describe them, including me, in the list of symptoms by nutrient. My muscle pains required sufficient MeCbl, AdoCbl, L-methylfolate and LCF. Each one of those affected muscle pains in a different way or of different types. LCF turned out to be key to removing all of them that were not neuropathic in origin and it even can even help that, and maybe works best in the presence of prolactin (hypothetically). Combining the two has only happened to people coincidently.
 

pemone

Senior Member
Messages
448
Despite my agreement with minerals, glutathione destroys AdoCbl and MeCbl about as fast and thoroughly as cyanide or nitrous oxide abuse (or other cause of daily use) and can cause demyelination of nerves starting in less than two weeks in some cases. It can be dangerous.

I keep seeing this claim made, but can anyone find any study in the research literature that confirms this?

Since the claim being made is simple chemistry, has any person making the claim ever done a blood test and proven that the claim is true for even N=1?

I am having problems finding any confirmation that this claim is true, and the chemistry is so straightforward that there is no way that this would not be in dozens of scientific papers if it were correct.

Glutathione makes me very sick. But I think that is because I have a thiole sensitivity, probably due to a mercury toxicity.

Here's another theory that would explain demyelination of nerves after you take Glutathione. And this theory actually makes sense if you care about the research literature. Glutathione stirs up mercury in cells without actually disposing of it out the kidney or liver. It therefore just redistributes mercury to new tissue locations, where new symptoms are created. There is very good research literature that shows mercury in the brain demyelinating neurons and causing loose tangles. Here is a great video that summarizes some Canadian research:


Some would argue that glutathione does not cross the blood brain barrier, but I have found studies arguing it both ways:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC296671/pdf/jcinvest00072-0311.pdf
 

Freddd

Senior Member
Messages
5,184
Location
Salt Lake City
I keep seeing this claim made, but can anyone find any study in the research literature that confirms this?

Since the claim being made is simple chemistry, has any person making the claim ever done a blood test and proven that the claim is true for even N=1?

I am having problems finding any confirmation that this claim is true, and the chemistry is so straightforward that there is no way that this would not be in dozens of scientific papers if it were correct.

Glutathione makes me very sick. But I think that is because I have a thiole sensitivity, probably due to a mercury toxicity.

Here's another theory that would explain demyelination of nerves after you take Glutathione. And this theory actually makes sense if you care about the research literature. Glutathione stirs up mercury in cells without actually disposing of it out the kidney or liver. It therefore just redistributes mercury to new tissue locations, where new symptoms are created. There is very good research literature that shows mercury in the brain demyelinating neurons and causing loose tangles. Here is a great video that summarizes some Canadian research:


Some would argue that glutathione does not cross the blood brain barrier, but I have found studies arguing it both ways:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC296671/pdf/jcinvest00072-0311.pdf


Hi Pone,

When lots of mgs appear in urine in the hours after taking glutathione if the person has enough unbound b12 in their body to be visible,. and it is repeatable over and over, and full predictable in the defined situation, a person would have to be literally blind to not see it. If you want to pay for all the blood tests, and the opaque blood draw kits for a cobalamin differential test and for all the MeCbl 30mg injections for pre-loading the body with unbound cobalamins, and then do a 12 hour urine collection and measure the amount of cobalamins. This would need to be done with those with known paradoxical folate deficiency, then a series of injections with methylfolate, then a series with some folic acid, then then a series with only folic acid causing partial methylation block and then a series of injections with glutathione only putting the person into methyltrap, you will have the blood work and the graduated excretion of cobalamin based on active folate effectiveness. I would imagine we could do this with say n=100; how deep is your wallet for funding this? We would demonstrate that more cobalamin is excreted than without glutathione. And we would nail down that it was in the serum before being in the urine. However, there are lots of studies on serum halflife that have been done, just not one with glutathione and sizable MeCbl injections that make it visible.

Then after letting the folate deficiency symptoms increase for long enough to be evident to everybody, but before causing demyelination damage, then reverse them with new b12 injections and l-methylfolate and AdoCbl.

It isn't difficult to do, conceive or understand why this is occurring. The trick is knowing to ask the question after having seen it occur with 10 people purposefully and hundreds accidently. You can find "glutathione detox" and "NAC detox" all over the place. There is a lack of understanding that "glutathione detox" responds to MeCbl, AdoCbl and L-methylfolate deficiency symptoms and can start responding in minutes.

Several hundred thousand dollars probably ought to be enough to finance such a study. You won't find any drug companies wanting to research that unless they think they can lock something up and charge a lot of money for it.

Honestly, I don't think it matters at all in this serum level of b12 discussion whether glutathione crosses the BBB or not. That is not relevant as to how it does the damage caused by methyltrap. The damage happens in the same way and as rapidly as survived cyanide poisoning treated with 5+ gram doses of HyCbl or daily nitrous oxide.

