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Liposomal Glutathione

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by Sallysblooms, Apr 23, 2011.

  1. richvank

    richvank Senior Member

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    Hi, AQ.

    Yes, I think they would. Another thing that I think would help, which is not too available in the U.S., is what Bianca did in Germany: hemapheresis. It's sort of like dialysis for kidney disease--blood is taken out and passed over binders like activated charcoal, and then put back in. I think heparin is added to it to prevent clotting. If a person's own detox system is not able to clear out the toxins, this may be the answer. I've seen a few papers about it in connection with treatment of acute poisoning, but I think it can be used for chronic toxicity, also. But passing binders through the digestive system would at least help with toxins that are excreted in the bile.

    Best regards,

    Rich
     
  2. Vegas

    Vegas Senior Member

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    Some of the usual things that significantly increase activity/expression like Curcumin & silymarin...as well as having a lot of other properties...but also a whole lot of other things like sulforaphane (Broccolli Seed Extract), Biotech's Extra Energy Enzymes (which has some of these same plant compounds), Rosemary, flavonoids like EGCG (catechins in green tea extract).

    I think these compounds, although obviously possessing many more properties that acting on a singular enzyme group, are backed by a good amount of research as being beneficial to some patients with chronic fatigue. Actually, if you take a look at substances that have been studied in the treatment of fatigue, there seems to be an over-representation of substances that stimulate this enzyme group. I've also notice a lot of relatively research into mercury toxicity pointing to specific GST SNP's.
     
  3. richvank

    richvank Senior Member

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    Hi, all.

    I very much appreciate the discussion going on here. As some of you know, for about 5 years (1999-2004) I advocated direct boosting of glutathione by a variety of modes. Most of this went on in the Yahoo CFSFMExperimental group. This was based on the experiences of Drs. Salvato, Cheney, and Enlander, which indicated that it could be helpful. Some people experienced temporary improvement in symptoms from this, while others found that it made their symptoms worse. For the ones for whom the symptoms got worse, some of us speculated about possible reasons, but we never knew for sure. The possibilities that were raised were: (1) a "herxheimer" reaction due to die-off of pathogens from activation of the immune system by glutathione; (2) catabolic breakdown of the glutathione, producing too much cysteine, which would auto-oxidize and make the oxidative stress more severe; (3) catabolic breakdown of the glutathione, which would present too much sulfite to the sulfite oxidase reaction, causing the sulfite to rise to toxic levels; (4) mobilization of toxins into the blood by the glutathione, and then dumping them, which would expose all the cells to the toxins; (5) oxidation of the glutathione to oxidized glutathione (GSSG), which would shift the redox potential in the oxidizing direction and deleteriously affect biochemical reactions that depend on it. Those are the ones that I can think of, and I'm not sure which if any of them explain what these people experienced. There hasn't been any clinical research to sort this out, unfortunately.

    When I learned about the involvement of the partial methylation cycle block in autism from the work of Jill James et al. in late 2004, I shifted my focus to treating to lift the partial methylation cycle block, which was found to raise glutathione automatically in autism, and the same was later found in ME/CFS by the clinical study that Dr. Nathan and I carried out and reported in 2009. So then it seemed to me that it wasn't necessary to boost glutathione directly.

    More recently, I have become concerned about the many reports of symptoms of excitotoxicity when people begin the methylation treatment. These include anxiety, nervousness, insomnia, a "wired" feeling, and hypersensitivity of the senses. Dr. Amy Yasko had already found this in autism, and had suggested protocols to deal with it. From reading some of her material, I learned that a lowering of glutathione in the astrocytes of the brain could account for the excitotoxicity, because it would cause the glutamate level to remain too high in the neuronal synapses, overstimulating the NMDA receptors. When I combined this with the experience reported by Dr. Cheney when he measured the IVRT changes in his patients on his echocardiograph machine, comparing the effects of methyl B12 with hydroxo B12, it dawned on me that raising the activity of the methionine synthase reaction would initially lower glutathione, and that could explain the initial excitotoxicity increase and the more severe change in IVRT caused by methyl B12 than hydroxo B12. The methyl B12 would have a more immediate effect on the methionine synthase reaction, because it did not need to be converted to serve as the coenzyme.

    So at that point, I began to think that it might help to add some glutathione to the methylation treatment, especially early on, to counter this initial drop in glutathione, and hopefully to relieve the excitotoxicity increase. So far, I'm not sure this has paid off for the people who have tried it, and there are clearly some for whom it made things worse, as reported on this thread. Why did that happen? I think it goes back to trying to understand why some of the people did not respond well to glutathione by itself. As has been mentioned here, maybe it was due to mobilization of toxins, which were then redistributed rather than taken completely out of the body. How would this happen? I think it's always important to keep in mind that in chemistry there is the concept of the dynamic equilibrium. This means that bonds are continuously being made and broken, and the average effect of all of this is what is reflected in chemical reactions. More to the point, the bond between a glutathione molecule and a toxic metal ion is not necessarily permanent. It can be broken. If there continues to be enough glutathione present, the toxic metal ions can be rebound, and the overall net effect is that they will be carried out, on the average. This dynamic equilibrium effect is the same reason Andy Cutler recommends taking alpha lipoic acid every three hours to chelate mercury. That keeps its concentration up in the blood, so that a mercury ion that become unbound can be bound again by another ALA molecule.

