Has Anyone Found Using Glutathione Helpful?

Discussion in 'Fibromyalgia Main Forum' started by equanimous, Jan 10, 2011.

  1. equanimous

    equanimous New Member

    So I'm constantly reading about PWCs who are made more sick by glutathione, which makes me wonder, has anyone actually had any success in treating their CFIDS with glutathione? I'm starting on liposomal glutathione because my levels are low and I'm possibly experiencing excitotoxicity from the methylation protocol, but I'm extremely skeptical.

  2. richvank

    richvank New Member

    Hi, Liz.

    I'll be curious to see what sort of responses you receive to this post.

    When I first understood that glutathione is depleted in CFS back in 1999 (from Dr. Cheney), I started encouraging PWCs to build glutathione directly, by various methods. This went on until about the end of 2004. Quite a few PWCs reported that this helped to lessen their symptoms, so long as they continued to do it, but if they stopped, their symptoms worsened again. There were others who found that it worsened their symtpoms, and they could not tolerate it, so they stopped.

    I began to suspect that there must be more to this. There must be a vicious circle that was preventing glutathione from staying up. I reported this at the 2004 conference of what was then the AACFS.

    A couple of months later, Jill James and colleagues published a paper in autism research that showed that there was a partial block in the methylation cycle, upstream of glutathione synthesis in the sulfur metabolism, and that when this was corrected, glutathione came up automatically, without direct support.

    At that point I saw the similarity between what was going on in the biochemistry in autism and what was going on in CFS. I then shifted to encouraging PWCs to treat to lift the methylation cycle block, and this turned out to help many people. Lab testing showed that indeed the glutathione level came up when this was done.

    However, as I discussed in my earlier post here today, this treatment tends to exacerbate excitoxicity in some people. As I wrote there, I suspect that temporary additional depletion of glutathione is responsible for that, and in addition to other measures I listed there, I have suggested directly building glutathione, expecially at first, by means of a liposomal glutathione supplement.

    It's true that some people have reported that building glutathione directly has made their symptoms worse. One person who has experienced this strongly is "freddd," who has posted on the Phoenix Rising forum. freddd has acknowledged there that he has an inborn error of metabolism involving the intracellular B12 processing enzymes, and I suspect that the reason why glutathione was detrimental to him was that it reacted with B12 to form glutathionylcobalamin, which is a normal reaction in the body that protects B12 at an intermediate stage of its metabolism, but in his case, his cells were not able to carry on the next steps to make methylcobalamin and adenosylcobalamin.

    I don't believe that this is a problem for most PWCs, because this mutation is reported to be rare. There are some other possible reasons why building glutathione might exacerbate symptoms. One is that it may increase the activity of the immune system and the detox system, killing pathogens and mobilizing toxins into the blood temporarily. Another is that it may overload the enzyme sulfite oxidase (this can be helped by adding molybdenum in many cases, which may be deficient). Another is that it may raise the cysteine level too high. Cysteine can auto-oxidize at high concentrations, making the oxidative stress more severe. We don't yet know which of these may be going on, and it may differ from one person to another.

    As I wrote in the earlier post, I haven't heard from anyone who has tried using liposomal glutathione during methylation treatment to counter excitotoxicity, so I don't know whether it will work.

    As always, I recommend working with a physician while doing this type of treatment.

    Best regards,


  3. hermitlady

    hermitlady Member

    My PCP doc was just talking to me about IV Glut treatments that he's done for Parkinson's pts. I had mentioned that my BIL was recently diagnosed w Parkinson's and my doc was pleased to report success in reducing symptoms on some of his pts w this treatment.

    My doc has an autistic son, and he is very involved in research etc in these complex areas of human body chem. I imagine him to someday be adding a lot of alternative type treatments to his practice. He is a wonderful doctor.

    Rich...have you heard of anything like this for Park pts?
    [This Message was Edited on 01/11/2011]
  4. richvank

    richvank New Member

    Hi, hermitlady.

    Yes. That treatment originated with Dr. Secchi in Italy and was picked up some years ago by Dr. David Perlmutter in Florida. Dr. Perlmutter has been using this treatment for quite a while. Recently he and some colleagues published a small clinical study of it. See below. Unfortunately, the results were not as positive as one might have hoped. Sounds as though they are planning to do a larger study.


    Mov Disord. 2009 May 15;24(7):979-83.
    Randomized, double-blind, pilot evaluation of intravenous glutathione in Parkinson's disease.

    Hauser RA, Lyons KE, McClain T, Carter S, Perlmutter D.