Glutathione makes me very sick. But I think that is because I have a thiole sensitivity, probably due to a mercury toxicity.

I'm not surprised glutathione makes a person very sick. It messes up every reaction using single carbon transactions first or second or third hand and deadlocks ATP production trashing hundreds of enzyme reactions that require ATP at one or many levels. As glutathione messes up potentially every ATP and methylation reactions, potentially everything using hormones, enzymes, neurotransmitters and so on, with research you could hang maybe 200 secondary biochemical reactions or lack there of on glutathione. It causes over a period of time well over 300 symptoms as it brings the whole system to deadlock. You could hang hundreds of results on it that look like causes until the reason for failure is understood.
 
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Sherpa

Ex-workaholic adrenaline junkie
Messages
699
Location
USA
Freddd,

Thanks for sharing your experience with glutatione. I am sorry to hear it caused damage or setbacks. I will be cautious with it and aim to avoid using it regularly.

My own personal experience with supplementing liposomal glutathione - based on mood and feelings - has been positive.

Long term: I took approximately 450mg of LivOn Labs GSH 2x daily for about 6 months when I was extremely ill, I had no trouble coming off it, and I felt much better after the course than before it.

Short term: Last night I was feeling unpleasant methylfolate side effects and woke up this morning with inflammation, periphrial neuropathy and terrible depression. Desperate for relief ASAP: I drank 500mg of liposomal glutathione and I felt a little better. Then an hour later I drank 12oz of coconut water (with 560mg potassium) and I felt almost immediate boost in mood and well-being. Another coconut water this aftenoon and I feel like I am back on track.

Conclusion: Electrolytes + glutathione does seem to relieve methylfolate side effects, as Dr. Lynch's article claims.
 
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pemone

Senior Member
Messages
448
Hi Pone,

When lots of mgs appear in urine in the hours after taking glutathione if the person has enough unbound b12 in their body to be visible,. and it is repeatable over and over, and full predictable in the defined situation, a person would have to be literally blind to not see it. If you want to pay for all the blood tests, and the opaque blood draw kits for a cobalamin differential test and for all the MeCbl 30mg injections for pre-loading the body with unbound cobalamins, and then do a 12 hour urine collection and measure the amount of cobalamins. This would need to be done with those with known paradoxical folate deficiency, then a series of injections with methylfolate, then a series with some folic acid, then then a series with only folic acid causing partial methylation block and then a series of injections with glutathione only putting the person into methyltrap, you will have the blood work and the graduated excretion of cobalamin based on active folate effectiveness. I would imagine we could do this with say n=100; how deep is your wallet for funding this? We would demonstrate that more cobalamin is excreted than without glutathione. And we would nail down that it was in the serum before being in the urine. However, there are lots of studies on serum halflife that have been done, just not one with glutathione and sizable MeCbl injections that make it visible.

How about doing it for n=1 and publishing the data? I mean if I am going to say something like "Taking 1000 mg of Vitamin C will destroy all magnesium in the body" then I measure magnesium before and after taking the vitamin c, and I am going to see some result in the blood test. That's not a true claim, but it was an example.

The thing is, your protocol doesn't need your claim that glutathione destroys mecbl to be helpful to people. I don't understand why you even bother to make the claim. It isn't supported by science.
 

Freddd

Senior Member
Messages
5,184
Location
Salt Lake City
The thing is, your protocol doesn't need your claim that glutathione destroys mecbl to be helpful to people. I don't understand why you even bother to make the claim. It isn't supported by science.

Hi Pone,
It isn't supported by science

I can show you various studies where methyltrap symptoms show up as side effects of NAC or glutathione. That these items produce those symptoms “as side effects” at various rates and intensities is well established. What isn’t recognized is that all these symptoms are partial methylation block and methyltrap symptoms.

That is like the Hypokalemia as a side effect from CyCbl recognized in the 50s, always a side effect, never as a sign of blood tissue formation except that it is mentioned but not recognized as a flag that it is working. That also included the CyCbl “startup” effects that the AMA dismissed as placebo effect. Isn’t that comforting to know that SCIENCE thinks that B12 startup effects are all placebo, ALL IN YOUR HEAD. Do you believe that? So people having startup effects of B12 are having a placebo experience and it’s all in their head. That’s SCIENCE for you. Their significance as a group is not recognized. And from the sound of it you seem to think that only big money can do SCIENCE It’s true that science needing expensive supplies and mass spectrometers, NMRs, electron scanning g microscopes, MRI etc. can only be done by big money.

