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Glutathione: Pro / Con arguments confuse me!

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by Jorlev, Feb 20, 2013.

  1. Jorlev

    Jorlev

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    Regarding glutithione, from past threads it seems Rich Vank is pro in that G is beneficial and protects B12 in some fashion and Fred is con saying G inceases excretion of B12 leading to deficiency. If one is taking 30mg of meCbl daily, is G really a threat to a dose of that size? Was taking NAC precursor to G but now I don't know if I should stop or not.

    Love these boards but it's tough when knowledgeable people disagree on protocols.

    What's the latest on G and how should I proceed?
    Very confused on this matter.
     
    golden likes this.
  2. Lynn_M

    Lynn_M Senior Member

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    This controversy is over the issue of whether taking supplemental glutathione is good or bad. In his earlier days, Rich Van K. was advocating supplemental glutathione for CFS. However, his views evolved and ultimately he thought it best to support the body's ability to make its own glutathione, and he no longer recommended taking glutathione. You should be able to find some of his posts at PR explaining his change in thinking.
     
  3. Dreambirdie

    Dreambirdie work in progress

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    In my case, glutathione is very helpful to clear toxic reactions when I get a chemical exposure from being out in the world. I have MCS in addition to CFS, and I use G as needed. I also use NAC. I have not had any problems with either one of them.

    Rich was much more accurate in his assessment of my health issues regarding methylation, so I ALWAYS go with his advice over Freddd's. He was also much more moderate in his approach, and that works much better for me. That said, everyone has to choose for themselves what works best for them.

    Good luck.
     
  4. Freddd

    Freddd Senior Member

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    Hi Jorlov,

    I will explain it as best I can. Glutathione combines chemically with the cobalamin, doesn't matter which one in this case. It's like cyanide. It combines with it. For whatever the reason once the glutathione combines with what appears to be about 100% of the unbound b12 in the body and flushes it out through the urine, very visiably if a person has any significant amount. The molecular mass of MeCbl is about 1350 (several variations). The CH4 stripped off is 1.3% of the mass , so the rest of the cobalamin is attached to glutathione making glutathionyl cobalamin. If a person takes causes 1000mg of glutathione to be made that could destroy 5000mg or more of MeCbl. Since a person has typically 1mg to 100mg in somebody using a lot, there is vasrt overkill of glutathione regardless of the exact amounts. When this b12 is swept from the body the person goes onto methyltrap, in 2-3 hours if the dose of glutathione is large enough. Now if the person is already in methyltrap, they don't notice a thing except perhaps some relief from neurological pain and whatever else the glutathione is doing. Glutathione, when I was taking 30mg a day, had a coloration equal to 60mg in the toilet bowl. The only thing comparable was taking multi hundred mg doses by injection as far as the coloration goes. The difference was that in that N=10 trial, was that everybody tjhat tried the glutathione was already sucessfully healing and was out of methyl block. Every one of us went back into methylblock in hours to a day (whey was way slower).

    You can experiment for yourself. First tun on healing. Start feeling pretty good for some months and then try glutathione and you will feel yourself being cast back into the pits of hell as symptoms return and getting worse by the day. In six weeks a person can go from health to very sick. If you use glutathione during methyltrap it will only make it worse but the person can't feel it. I found the arguments strong enough to convinve me to try it with 9 other people. I was very hopeful it would work. I was looking what would fix me and others. The omne thing I can tell you for sure. The people taking glutathione do not get well as long as they are taking it. They may quibble about how they feel. They do not largely heal in year. Healing does not turn on while they are taking it. As some others found out who had never had healing turn on when they discontinued the glutathione already being taken at the same time as MeCbl etc they didn't heal until some while after stopping glutathione and taking the reversal doses.
     
  5. golden

    golden Senior Member

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    This is the very reason I am wary of supplements.

    Not omly are they synthetic but also its such a complicated process adding in this to combat that and the body isnt fully understood nor is the illness.

