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Suggestions and Questions for Dr Ron Davis

Discussion in 'General ME/CFS Discussion' started by Jesse2233, Mar 20, 2017 at 12:44 PM.

  1. Jesse2233

    Jesse2233 Senior Member

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    Hi everyone,

    It occurred to me that with all the knowledge on this board, we might put together a thread with suggestions and questions for Dr Davis.

    @Rose49 has indicated that he's interested in our ideas, so this could be a good opportunity to collate hypotheses, questions, and personal experiences in an organized way and directly help with Dr Davis' research

    Edit:

    Tagging some people whose posts I benefit from that might be interested:

    @Hip
    @eljefe19
    @nandixon @halcyon @alex3619
     
    Last edited: Mar 20, 2017 at 9:04 PM
  2. Jesse2233

    Jesse2233 Senior Member

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    I'll start...

    - Will your electronic testing assay be able to assess whether something upstream / beyond the serum is the producing the problem?

    E.g. something like a virus, malfunctioning lymph, or epigetically altered organ

    - Will you be testing Dr Jay Goldstein's "rapid remission" drugs such as ketamine and lidocaine on the serum?

    See this link for more Dr Goldstein drugs

    See this thread with a diagram (third post down) of Dr Goldstein's protocol

    - Does your research encompass potential causal factors such as dysfunction of the ANS / brain, or ongoing environmental poisoning (be it from myotoxins or synthetic chemicals)?
     
    Last edited: Mar 20, 2017 at 9:08 PM
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  3. ScottTriGuy

    ScottTriGuy Stop the harm. Start the research and treatment.

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    How, if at all, does De Vega's epigenetic research dovetail with your findings?

    Our results indicate DNA methylation modifications in cellular metabolism in ME/CFS despite a heterogeneous patient population, implicating these processes in immune and HPA axis dysfunction in ME/CFS. Modifications to epigenetic loci associated with differences in glucocorticoid sensitivity may be important as biomarkers for future clinical testing. Overall, these findings align with recent ME/CFS work that point towards impairment in cellular energy production in this patient population."

    https://bmcmedgenomics.biomedcentral.com/articles/10.1186/s12920-017-0248-3
     
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  4. Helen

    Helen Senior Member

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    - Did you get any results from the analyzes with the new method that, according to Ian Lipkin, should detect any possible microbe and ongoing infection? In other words, are the patients having infections compared to the controls, or not?

    - Do you have a hypothesis how comes that Whitney as well as many PWME had a severe vitamin B2 deficiency? I donĀ“t know if it was about a riboflavin deficiency or the converted, bio-active form of B2.
     
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  5. eljefe19

    eljefe19 Senior Member

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    Jesse I don't know if anyone you tagged got a notification because I didn't.
    I think nandixon has been good at contacting Prof Davis with any new theories regarding mTOR.

    I'm curious what he thinks of Dr. Chia's work, and if he think enteroviruses could cause the metabolic issues found in Naviaux/F&M.
     
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  6. Sushi

    Sushi Moderator and Senior Member Albuquerque

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    Note: you can't edit in a tag--that is why you didn't get one. @Jesse2233
     
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  7. eljefe19

    eljefe19 Senior Member

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    Here Jesse;

    @Hip
    @nandixon @halcyon @alex3619
     
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  8. alex3619

    alex3619 Senior Member

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    One thing I would like to see is a full metabolic chart for patients that are not coloured blue or red but colour coded by standard deviation from normal.
     
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  9. Neunistiva

    Neunistiva Senior Member

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  10. Jesse2233

    Jesse2233 Senior Member

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    Fair point, we should all submit our questions via email as well. But I also think there's value in publically sharing them so we can build on each other
     
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  11. eljefe19

    eljefe19 Senior Member

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    Alright Jesse, in the interest of building on each other, my question is this.