However, lots and lots of science has been done via observation. For instance watching people heal day by day in front of your eyes can be much more convincing than knowing that their MCV dropped from 100.0 to 99.9 and so they no longer have macrocytic anemia. Say what? There is lots of naked eye science. Most of it depends on clear thinking and recognizing what matters, and build valid logic structures on the data. So instead of detailing the 600+ biochemical malfunctions in the body caused by B12 and look for a different drug to “fix” each broken item, I found the forms of B12 and cofactors that restores these 600 biochemical malfunctions to a more normal state.

In the group health business there is never an assessment of the patients’ health. However, when their pharmacy bill goes down from $1500/month to $50/month, and the physician utilization falls off 90% and they go back to work that usually means they got a lot better. These are direct measures of utilization but all indirect measures of health. And the company does this for the entire group each year to calculate what the new premium is to be.
Right now people who get genuinely better from these chronic diseases are rare. In my opinion these are the people that need to be studied. You and I and everybody else here has already proven that SCIENCE has not provided them understanding of their condition or cured them of it. If it had we would not be here. We are outside the 95% mark. We are more than 2 standard deviations from “average”. 95% medicine doesn’t include us. I would have spent my life doing something other than dealing with this disease. I was all set to be an on-snow ski area photographer and a red light runner changed all that.

So perhaps “It isn't supported by science” might be more accurately stated “it isn’t supported by science by my understanding of science which does not include an understanding of the scientific method”.

I don't understand why you even bother to make the claim.

That's obvious. John W. Campbell Jr, editor of Astounding Science Fiction and ANALOG once said "The art of science is making the obvious so to everybody." Twelve years ago, after almost 16 years of being down with severe CFS, FMS and congestive heart failure, eleven years into CHF with an 80% mortality rate in the first 10 years from diagnosis, I started looking seriously, full time, to solve this problem. Instead of assuming I came down with 20 or so disorders all at the same time I assumed that I had one thing. In December I got hit with methytrap and a more severe partial ATP block. Why? So what happened, I got told it was all in my head. I got kicked out of practices for insisting there was really something genuinely wrong and no doubt treatable. I had solved the problem for the first time in 1978-79 but nothing but liver was available. In 1987 MeCbl and AdoCbl and l-methylfolate were still not available.

You seem to think that I am here promoting or pushing or whatever a protocol. A lot of people here seem to look at this protocol has some fixed definition, something cast in concrete. Instead it is a description of a course of healing and the combinations of nutrients that promote or stop healing at various levels, body systems or whatever. I am working on a systems level understanding of ME, CSF, FMS, SACD, MS, Parkinson’s, Supra Nuclear Palsy and a few others all of which have partial methylation block, methyltrap and partial ATP block, all in different combinations and intensities and with unknown additional and/or resultant comorbidities. It appears that any of 5 or 6 or so varieties of paradoxical folate deficiency are at the most base root of all of these disorders, because of the many polymorphisms on folate affecting genes. The hypothesis follows from the pragmatic results.

When you get rid of all the labels, and look only at symptoms and so on, all of these have symptoms sets that all come from the same universe. What distinguishes them is where the worst damage is done. It’s like humans and chimps, something like 99% overlap genetically. Can you recognize the branches that go towards Parkinson’s or Supra Nuclear Palsy or MS or SACD? Why does it matter what one cause of demyelinating diseases is? Is it a major or minor contributor.? I don't know. Nobody does. That could come out of a well done double blind placebo study. Of course to replicate the results they would first have to get 100 or so people healing well with the active b12/folate protocol so they can pull the rug out from under them and prove it. Does it matter to you that some of us that today have functional malfunctions that have not yet damaged the nervous system beyond repair will have such demyelization in the next year or decade and move over to the “incurables” diseases? That’s a reason it’s good to know what CAN cause demyelization. It’s also good to know how to turn on methylation and ATP generation, breaking the 4 way deadlock on our body’s biochemistry. Those who understand the urgency of getting out of methyltrap can do so. Those that would rather tickle the dragon of methyltrap are also free to do so.

For starters, the current hypothesis, as to how/why glutathione causes methyltrap is one that has evolved over a 9 year period and something in excess of 6000 injections observed under perhaps 6 folate situations. These MeCbl injections took place in and out of methyltrap, in and out of all the various forms of paradoxical folate deficiency I have run into so far. There is zero doubt that glutathione can cause methyltrap in people who have previously had methyltrap and then intentionally healed and recovered from methyltrap. Methyltrap makes people sick, generally hard and fast. It's pretty much like flicking a switch. It isn't an easily feathered item either. It's more of a gate, on or off. I had skied the previous day and woke up terribly sick the next day with sudden onset CFS with which many here are familiar.

