Phoenix Rising tells QMUL: release the PACE trial data
Mark Berry, Acting CEO of Phoenix Rising, presents the Board of Directors’ open letter to Queen Mary University of London (QMUL) urging them to release the PACE trial data, and hopes that other non-UK organisations will join British charities in the same request...
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new Alan Light paper... alpa-2a, glutocorticoid implication

Discussion in 'Latest ME/CFS Research' started by voner, Oct 8, 2013.

  1. lansbergen

    lansbergen Senior Member

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    I understand that it is a muscarine receptor. My immunemodulator acts on the a7 nicotine receptor.

    As B1 cells pump out large amounts of none specific anitbodies there could be some that can bind to acetylcholine receptors.

    Then there is less acetylcholine release and receptors blocked by antibodies.
     
  2. Snow Leopard

    Snow Leopard Hibernating

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    That and a million other things (as is usual in biological systems). It's all speculation from here on out.

    The first question that comes to mind is whether the increased Alpha-2A receptor expression is serving a positive response or not. But the only way you'd really find out is by using an antagonist and associating a reduced Alpha-2A receptor function with reduced post-exertion severity.
     
  3. voner

    voner Senior Member

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    Thanks. I'm sure this is much much more complex and we should use caution in individual interpretation of these receptor studies. I wrote a blog about a presentation given by Dr. Bateman in Denver this summer where she discussed the various results of earlier studies by Dr. Light. She showed slides for individual patients and it became pretty apparent that patient to patient the responses of these receptors after exercise varied immensely. While most of the patients (with ME/cfs and fibromyalgia and NO orthostatic intolerance) had a similar response of increased alpha-2a receptor expression, there was a subset of patients with ME/cfs and fibromyalgia AND orthostatic intolerance who had a decrease in alpha-2a receptor expression.

    http://www.cortjohnson.org/blog/201...yndrome-subset-if-doctors-will-just-look-for/

    The impression given was that this decrease in the alpha-2a receptor receptor expression was correlated with orthostatic intolerance. I remember she said that the patients averaged a increase in heart rate upon standing of 28 beats per minute, thus she was forced to not call it POTS, rather "orthostatic intolerance", although she indicated clinically and symptomatically it was all the same.

    I suspect the doctor Light group is also trying to ferret out what is evidence of pain pathways being activated and what is the evidence of fatigue pathways being involved, if any.
     
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  4. MeSci

    MeSci ME/CFS since 1995; activity level 6?

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    Safer to use electronic cigarettes, I would think, and you can control the nicotine hit better with them.
     
  5. MeSci

    MeSci ME/CFS since 1995; activity level 6?

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    From a quick look I didn't see anything about control groups in this paper. Also, it says
    so a minority, and would it be different from control groups?
     
  6. Valentijn

    Valentijn Activity Level: 3

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    I've been using the most potent antagonist, Yohimbe, and thus far it seems like it's reducing PEM. But I haven't really tried to provoke an episode, aside from a 10 hour flight + airport time (with wheelchairs).
     
  7. voner

    voner Senior Member

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    @Valentijn ..... How has your Yohimbe trial turn out? I would love an update...
     
  8. Valentijn

    Valentijn Activity Level: 3

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    Still generally helpful, but doesn't prevent my episodes where I end up bedbound for a week or three due to intense OI. I had a couple of those happen a while ago, and had hoped that the Yohimbe was keeping them away! Still, I definitely do a lot better with the Yohimbe.
     
  9. ukxmrv

    ukxmrv Senior Member

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  10. alex3619

    alex3619 Senior Member

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    I doubt it. However over-expression might set in motion feedback effects leading to other problems.
     
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