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Supplement Glutathione to protect supplemented b12

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by Adster, Dec 25, 2011.

  1. Adster

    Adster Senior Member

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    I've read here and there about the need for Glutathione to "protect" b12. If we are low in Glutathione, does it mean that much of the b12 we are supplementing in order to raise Glutathione is in fact rendered useless in the body? Do we then need to supplement Glutathione with the b12 in some cases, then taper off, in order to bring the cycle back up?

    I'm probably wrong, but worth asking!
     
  2. RustyJ

    RustyJ Contaminated Cell Line 'RustyJ'

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    I was having lower intestinal issues with embarrassing "leakage" and severe flatulence while on B12 protocol - over several months. On the day I began. Not sure what this means. I have only been taking the glutathione for a week, so I am curious as to what longer term benefit this might have.

    Perhaps the B12 was not helping to build up glutathione levels sufficiently? Or was further depleting them?
     
  3. Freddd

    Freddd Senior Member

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    Hi Adster,

    The glutathione will protect you from both active forms of b12 hustling them out of the body much more rapidly than without the glutathioone and also inducing a severe folate deficiency in many. Taking the mb12 and Metafolin will alloow the needed levels of glutathione to be formed in the body. Taking glutathione or precursors like NAC will induce b12 and folate deficiencies rapidly and severely.

    IBS is one of the symptom sets that is caused by folate deficiency, natural or induced.
     
  4. Adster

    Adster Senior Member

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    Hi Freddd, welcome back :) Do you have a proposed or reported biological "mechanism" for glutathione supplementation draining b12? How is the supplemented glutathione different to the "naturally formed" glutathione? Cheers :)
     
  5. Freddd

    Freddd Senior Member

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    Hi Adster,

    For starters, because of a lack of data I have no idea what percentage of people this occurs in. As far as I can tell, essentially 100% of those having response to mb12/adb12/metafolin who then take glutathione then lose the response they were having and have rapidly increasing returning symptoms that are generally called "detox". When the glutathione or precursors are discontinued and 8mg or so doses of Metafolin are taken until the returned symptoms retreat once again and then titrate down on Metafolin until it ceases working and go back up a bit.

    The mechanism is obvious if a person has been taking relatively larger doses of mb12/adb12 because the urine turns far pinker as the amount of cobalamin in the presumed form of glutathionylcobalmin (but the form doesn't matter) is far more rapidly excreted by the kidneys. The hypothesis being that the lack of active b12 in the cells as needed then appears to cause the flushing out of methylfolate from the cell in a process called the "methyl trap". This causes the appearance of folate deficiency starting to be apparant often with hours of the glutathione dose.

    How is the supplemented glutathione different to the "naturally formed" glutathione?

    Since precursors as well as glutathione have been demonstrated to cause identical effects the difference is not a qualitative factor of "naturally" formed or anything. It appears to be strictly a dose related quantitative item. Presumably there is an ideal level of glutathione that is enough for the body's needs without leaving so much excess that it is immediately bound to the cobalamins. This appears to be a simple chemical reaction that directly happens taking the b12 to a more oxidized state and requires no enzyme for this downhill transaction. If the conversion of the inactive glutathionylcibalamin is the same as in converting the inactive hydroxycobalamin and the inactive cyanocobalamin methylb12 then to convert the glutathionylcobalamin back to the active form of mb12 requires an input of energy in the form of ATP and an enzyme. The ATP is produced by adb12 which is also destroyed by the glutathione so that the ability to create the ATP to change it back also becomes impaired. Since the methylb12 is an effective detoxifier it might be said that the mb12 is part of the feedback system maintaining glutathione below a certain level or it is removed from the body by the mb12 which, like when mb12 detoxifies cyanide, the mb12 is destroyed in the process. It is converted to the inactive cyanocobalamin or in this case, the inactive glutathionylcobalamin. The mb12 is also part of the operation to create the glutathione in the first place. It is a delicate balance that is destroyed by too much glutathione.


    In my own experience the rate of excretion of the b12 with glutathione is matched in the urine by the amount excreted by a dose 4 times as large without the glutathione.