As CFS/FMS/ME sits on a foundation of partial methylation block, methyltrap and partial ATP block which can deadlock both methylation reactions and ATP reactions in numerous combinations of between 8 or 10 compartments (pharmacokineticly speaking) in body and CNS, anything that can start methyltrap in hours and start partial ATP block in a month or two predictably and cause additional sub acute combined degeneration damage in 2 weeks is very important. Perhaps this could allow researchers to have an animal model in which FMS, CFS and ME can be caused in weeks or months and then reversed. It would be very educational and oh so scientific to give mice CFS and FMS and cure them again.

Whether you like to believe it or not real science can be done at home. Further in my going to more than 100 doctors and read I don’t know how many thousands of journal articles, since folic acid and CyCbl are routinely thought to be fully effective B12 and folate through the past 60 years of mistaken research built on top of a fairy tower in the sky of the lab mistake that won a Nobel Prize. They have all sorts of microscopic evidence “proving” how effective CyCbl and folic acid are. All logic structures based on these are WRONG. None of these people can be trusted to do my thinking for me. They literally are incapable of understanding the problem or solution because of how they think about it. I am perfectly capable of doing my own thinking. I know and apply the scientific method. I spent my working life being hired to do the thinking for people who couldn’t. Why should I stop thinking just because I got sick. I changed my focus to solving ME, CFS, FMS, MS, Parkinson’s, SNP and so on. Not one of the 100 plus doctors I had hired to do my thinking on my health were capable of doing so by their own demonstration. So who would you hire to do your thinking for you?

The thing is, your protocol doesn't need your claim that glutathione destroys mecbl to be helpful to people

So the people being damaged by glutathione shouldn’t be told about it? Why would you want to see them continue to be damaged? Why shouldn’t they have an opportunity to heal? Without somebody outside the group think how long do you think it would take to have SCIENCE asking this question? 50 years? 100 years? Never?

Alongside my N=10 private study of glutathione was a sort of side car. The was an N=3 group that had methyltrap symptoms (CFS, FMS, ME) and were already taking glutathione or precursors that worked and were having zero success with the MeCbl, AdoCbl and Methylfolate they were taking already. They had never had startup and healing. A month after quitting glutathione they all had had startup and were actively healing, as the initial hypothesis stated. There was no need for a revised hypothesis and another iteration.
Solving the problem of CFS, ME, FMS, MS, Parkinson’s etc requires the recognition that excess glutathione could be a cause of disease for some people, that it can do serious damage.
 

pemone

Senior Member
Messages
448
I can show you various studies where methyltrap symptoms show up as side effects of NAC or glutathione. That these items produce those symptoms “as side effects” at various rates and intensities is well established. What isn’t recognized is that all these symptoms are partial methylation block and methyltrap symptoms.

So publish URLs to those studies? That was really all I was asking.

The thing is, your protocol doesn't need your claim that glutathione destroys mecbl to be helpful to people

So the people being damaged by glutathione shouldn’t be told about it? Why would you want to see them continue to be damaged? Why shouldn’t they have an opportunity to heal? Without somebody outside the group think how long do you think it would take to have SCIENCE asking this question? 50 years? 100 years? Never?

I think at the level you are doing things, you could simply say something like "Glutathione appears to make a sizeable percentage of people very sick, for reasons that are not entirely clear." It's hard to argue that point. What's not clear is the exact mechanism. For some people it is a methylation defect. For others, it is some obscure SNP. For most of us, I think, it is a side effect of mercury toxicity, just a straightforward sensitivity to excess thiols.
 
Messages
1
Hi @pone,

I think I can confirm NAC and glutathione quickly removing all B12 from the body from my own experience.

I've been on the Active B12 Protocol since august. One of my symptoms was my hands feeling a bit numb, like wearing gloves. The numbness is gone since starting the protocol and staying on the protocol.

A few weeks ago I decided to try NAC. I won't go into the reason why I tried the NAC here. A few hours after the first 600mg capsule my hands started to go numb again like before I started the protocol. I think this confirms what @Freddd wrote about NAC in his posts: The NAC, a glutathione precursor, binds to the B12 and you become B12 deficient again instantly.

I took 2 NAC capsules per day for five days before giving up. After that it took weeks for my hands to feel normal again.
 

Freddd

Senior Member
Messages
5,184
Location
Salt Lake City
Hi Pone,

Here is a short listing of what I have been doing since I had to do a disability retirement. The Glutathione wasn't of of the blue. I will have more complete response to you after family activities. I've done more research in 11 years post disability, of the type we can do with vitamins than most do in a career. I've gotten well and recovered based on these "you bet your life" studies.

