The Power and Pitfalls of Omics: George Davey Smith’s storming talk at ME/CFS conference
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Changes in Gut and Plasma Microbiome following Exercise Challenge in ME/CFS

Discussion in 'Latest ME/CFS Research' started by Kyla, Dec 18, 2015.

  1. Kyla

    Kyla ᴀɴɴɪᴇ ɢꜱᴀᴍᴩᴇʟ

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    http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0145453
    Open access


     
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  2. John Mac

    John Mac Senior Member

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    Blood samples after 15 minute exercise

    [​IMG]

    This looks striking.
    Should these levels always be zero in the blood?
     
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  3. Marky90

    Marky90 Science breeds knowledge, opinion breeds ignorance

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  4. halcyon

    halcyon Senior Member

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    It would have been really interesting to see some other diseases thrown in as controls.
     
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  5. A.B.

    A.B. Senior Member

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    Very interesting to see such a marked difference between patients and controls, but this is a small pilot study so results need to be interpreted with some caution.

    Could a transient presence of bacteria in the blood explain the findings by Alan Light? (altered gene expression in white blood cells after exercise)
     
  6. halcyon

    halcyon Senior Member

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    I'm guessing that it probably has to do with exertion induced cytokine release. It looks like proinflammatory cytokines are known to disrupt epithelial barrier function.
     
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  7. A.B.

    A.B. Senior Member

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    I believe exercise increase intestinal permeability. Could anyone confirm this with a good source?

    Then again this alone cannot explain the difference between patients and controls.
     
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  8. Marky90

    Marky90 Science breeds knowledge, opinion breeds ignorance

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    I like that idea!
     
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  9. Crux

    Crux Senior Member

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    Exercise, stress,etc. increase catecholamines, such as, adrenaline and noradrenaline.

    Bacteria use these and other hormones for growth.

    It seems to explain, possibly, why we feel poorly, PEM, after exercise and stress of any sort.

    It also seems to explain why stimulant type interventions can cause side effects. Stimulants increase adrenaline, noradrenaline, etc., then bacteria utilize them for growth, thereby producing toxic products, causing host disease.

    http://www.microbemagazine.org/inde...crobial-endocrinology-comes-of-age&Itemid=263

    http://www.hindawi.com/journals/scientifica/2013/361073/
     
  10. SB_1108

    SB_1108 Senior Member

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    Would this be similar to a very low-grade sepsis-like infection?
     
    Last edited: Dec 18, 2015
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  11. bel canto

    bel canto Senior Member

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    I'm thinking that this chart is not showing zero levels, but is showing that these bacteria don't change in controls, but do change by the specified %'s in the patients.

    It's confusing the way it's described as "relative abundance" on one axis.
     
  12. alex3619

    alex3619 Senior Member

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    I would really like to see a better graph than the one shown. We should be well aware of outliers as a problem in CFS and ME research by now. If we had used scatter plots not neat lines, with perhaps neat lines superimposed, then we might have picked up on subgroup problems long ago.

    However it is NOT normal for high levels of bacteria in the blood. It can cause cytokine and chemokine shifts, inducing immune cell migration and this includes drawing cells away from other places they are needed. Such changes can be persistent, or have persistent secondary effects.

    If NK cells or other immune cells are constantly fighting this its no wonder they get exhausted.

    The time frame is suggestive of a link with PEM, but we need more research to say much here.

    This is only a small initial study. A larger better study might tell us a lot.

    It might suggest that the use of NSAIDs is undesirable in us.
     
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  13. ScottTriGuy

    ScottTriGuy Stop the harm. Start the research and treatment.

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    Last edited: Dec 18, 2015
  14. Kati

    Kati Patient in training

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    Why do you suggest that? (Not that it's been useful anyways)
     
  15. alex3619

    alex3619 Senior Member

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    Because aside from COX-2 inhibitors they all detract from the repair status of the gut lining. In fact this is the leading cause of gut ulcers after H. pylori. Its because they block the synthesis of eicosanoid hormones needed in the repair process.
     
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  16. adreno

    adreno PR activist

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    Leaky gut?
     
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  17. Kati

    Kati Patient in training

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    At this point, jut as in HIV (correct me if I'm wrong) we don't know why there is a change in the microbiome of affected patients. Is there a causality relationship? Cause and effect? Can it be altered? Should it be treated?

    Food for thoughts.

    http://www.ncbi.nlm.nih.gov/pubmed/26540050
     
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  18. msf

    msf Senior Member

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    It´s not surprising at all if you have been following Maes and De Meirleir´s work, or that of Montoya and Younger.

    It´s good that other groups are confirming their findings now though.
     
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  19. alex3619

    alex3619 Senior Member

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    This kind of finding will substantiate leaky gut theory. Definitively if its repeatedly and independently replicated. However it might show that the problem is transient, and has triggers, rather than continuous.
     
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  20. adreno

    adreno PR activist

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    Yes, as has been said before, exercise increases intestinal permeability.
     
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