    If you do some back and forth trials satisfying the conditions stated you will see very obviously if that happens in you. The people who had no apparant reaction to the glutathione didn't have a return of symptoms because they had never gone away in the first place on hydroxycobalamin and folic/folinic acid.

    Also, for those taking glutathione (precursors) in the first place there are generally no startup effects from mb12/adb12/Metafolin and no benefit until after the glutathione (precursors) are stopped. It is quite clear that it blocks acdtive b12s and active folate.
     
  6. Adster

    Adster Senior Member

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    Thanks Freddd :) I and others do benefit from appropriate doses of NAC or glutathione, and for me personally more than mb12/mfolate supplementation so far. NAC usage short term brings me significant quality of life improvements in that it allows me to deal with chemical exposures that I would normally have to avoid due to the crash they induce.

    I think it's a good idea to assume that we are all different here and won't all have the same response to supplements. I avoided NAC on your advice for a while, but am glad I've tried it again as it's given me back significant freedoms that I'd lost due to the progression of this illness. That's not to say your advice isn't appreciated, you clearly devote a lot of time to helping people and that's a good thing :)

    I'd be interested in hearing how you go with the glutathione supplementation RustyJ.
     
  7. Freddd

    Freddd Senior Member

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    Hi Adster,

    To add to my data, what kind of folate and b12 do you take?
     
  8. Adster

    Adster Senior Member

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    Either Jarrows 1mg or Thorne 1mg and Solgar Metafolin 400mg.
     
  9. RustyJ

    RustyJ Contaminated Cell Line 'RustyJ'

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    Adster, after reading Fredd's response I decided to discontinue the glutathione. I did notice my urine contained much more b12, which supported what Fredd was saying. I didn't like seeing all the money I was spending on the vitamins pissing down the toilet, so it was either give up the B12 or give up the glutathione.

    I have been on Fredd's protocol for about 4 months. Have not improved mentally or stamina wise enough to convince myself the B12 was going to work. Have had to cut back my hours of work also, which has not made me a little despondent.

    I have put on some weight which I am real happy about. And I look and feel better for it - don't feel like the wind will blow me over (maybe that is a mental stamina improvement in itself). And I am able to persist with light weights. The problem is I think the weights might be at the expense of the work hours I had to give up. I am pushing to the limits physically, but those limits don't seem to have expanded at all.

    I have had me for 20 odd years, so I am wondering if any damage I have incurred would take some time to reverse. If it is a retrovirus causing glutathione and B12 deficiencies, then I am concerned that only high levels of glutathione will inhibit viral levels.
     
  10. richvank

    richvank Senior Member

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    Hi, all.

    The question of whether to supplement glutathione in some way in conjuction with treatment of the partial methylation cycle block in ME/CFS often comes up. There is some recent research that appears to shed some light on this issue, so I would like to
    review the status of at least my understanding of it.

    As I see it currently, there are three groups of people with respect to their response to
    adding glutathione to methylation treatment:

    1. There is a group who benefit from this addition, in terms of their symptomatic response.
    2. There is a group who benefit initially, but as time goes on, it causes their symptoms to worsen.
    3. There is a group who experience immediate worsening of their symptoms.

    I dont know what fraction of the ME/CFS population is in each group.

    I would like to suggest what I think is going on in each of these groups.

    I suggest that the first group have inherited normal genotypes of their intracellular B12 processing enzymes, and they also have normal status of vitamins B2 and B3. In this group, the glutathione can be recycled at a normal rate when it becomes oxidized by reactive oxygen species that are part of the oxidative stress in ME/CFS, by the glutathione reductase reaction, which requires both B2 and B3. Furthermore, glutathione
    is able to play its normal roles with respect to the intracellular processing of vitamin B12.
    In particular, the Cblc enzyme (also known as MMACHC) uses glutathione to remove the upper ligand from incoming forms of B12 (cyano-, methyl- or adenosyl-) by the formation of glutathione conjugates of these ligands (PMID: 19801555).
    In addition, it appears that glutathione also reacts with the resulting aquocobalamin to form glutathionylcobalamin. Glutathionylcobalamin is chemically more stable than the other forms of B12, but Cbcl is normally able to retrieve cobalamin from glutathionylcobalamin so that the cobalamin can be used to form methylcobalamin and adenosylcobalamin in the amounts needed by the cell (PMID: 21429294).
    Thus, glutathione appears to serve not only as a reactant in the metabolism of B12, but also as a protector of B12 from reactions with toxins, and a buffer to store B12 until it is needed by the cell.