As FrankVand points out, my hypothesis can be tested for both causing the problem and hopefully reversing the damage. You don't have to take anything I say on faith and I wouldn't want you to. I have provided exacting descriptions on how to duplicate the results. It doesn't take years of suffering on faith in some hypothesis to know. A person can know in days or weeks in both directions. That's why it took 5 years to define the deadlock quartet, pragmatically and 6 more years so far understanding paradoxical folate deficiency and why and how it all fits together, including glutathione.


PRIVATE STUDIES and COMPILATIONS
  1. N=1000 symptoms questionnaire with < 2 hour response to mb12, adb12 and mb12 & adb12.
  2. Mb12 urine colorimetry, 1-10mg sc injection series, 10-25mg series, 10-60mg series. 1-100mg sublingual series, determination of percentage of sublingual absorption.
    1. Folic acid
    2. Folinic acid
    3. Methylfolate
    4. Glutathione
  3. N=5 mb12 hypersensitive persons, 10 brand comparison testing.
  4. N=10 glutathione/precursors trial
  5. Titration trials, balance of methylfolate, adb12, mb12, potassium
  6. Light exposure required to ruin mb12
  7. Overcoming Types 1, 2 and 3 paradoxical folate deficiency/insufficiency titration trials
  8. Determination of CNS threshold effectiveness dose for adb12 and mb12 independently, both sublingually and injected SC.
  9. Five batch injectable mb12 comparison testing against 5 star batch.
  10. Composite international list of b12/folate symptoms
  11. Distinguishing the four specific forms of b12 deficiency and pharmacokinetic modeling.
  12. Family tree of methylfolate, adb12 and mb12 deficiency diseases
  13. Three types CSF/CNS cobalamin deficiencies
  14. Mb12, ADb12 and Methylfolate Insufficiency vs Deficiency
  15. Metanx, Deplin and Cerefolin-NAC and side effects.
  16. CSF/CNS penetrating doses of adb12 and mb12 for those with low CSF cobalamin levels.
  17. ZONES of healing by type and quantities of cobalamin
  18. The 95% reasons why b12 and folate therapies fail
  19. The body’s levels of healing illustrating the body’s internal triage system of distributing the most limiting nutritional factors.
 

pemone

Senior Member
Messages
448
Hi @pone,

I think I can confirm NAC and glutathione quickly removing all B12 from the body from my own experience.

I've been on the Active B12 Protocol since august. One of my symptoms was my hands feeling a bit numb, like wearing gloves. The numbness is gone since starting the protocol and staying on the protocol.

A few weeks ago I decided to try NAC. I won't go into the reason why I tried the NAC here. A few hours after the first 600mg capsule my hands started to go numb again like before I started the protocol. I think this confirms what @Freddd wrote about NAC in his posts: The NAC, a glutathione precursor, binds to the B12 and you become B12 deficient again instantly.

I took 2 NAC capsules per day for five days before giving up. After that it took weeks for my hands to feel normal again.

All this shows is that NAC produced a symptom. I have no problem with the idea that glutathione and its precursor NAC cause many people many problems.

Both of these lead to formation of single-thiol metabolites that would cause a mercury toxic person to stir up mercury and eventually it would resettle in new places and create symptoms, sometimes awful symptoms. But that is my inference and it is a suggestion of one possible reason for the symptom.

You can't state as a scientific fact that an amino acid completely uses up or destroys a vitamin B12 unless you have a measurement. Did you measure your B12 or any B12-metabolites before and after you took NAC? If yes, publish the data. If no, then you have an opinion about a reason for a symptom you had. That's fine. Just don't confuse opinions with facts.
 

pemone

Senior Member
Messages
448
Hi Pone,

Here is a short listing of what I have been doing since I had to do a disability retirement. The Glutathione wasn't of of the blue. I will have more complete response to you after family activities. I've done more research in 11 years post disability, of the type we can do with vitamins than most do in a career. I've gotten well and recovered based on these "you bet your life" studies.

As FrankVand points out, my hypothesis can be tested for both causing the problem and hopefully reversing the damage. You don't have to take anything I say on faith and I wouldn't want you to. I have provided exacting descriptions on how to duplicate the results. It doesn't take years of suffering on faith in some hypothesis to know. A person can know in days or weeks in both directions. That's why it took 5 years to define the deadlock quartet, pragmatically and 6 more years so far understanding paradoxical folate deficiency and why and how it all fits together, including glutathione.


