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ME/CFS and the Magic of the Canine Factor
There's been plenty of research indicating that having pets is good for your health. I never really noticed any particular benefits to having cats, though that may have had more to do with my cats. They've been fairly indifferent to my presence and we've shared a live-and-let-live...
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Autoimmune Inflammation and Monoamines

Discussion in 'Antivirals, Antibiotics and Immune Modulators' started by pgoody, May 14, 2013.

  1. pgoody

    pgoody

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    Here's a very interesting recent pubmed article for anyone that suffers from a wide range of psychiatric disorders mentioned in this article. This article discusses the Kynurenine metabolic pathway of tryptophan, where much of our tryptophan goes. An imbalance of autoimmune response or aggravation of a certain type can affect the metabolites in this pathway, which act on our glutamatergic NMDA receptors, and can deplete our serotonin (through lack of tryptophan or increased metabolism of it). Just some food for thought: (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3626880/)
    Emootje, alex3619 and katim like this.
  2. Enid

    Enid Senior Member

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    Very interesting pgoody - "pathogenic clues" being revealed - hope all the psychos now listen and well learn the lesson - not all in your mind (imagination) attributed to everything they do not understand.
  3. Bob

    Bob

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  4. alex3619

    alex3619 Senior Member

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    Symptoms associated with these disorders (see Table 1 in the paper):

    Common and pronounced: Anxiety, agitation, paranoid delusions, perceptual changes, erratic behavior, speech changes, severe psychosis Agitation, anxiety, panic-attacks, depression, psychosis, hallucinations, delusions, delirium, confabulation Atypical psychosis, which can be isolated Paranoia, behavioral changes Depression, atypical psychosis (case reports)

    Neurological Features Early features: seizures, cognitive/memory impairment; Late features: catatonia, orofacial and limb dyskinesia, dystonia, autonomic dysfunction, reduced level of consciousness, aphasia, central hypoventilation LGI1: limbic encephalitis (more common): amnesia temporal lobe seizures, tonic seizures, and hypernatremia. Extrapyramidal symptoms (choreoathetosis) and extra-temporal (faciobrachial dystonic) seizures (less common). CASPR2: limbic encephalitis, Morvan's syndrome (neuromyotonia, REM disorder, insomnia, and autonomic dysfunction). Memory impairment, temporal lobe seizures Prominent temporal lobe seizures, memory impairment, concomitant glutamic acid decarboxylase autoantibodies Stiff-person syndrome, cerebellar ataxia, cognitive/memory impairment, epilepsy (often mesial temporal)
    Bob likes this.
  5. Bob

    Bob

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    Intriguing. How many of those symptoms do we hear discussed on this forum?!
  6. alex3619

    alex3619 Senior Member

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    Any and all of our cognitive/emotional/behavioural symptoms can be induced by these kinds of neuroimmune disorders. What a surprise! Even some our non-central symptoms can be induced by these things, if peripheral or spinal nerves are damaged.
  7. warriormom

    warriormom

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    I believe that Mady Hornig at Columbia, via the CFS Initiative, is investigating the nexus between neuroimmune disorders like ASD and PANDAS, and ME/CFS. I personally emailed her about my belief in a connection between the two, and she told me I was "astute".
    alex3619 and ukxmrv like this.
  8. Marco

    Marco Old blackguard

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    Near Cognac, France
  9. Marco

    Marco Old blackguard

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    Pgoody

    Great paper by the way.

    Thanks:)
  10. pgoody

    pgoody

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    Another good article similar to the last: (http://www.ncbi.nlm.nih.gov/pubmed/23336044)
    direct article link: (http://pubs.acs.org/doi/pdf/10.1021/cn300186b)
    Honestly I am not literate enough to understand this article, I just found it and thought some others might find interest in it. I will probably look through it when I have more time.

    Here's the part where it echoes that last paper:
    "Pro-inflammatory cytokines, including IFN-β1b and IFN-γ (with a synergistic effect of TNF-α
    76), have been shown to reduce the availability of tryptophan, which is required for 5-HT synthesis, through activation of indoleamine-2,3-dioxygenase (IDO),77−79 a tryptophan-degradingenzyme, and elevate kynurenine metabolites, that can be neurotoxic.80 Changes in tryptophan, through manipulation of IDO, influence brain 5-HT. Upregulation of IDO by IL-6 has been shown to reduce 5-HT/tryptophan ratios, increase kynurenine/tryptophan ratios in hippocampus, and produce a depressive-like effect on behavior that is lost in IDO knockout mice.81"

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