    So if this is what is going on, perhaps the application of glutathione would need to be more frequent. This may be why I.M. application of glutathione, as practiced by Dr. Salvato, might work better, because the release to the blood would be slower than by I.V.

    On the other hand, if the glutathione is producing too much sulfite, maybe more molybdenum supplementation would help. 2000 micrograms per day is the upper limit recommended by the Institute of Medicine.

    If glutathione is being oxidized, perhaps more supplementation with B-complex would help, because B2 and B3 are needed by the glutathione reductase reaction.


    The other new thing that has come into this picture recently is the research published a few months ago from Korea, which showed that glutathione has a major effect on the affinity of part of the intracellular B12 processing system for the B12 molecule (the CblC complementation group). I think this is probably the reason why we have had to use such high dosages of B12 (compared to the RDA dosage) to treat ME/CFS, where glutathione has become depleted. This has suggested to me that if glutathione could be raised sooner in the cells during the methylation treatment, it might work better, because the B12 would be processed more rapidly by the cells. So that's another reason I've been thinking that adding glutathione might help.

    As you know, Freddd has been adamantly opposed to supplementing with glutathione, based on his personal experience with it, and the experiences of some others. As I've posted in the past, I think that Freddd himself has a polymorphism in his CblC complementation group. This is the part of the intracellular B12 processing system that normally uses glutathione. In Freddd's case, I think that what happens is that glutathione binds his B12 to form glutathionylcobalamin, and his CblC group is not able to reclaim the cobalamin, to use it to make methy and adenosyl B12, which it normally does. I don't know how many people have such a polymorphism, but the published literature says it is rare. Nevertheless, this could be another way in which glutathione causes problems for some PWMEs.

    With regard to the ways of boosting glutathione, most of them that have been used do not actually get glutathione into the cells in general. For example, I.V. glutathione is of course put directly into the blood, but it doesn't stay in the blood very long. About 80% of it is removed by the kidneys, and about 10% by the lungs. The rest goes to various other cells, tissues and organs. Most cell types do not import glutathione. Instead, it is broken down into its amino acids. Some of them are imported, and glutathione may be re-formed from them inside the cells.

    To actually get glutathione into the cells in general, liposomal or acetyl glutathione are the forms that should work. Another approach is to give the cells the amino acids needed, so that they can make glutathione. The rate-limiting amino acid is usually cysteine, though I have seen quite a few PWMEs who are low in glycine, also. Cysteine can be given orally as N-acetylcyteine, which the liver cells will import. However, there has been controversy about use of NAC in ME/CFS, on the grounds that it can move mercury into the brain. There has not been a clinical study of this.

    Selenium is needed by some of the glutathione peroxidase enzymes. These enzymes convert hydrogen peroxide to water, in the process oxidizing glutathione to GSSG. This is separate from the conjugation of glutathione to toxins by the glutathione S-transferase enzymes.

    At this point, I'm not sure what to recommend about using glutathione together with the methylation treatment. It does seem to help some people, but I don't know how to predict whether it will help a given person or not. I appreciate people's input on this issue.

    Best regards,

    Rich
     
    Sidereal, RosieBee, nanonug and 2 others like this.
  4. Sallysblooms

    Sallysblooms P.O.T.S. now SO MUCH BETTER!

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    I have found that using all of my supplements together was the only way I got better. I do it all, all at the same time and the improvement in CFS is wonderful.

    I went to see Dr. Salvato just one time. I could not wait to leave. Thank goodness I do have a good doctor that helped my CFS and now we are working to heal my POTS.

    For me, there was not just one area to work on. I needed many supplements and foods to heal my CFS. Glutathione, NAC, Alpha Lipoic Acid, Benfotiamine, pregnenalone, 7 keto......SOOOO many things on my supplement list. They all were needed. I hope everyone can find the supplements they need.

    Thank you Rich for all of your work! I love reading your posts, so much to learn from them.
     
    LivingwithFibro likes this.
  5. lizw118

    lizw118 Senior Member

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    Hi everyone,
    I just wanted to add an update with my glutathione supplements. I read Rich's long post and decided to spread one packet of glutathione out over the entire day. It seems to have made a difference. I also cut back on some estriol I was taking, which I believe has helped my thyroid medicine work better, which in turn also seems to help (not sure why). Anyway, now I am seeing benefits from the glutathione. I will update as I go
    Liz W
     
    RosieBee likes this.
  6. nanonug

    nanonug Senior Member

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    I take S-acetyl-glutathione, 100mg three times daily on an empty stomach.
     
