New Atmosphere, New Vision: Gibson and Whittemore Kick Off Invest in ME Conference 2016
Mark Berry reports on Dr. Gibson's introduction and Dr. Whittemore's keynote speech, at the 11th Invest in ME International ME Conference in London.
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Supplement help

Discussion in 'General Treatment' started by MAOAr297r, Oct 21, 2017.

  1. MAOAr297r

    MAOAr297r

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    Seattle
    Hey guys,

    I have just started taking NADH at 20mg and it noticed it helps a bit. What dosages do you guys like to use for NADH and how many times a day do you take it?

    I just receive Pyruvate I ordered it after hearing Ron Davis speak about it. I'm going to try a low does as I know it can make you worse sometimes, especially at too much.

    Last I just purchased D-ribose and CoQ10 but I have no idea how much is the therapeutic dose for us ME/CFS people. Any tips or advice would be highly appreciated!

    Thank you :)
     
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  2. rodgergrummidge

    rodgergrummidge

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    upload_2017-10-22_16-20-27.png
    10mg/day resulted in improvement in this trial (above), but the overall individual response-rate (only 31%) was low. Sounds like you are one of the lucky people who responds to NADH treatment @MAOAr297r ! Some trials have suggested that including CoQ10 with NADH can also assist in CFS. Something to consider?

    cheers

    Rodger
     
    pattismith likes this.
  3. Learner1

    Learner1 Professional Patient

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    Pacific Northwest
  4. echobravo

    echobravo Keep searching, the answer is out there

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    Norway
    I am not sure that pyruvate supplementation is beneficial for someone with ME, what did Ron Davis have to say about it?

    A key finding of Fluge & Mella last year was that oxidation of pyruvate to acetyl-coa seems to be blocked in the inner mitochondrial membrane, due to a blockage in the PDH enzyme complex.

    Then, because the main source of acetyl-coa into the Krebs cycle is blocked, any excertion (cells needing more energy (ATP)) will lead to a buildup of pyruvate in ppl w ME. The body will further convert (some of the?) excess pyruvate into lactate, a major contibutor to PEM symptoms.

    I am sure I don’t have the whole picture, so it would be nice to hear other peoples opinion on this.

    PS! Since methylglyoxal (MG) seems to be closely linked to the glycolysis process (pyruvate, lactate) in cellular cytoplasma, how is the concentration of MG affected as pyruvate and lactate builds up (from PDH defect)? I would guess higher MG would contribute to the PEM symptoms as well, the feeling of being “poisioned inside”..?

    “Methylglyoxal, the dark side of glycolysis”
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4321437

    https://en.wikipedia.org/wiki/Methylglyoxal_pathway

    https://upload.wikimedia.org/wikipe...e.png/700px-Methylglyoxal_pathway_picture.png

    Excess sugar in the cell supposedly triggers the methylglyoxal pathway. Question is, what happens in that pathway when pyruvate builds up (see figure above)?

    Edit: Also, wouldn't D-Ribose add to the glucose load in cells and cause even more pyruvate to be created?
     
    Last edited: Oct 22, 2017
    pattismith likes this.

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