    Department of Neurology, University of South Florida, Tampa, Florida 33606, USA. rhauser@health.usf.edu

    Comment in:

    * Mov Disord. 2010 May 15;25(7):962; author reply 962-3.
    * Mov Disord. 2010 May 15;25(7):961-2; author reply 962-3.
    * Mov Disord. 2010 Nov 15;25(15):2690-1.


    The objective of this study was to evaluate the safety, tolerability, and preliminary efficacy of intravenous glutathione in Parkinson's disease (PD) patients. This was a randomized, placebo-controlled, double-blind, pilot trial in subjects with PD whose motor symptoms were not adequately controlled with their current medication regimen. Subjects were randomly assigned to receive intravenous glutathione 1,400 mg or placebo administered three times a week for 4 weeks. Twenty-one subjects were randomly assigned, 11 to glutathione and 10 to placebo. One subject who was assigned to glutathione withdrew from the study for personal reasons prior to undergoing any postrandomization efficacy assessments. Glutathione was well tolerated and there were no withdrawals because of adverse events in either group. Reported adverse events were similar in the two groups. There were no significant differences in changes in Unified Parkinson's Disease Rating Scale (UPDRS) scores. Over the 4 weeks of study medication administration, UPDRS ADL + motor scores improved by a mean of 2.8 units more in the glutathione group (P = 0.32), and over the subsequent 8 weeks worsened by a mean of 3.5 units more in the glutathione group (P = 0.54). Glutathione was well tolerated and no safety concerns were identified. Preliminary efficacy data suggest the possibility of a mild symptomatic effect, but this remains to be evaluated in a larger study.
    (c) 2009 Movement Disorder Society.

    PMID: 19230029 [PubMed - indexed for MEDLINE]
  5. heapsreal

    heapsreal New Member

    My wife and i have medical backgrounds although not doctors, i wish, but would be able to do our own infusions. Can someone point us to a good source of IV glutathione. Alot of sources seems directed at asians who use it to whiten their skin, so mark up the price.

  6. hermitlady

    hermitlady Member

    Thank you for the info, I will be fwding it to my BIL. He is seeing folks thru the VA hospital etc, filing govt comp claims for vets. I guess Parkinson's is quite common in Vietnam Vets who were exposed to Agent Orange as he was. Poor guy has had so many health problems many of which have been related to being in that hideous war. He was only 18 when he went over there, and now he is in his mid 60's. I hate seeing how quickly he has been deteriorating over the past year, so sad for such an active person.

    If you possibly have any other Parkinson's related info, links, etc, I'd really appreciate anything. Sorry to be off topic here, just kind of stumbled into this. The knowledge that you share here is soooo greatly appreciated![This Message was Edited on 01/12/2011]
  7. wrthster

    wrthster New Member


    I have tried NAC 600 MG. I have no problem tollerating but some do. You can buy at any health food store any brand and go slow to see. I have had some benefit from it but limited.
  8. richvank

    richvank New Member

    Hi, hermitlady.

    Dr. Amy Yasko has reported that before she began to focus her efforts on autism, she had a local practice in which she treated cases of adult neurological diseases, including Parkinson's.
    She found that treating the methylation cycle was helpful in these diseases, also, and that's actually how she got started using this approach.

    It would probably be difficult to get tested for this through the VA, but it might be helpful if your BIL could have the Health Diagnostics and Research Institute methylation pathways panel run to see if he does in fact have a partial methylation cycle block and depleted glutathione. Contact info and an interpretive guide are pasted below.

    Before I learned about the partial methylation cycle block in autism and realized that it must also be present in CFS, which subsequent testing has abundantly shown, I used to encourage PWCs to try to build up their glutathione by more direct methods, including IV glutathione. This was only temporarily helpful in those it did help. The problem is that the partial methylation cycle block holds glutathione down. So it's necessary to fix that first.

    I think it might be possible that the same situation applies in Parkinson's disease, only on a more local level, i.e. confined primarily to the basal ganglia in the brain.

    As you know, I am a researcher, not a licensed physician, and I cannot recommend individual treatment unless a physician is on board to review my suggestions. However, from a scientific point of view, I think it would be interesting to see how Parkinson's patients respond to a methylation-type treatment. There are several of them in use now. One is even a prescription "medical food"--Cerefolin-NAC, produced by PamLab. Mainstream physicians may be more comfortable with using this treatment, since it is an FDA-approved prescription treatment. But it basically includes similar supplements (no actual drugs) to what quite a few alternative/complementary physicians are using in the over-the-counter methylation treatments for CFS and autism now, i.e. B12, folate and N-acetylcysteine.

