Volunteer opportunity: Organizing Phoenix Rising articles
This section contains all the articles that have been published by Phoenix Rising over the years. As you will see if you browse here, some of the articles are outdated--either the research has been superseded or retracted or the article features an event or campaign that is now in...
Discuss the article on the Forums.

Normal glutathion means methylation is not the problem?

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by cigana, Dec 6, 2011.

  1. cigana

    cigana Senior Member


    I wonder if someone can help. I have my glutathione results back showing my Red Cell and Plasma GSHPx in the normal range (with SOD also normal in red cells).

    Does this mean that methylation is not my problem and I don't need to go on the methylation protocol, or could it be that as I am taking B-vitamins and large B12, that this has temporarily fixed my glutathion issue making it appear as though I don't have a problem?


  2. xrunner

    xrunner Senior Member

    Very good question. I happen to be in that same group, although my gsh, gshpx, sod etc have normalised via other treatment, and would also like to know.
    And if I may ask a related question, when glutathione levels appear normal, is there any other additional benefit in doing the methylation protocol?
  3. Valentijn

    Valentijn Senior Member

    From what I understand, methylation lowers homocysteine by converting it back to methionine. High homocysteine is generally considered bad, though I'm not sure if it's harmful itself or if it just reflects other problems, like trouble producing cysteine.
  4. richvank


    Hi, all.

    I'm guessing that you are citing results from Acumen Lab in the UK. This is a wonderful lab. I correspond with Dr. Howard there often and am an admirer of his work on developing mitochondrial testing. However, the test that he runs for glutathione is a red blood cell total glutathione measurement. If this measurement comes out low, it is a good indication that the tissue cell reduced glutathione is likely low. However, if this measurement comes out in the normal range, one cannot be sure that the tissue cell reduced glutathione is in the normal range. There are two reasons for this: First, the red blood cells are normally producers and net exporters of glutathione. They are thus likely to have a better glutathione status than tissue cells (such as in the skeletal muscle). Second, the measurement of total glutathione contains oxidized glutathione, and such a measurement does not distinguish reduced glutathione, which is the active, usable form.

    It is much easier to measure red blood cell glutathione than plasma glutathione, because it is about 1,000 times as high. Also, it is much easier to measure total glutathione than reduced glutathione, because reduced glutathione will oxidize during shipping and storage of blood samples, unless a combination of certain enzyme blockers are in the sample vial. As far as I know, only the European Laboratory of Nutrients in the Netherlands and the Health Diagnostics and Research Institute in New Jersey, USA, use these enzyme blockers and are able to measure reduced glutathione in shipped samples. They keep the formulation proprietary for business reasons. They put considerable effort into developing this formulation.

    Beyond this, I think it is still possible for a person to have normal tissue cell reduced glutathione (as inferred from plasma measurement of reduced glutathione) and still have a partial methylation cycle block. This can occur if the person has genetic polymorphisms in the enzymes that use glutathione (the glutathione peroxidases and/or the glutathione transferases). I have seen a few Spectracell lab reports (this is a lymphocyte functional test offered in Houston, Texas, USA) in which the glutathione came out normal, but the total antioxidant capacity was low. I suspect that these people fit into this category. For most PWMEs, though, I see both a partial block in the methylation cycle and depletion of reduced glutathione, based on the methylation pathways panel offered by ELN and HDRI, mentioned above.

    Best regards,

    taniaaust1 likes this.
  5. xrunner

    xrunner Senior Member

    Hi Rich,

    thanks for the explanation. My tests were at Biolab and they measured:
    Rbc GSHPx-1
    Plasma Glutathione peroxidase GSHPx-3
    Serum Glutathione-S-Transferase
    RBC Superoxide dismutase

    all normal.

    From what you wrote, does it mean that in cases where GSH peroxidase and transferase seem ok, then it's unlikely that tissue GSH would be deficient and that a partial methylation cycle block was present? or one still needs to run one of those methylation panels to make that conclusion?
  6. Freddd

    Freddd Senior Member

    Salt Lake City
    Hi Cigana,

    Methylb12 specifically and Metafolin specifically will turn methylation on in the absence of any cause for induced or paradoxical folate deficiency. They are the heart of a mehtylation protocol. They increase glutathione. However, as mb12, Metafolin and adb12 do hundreds of other things such as startup of mitochondria it's good to have all the cofactors. The "glutathione problem" is a RESULT of low mb12 and low methylfolate, not a freestanding problemn that pops up separately from those lacks. It can result from taking cyanocbl/hydroxycbl and folic acid becasus those may not fill a need. Every time I go into paradoxical folate deficiency the cell reproduction stops and I have tissue breakdown. Presumably that deficiency stops at least some methylation very quickly.

    making it appear as though I don't have a problem

    If methylation is working you don't have that problem. Lack of mb12/methylfolate CAUSE glutathione to be low, not the other way around. It sounds like conceptually you have the cart before the horse.

See more popular forum discussions.

Share This Page