    I see Asparagus is very high in glutathione and turmeric is a good source of it.

    Having bax reactions to most supplements I think I will follow the detox methods, mercury removal and increasing foods with these nutrients in.
     
  6. Lotus97

    Lotus97 Senior Member

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    Most people don't have a bad reaction to taking glutathione, but there are better ways of raising glutathione besides taking glutathione. The only convincing argument I've heard against taking glutathione is that it might send a message to your body to stop producing glutathione on it's own. As far as I know, this theory has yet to be proven in any study. I don't think NAC would pose the same problem. Some people caution the use of NAC since it is a chelator of mercury.
     
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  7. Lotus97

    Lotus97 Senior Member

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    What Rich says about Glutathione and B12
    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
     
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  8. Dreambirdie

    Dreambirdie work in progress

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    Thanks Lotus97, for digging up Rich's take on the glutathione. I use the G only infrequently, but am glad to have that option when I am overloaded with toxins. It helps me clear them out much quicker.
     
  9. Lotus97

    Lotus97 Senior Member

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    Once I learned that improving mitochondrial function and getting the Krebs Cycle and ATP going raises glutathione I decided I might not need glutathione. A few months ago, I stopped taking NAC after thinking I was exposed to mercury when my tooth with an amalgam cracked, but I realized my symptoms were from taking methylfolate rather than mercury (although I haven't completely ruled out some exposure to mercury). I think I'm going to continue with NAC though. I have Lyme and Rich said that borrelia can deplete their hosts or cysteine. Maybe once I get methylation going I can stop NAC also.
     
  10. Freddd

    Freddd Senior Member

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    The one thing I will be clear about is that aside from ignoring hypokalemia and calling it detox, the most potentially damaging thing a person can do is take glutathione above a certain unknown level and keep taking it. In 6 weeks it can cause or worsen brain and cord damage in Subacute combined degeneration and it's first cousin, MS is also likely rapidly increased damage. It can cause high MCV and high MCH and half a dozen other blood changes on the first 3 months (the problems happen right away but blood cells stick around 3-4 months so it takes a while ot see). Doing a risk assessment of this is probably a good idea. A researcher I have spoken with who has approiached these matters from a different direction told me, in person and on the phone, that "There is probably no safe way to take glutathione."

    The subjective benefits I too have felt. When there is neurological pain, it reduces the neurological pain by damaoing the nerves to numbness so even perveived benefit is dangerous and damaging. That can be perceived in the first days, as I perveived it, before the effects of methyltrap become felt. Those who are not in methyltrap and are doing welll will be the ones who will feel the worst onset of glutathione.

    Rich Said:
    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.

    Since Rich is basing this hypothesis on me, based on old incorrect hypothses concerning my own supposed inborn error in the CblC enzyme whic isabsolutely 100% wrong for me and all of the N=10 group, all logic flowing from this assumption is 100% wrong.

    In addition, this group is unable to make use of hydroxocobalamin as their B12 supplement
    This assumption is also 100% wrong concerning the people in the N=10 group trial. Some of those were vegetarians. One man had such amazingly good response to HyCbl that it got him out of a wheelchair but the HyCbl could take it no further. He needed MeCbl and AdoCbl to get rid of the walker frame and return to work.

    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.
    Again, all of this is based on assumptions that are 100% WRONG!

    , 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).
    While this may be sort of correct in terms of normal amounts of glutathione, in these much larger doses beiong taken, this is NOT CORRECT. The glutathione combined dirrectly with AdoCbl and MeCbl that is in serum or cells and changes there again and again faster than the body can convert it back to usable forms, This is demonstrable. No amount of injected MeCbl taken with large amounts of glutathione survive to be used.