    I suggest that the second group have inherited normal genotypes of their intracellular B12 processing enzymes, but they have a deficiency in B2 or B3 or both, so that the rate of the
    glutathione reductase reaction is too slow to keep up with the oxidation of the glutathione. As a result, though the supplemented glutathione is initially beneficial to them, over time it becomes a detriment, because the ratio of reduced to oxidized glutathione drops too low, and this worsens the oxidative stress of the cells.

    I suggest that the third group has inherited an inborn error of metabolism involving the Cblc enzyme. As a result of this, when glutathione reacts with B12 to form glutathionylcobalamin, their genotype of the Cblc enzyme is unable to retrieve the cobalamin from the glutathione to use it to form methylcobalamin and adenosylcobalamin. If glutathione is supplemented, this situation is made worse for this group. In addition, this group is unable to make use of hydroxocobalamin as their B12 supplement
    (PMID: 21497120), because it is converted to glutathionylcobalamin in their cells (even without supplementing glutathione) and is therefore made inaccessible. I suggest that Freddd is in this group, and this explains why he cannot tolerate supplementing glutathione, why he cannot make use of cyanocobalamin or hydroxocobalamin, and why he must use high dosages of methylcobalamin and adenosylcobalamin, applied either sublingually or by injection. This raises the concentration of these species in the blood stream, and enough of them is able to diffuse into the cells through their plasma membranes to be used directly without intracellular processing, thus supplying the need of his cells for methylcobalamin and adenosylcobalamin.

    Best regards,

    Rich
     
    Lotus97, Adster and anne_likes_red like this.
  11. Freddd

    Freddd Senior Member

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    Hi Rich,

    I may not have been posting for a while but I haven't been asleep. I have found some additional questions to ask you, some additional understandings in this area, we can hopefully hash out.

    I suggest that the third group has inherited an inborn error of metabolism involving the Cblc enzyme. As a result of this, when glutathione reacts with B12 to form glutathionylcobalamin, their genotype of the Cblc enzyme is unable to retrieve the cobalamin from the glutathione to use it to form methylcobalamin and adenosylcobalamin

    There are several problems with that as a freestanding explanation. First that could hardly account for the relatively large number of people who have this response. Second, there is the cobalamin dumping that occurs. While nobody has done a peer reviewed study of serum and body levels of cobalamin with and without glutathione, the effect I'm speaking of is as obvious as Jimmy Durantee's nose. I ran a number of urine colorimetry trials that allowed me to calibrate injected dose of mb12 to the color of urine from sublingual doses because cobalamin is intensly colored and shows up very clearly. It is almost pure magenta in coloration which no other nutritional factor affects. The amount of magenta is directly proportionate to dose of cobalamin. Concentration doesn't affect the relative color because the yellow components are equally diluted. It is purely the relative amount of magenta to yellow and cyan. Further it is a very easy naked eye comparison. The glutathione causes the amount of cobalamin excreted in the urine at 30mg injected daily to approximately match the urine excretion of 120-160mg of daily injection. RustyJ noticed this change "I did notice my urine contained much more b12," as do others who are taking enough to be above the threshold of naked eye visibility. If nothing else this dramatically lowers serum and probably tissue level and limits the amount of diffusion that can take place, even if it does nothing more than cause it to exit 4-6 times as rapidly. In me that caused a lack of penetration to the CNS and provoked rapid neurological deterioration.

