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NICEGUIDELINEBLOG = study points 95% PWCs have autoimmune disease

Discussion in 'Latest ME/CFS Research' started by Nielk, Oct 30, 2011.

  1. Nielk

    Nielk

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    Jacque likes this.
  2. Sasha

    Sasha Fine, thank you

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    Thanks for posting - yes, weird this is a 2009 study and we've never heard of it.
  3. fla

    fla Senior Member

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    I joined the National CFIDS Foundation almost a year ago because they were the only ones investigating the auto-immunity link in M.E. When I joined they mentioned a test at the University of Hawaii but I declined to take it since it would also be positive if you have other auto-immune diseases also and I do but if M.E. is your only disease you might consider it.
  4. Nielk

    Nielk

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    This was published in 2009!
    redrachel76 likes this.
  5. Smulan

    Smulan

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    Very interesting. Wonder if the Norwegian doctors now of this study....
  6. Waverunner

    Waverunner Senior Member

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    This is really crazy. They pinpointed towards treatment with Rituximab in 2009 and we have proof now that they made a very valid point.
  7. Battery Muncher

    Battery Muncher Senior Member

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    Good Lord. Someone send that to Mella and Fluge, pronto!
  8. sensing progress

    sensing progress Senior Member

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    Probably as this was around the time when the XMRV paper came out in Science and it overshadowed it.
  9. currer

    currer Senior Member

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  10. Enid

    Enid Senior Member

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    Thanks Nielk - what a find !
  11. Vitalic

    Vitalic Senior Member

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    Has anyone thought about how the autoimmune aspect might be reconciled with the gene expression alterations detected by Light et al?

    At first glance I can't see an obvious way that the two could fit together, ACA autoantibodies attacking mitochondria can explain a portion of the symptomatology but not all, and I struggle to see how pain/fatigue receptors would be upgregulated as a result of these autoantibodies. That said, my knowledge of autoimmune diseases is very limited so I'd love it if someone could enlighten me.
  12. fla

    fla Senior Member

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    My guess would be that in a subgroup the autoimmunity is causing extreme oxidative stress which ends up depleting glutathione which then causes excessive gene expression.
  13. kurt

    kurt Senior Member

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    Wow, I just told someone earlier today that if we have an autoimmune condition it must be attacking the mitochondria. Holy cow, that's probably exactly what is happening! The triangulation now with the Mella and Fluge study should really push this 2009 study into the mainstream of ME/CFS research.

    So basically, if I am interpreting this correctly, any time our B cells become activated, such as a re-exposure of a viral insult for which we already have antibody memory, then our mitochondria will be attacked by autoantibodies? If EBV is somehow staying semi-active, then it stands to reason that anything that aggravates the EBV (stress is known to do that, or modulation of immune function) would then set of a cascade of events, since there is plenty of antibody memory of EBV right in the B cells! Wow, that could really make the ME/CFS model simple, Occam would approve...

    Regarding the Lights' studies, IF the pain receptors are down-stream of a mitochondria insult (I believe there is research showing that to be true), then attacking the mitochondria might lead to some type of release of signals from the mitochondria to the pain/fatigue receptors. Just speculating, but I don't think it will be difficult at all to connect those two factors (pain/fatigue receptors and mitochondria).

    see: http://www.jneurosci.org/content/31/36/12982.abstract
  14. kheopz

    kheopz

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    Ok its sent :)

    Doesnt this point to what Ken Lassesen has been saying all alone. The microthrombosis theory. Chronic low level hypercoagulation in this disorder. This would be an effect of the anti cardiolipin antibodies and could
    in turn produce many of the cfs symptoms, hypoperfusion, memory problems, autonomic issues, maybe also gut, liver and kidney issues.

    "Antiphospholipid syndrome

    Patients with anti-cardiolipin antibodies (Antiphospholipid syndrome) can have recurrent thrombotic events even early in their mid- to late-teen years. These events can occur in vessels in which thrombosis may be relatively uncommon, such as the hepatic or renal veins. These antibodies are usually picked up in young women with recurrent spontaneous abortions. In anti-cardiolipin-mediated autoimmune disease, there is a dependency on the apolipoprotein H for recognition.[29]"

    I know a patient story with the same distinct improvement as in the norwegian study, however it was an immediate response.
    A swedish guy got clopidogrel for some heart issue and as soon as he took it his CFS symptoms disappeared.
    He took it until his doctor didnt allow it anymore and he returned with to the same cfs state.
  15. Vitalic

    Vitalic Senior Member

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    Another thing I just realised, if this is indeed getting close to the central pathological mechanism of the illness, then Low Dose Naltrexone surely becomes a must-try treatment for anyone that believes they may fit within that subgroup:

    LDN might be having the same effects as Rituximab but obviously in a less drastic way.
  16. FunkOdyssey

    FunkOdyssey Senior Member

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    In one of the multiple sclerosis studies that tracked beta-endorphin levels, LDN raised beta-endorphin ~100% over baseline IIRC.

    In another study that looked at 3 month and 6 month time points, beta-endorphin levels were STILL rising SIX months after initiation of therapy. It kills me every time I read someone tried LDN for a few weeks and dropped it because they didn't think it was doing anything. This a marathon, not a sprint.
  17. FunkOdyssey

    FunkOdyssey Senior Member

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    In addition to beta-endorphin, opioid growth factor is another endogenous opiate whose production is upregulated by LDN, arguably more important than beta-endorphin (especially if you ask Ian Zagon):

  18. Vitalic

    Vitalic Senior Member

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    Interesting, thanks for that. I'm fairly sure I'm going to start this treatment as soon as possible, as long as my test results support the hypothesis. I'm guessing cytokine profiles, NK cell function and presence of TH1-TH2 shift are going to be the best indicators?
  19. Waverunner

    Waverunner Senior Member

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    Thanks for your input, Vitalic. I didn't know that LDN decereases B-cell activity.
  20. Smulan

    Smulan

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    Great thank you :)

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