    The whole thing is based on a first approximation understanding that upon more iuderstanding has been proven totally wrong. Rich was unwilling to reconsider my situation because it fit his theories so nicely. As everything he thinks about my biochemistry as regards B12 and folates is wrong, all of his suggestions and conclusions based on that are wrong. This entire statement is too badly flawed to be any valid usage and anybody basing what they do on it is at risk of doing unintentional damage to themselves.

    That entire statement is so flawed that I'm not sure any of it is salvagable.
     
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  11. Lotus97

    Lotus97 Senior Member

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    I can't say for sure who is right, but it's good to have more than just one point of view in these forums
     
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  12. Freddd

    Freddd Senior Member

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    I would like it much better if somebody knowledgeable could write an understanding of it that isn't based on me as an example and my presumed genetic characteristics and ignore entirely the other 9 in the trial. I have been extremely specific about those who tried it and found the reversal. FIRST they had to have effectiveness of the Active B12 protocol. So whatever argument made can't be about a specific set of rare genes because the people in the N=10 are quite varied, including a vegetarian, using every form. That every form of precursors were approximately as effective as glutathione IV, including NAC alone in some people, shows that it isn't difficult at all to get glutathione into the body. Any explanation has to able to include the actual pragmatic examples within a suitable hypothesis. You can't throw out every bit of contrary information and form the hypothesis on wrong statements and misunderstandings. The above fails that test. When all the logic on who it happens to disappears and even reverses from his statements, there is nothing valid there. It may be possible to form a valid hypothesis from all this that supports glutatathion at certain minimal doses for a short time in people who haven't achieved methylation startup and who are still in methyltrap and not yet achieved ATP startup. If Rich had been willing to discuss this matter and revise his opinions about what is wrong with me based on all the folate information he got me started on, this is what I would have tried to work out with him. As he came to believe that glutathione shouldn't generally be given in any case, he was likely near to be willing to discuss. It was perhaps my disappearing for some months that prevented that. You may not understand how we were interacting. We exchanged information and data. He brought to my attention a variety of flaws, all of which I corrected. I brought flaws to his attention. SOme he considered and made alterations. Some he ignored 100% despite repeated explanation. His hypothesis appeared far more important to him than mine is to me. For me what is important how to solve the probelm, not the specific details of the solution. In order to get good answers one must ask good questions. If there isn't some ancient wisdom to that effect there should be. In the computer age it has been summerized GIGO; Garbage In Garbage Out. That is logic based on flawed assumptions and incorrect data doesn't yield valid results except by accident. In computers if you do everything that wrong the program doesn't run or gives lots of interesting and weird errors.

    I'm playing "you bet your life" in this 100%. My life is literally at stake in all this, as is yours. Rich was playing science. He was a disinteresrted observer except for protecting his theoretical turf. His life wasn't at stake. His theory was. "Old scientists never die, they just loose track of their data". You know, "Old gymnasts never die, they just can't remount in 30 seconds."

    I ask questions nobody else who hasn't lived through it can ask. I have possible answers that require experienceto have . In the end a valid hypothesis can explain you and me and Dan and Dbkita et al and have each of us described accurately and predictably. There is a lot to account for, not a lot to throw out or ignore.
     
  13. Freddd

    Freddd Senior Member

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    As far as understanding MeCbl better: http://health101.org/art_methylcobalamin.htm and it has footnotes. It was written before l-methylfolate and has some things that could be changed. A sample paragraph.

    The coenzyme form of vitamin B12 is known as methylcobalamin or methyl B12.It's the only form of vitamin B12 which can directly participate in homocysteine metabolism.In addition, converting homocysteine to methionine via methyl B12 generates an increased supply of SAMe (S-adenosyl methionine), the body's most important methyl donor.Indeed, some of the benefits of methyl B12, such as protection from neurotoxicity, appear to derive from increased production of SAMe8, 9.Methyl B12 has also been reported to be neurotrophic or growth-promoting for nerve cells10, 11, a property which may help regenerate central and peripheral nervous tissues damaged in disorders such as amyotrophic lateral sclerosis12 and diabetic peripheral neuropathy13.
     
