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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Fundraiser: A Novel Proposal for the Treatment of ME/CFS

Discussion in 'Fundraising' started by AndyPR, Jan 26, 2017.

  1. AndyPR

    AndyPR Senior Member

    http://www.crowdfunder.co.uk/a-novel-proposal-for-the-treatment-of-mecfs

    Personally I'd need more details before I'd put any money in but it's a least one example of researchers not being put of from ME research.

    Tagging @Hip as Myhill studies are referenced on the Crowdfunder page.
     
  2. AndyPR

    AndyPR Senior Member

    Also saw this as it was shared on the MEA's Facebook page. Hopefully now we'll see the MEA regularly sharing details of all studies that need funding?? ;)
     
  3. ukxmrv

    ukxmrv Senior Member

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    I've lost the link to his Facebook page but last night I saw a new post there explaining his hypothesis in a little more detail. It's about ATP but my brain problems stopped me from reading it properly.
     
  4. charles shepherd

    charles shepherd Senior Member

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    A CROWD FUNDER FOR GARETH ETTERIDGE'S RESEARCH PROJECT

    Helen Hyland, MEA fund-raising manager, writes:

    Gareth is a keen and long standing supporter of The ME Association. We sincerely hope that his 'novel' research secures all the funding it needs to proceed.

    http://www.crowdfunder.co.uk/a-novel-proposal-for-the-treat…

    Gareth was one of the students that we funded to attend the 2016 CMRC conference in Newcastle
     
  5. AndyPR

    AndyPR Senior Member

    Details are on his Crowdfunder page, both for his Facebook, Twitter and blog, and his slightly-expanded theory, which in a nutshell is that "This project aims to give rise to a method by which ATP can be provided to body cells, with the view of acting to ease patient suffering.".

    Personally I'm not convinced by that at the moment as Fluge and Mella are pointing out a problem converting glucose before the ATP stage - I don't believe more ATP will fix this issue, if Fluge and Mella are correct.
     
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  6. charles shepherd

    charles shepherd Senior Member

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  7. Joh

    Joh Inactivist

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    From the crowdfunder page:
     
  8. Joh

    Joh Inactivist

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    Just started watching his crowdfunder video. His girlfriend Chloe has ME and he is determined to help her. Romantic! :heart:
     
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  9. Hip

    Hip Senior Member

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    Looks like an interesting concept: rather than fixing the energy metabolism dysfunction in ME/CFS to that patients can produce sufficient ATP energy in their cells, this PhD research appears to be about trying to supply ATP energy to the cells by alternative means, to help make up for the shortfall.

    It says this at the bottom of the proposal:

    Note that this PhD research I don't think will be about just supplying ATP as a supplement (you can buy ATP as a supplement anyway), because the average human body gets through around 100 kilograms of ATP each day to meet its energy needs (more than your own body weight in ATP).

    This is why the energy metabolism constantly recycles spent ATP, so in fact the same ATP molecules are used to supply energy over and over again. But if it were not for this recycling, you would need to consume 100 kilograms of ATP each day, which is obviously completely impossible.

    So I imagine that this PhD proposal will be more about a treatment that helps recycle the ATP in order to provide energy.
     
  10. AndyPR

    AndyPR Senior Member

    @Hip So has it been shown that we are deficient in ATP then? My, admittedly very limited understanding, of the recent Fluge and Mella results indicate a constriction of the processing of glucose into the mitochondria but, from memory, didn't have anything to say about quantity of ATP itself. My interpretation was that there is a shortage of fuel, converted glucose, not necessarily a shortage of fuel transporters, ATP.
     
  11. Hip

    Hip Senior Member

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    The Myhill, Booth and McLaren-Howard studies certainly measured and demonstrated a shortage of ATP in the cells of ME/CFS patients — and also discovered why not enough ATP is being produced in ME/CFS: they showed this is likely due to blockages in ATP recycling in the mitochondria (oxidative phosphorylation), and blockages in the translocator protein (translocator protein transports ATP made in the mitochondria into the cell).

    The recent Fluge and Mella metabolomic study did not directly measure ATP levels in the cell, but as you point out, found a blockage in the processing of glucose into the mitochondria, which would most likely lead to a shortage of ATP.
     
    Last edited: Jan 26, 2017
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  12. Murph

    Murph :)

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    FWIW Naviaux found women had ATP levels at 97% of controls, according to my analysis of his metabolite data. For some reason the molecule was not measured in men.

    I respect Mr Ettridge's genius and his motivation, and I've donated. Nevertheless, from what I know of science PhDs you're lucky if your experiments hold up well enough to learn anything about your hypothesis, and to get a paper or two accepted about your methods. Inventing novel treatments in your first independent project is probably not unheard of but not exactly common.
     
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  13. Hip

    Hip Senior Member

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    Can you point out where in Naviaux's study you got that from please.
     
  14. alex3619

    alex3619 Senior Member

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    Yes. ATP is created and destroyed and recreated so fast that the total number of molecules in a day is staggering. You can alter the AMP and ADP pools, but you still need to be able to create ATP. Supplementing ATP is useless from an energy perspective, but might be useful as an extracellular trigger if that is what you want to do. Increasing the total pool that is being turned over may have some impact though, its hard to assess until somebody finds out what effect that has in ME patients.
     
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  15. alex3619

    alex3619 Senior Member

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    Using ATP levels as a direct measure of energy available has problems, its more about how much is being utilized over a given time frame than the total quantity. If you have less ATP synthesis but use much less then ATP levels might even be high. Yet you still wont have energy.
     
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  16. Murph

    Murph :)

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    The paper itself included the key metabolites, but the data made public here had all of them:

    http://www.metabolomicsworkbench.org//data/DRCCMetadata.php?Mode=Study&StudyID=ST000450

    I've done my own simple analyses of several of them and shared them in a few threads here.

    Here's a chart of the raw data for ATP levels in female patients and controls. I've not tested for statistical signifcance, but the ratio of the means is .97. Just by eye-balling you can see there's only a minor difference.

    Screen Shot 2017-01-27 at 11.33.38 AM.png

    @Hip If you've not seen it in the other thread I put it in you might be interested in this analysis of amino acids I took from the same dataset. Like Fluge and Mella it shows that sufferers have higher concentrations of Group I aminos than of group II. Unlike Fluge and Mella it shows Group I aminos higher in sufferers than controls, while group II are roughly equal in sufferers and controls.
    Screen Shot 2017-01-27 at 11.38.22 AM.png
     
    Last edited: Jan 26, 2017
  17. Hip

    Hip Senior Member

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    @Murph
    Did Naviaux et al measure the ATP levels from cells directly taken from ME/CFS patients, as opposed to cells taken from ME/CFS patients and then grown in culture, because the latter method is known to produce errors (see this post).


    If you look at Figure 2A from the Myhill, Booth and McLaren-Howard 2009 study, they found healthy controls had on average ATP levels around 2 fmol per cell, whereas ME/CFS patients had on average around 1.2 fmol per cell, with some patients having as little as 0.9 fmol per cell.

    So as a percentage, ME/CFS patients on average have only around 60% of the ATP of healthy controls, according to the measurements made in the Myhill, Booth and McLaren-Howard studies.
     
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  18. Murph

    Murph :)

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    I *think* all the Naviaux data is based on plasma levels of metabolites. is that right? What that might infer about the levels of various metabolites we'd expect as compared to in the cytosol or within mitochondria is way beyond my pay-grade.
     
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  19. AndyPR

    AndyPR Senior Member

    Posted on the fundraising Facebook page

     
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