PRIVATE STUDIES and COMPILATIONS
  1. N=1000 symptoms questionnaire with < 2 hour response to mb12, adb12 and mb12 & adb12.
  2. Mb12 urine colorimetry, 1-10mg sc injection series, 10-25mg series, 10-60mg series. 1-100mg sublingual series, determination of percentage of sublingual absorption.
    1. Folic acid
    2. Folinic acid
    3. Methylfolate
    4. Glutathione
  3. N=5 mb12 hypersensitive persons, 10 brand comparison testing.
  4. N=10 glutathione/precursors trial
  5. Titration trials, balance of methylfolate, adb12, mb12, potassium
  6. Light exposure required to ruin mb12
  7. Overcoming Types 1, 2 and 3 paradoxical folate deficiency/insufficiency titration trials
  8. Determination of CNS threshold effectiveness dose for adb12 and mb12 independently, both sublingually and injected SC.
  9. Five batch injectable mb12 comparison testing against 5 star batch.
  10. Composite international list of b12/folate symptoms
  11. Distinguishing the four specific forms of b12 deficiency and pharmacokinetic modeling.
  12. Family tree of methylfolate, adb12 and mb12 deficiency diseases
  13. Three types CSF/CNS cobalamin deficiencies
  14. Mb12, ADb12 and Methylfolate Insufficiency vs Deficiency
  15. Metanx, Deplin and Cerefolin-NAC and side effects.
  16. CSF/CNS penetrating doses of adb12 and mb12 for those with low CSF cobalamin levels.
  17. ZONES of healing by type and quantities of cobalamin
  18. The 95% reasons why b12 and folate therapies fail
  19. The body’s levels of healing illustrating the body’s internal triage system of distributing the most limiting nutritional factors.

It would take you less time and effort to just do a challenge test and measure B12 before and after a glutathione challenge. I mean honestly why do you resist just doing something so simple? You seem to have a love of hypothesis and a complete disdain for any form of proof that is not based on subjective symptoms.

When I had high homocysteine, one of my naturopaths had me do a methionine challenge. Methionine becomes homocysteine. He had me fast for 12 hours and go in for a homocysteine test. Then I immediately ingested 2.5G of methionine, continued the fast, and waited four hours. I then went in for a second homocysteine test.

My first homocysteine was "normal" around 8. My post-challenge homocysteine was quite high, around 16. That was factual proof that I have a methylation problem. When I metabolically create high homocysteine, my body is not disposing of it efficiently.

That's how science should work. If you have a theory about a symptom, you come up with a test and measurements to prove the theory true or false. I don't understand why you can't test your theories using the same kind of ultra-simple and practical testing. You would amplify the power of your theories 100-fold just by backing up your claims with hard scientific facts, not subjective interpretation of subjective claims by a biased population.
 

Freddd

Senior Member
Messages
5,184
Location
Salt Lake City
It would take you less time and effort to just do a challenge test and measure B12 before and after a glutathione challenge. I mean honestly why do you resist just doing something so simple? You seem to have a love of hypothesis and a complete disdain for any form of proof that is not based on subjective symptoms.

When I had high homocysteine, one of my naturopaths had me do a methionine challenge. Methionine becomes homocysteine. He had me fast for 12 hours and go in for a homocysteine test. Then I immediately ingested 2.5G of methionine, continued the fast, and waited four hours. I then went in for a second homocysteine test.

My first homocysteine was "normal" around 8. My post-challenge homocysteine was quite high, around 16. That was factual proof that I have a methylation problem. When I metabolically create high homocysteine, my body is not disposing of it efficiently.

That's how science should work. If you have a theory about a symptom, you come up with a test and measurements to prove the theory true or false. I don't understand why you can't test your theories using the same kind of ultra-simple and practical testing. You would amplify the power of your theories 100-fold just by backing up your claims with hard scientific facts, not subjective interpretation of subjective claims by a biased population.

HI PONE,

The cobalamin is extremely visible in the urine. The amount of cobalamin in the urine can be measured by color. As low b12 causes over 600 biochemical malfunctions, it is highly likely that your favorite mercury and thiols uses ATP and/or methylation in the process is is one of hundreds of malfunctions. \

It is not possible to see the cobalamin in the urine if it isn't there. The amount is proportional, from almost none with only methylfolate (in a qualifying person) to more with folic acid and methylfolate and more again with folic acid only and more again with glutathione/NAC. With the glutathione/NAC there is more cobalamin in the first days urine than is injected that day.

With that comes folate deficiency symptoms and B12 deficiency symptoms that can be easily demonstrated to be reversed by taking MeCbl, AdoCbl and l-methylfolate. You can even repeat that over and over and get the same results in both directions, over and over.