    Then in looking at the actual process of conversion of inactive cobalamins to methylb12 there are several potential roadblocks. This requires an enzyme that is available in limited quantities. This conversion also requires ATP. This produces a potential deadlock preventing conversion. If the person in question has certain types of muscle pain and severe fatigue (as in FMS and CFS) indicating mitochondrial failure from lack of adenosylb12 or l-carnitine fumarate or other causes, the ATP may not be available for the conversion. As many processes break down for all we know the enzyme, which is severely limited in quantity at best, itself might not get made without mb12. I haven't been able to track that down yet. As the conversion pathway is generally inactive cobalamin + enzyme + ATP >> methylb12, methylb12 + enzyme + ATP? >> adenosylb12, the ATP needed for the conversion from inactive to mb12 might not happen without priming the pump with adb12 and/or l-carnitine fumarate and/or D-ribose and/or unknown other factors, in the first place.

    In my own case, I certainly converted some mb12 to adb12, enough to knock me for a loop de loop (in noodle soup?). However, it was nowhere near complete no matter how much mb12 I took for 9 months thereby producing a completely separate startup effect from Adb12. And another huge further startup with l-carnitine fumarate. So I had three ramp-ups of ATP. Without sufficient ATP I could NOT convert inactive cobalamins more than just a little for all those years. I did however convert cyanocobalamin all those years sufficiently to keep my MCV < 100 which is more than 1/3 of subjects in studies can't do. So I doubt the complete lack of the enzyme in my body. I did not die as a child. I did not have failure to thrive as an infant. The problem may not have occurred at all except that I became a vegetarian robbing my body of that pump-primimg amount of ATP. Before becoming a vegetarian I could jog 5 miles in 40 minutes and 10 miles in 90 minutes. I was a professional ski patrolman and could ski 2600 vertical feet without stopping and could do that all day every day. My EARLY symptoms, before becoming vegetarian were mostly methylfolate deficiency, CNS-mb12 and CNS-adb12 symptoms and a weak immune system which vitamin C strengthened at age 23 when I started vit C.



    As I see it currently, there are three groups of people with respect to their response to
    adding glutathione to methylation treatment:

    1. There is a group who benefit from this addition, in terms of their symptomatic response.
    2. There is a group who benefit initially, but as time goes on, it causes their symptoms to worsen.
    3. There is a group who experience immediate worsening of their symptoms.

    I dont know what fraction of the ME/CFS population is in each group.


    I would generally agree with this but think that there may be another group or two, or maybe actually subgroups of one or more specified above. Let me try a different logical grouping. An assumption is that potassium is given as needed so that doesn't have to be dealt with as a response. This may be a sparsely populated matrix without all positions filled


    I. There is a group who have a large startup response to each of mb12/adb12/Metafolin with a large reduction of symptoms over a period of a year or more.

    A. There is a group who experience immediate worsening of their symptoms, typically a RETURN OF SYMPTOMS, specifically folate deficiency symptoms intially followed by mb12 deficiency symptoms followed by adb12 deficiency symptoms which are typically called DETOX.

    B. There may be a group who benefit initially, but as time goes on, it causes their symptoms to worsen as mb12 deficiency symptoms followed by adb12 deficiency symptoms which are typically called DETOX.

    C. There may be a group who benefit from this addition, in terms of their symptomatic response

    II. There is a group who have a large startup response to each of mb12/adb12 with a large reduction of symptoms over a period of a year or more.

    A. There may be a group who experience immediate worsening of their symptoms, specifically folate deficiency symptoms intially followed by mb12 deficiency symptoms followed by adb12 deficiency symptoms which are typically called DETOX.

    B. There may be a group who benefit initially, but as time goes on, it causes their symptoms to worsen as mb12 deficiency symptoms followed by adb12 deficiency symptoms which are typically called DETOX.

    C. There may be a group who benefit from this addition, in terms of their symptomatic response

    III. There is a group who have little or no startup response to each of mb12/adb12/Metafolin with a little reduction of symptoms over a period of a year or more.

    A. There may be a group who experience immediate worsening of their symptoms, specifically folate deficiency symptoms intially followed by mb12 deficiency symptoms followed by adb12 deficiency symptoms which are typically called DETOX.

    B. There may be a group who benefit initially, but as time goes on, it causes their symptoms to worsen as mb12 deficiency symptoms followed by adb12 deficiency symptoms which are typically called DETOX.

    C. There may be a group who benefit from this addition, in terms of their symptomatic response

    IV. There is a group who have some or no startup response to each of hycbl/cycbl/Folic-folinic acid with perhaps some reduction of symptoms over a period of a year or more.