  7. nanonug

    nanonug Senior Member

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    This interests me a lot!

    Do you happen to know what these SNPs are?

    Thanks!
     
  8. nanonug

    nanonug Senior Member

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    A few years ago, I used to get glutathione shots followed by a Myer's cocktail. The problem with glutathione is that its half-life is measured in minutes (if memory serves me right). So you may end up in a situation in which you may take too much for a short period of time and not enough for a much longer period. That's why I now do the oral route spread throughout the day.
     
  9. nanonug

    nanonug Senior Member

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    It is almost impossible to add anything of value to Rich's excellent posts but I am going to try anyway! :)

    Based on this study, "Lipoic acid increases de novo synthesis of cellular glutathione by improving cystine utilization", it would appear that supplementing with alpha-lipoic acid (or preferably the R form) and undenatured whey protein (a source of cystine) would also result in increased levels of naturally produced glutathione.
     
  10. RosieBee

    RosieBee

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    Hi Liz, How did this go?
    RosieBee
     
  11. Athene

    Athene ihateticks.me

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    I have been spreading my liposonal glutathione out throughout the day too, and it works really well like that.
    I have also tried stopping it for a few days at a time and taking it on an "as needed" basis, in the hope that will also help prevent the day when it just stops working. I take it whenever I feel the symptoms of low glutathione. So far that has been working really well for me too.
    I've been doing this for 10 weeks so far.
     
    Hanna likes this.
  12. dsnrbec

    dsnrbec

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    With much trepidation, I took 1 tsp yesterday and now, 24 hours later, I still smell it strongly in my urine. Has anyone else experienced this? I take lots of supplements but have never smelled anything in my urine. I must admit I'm a little freaked out!
     
  13. Sparrow

    Sparrow Senior Member

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    Certain ones smell in my urine. There's not anything necessarily wrong with that. The smell just means that there's some part of what you've taken that doesn't get broken down by the body (in a similar way to components in asparagus or coffee or certain other foods that make pee smell).

    I'm not qualified to give medical advice of any kind, but in my unprofessional opinion, I wouldn't be freaked out about it. It isn't one of the signs I know of that your kidneys aren't doing well or anything. Just that the supplement is maybe still in your system (which isn't a bad thing), and that part of it get excreted through the urine (which is at worst a neutral). Some things have their natural "exit" through the feces, and some through the urine, and that's perfectly normal.

    Is there a part of it in particular that's worrying you? Sorry you're feeling concerned.
     
  14. dsnrbec

    dsnrbec

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    Just that I know there is a lot of controversy about glutathione and I was already nervous about trying it. Like many, I react to a lot of supplements so it's always a crap shoot when I try something new, especially if its "iffy". Still not sure if I will take it again since I'm very mercury toxic.
     
  15. Lotus97

    Lotus97 Senior Member

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    Yes, I would like to know others' experiences too. Also, I was wondering if anyone has tried both liposomal/lipoceutical Glutathione and Acetyl Glutathione since both types promise increased oral absorption compared to regular reduced glutathione.
     
  16. Lynn_M

    Lynn_M Senior Member

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    Nanonug, although it's been 11 months since you asked and I've also been wondering, I just found out tonight what SNPs are involved in glutathione s-transferase genes. Based on information in geneticgenie.org and the Genova Detoxigenomics sample report, GSTP1 I105V and GSTP1 A114V are two SNPs involved in glutathione s-transferase. The I105V is rs1695, with wild type TT. The A114V is rs1138272 with wild type CC. There's also a GSTM SNP, but 23andMe doesn't test for it.

    Lynn
     
  17. Zensational

    Zensational

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    I just started my first Liposomal Glutathione and Liposomal Vit C combo today. We are making it based on this technology.

    I took 6 ounces total first thing this morning. I will keep you posted on my progress.
     
  18. drob31

    drob31 Senior Member

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  19. PeterPositive

    PeterPositive Senior Member

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    I have used the least absorbable form of GSH for quite some time, which is oral reduced glutathione with decent results. It helps with bowel inflammation. I normally take 3x 500mg. capsules (by Jarrow) during the day.

    I also tried the acetyl form, which seems promising, but at the max suggested dosage ( 300mg ) it doesn't do anything for me. In fact when I go back to the Jarrow supplement I feel better within an hour... Very puzzling.

    One thing it's not clear to me is the noteworthy difference in recommend dosage between regular GSH and the acetyl form. Taking 1500mg of the former vs only 300mg of the latter seems a pretty significant difference.

    Do you know of a reason why acetyl-GSH is recommended at such a lower dosage?

    Thanks
     
  20. Hanna

    Hanna Senior Member

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    Has someone tried the LivOn liposomal Glutathione ?
     

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