    As always, I want to emphasize that methylation-type treatments should be done under the supervision of a physician, since a small number of people have reported serious adverse effects while on them. More information is available at www.cfsresearch.org by clicking on CFS/M.E. and then on my name.

    Best regards,


    Methylation Pathways Panel

    This panel will indicate whether a person has a partial methylation cycle block and/or glutathione depletion. I recommend that this panel be run before deciding whether to consider treatment for lifting the methylation cycle block. I am not associated with the lab that offers this panel.

    The panel requires an order from a physician or a chiropractor. The best way to order the panel is by fax, on a clinician’s letterhead.

    Available from:

    Health Diagnostics and Research Institute
    540 Bordentown Avenue, Suite 4930
    South Amboy, NJ 08879
    Phone: (732) 721-1234
    Fax: (732) 525-3288

    Lab Director: Elizabeth Valentine, M.D.

    Dr. Tapan Audhya, Ph.D., is willing to help clinicians with interpretation of the panel by phone, or the guide below can be used:

    Interpretation of the Health Diagnostics and Research Institute
    Methylation Pathways Panel

    Rich Van Konynenburg, Ph.D.

    Several people have asked for help in interpreting the results of
    their Health Diagnostics and Research Institute methylation pathway panels. Here are my suggestions for doing so. They are based on my study of the
    biochemistry involved, on my own experience with interpreting more
    than 120 of these panel results to date, and on discussion of some of
    the issues with Tapan Audhya, Ph.D., at the Health Diagnostics and Research Institute.

    The panel consists of measurement of two forms of glutathione
    (reduced and oxidized), adenosine, S-adenosylmethionine (SAM) , S-
    adenosylhomocysteine (SAH), and seven folic acid derivatives or

    According to Dr. Audhya, the reference ranges for each of these
    metabolites was derived from measurements on at least 120 healthy
    male and female volunteer medical students from ages 20 to 40, non-
    smoking, and with no known chronic diseases. The reference ranges
    extend to plus and minus two standard deviations from the mean of
    these measurements.

    Glutathione: This is a measurement of the concentration of the
    reduced (active) form of glutathione (abbreviated GSH) in the blood
    plasma. From what I've seen, most people with chronic fatigue
    syndrome (PWCs) have values below the reference range. This means
    that they are suffering from glutathione depletion. As they undergo
    the simplified treatment approach to lift the methylation cycle
    block, this value usually rises into the normal range over a period
    of months. I believe that this is very important, because if
    glutathione is low, vitamin B12 is likely unprotected and reacts with toxins
    that build up in the absence of sufficient glutathione to take them
    out. Vitamin B12 is thus “hijacked,” and not enough of it is able to
    convert to methylcobalamin, which is what the methylation cycle needs
    in order to function normally. Also, many of the abnormalities and
    symptoms in CFS can be traced to glutathione depletion.

    Glutathione (oxidized): This is a measurement of the concentration
    of the oxidized form of glutathione (abbreviated GSSG) in the blood
    plasma. In many (but not all) PWCs, it is elevated above the normal
    range, and this represents oxidative stress.

    Adenosine: This is a measure of the concentration of adenosine in the
    blood plasma. Adenosine is a product of the reaction that converts
    SAH to homocysteine. In some PWCs it is high, in some it is low, and
    in some it is in the reference range. I don't yet understand what
    controls the adenosine level, and I suspect there is more than one
    factor involved. In most PWCs who started with abnormal values, the
    adenosine level appears to be moving into the reference range with
    methylation cycle treatment, but more data are needed.

    S-adenosymethionine (RBC) (SAM): This is a measure of the
    concentration of SAM in the red blood cells. Most PWCs have values
    below the reference range, and treatment raises the value. S-
    adenosylmethionine is the main supplier of methyl groups in the body,
    and many biochemical reactions depend on it for their methyl
    groups. A low value for SAM represents low methylation capacity, and
    in CFS, it appears to result from a partial block at the enzyme methionine
    synthase. Many of the abnormalities in CFS can be tied to lack of
    sufficient methyation capacity.

    S-adenosylhomocysteine (RBC) (SAH): This is a measure of the
    concentration of SAH in the red blood cells. In CFS, its value
    ranges from below the reference range, to within the reference range,
    to above the reference range. Values appear to be converging toward
    the reference range with treatment. SAH is the product of reactions
    in which SAM donates methyl groups to other molecules.

