New era for ME/CFS research as top cytokine study attracts media headlines
The immune systems of patients who have recently developed ME/CFS look markedly different from those who have been ill for much longer, according to a major new study from Drs. Ian Lipkin and Mady Hornig at Columbia University. This shift in immune function hadn’t been seen before.
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Brain Cells Making us Sick? The microglia connection in ME/CFS & Fibromyalgia

Discussion in 'Phoenix Rising Articles' started by Simon, May 30, 2014.

  1. searcher

    searcher

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    I thought it may be useful to see a list of the microglia modulators that Dr Younger shared at the Stanford conference (http://forums.phoenixrising.me/inde...-me-21-march-day-two.29098/page-3#post-443598)
    I think that LDN and minocyline (and possibly rifampin) are probably the most commonly used prescription drugs for reducing microglial activation. Reishi may be studied soon in Gulf War Illness.

    Note: Dr Younger compiled this list by looking at research on potential microglia modulators; only a few have been studied in humans for their ability to modulate microglia.

    Drugs:
    • Naltrexone
    • Dextro-naltrexone
    • Minocycline
    • Ibudilast
    • Dextromethorphan
    • Rifampin
    • Propentofylline
    • Ceftriaxone
    • Glatiramer acetate
    • 3-hydroxymorphinan
    • Dilapimod
    • ATL313
    • BAY 60-6583
    • FP-1 Resolvin D1
    • Resolvin E1
    Supplements:
    • Luteolin
    • Panax ginseng
    • Turmeric
    • Resveratrol
    • Gastrodia elata
    • Obovatol
    • Inflexin
    • Piper kadsura
    • Ganoderma lucidum (Reishi)
    • Berberine
    • Epimedium brevicornum
    • Isodon japonicas
    • Stephania tetrandra
    • Stinging nettle
    • Fisetin
    • Pycnogenol
    • Boswellia
    • Kratom
     
    Last edited: Jun 1, 2014
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  2. Marco

    Marco Old blackguard

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    Might also consider CoQ10, beta blockers, N acetylcysteine, certain anti-virals and ... Rituximab :

    http://www.turkishneurosurgery.org.tr/pdf/pdf_JTN_1230.pdf
     
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  3. cigana

    cigana Senior Member

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    There is something I don't understand. Isn't there a contradiction between the cause of our fatigue being "sickness syndrome" and the research that has shown mitochondrial dysfunction (e.g. Sarah Myhill)? I mean one says we feel fatiguebecause chemical messengers are being fired which increase the perception of fatigue, whereas the other is saying we feel fatigue because we actually cannot produce energy at a sub-cellular level.
     
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  4. Valentijn

    Valentijn Activity Level: 3

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    I don't think anyone is claiming that sickness response is responsible for all ME symptoms, but might be involved in some symptoms.
     
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  5. A.B.

    A.B. Senior Member

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    What makes you think that the cytokines responsible for sickness behaviour don't induce it by acting on mitochondria? Maybe the perception of fatigue isn't just a brain thing but is actually fatigue. In any case, one doesn't necessarily exclude the other. As usual, the situation is unclear and we need more research.
     
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  6. cigana

    cigana Senior Member

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    I considered that might be the case, but the way sickness behaviour is usually explained is as a mechanism to "tell the body it needs to rest to conserve energy to fight the infection" etc. Actually damaging/impairing mitochondria seems like it would not be the best way of telling us we need to rest :)
     
  7. MeSci

    MeSci ME/CFS since 1995; activity level 6

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    No need for apology
    To those who LOVE biology!

    (Like me)

    :)
     
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  8. Leopardtail

    Leopardtail Senior Member

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    Two thoughts spring to mind here:
    1. This explains why we FEEL sick...
    2. How could this explain genuine exhaustion in which one CANNOT override the feeling is is forced to stop (e.g. total loss of muscular strength).

    Any thoughts Simon?
     
  9. Leopardtail

    Leopardtail Senior Member

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    High levels of mito activity are needed for immune response (both humeral and febrile). Hence sickness response forcing rest makes biological/evolutionary sense) but sickness repsonse lowering energy production does not - it would destroy immune response as occurs in ME patients.
     
  10. Leopardtail

    Leopardtail Senior Member

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    I am inclined to agree Cigana, poor mito function inducing sickness response would make sense to protect vital functions. Poor mito function reducing immune response and cause extended symptoms via sickness response would also make sense. Sickness response causing poor mito function would be an evolutionary disaster other than by safe mechanisms such as thyroid hormones and melatonin.
     
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  11. Simon

    Simon

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    Couple of thoughts from me
    1. Microglia/sickness response is unlikely to be a complete explanation. As Jarred Younger stressed in his presentation in California, there is considerable overlap between sickness response and mecfs/FM, but it isn't complete by any means.
    2. Also, sickness response doesn't have a single level: it can be mild and it can also be severe and incapacitating. I'm not quite sure of the difference between exhaustion and 'genuine' exhaustion, but it's possible that severe sickness response could explain genuine exhaustion too. So far, though, this central role of sickness response in mecfs is very much a plausible but untested hypothesis.
     
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  12. Leopardtail

    Leopardtail Senior Member

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    I think we are pretty much on the same page given your response above Simon.

    I refer to "genuine" exhaustion in the true meaning of the term - absolutely no energy left if the house were burning down, one would have to be carried out. I did used to experience that degree of exhaustion as opposed to the severe fatigue accompanying heavy infection that may be mis-labelled as exhaustion.

    Hyperbole in general use of language sometimes makes finding the right phrasing with severe ME difficult doesn't it?
     
  13. Ema

    Ema Senior Member

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