  14. dannybex

    dannybex Senior Member

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    Hi Fred,

    Above you stated: "the most potentially damaging thing a person can do is take glutathione above a certain unknown level and keep taking it."

    Can you explain then, the marked improvement of patients of Dr. David Perlmutter M.D.'s Parkinson's patients after receiving IV glutathione?

    Also, did you ever do IV glutathione, or was it just precursors like NAC and/or whey -- which can indirectly increase glutathione if many other factors are present, but aren't the same thing as glutathione. If not, then I think it would be helpful to differentiate between the two, and perhaps say 'NAC or Whey protein', instead of glutathione.

    You also state emphatically that Rich was '100 percent wrong' (which he may have been) when it came to his hypothesis that you may have some sort of genetic issue involving a Cblc enzyme. Just curious if you ever tested for that to make sure?

    Thanks Fred,

    Dan
     
  15. dannybex

    dannybex Senior Member

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    Come on now Fred. That bolded statement is at the very least inaccurate, but also highly insulting to a man who spent the last 15 years of his life dedicated to finding answers for folks with ME/CFS, all because he wanted to help a friend of his who was suffering w/ME/CFS.

    A 'disinterested observer' doesn't cry at night because he's received an email from a patient who's having a bad reaction from his recommendations. During the phone-in memorial tribute to Rich, several people spoke about how he gave them their lives back, many were in tears.

    His work resulted in a published clinical study with Dr. Neil Nathan involving 30 patients, 2/3rds of whom improved during the study period.

    I know your protocol has worked for the most part for you, and for others as well, but that doesn't mean it will work for everyone, just like Rich admitted repeatedly that his protocol was probably not enough -- that infections, environmental issues also may need to be addressed. I guess my point is that I don't think you'd appreciate it if the same were said about you -- that you're protecting your theoretical 'turf'. I know I'm a broken record on this subject, but with any protocol -- yours, or Rich's, or Martin Pall's -- what works for one person might be poison for another. There is no one-size-fits-all answer, just like there is no one-size-fits-all diet. One person will need more protein, one will need more fat, and others will need more carbs -- and vice versa.

    I'm sure you didn't mean to insult his memory, but I think you did, and you owe his family an apology.
     
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  16. Freddd

    Freddd Senior Member

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    Hi Dan,

    I'll try.

    Can you explain then, the marked improvement of patients of Dr. David Perlmutter M.D.'s Parkinson's patients after receiving IV glutathione?

    The explanation I can give you may not be what you want. There is nothing I have said that says it can't cause improvements. In fact, there is no reason at all that it can't cause some improvments or perceived improvments in such a damaged neurology . I felt some too, especially on neurological pain. Now let's consider Parkinson's. Research has shown low CSF cobalamine and specifically elevated MMA. This is broken mitochondria. It is known that Parkinson't damages the limbic system. The damage is hypothecized to be caused by 20 years or more of malfuntioning mitochondria in the neurons of the brain, and the limbic system is the area damaged. It is inflammed or irritated or something in Parkinson's. Occasionall hyper resoonse to MeCbl, more frequent hyper response to AdoCbl and increadibluy hyper response to L-carnitne is very likely. This hyper response is typically something like a progression of extreme anxiety, fear, panic, anger, rage, homicidal rage, severe depression on as little as 1mg of l-carnitine and is quite intolerable. I would bet that glutathione would relieve perhaps that inflammation or irritability or something. It certainly affects the neurological aspects. My hypothesis says that it is at a potential long term cost. That cost may releate to actual effective dose of glutathione and rthe frequency.

    Anyway, there is an extreme response with ATP startup which appears to quickly affect dopamine too or maybe be the dopamine effect.

    Also, did you ever do IV glutathione, or was it just precursors like NAC and/or whey -- which can indirectly increase glutathione if many other factors are present, but aren't the same thing as glutathione. If not, then I think it would be helpful to differentiate between the two, and perhaps say 'NAC or Whey protein', instead of glutathione.