    Question; Is Prof Davis aware that certain viruses can inhibit Akt/mTOR?
    A quick google search of "Coxsackievirus B mTOR" revealed a couple of sources about Coxsackievirus A16 inhibiting Akt/mTOR (Here and here).

    That first source says the following;
    Coxsackievirus B has some evidence of causing ME/CFS whereas I don't believe there is any links with Coxsackie A, yet. My doctor tested for both, and my Coxsackievirus A titers (including A16) were way more elevated than CVB.

    Question; If CVA16 can inhibit Akt/mTOR, can it be surmised that CVA16 can cause ME/CFS?
     
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  12. eljefe19

    eljefe19 Senior Member

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    Here's some more circumstantial evidence for Coxsackievirus causing ME/CFS.

    https://www.ncbi.nlm.nih.gov/pubmed/25755782
    So we've got this study here, that relates CVB3 infection to IL-10 producing B cells. Perhaps this is the B cell mediated feedback loop discussed in the mTOR thread, at least for a subset of patients.

    Hypothesis;
    CVB3 (and other enteroviruses) can cause ME/CFS by increasing IL-10 producing B cells which enable the virus to remain chronically activated while it simultaneously inhibits Akt/mTOR. Therefore, Rituximab cures those with IL-10 producing B cell dependent enterovirus infections causing Akt/mTOR inhibition and ME/CFS.
    According to this source, CVB3 induces a direct cytopathic effect (CPE) and apoptosis on infected cells (bad). Treatment with Rapamycin (a strong mTOR inhibitor) made the CPE and Apoptosis worse, indicating that mTOR plays a role in the pathogenesis of the CVB3 virus.

    Another source; https://www.ncbi.nlm.nih.gov/pubmed/23406864
     
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  13. eljefe19

    eljefe19 Senior Member

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  14. eljefe19

    eljefe19 Senior Member

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    BUMP...

    Because I believe this is really good idea for a thread. It's the perfect place to generate, and coordinate, our communication to Ron Davis.

    Does anyone have any opinions on the research I found last night???
    It seems Coxsackievirus of several types can inhibit Akt/mTOR and induce autophagy instead. @nandixon has the potential domino effect causing ME/CFS narrowed down to these two options. See below;


    IMG_2660.PNG

    So if we go with option two, why could the initial cause, which is currently '????' not be a chronic enterovirus infection?
    It directly causes the next step in the domino effect....

    Furthermore, CVB3 (Reference) has been found to evade the bodies' normal defenses by an IL-10 B-cell dependent mechanism (possible Rituximab connection?).

    I presented evidence that both CVA16 and CVB3 can disturb Akt/mTOR signaling, above.

    I believe that Prof Davis should prioritize drugs for his new device that have antiviral action against certain enteroviruses, such as CVA/CVB/Echovirus/EV71. I can produce a list of these with a little help from @Hip 's great antiviral post. I'll edit in later.
     
  15. Jesse2233

    Jesse2233 Senior Member

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    I like this, but how to explain those with no evidence of enteroviruses? Different subgroup?
     
  16. eljefe19

    eljefe19 Senior Member

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    Yup. I imagine a few things can start the feedback loop that involves Akt/mTOR inhibition upstream of everything else.
     
  17. eljefe19

    eljefe19 Senior Member

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    I thought of another couple.

    QUESTION: Shouldn't Prof Davis test things like Leucine (a pure mTOR activator and direct AMPK inhibitor) and other known activators that aren't FDA approved drugs?

    He tested Pyruvate and ATP so I don't see why not. Leucine, NAC, various aminos, Insulin, Myostatin inhibitor Myo-X, Follistatin, growth factors etc.

    QUESTION: Would something like Rituximab, which takes months to exert clinical benefit on average, work to stop impedance in Ron's device?

    I suppose I will email some of these to Ron and Janet, but do you guys have any feedback first???
     
  18. BurnA

    BurnA Senior Member

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    Did you watch the latest video's, AFAIK he will test everything he can in vitro.
     
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