You may or may not be a person that responds in this way. You can verify for yourself if you do, or if you don't, by running trials yourself. You are free to buy what products you want and use them according to any theories you want to. I did that myself based on thousands of trials over 35 years. Sixty years of research on folic acid and CyCbl have corrupted the scientific process and is no longer are able to recognize most folate deficiencies or B132 deficiencies. When these vitamins are not working right lots of things go wrong in the body including quite probably your beloved mercury problems. There are hundreds and hundreds of things that go wrong from the same primary cause. I have healed myself of CFS and FMS and surprising to me initially, congestive heart failure. There are hundreds of comorbid conditions that are caused by B12 and folate deficiencies. Anybody taking sufficient B12 to be visible in their urine daily can see the effects of various folates, depending upon how they react to the folates, in their urine. They can see the effects of glutathione/NAC on the cobalamin content in their urine. If a person is taking enough B12 to be visible the difference with glutathione is very apparent to anybody who isn't literally blind. Now you can apply any hypothesis you wish to explain WHY the cobalamin is excreted rapidly following glutathione consumption there is no way to deny the visibility of the cobalamin. It doesn't take repeated expensive blood tests to show that there is excretion of cobalamin taken by the kidneys out of serum and into urine. I found that stopping the glutathione/NAC induced loss of B12 in mass quantities allowed the induced symptoms to go away and for healing to resume. Perhaps someday you will find a useable hypothesis that will allow you to heal. I call it the way I see it, based on decades of research, paper and pragmatic as you are also describing your hypothesis. Personally I have been evolving my hypotheses for 35 years or more and have found what works for me and it is very inclusive because it includes all the hundreds and hundreds of things that go wrong with partial methylation block, methyltrap and partial ATP block.
 

Freddd

Senior Member
Messages
5,184
Location
Salt Lake City
that an amino acid completely uses up or destroys a vitamin B12
PONE,
That is your claim, not mine. So have a happy straw man disagreement with yourself. Glutathione is not an amino acid. Glutathione does not “use up” B12. Glutathione does not destroy b12. So, why not try to restate it again until you get it right. If this is what you think I am saying you clearly don’t understand it at all. For starters, here is a list of amino acids.
http://www.cryst.bbk.ac.uk/education/AminoAcid/the_twenty.html
Sometimes it is not possible two differentiate two closely related amino acids, therefore we have the special cases:
  • asparagine/aspartic acid - asx - B
  • glutamine/glutamic acid - glx - Z
 

pemone

Senior Member
Messages
448
PONE,
That is your claim, not mine. So have a happy straw man disagreement with yourself. Glutathione is not an amino acid. Glutathione does not “use up” B12. Glutathione does not destroy b12. So, why not try to restate it again until you get it right.

I apologize for misquoting you. You say in this thread, and it is repeated in dozens of other threads that "...glutathione destroys AdoCbl and MeCbl about as fast and thoroughly as cyanide or nitrous oxide abuse (or other cause of daily use) and can cause demyelination of nerves starting in less than two weeks in some cases."

http://forums.phoenixrising.me/inde...t-inspired-what-next.32898/page-2#post-536979

I'm not arguing that glutathione supplementation makes many people ill. But you are making really really specific factual claims and then trying to prove them by saying things like "I can see it in my urine". Why not just test the metabolites that you think are being destroyed and document for posterity what the actual numbers are before and after a glutathione challenge?
 

Freddd

Senior Member
Messages
5,184
Location
Salt Lake City
Hi Pone,
This is a matter of semantics. I apologize for not being more completely clear. When MeCbl and AdoCbl are “destroyed” by cyanide, there is by definition no destruction of “B12”, there is the creation of “B12” from two “b12 analogs”. There is a conversion of AdoCbl and MeCbl to CyCbl. CyCbl is the official B12. While MeCbl and AdoCbl are deactivated, according to the official definitions they are converted from a “b12 analog” to “B12”. So “B12” is not destroyed, it is actually created. However, they are converted to a more highly oxidized less active form. Glutathionylcobalamin is also considered a “b12 analog” as is HyCbl. By official definitions no b12 is destroyed, only “b12 analogs” are changed.
Having done more than 6000 injections it became apparent that something was affecting how much b12 was visible in my urine. I calibrated the toilet bowl and made a conversion table to mgs of cobalamin compounds visible. It is the inexpensive way to measure the amount of something highly visible in the urine. There is no way for B12 to get from a syringe into subcutaneous tissues and out in the urine without going through the serum. It just isn’t possible. So here is a small compilation of the effects. There is a clear relationship to visible cobalamin in urine to folate deficiency symptoms. Glutathione maintains methyltrap making all injected cobalamins useless while taking glutathione.
Setting a 1-10 scale, Just Noticeable difference is 1/3 of a doubling, subcutaneous injections
  1. Ample methylfolate (14.4mg), no signs of PFD, just barely visible cobalamin amounts in urine in 8 hours after injection, at 10mg 3x per day, designated 1 on 1-10 scale.
  2. Mixture of folic acid and 400mcg Methylfolate, some PFD symptoms Just barely visible at 4.4mg injection 3x per day, scale 1.
  3. Folic acid, many PFD symptoms, 2.5mg injection, just barely visible, scale 1
  4. Folic acid and 8mg Methylfolate, some PFD symptoms, 10mg 3x day injections, visible scale 3
  5. Folic acid, many PFD symptoms, 10 mg 3x per day injection visible, scale 5
  6. Folinic Acid and 400mcg methylfolate, many PFD symptoms, 10mg 3x per day injections, scale 6
  7. Glutathione, 14.4mg methylfolate, 10mgx 3x daily MeCbl severe folate deficiency symptoms, visible scale 10 for first couple of days and then fades to scale 7-8 as the body is exhausted of b12 that isn’t nailed down
  8. 14.4mg methylfolate, 60mg mecbl 3x per day, no PFD, visible scale 8
  9. 14.4 methylfolate, 100mg MeCbl once, no PFD visible scale 10
  10. 14.4 methylfolate, 500mg MeCbl once (different person), visible scale 10 for 2-3 days – note: another person did similar trials with similar results. Being a paramedic he did an IV infusion of 500mg. It had the characteristic of reaching a ceiling of excreted cobalamin just as my trials did. He was taking the methylfolate too. Our other parts of the scale all lined up too with minor variations of “just visible” amounts.
On the 1 to 10 scale 10 is the maximum excretion amount in urine which appears to be 10-20mg/hour. There is not any pharmacokinetic data of large doses. All research indicated serum halflife that varies by serum concentration. The large variability seen in research of serum halflife appears to relate to Methylfolate effectiveness in the body.