    Sum of SAM and SAH: When the sum of SAM and SAH is below 268
    micromoles per deciliter, it appears to suggest the presence of
    upregulating polymorphisms in the cystathione beta synthase (CBS)
    enzyme, though this may not be true in every case.

    Ratio of SAM to SAH: A ratio less than about 4.5 also represents low
    methylation capacity. Both the concentration of SAM and the ratio of
    concentrations of SAM to SAH are important in determining the
    methylation capacity.

    5-CH3-THF: This is a measure of the concentration of 5-methyl
    tetrahydrofolate in the blood plasma. It is normally the most
    abundant form of folate in the blood plasma. It is the form that
    serves as a reactant for the enzyme methionine synthase, and is thus
    the most important form for the methylation cycle. Many PWCs have a
    low value, consistent with a partial block in the methylation cycle.
    The simplified treatment approach includes FolaPro, which is
    commercially produced 5-CH3-THF, so that when this treatment is used,
    this value rises in nearly every PWC. If the concentration of 5-CH3-
    THF is within the reference range, but either SAM or the ratio of SAM
    to SAH is below the reference values, it suggests that there is a
    partial methylation cycle block and that it is caused by
    unavailability of sufficient bioactive B12, rather than
    unavailability of sufficient folate. I have seen this frequently,
    and I think it demonstrates that the “hijacking” of B12 is the root
    cause of most cases of partial methylation cycle block. Usually
    glutathione is low in these cases, which is consistent with lack of
    protection for B12, as well as with toxin buildup.

    10-Formyl-THF: This is a measure of the concentration of 10-formyl
    tetrahydrofolate in the blood plasma. It is usually on the low side in PWCs.
    This form of folate is involved in reactions to form purines, which
    form part of RNA and DNA as well as ATP.

    5-Formyl-THF: This is a measure of the concentration of 5-formyl
    tetrahydrofolate (also called folinic acid) in the blood plasma.
    Most but not all PWCs have a value on the low side. This form is not used
    directly as a substrate in one-carbon transfer reactions, but it can
    be converted into other forms of folate. It is one of the
    supplements in the simplified treatment approach, which helps to
    build up various other forms of folate.

    THF: This is a measure of the concentration of tetrahydrofolate in
    the blood plasma. In PWCs it is lower than the mean normal value of 3.7
    nanomoles per liter in most but not all PWCs. This is the
    fundamental chemically reduced form of folate from which several
    other reduced folate forms are made. The supplement folic acid is
    converted into THF by two sequential reactions catalyzed by
    dihydrofolate reductase (DHFR). THF is also a product of the
    reaction of the methionine synthase enzyme, and it is a reactant in
    the reaction that converts formiminoglutamate (figlu) into
    glutamate. If figlu is high in the Genova Diagnostics Metabolic
    Analysis Profile, it indicates that THF is low.

    Folic acid: This is a measure of the concentration of folic acid in
    the blood plasma. Low values suggest folic acid deficiency in the
    current diet. High values are sometimes associated with inability to
    convert folic acid into other forms of folate, such as because of
    polymorphisms in the DHFR enzyme. They may also be due to high
    supplementation of folic acid.

    Folinic acid (WB): This is a measure of the concentration of folinic
    acid in the whole blood. See comments on 5-formyl-THF above. It
    usually tracks with the plasma 5-formyl-THF concentration.

    Folic acid (RBC): This is a measure of the concentration of folic
    acid in the red blood cells. The red blood cells import folic acid
    when they are initially being formed, but during most of their
    approximately four-month life, they do not normally import, export, or use
    it. They simply serve as reservoirs for it, giving it up when they
    are broken down. Many PWCs have low values. This can be
    caused by a low folic acid status in the diet over the previous few
    months, since the population of RBCs at any time has ages ranging
    from zero to about four months. However, in CFS it can also be
    caused by damage to the cell membranes, which allows folic acid to
    leak out of the cells. Dr. Audhya reports that treatment with omega-
    3 fatty acids can raise this value over time.

  9. hermitlady

    hermitlady Member

    We'll take any info we can get, anything could be potentially helpful.

    I know you probably don't remember, but I'm the one who was born and raised in Livermore, my dad worked at LLL many yrs ago. We "Livermorons" must stick together ;)

    Glad we all have someone like you who is sincerely dedicated to helping us. xoxoxo
  10. richvank

    richvank New Member

    Hi, hermitlady.

    Yes, I do remember. Amen! Let's hear it for the Livermorons! :)-) And the Vietnam vets, too!