    A. There may be a group who experience immediate worsening of their symptoms, specifically folate deficiency symptoms intially followed by mb12 deficiency symptoms followed by adb12 deficiency symptoms which are typically called DETOX.

    B. There may be a group who benefit initially, but as time goes on, it causes their symptoms to worsen as mb12 deficiency symptoms followed by adb12 deficiency symptoms which are typically called DETOX.

    C. There may be a group who benefit from this addition, in terms of their symptomatic response

    D. There may be a group with no change at all as their folate, mb12 and adb12 deficiency symptoms continue unchanged

    V. There is a group who have "DETOX" symptoms (methylfolate deficiency) in response to hycbl/cycbl/Folic-folinic acid.

    A. There may be a group who experience immediate worsening of their symptoms, specifically severe worsening of folate deficiency symptoms intially followed by mb12 deficiency symptoms followed by adb12 deficiency symptoms which are typically called DETOX.

    B. There may be a group who benefit initially, but as time goes on, folate deficiency symptoms remain about the same and their symptoms to worsen as mb12 deficiency symptoms followed by adb12 deficiency symptoms which are typically called DETOX.

    C. There may be a group who benefit from this addition, in terms of their symptomatic response, despite the continuing folate deficiency symptoms.

    D. There may be a group with no change at all as their folate, mb12 and adb12 deficiency symptoms continue unchanged

    Vi. There is a group who start glutathione or precursors prior to starting any cobalamin or folate.

    A. There may be a group who experience immediate worsening of their symptoms, specifically folate deficiency symptoms intially followed by mb12 deficiency symptoms followed by adb12 deficiency symptoms which are typically called DETOX.

    B. There may be a group who benefit initially, but as time goes on, it causes their symptoms to worsen as mb12 deficiency symptoms followed by adb12 deficiency symptoms which are typically called DETOX.

    C. There may be a group who benefit from this addition, in terms of their symptomatic response

    D. There may be a group with no change at all as their folate, mb12 and adb12 deficiency symptoms continue unchanged

    VII. There is a group who start glutathione or precursors prior to starting any cobalamin or folate who then later start mb12/adb12/Metafolin.

    A. There may be a group who experience immediate worsening of their symptoms, specifically folate deficiency symptoms intially followed by mb12 deficiency symptoms followed by adb12 deficiency symptoms which are typically called DETOX.

    B. There may be a group who benefit initially, but as time goes on, it causes their symptoms to worsen as mb12 deficiency symptoms followed by adb12 deficiency symptoms which are typically called DETOX.

    C. There may be a group who benefit from this addition, in terms of their symptomatic response

    D. There may be a group with no change at all as their folate, mb12 and adb12 deficiency symptoms continue unchanged.

    E. There may be a group who benefit from this addition, in terms of their symptomatic response and then improve again after starting amb12/adb12/Metafolin

    F. There may be a group who benefit from this addition, in terms of their symptomatic response and then no change after starting amb12/adb12/Metafolin
     
  12. Freddd

    Freddd Senior Member

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    Hi Adster,

    In the matrix I layed out in the previous post, which pattern do/did you follow or is there a different pattern yet that you followed?
     
  13. Adster

    Adster Senior Member

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    Sorry Freddd, that matrix is too much text in one slab for me to comprehend! For me, there is no benefit in higher doses of metafolin, and no gain then a slow general worsening of symptoms, kidney pain, infected follicles and loss of proper taste sensation if I add more mb12. SAM-E helps greatly in higher doses than ~200mg for a short while then dulling and slowing of senses and subsequent depression sets in. I respond well to DMSA chelation, but am yet to determine if I have a body burden of mercury or if the DMSA is helping me in a different way.
     
  14. Freddd

    Freddd Senior Member

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    Hi Adster,

    Thankyou for the info. So you are saying that at best you had a minor response to mb12/metafolin without a lot of startup and relief of symptoms? So there are not the previously removed symptoms by mb12/adb12/metafolin coming back rapidly? Basically the only predictable response was for the cagtegory of people who had strong immediate response to mb12/adb12/Metafolin and large decrease of symptoms prior to trying glutathione (precursors) and you don't appear to fit that category as far as I understand from what you said.