    In the N=10 trial 100% had the same results, the already defined "Glutathione Detox" reaction that I had heard of but didn't think anythong of it. It happened for each of the different pathways people were trying, identically within normal variations of speeds and intensities. Some started a little faster. Some had more improvement or less perceived benefit in the first few days, and by the end of 6 weeks all 10 were eager to call it off halfway through the planned 3 months becasue of the severity and universality of responses. Only the whey was a few days slower in onset. IV or precursors were all the same. I have distinguised glutathione (percursors) in this way dozens of times. I don't believe that there is an utter necessity of repeating everything in every possible detail in every post. It just isn't possible. Every post would be a dense 100 pages. For instance, I only say "b12" these days when I am speaking of it in a general way. I use a specific cobalamin for all specific intances. SInce the form made no difference at all and for many NAC alone was identical, I see no reason that the distinctions need to be made every time. I do specifiy the single precursor NAC because that is often hidden in "neurological formulas" and causing people problems unbeknownst to themselves aznd is less certain. It won't make any difference in a practical sense. I hope people read and remember.


    You also state emphatically that Rich was '100 percent wrong' (which he may have been) when it came to his hypothesis that you may have some sort of genetic issue involving a Cblc enzyme. Just curious if you ever tested for that to make sure?

    For starters I didn't die from "failure to thrive". I NEVER had flagrant b12 issues of the type that lead people to get tested. I was tested for hypothyroid at 8 and may have been since near birth. And treatment started the next day. It turns out that I have a quite normal response to CyCbl, I just didn't know it.. That was because I accepted the theory that folic acid was "folate". In the original list folate and b12 deficiencies are mixed together because they can all be caused by both but in different sequences. Now aware of all these many folate problems, that fits my history. And to cap it off MeCbl didn't affect my MCV in any way l-methylfolate lowered it. CyCbl outperformed the folic acid. How were any of us going to find that out until l-methylfolate could be tried. HyCbl gives me pimples becasue it doesn' satisfy the need for for MeCbl and starts a methylation block. Somebody with CblC problems has absolutely no response to CyCbl, especially not maintaining MCV and other things. CyCbl works about average in me. I didn't have methyltrap except ocaasionally for a limited time. Until age 39 I always recovered. Then I got traped in methytrap and partial ATP blockage, after 7 years as a vegetarian.

    Rich's errors in premise are precisely because of 60 years of inactive cobalamin research predominating the understanding. That is why our docs mostly are so useless in this. Their undeerstandoings are flawed with folic acid and inactive cobalamins at the root. He was a revolutionary for working on FMS/ME/CFS at all. He still formed his entire set of fundamental understandings on the inactive cobalamins and folic acid. Everything they touch are poisoned in understanding. I've been working on this other understanding for more than 30 years. And I keep advancing them. I'm not "freezing" them for release like a software product gets frozen for release, and still get weekly updates for all sorts of software. Each weeks release is frozen instead of each years.
     
  17. Freddd

    Freddd Senior Member

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    I don't agree with you. I meant "disinterested" to distinguish his scientific objectivity. Come on don't make insult out of compliment. He wasn't " an honest politician, one who stays bought". He wasn't mistating research to get a marketing result. As most researchers he was fond of his theory. I would not have hesitated to invite him to consult on a suitable contract if it had come up.
     
  18. dannybex

    dannybex Senior Member

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    Well, I think you may find that others may interpret it as an insult, so I didn't "make" it one, that's just the way it read to me. Maybe your explanation will clear things up. I do agree he was fond of his theory, just as you are fond of yours, and Martin Pall and others are fond of theirs. :)
     
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  19. dannybex

    dannybex Senior Member

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    Thanks for your replies to my other post. I didn't see many direct answers to my questions, but I'll try to read it over in the next few days so I can hopefully decipher what you were attempting to say. I appreciate you taking the time to reply Fred.
     