I apologize for misquoting you. You say in this thread, and it is repeated in dozens of other threads that "...glutathione destroys AdoCbl and MeCbl about as fast and thoroughly as cyanide or nitrous oxide abuse (or other cause of daily use) and can cause demyelination of nerves starting in less than two weeks in some cases."

As I have noted previous the semantic misunderstandings here, the rest of my statement stands as accurate. Glutathione has the same effects as cyanide and nitrous oxide on MeCbl and AdoCbl in at least the group that responds to the deadlock quartet, whether they like the responses or not, whether the person can manage the induced deficiencies or not, regardless of whether they find ATP startup intolerable or not and regardless of what labels they put on the responses, like “glutathione/NAC detox”. The two weeks for MS type (and SACD) demyelinations comes from journal reported studies and case histories from cyanide exposure, 5-20gram HyCbl exposure, nitrous oxide exposure on a daily basis.

These are predictable and repeatable though who would want to repeat the demyelination experience I can’t imagine. Do you want to do some trials that could leave you with brain and cord damage? I experienced that multiple times, once with glutathione and stopped the glutathione as soon as it was recognized. And no, I didn’t have before and after MRIs to show the new demyelinations.

I got into trouble with the car wreck where I was hit by a red light runner. I didn’t have before x-rays showing I didn’t have damaged disks and vertebras I had after. That was long before side impact injury research was done. I was screwed in court because there was no proof that the collision did it because I wasn’t laying there bleeding after the collision so there was no presumption of injury, literally.

Now that I don’t have any symptoms of FMS and CFS to distract my new doctor (previous retired), she is starting to talk about spinal draws and other testing to determine what exact form of CNS demyelinations I have. She suspects MS or SACD or something, can you imagine that?. We will talk about that on my next appointment. She has a special interest in FMS/CFS and wants that kind of patient. However, I’m not one of them, despite the diagnoses I have in the folder. That stuff is all gone. My new doc wouldn’t even suspect those as my diagnoses any more. And with my BP 120/70, no edema to speak of and a healthy heart there is no trace of CHF either.

You know, I think I am on the home stretch of understanding what is wrong with me, and thousands of others posting or reading here.
 

SDSue

Southeast
Messages
1,066
Pardon my my inability to wade through the details of this thread, but what becomes of those of us who've been "poisoned" by glutathione?

One IV nearly 3 years ago took me from a 5-6 on the function scale to bed bound within hours. I've "recovered" to mostly housebound. It seems now that any tinkering with my methylation leaves me extremely wired, irritable, depressed, and nearly suicidal.

Anyone have thoughts on this? Suggestions? Theories? Thanks.
 

Freddd

Senior Member
Messages
5,184
Location
Salt Lake City
Pardon my my inability to wade through the details of this thread, but what becomes of those of us who've been "poisoned" by glutathione?

One IV nearly 3 years ago took me from a 5-6 on the function scale to bed bound within hours. I've "recovered" to mostly housebound. It seems now that any tinkering with my methylation leaves me extremely wired, irritable, depressed, and nearly suicidal.

Anyone have thoughts on this? Suggestions? Theories? Thanks.

Hi SDSue,

Yes, I have mostly recovered.