    Just look at the Roman numeral lines and find the category that fits you and then pick the a,b,c,d etc line that fits best. Good luck
     
  15. Adster

    Adster Senior Member

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    I would say that I have had a moderate initial improvement with mb12/mf and then a plateau with pre mb12/mf variations in health remaining, so it certainly does help to some degree but doesn't appear to be my main problem, or perhaps the methylation block and glutathione depletion remains regardless of the mb12/mf supplementation. I don't recall any significant start up effects. adb12 seems to give some energy but can cause excitotoxicity if I take much more than 1/4 of a tab weekly.

    The only co factor I haven't tried is TMG which I have here to try soon. The only thing that makes me reasonably normal is contracting a common head cold, which my gp thinks might be due to a Th2 dominant immune system issue. Of course as you would know that this can be caused, amongst many things, by glutathione depletion. Oh, 500mg of NAC daily will make me feel almost as healthy as the head cold will, but if I take it for more than a few week or two I crash with excitotoxity symptoms, and it also causes problems with mucous membranes. I'm currently experimenting with low doses of glutathione which are showing some promise.

    I'll let you pick the category in to which I fit :) Thanks for your time Freddd.
     
  16. Freddd

    Freddd Senior Member

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    NBasically what I seem to hear in what you are saying is that with the glutathione and/or NAC in your system you don't have and haven't had a major response to mb12 and metafolin. OF coursr not. It appears to fit the presented model quite exactly. NAC and/or glutathione prevent mb12 and metafolin effectiveness.


    if I take it for more than a few week or two I crash with excitotoxity symptoms,

    That is the effect of the induced methylfolate deficiency and if continued the induced mb12 deficiencies.

    This is excellent information that fits the model I presented with exactitude. It's just a matter of recognizing where it fits in.


    VII. There is a group who start glutathione or precursors prior to starting any cobalamin or folate who then later start mb12/adb12/Metafolin.
    B. There may be a group who benefit initially, but as time goes on, it causes their symptoms to worsen as mb12 deficiency symptoms followed by adb12 deficiency symptoms which are typically called DETOX.
     
  17. Adster

    Adster Senior Member

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    Sorry to be confusing Freddd. The NAC/glutathione was introduced only recently, 18months-2 years after starting the mB12/mF so the two aren't linked. The excitotoxicity symptoms that I describe are different to what I would call "detox" symptoms, which I've experienced before when starting things like Nystatin. Excitotoxity symptoms are typically the same as if I were to experience a chemical exposure, or overexercise; initially feeling quite good, then feeling "poisoned", wired, anxious, unable to relax muscles, poor sleep then a period of days with very low energy etc. "Detox" symptoms I would describe as feeling "fluey", headachey, drained of energy but not in a wired way etc. Cheers :)
     
  18. Freddd

    Freddd Senior Member

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    Hi Adster,

    Quite right so-called detox is typically potassium deficiency or induced folate deficiency and is not the same as mb12 nervous system excitation. However, for the "return of symptoms" after starting glutathione (precursors) they have to have gone away in the first place. The symptoms that start up after a week or two on NAC are induced deficiencies. People that already have all those symptoms see no negative effect. Those that didn't have a profound relief of those sysmptoms don't see them "return" strongly.

    The first few days on glutathione precursors I did feel a bit better at the same time various symtpoms started shifting around. It wasn't clear what was happening until it had gone on a while. Changes are just changes ubtil one can see the direction and mb12 and methylfolate cause all sorts of symptom shifting which clear up over time even though intensified (perception) initially. Something that makes the nerves less sensitive feels better at first until one realizes that the pain is less becasue the nbnerves are stopping working.

    A hypothesis that mb12 is causing glutatmate toxicity just doesn't hold water as all the literature says it prevents glutamate toxicity and is protective. An interesting thing with food allergies is that people are often very attracted to those very foods that cause them the most problems. Man of the people who really like hyrocodone and get in trouble on it is that in addition to pain relief they get stimulated by it because of the histamine production which is perceived as a stimulant.
     