  20. Freddd

    Freddd Senior Member

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    Hi Dan,,

    His work resulted in a published clinical study with Dr. Neil Nathan involving 30 patients, 2/3rds of whom improved during the study period.
    Yes, I read it. He also sent me the rawest data he had and I did some rearrangements and reinterpretations, sent that to him and a lot of my data. In a general way, and it had to be because they collected only some very specific symptoms, becasue it has to be frozen before it is started, before it goes in front of the IRB. In any case, at the level of granularity of information he had, I could do only limited things. "Improved" is a relative term. What I was able to do was group the relative reponses and relative lack of responses by specific nutrient(s). Very interesting. While I can't release my analysis, I will be posting the reponsive symptoms by nutrients data when I figure out how to do it understandably and somehow readably with the limited formatting we have in a text box. Then anybody can read the article and do a somewhat different level of results and groupings. It's nothing mindblowing. It fits nicely into my arrangement of information. It doesn't change anything, just a different understanding of the same data.

    I know your protocol has worked for the most part for you, and for others as well, but that doesn't mean it will work for everyone, just like Rich admitted repeatedly that his protocol was probably not enough -- that infections, environmental issues also may need to be addressed. I guess my point is that I don't think you'd appreciate it if the same were said about you -- that you're protecting your theoretical 'turf'. I know I'm a broken record on this subject, but with any protocol -- yours, or Rich's, or Martin Pall's -- what works for one person might be poison for another. There is no one-size-fits-all answer, just like there is no one-size-fits-all diet. One person will need more protein, one will need more fat, and others will need more carbs -- and vice versa.
    Please also note I am going WAY WAY WAY beyond what Rich claims he was dealing with, specifically partial methylation block. Rich says so in a number of posts. Again, Rich points at partially blocked methylation causing low glutathione and hence CFS/FMS/ME. I say that there is a common cause of CFS/FMS/ME that causes the partial methylation block that casues low glutathione. I maintain that is one of hundreds of biochemical changes, a result not a cause though it does cause a group of symptoms. The study only used about 30 or so symptoms. I'm going after the whole hierarchy of partial methylation block, methyltrap and Partial Mito Blockage in both body and CNS. Going specifically after glutathione misses the forest for all the trees in the way All six of the blockages need to be dealt with. Dealing with one of them doesn't usually do much relative to the whole. There is no one size fits all answer. Quite right. I know enough about permutations, combinations and all that good stuff. And you know. When I started all this I said it needs a lot of customizing which if explained was lots of comparison titrations to effect. Now I can say it needs lots of A-B trial titrations to effect. So far I've identified several main branches and can distinguish between them with a questionaire and by effects of substances. There are several more branches that are not defined. This 6 blockage conceptualization is just happening now because of this discussion. It's another way to rearrange data to see of there are some other understandings to find in it and maybe new predictablity. The 4 cobalamin deficiencies and methylfolate deficiency and LCF is another 6 items in combination, the various blockages are 6 more complex things but they are functional statements which may help understanding differently. I would like to bring the other 5 up to the same and better understanding tham partial methylation block exists. You know that Rich pointed out to me where what I was thinking at the time wasn't very proabable. It was missing folate in it's confusing role.


    The oldest historical approach I can find is the "Tantric meal" of the beefsteak, fish, whole grain items specifically and other fruits and veggies chosen for various reasons. The point is in India, with lots of lifelong vegetarians, they had a lot of hyper-responsive people to AdoCbl, MeCbl, l-methylfolate, carnitine, high quality proteins, b-complex, omega3 oils. It was known for it's "magical effects" for tantric spiritual/sexual practice. From the description people had some mild startup for a day, a brightening of mood and increase in energy. That goes back more than a thousand years in a form that could be done at the time in a practice that incuded herbs special foods and healing.
     

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