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Maes paper on autoantibodies in ME/CFS and depression

Discussion in 'Latest ME/CFS Research' started by alex3619, Jun 20, 2012.

  1. alex3619

    alex3619 Senior Member

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    http://www.springerlink.com/content/g72153265k3t523j/

    Metabolic Brain Disease
    2012, DOI: 10.1007/s11011-012-9316-8

    IgM-mediated autoimmune responses directed against anchorage epitopes are greater in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) than in major depression

    Michael Maes, Ivana Mihaylova, Marta Kubera, Jean-Claude Leunis, Frank N. M. Twisk and Michel Geffard

    Partially overlapping pathways, i.e. increased IgM antibodies to a multitude of neo-epitopes, underpin both ME/CFS and depression, while greater autoimmune responses directed against anchorage molecules and oxidatively modified neo-epitopes discriminate patients with ME/CFS from those with depression. These autoimmune responses directed against neoantigenic determinants may play a role in the dysregulation of key cellular functions in both disorders, e.g. intracellular signal transduction, cellular differentiation and apoptosis, but their impact may be more important in ME/CFS than in depression.

    [source deleted pending clarification of citation]
  2. alex3619

    alex3619 Senior Member

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    This paper ties in with the methylation and autoimmune theories of CFS. Let met give an example, using other models. A severe viral infection, particularly if the patient is not eating enough antioxidants and protein while ill, results in depletion of antioxidants. The immune system is already highly primed by severe infection. The increased oxidative stress results in oxidative damage to many molecules. Some of these are matched by B cells which are then sensitized and pump out the antibodies. These antibodies damage neurological and other control mechanisms, the nature of which are still debatable.

    I have not read the full paper as its behind a paywall.

    This may explain why methylation treatments do not have full effect. They reverse the trigger for the autoimmune condition, but not the autoimmune issue itself. So correcting oxidative stress (and this would include antioxidant protocols other than methylation protocols, including dietary ones) sets the condition for recovery but is not sufficient.

    An implication of this is that action to suppress the production of autoantibodies, including Rituximab, would be much more powerful if done on a strong antioxidant protocol.

    This is all hypothetical of course, not validated, but very interesting. In particular it is impossible to say if the Maes data shows a real but trivial issue that is not causal. Its another interesting path to pursue, and if correct may improve existing treatments a lot.

    Bye, Alex
    heapsreal, WillowJ and adreno like this.
  3. kaffiend

    kaffiend Senior Member

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    I posted a link to the full text on Google Docs in the PR research library.
    alex3619 likes this.
  4. user9876

    user9876 Senior Member

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    alex3619 likes this.
  5. alex3619

    alex3619 Senior Member

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    I thought this summed up the main point in the full paper:
    "The integrated index of oxidative, but not nitrosative, stress was significantly higher in ME/CFS than depression, suggesting that ME/CFS is accompanied by more severely and/or persistently elevations in oxidative stress than depression. Thus, the damage to lipids is more pronounced in ME/CFS, whereas protein nitrosation occurs equally in ME/CFS and depression. The auto-antibodies measured here are non-specific since they are detected in other autoimmune conditions, e.g. remitting-relapsing multiple sclerosis (Boullerne et al. 1996; Geffard et al. 2002; Bodet et al. 2004)."

    This was also interesting: "The autoimmune responses directed against acetylcholine did not differ between ME/CFS and depression but were significantly higher in all patients than in controls. These antibodies may interfere with acetylcholinergic neurotransmission."
    WillowJ likes this.
  6. alex3619

    alex3619 Senior Member

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    I have been thinking about this more, and it explains more than I had thought. The selection of targets for autoantibodies would be semi-random. Hence the actual targets (through cross matching) would be highly variable. So in this model (still hypothetical) ME and CFS would be a disorder in which a range of autoantibodies are created. While some of these might single out ME or CFS, others would be highly variable between patients. So therefore symptoms would be.

    Furthermore if key antibodies were absent, and perhaps other important ones were present, then you could have other similar disorders. Perhaps fibro, mcs, etc. ? Its just speculation as I said, but its an interesting idea. So these illnesses would, under this hypothetical model, represent different multidimensional subsets within a larger disorder spectrum.

    This has an interesting potential caveat. The disorder is not characterized by the variations but by its ultimate causes. So if the cause/s is/are the same, then diseases we have been thinking might be different might actually be the same, its just that the specific expression of the disease is different. This could open up a whole can of Acme Research Worms.

    Bye, Alex
    Waverunner likes this.
  7. WillowJ

    WillowJ Senior Member

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    this is a cool thought, Alex, because we have a hard time telling autoimmune diseases apart anyway. We have mixed connective tissue disease for "well it has components of several but doesn't fit into any single box" and undifferentiated connective tissue disease for "well it smells like one of these but it's not like the others".
    Similarly atypical MS...
  8. ramakentesh

    ramakentesh Senior Member

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    Im confused how autoimmunity has anything to do with antioxidant status or methylation, in fact Id wager that increased innate immune system activation would cause reduced antioxidant status as some inflammatory markers have large effects on iNOS which can directly effect endothelial function through catabolism into super oxides and other free radicals.
  9. alex3619

    alex3619 Senior Member

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    Nobody can yet separate autoinflammatory issues and autoantibody issues in ME. They have similar effects, and both are present. We do not definitively know the relative importance of each, and there are likely to be other factors involved too.
    merylg likes this.
  10. A.B.

    A.B. Senior Member

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    An active immune system has a pro-inflammatory effect on its own. Cytokines released with immune system activation can cause severe fatigue and all the symptoms of clinical depression.
    merylg likes this.
  11. GaryK

    GaryK

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    Thanks Alex a Very interesting take on this paper. Thanks for your take and thoughts on this subject too always enjoy your thoughts and Ideas Alex:)

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