  19. Adster

    Adster Senior Member

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    The symptoms I would call excitotoxicity have certainly been experienced many many times before my improvement on mb12/mF, so I would disagree that it is caused NAC undoing any gains from mb12/mF in this case. Before I started chelation pretty much every supplement I tried, except for a select few, caused it, just like foods/chemicals etc. Potassium deficiency doesn't appear to be an issue with me, unless it is a functional one, as when I supplement it I feel considerably worse. I'm not suggesting that mb12 causes glutamate toxicity. Cheers :)
     
  20. Freddd

    Freddd Senior Member

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    Hi adster,

    I'm not suggesting that mb12 causes glutamate toxicity. Cheers


    OOPs sorry. Sometimes I get things crossed up dealing with many different threads. I also see that this isn't where I put the protective against glutamate toxicity links. I wasn't saying potassium deficiency is your problem. That results AFTER a person has a major response to the mb12/adb12/mb12. I was just saying that it is often called "detox" contributing to definitional overload. I do want to say that the balance between the two b12s is important. As the ONLY function adb12 has is processing fats for use in myelin as a minor function and using them for ATP generation as it's major function, any excitation caused by adb12 is purely concerned with ramping up energy generation in the mitochondria to normal. I honestly don't think that there is any way adb12 can cause "excitotoxicity" so I would say that there is a definitonal problem here, a problem of words. Staying pegged on that usage of that word makes it very difficult to try to come up with a feasable hypothesis to test. I would say that I am asking you to expand your range and try to find an explanation that fits the way these things function. I'm trying to find the hypothesis that leads to your having a good response.

    Let me use the word "detox" to demonstrate the problem. When "detox" means pragmatically determined low potassium in one set of circumstances and when "detox" means pragmatically determined paradoxical folate deficiency in another case and pragmatically determined induced folate deficiedcy in another case and mercury or other actual toxins mobilizing in another case and who knows how many other "special" meanings it becomes so overloaded as to mean almost nothing. The word by itself says nothing.

    http://en.wikipedia.org/wiki/Excitotoxicity
    Excitotoxicity is the pathological process by which nerve cells are damaged and killed by excessive stimulation by neurotransmitters such as glutamate and similar substances. This occurs when receptors for the excitatory neurotransmitter glutamate (glutamate receptors) such as the NMDA receptor and AMPA receptor are overactivated. Excitotoxins like NMDA and kainic acid which bind to these receptors, as well as pathologically high levels of glutamate, can cause excitotoxicity by allowing high levels of calcium ions[2] (Ca2+) to enter the cell. Ca2+ influx into cells activates a number of enzymes, including phospholipases, endonucleases, and proteases such as calpain. These enzymes go on to damage cell structures such as components of the cytoskeleton, membrane, and DNA.

    Excitotoxicity may be involved in spinal cord injury, stroke, traumatic brain injury, hearing loss (through noise overexposure or ototoxicity) and in neurodegenerative diseases of the central nervous system (CNS) such as multiple sclerosis, Alzheimer's disease, amyotrophic lateral sclerosis (ALS), Parkinson's disease, alcoholism or alcohol withdrawal and Huntington's disease.[3][4] Other common conditions that cause excessive glutamate concentrations around neurons are hypoglycemia[5] and status epilepticus.[6]


    To say that mb12 and adb12 have something to do with this is NOT actually backed up by any research and in fact research indicates just the opposite, that methylb12 is protective against excitotoxicity with many toxins. Adb12 has no involvement at all. As a hypothesis as to methylb12 and/or adb12 causing it is a hypothesis that leads nowhere. A hyopothesis such as "NAC" causes methylfolate, mb12 and adb12 if continued long enough in high enough doses is a hypothesis that can be tested. You appear to have experienced it after a couple of weeks. It's a testable hypothesis for each person in each set of circumstances and is either demostrable as accurate or not accurate. A hypothesis of excitotoxicity from mb12 and or adb12 is not testable and doesn't make sense. What is the mechanism? Unless of course your biochemisry is alien and have exactly the opposite effects that these things generally have. Then the question is how do you produce ATP and have DNA transactions?
     

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