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Depression might be autoimmune, Maes study

Discussion in 'Other Health News and Research' started by alex3619, Dec 16, 2011.

  1. alex3619

    alex3619 Senior Member

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    Logan, Queensland, Australia
    J Affect Disord. 2011 Dec 12. [Epub ahead of print]
    Increased autoimmune activity against 5-HT: A key component of depression that is associated with inflammation and activation of cell-mediated immunity, and with severity and staging of depression.
    Maes M, Ringel K, Kubera M, Berk M, Rybakowski J.

    http://www.ncbi.nlm.nih.gov/pubmed/22166399

    This study shows that over half of depressive patients (in a smallish sample size) have antibodies that might induce it. This includes anticardiolipin antibodies, which are also often found in ME, see the link below. So it may turn out that much of the depression in ME is attributable to autoantibodies. The authors suggest that a driving force behind depression, including in CFS, is an increasing autoimmune response.

    Here is an earlier study:
    Autoimmunity in depression: increased antiphospholipid autoantibodies

    M. Maes1,2,3,*,
    H. Meltzer1,
    J. Jacobs4,5,
    E. Suy2,
    J. Calabrese1,
    B. Minner2,
    J. Raus4

    Article first published online: 23 AUG 2007

    DOI: 10.1111/j.1600-0447.1993.tb03349.x

    http://onlinelibrary.wiley.com/doi/10.1111/j.1600-0447.1993.tb03349.x/abstract

    Bye, Alex
     
    WillowJ and L'engle like this.
  2. taniaaust1

    taniaaust1 Senior Member

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    Very interesting. thanks Alex

    Maybe it wont be long till the psychs loose most of their patients :)
     
  3. Waverunner

    Waverunner Senior Member

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    Great post, thanks.
     
  4. Glynis Steele

    Glynis Steele Senior Member

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    Newcastle upon Tyne UK
    I remember Maes' study on LPS and depression, and being sooo excited about it. It seems so long ago now. It's called The Gut-Brain Barrier in Major Depression: Intestinal Mucosal Dysfunction with an Increased Translocation of LPS from Gram Negative Enterobacteria (leaky gut) plays a role in the inflammatory pathophysiology of Depression.

    I tried to post a link, but it doesn't work, if you use google scholar and type in the title above, you can probably find it.
     
  5. Waverunner

    Waverunner Senior Member

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  6. Tony Mach

    Tony Mach Show me the evidence.

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    Upper Palatinate, Bavaria
    I think the results that Michael Maes produces in his research are interesting.

    Alas, some things worry me very much by now about his work:

    First, the supposed "Intestinal Mucosal Dysfunction" (compromisation of the gut-blood barrier) is his interpretation. I have seen no direct evidence for this disease-mechanism, and the things he finds can be explained by different mechanisms (e.g. systemic infection or autoimmunity via molecular mimicry to dietary components). I have not seen a discussion of other possible mechanisms by him that could explain his results.

    Yet he makes a impression in his work as if "THIS IS IT".

    Secondly, he seems to find the same (or similar) mechanisms in many different disease. This could very well be, yet it could be that he has one hammer and everything looks like a nail to him

    What I would like to see is replication of this tests by other researchers and some elaboration on other disease mechanisms that could produce the same anomalies.

    Furthermore, I find his treatment regime for this supposed gut-barrier disfunction suspect. He gives no rationale for why he uses all the stuff he uses. Some things make sense (like changes in nutrition ala Terry Wahls), but some things I find very dubious without an explanation why he uses them and I have seen no explanation by him.
     
  7. Enid

    Enid Senior Member

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    This sort of study worries me too - what is their definition of "depression" for starters - can't recall anything in my 12 years except what is known as clinical. No ordinary - gosh I feel fed up sort of thing very possible to snap out of.
     

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