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My Current Understanding of ME

Discussion in 'General ME/CFS Discussion' started by msf, May 9, 2017.

  1. msf

    msf Senior Member

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    I´ve just written the first part of a blog about this, so I thought I would put the link in a thread since I often go months without remembering to look at the blog section, and I would like the blogs to start a discussion about some of the things I have been looking into recently.

    Unfortunately, however, I started in chronological order, so the first one is probably the least relevant to most people, as it covers the onset of my ME and the particular trigger that led to it.

    http://forums.phoenixrising.me/inde...nding-of-me-part-1-what-the-hell-hit-me.2164/

    The other parts should create a bit more discussion: they will be on sleep, the gut, and lactic acid/exercise.
     
  2. MEMum

    MEMum Senior Member

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    Nice to hear from you again msf.
     
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  3. msf

    msf Senior Member

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    Thanks, I have been busy recently, so although I have been checking PR quite regularly, I haven´t posted as much.
     
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  4. msf

    msf Senior Member

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    Ok, part 4 (I explain in the blog) is up guys, and it´s one you can really dig (or put the boot) into!

    I am posting this because a.) I hope that at least some of it is true, and b.) by doing so I hope to generate a debate about some of these ideas, which should in turn lead to better ideas.

    http://forums.phoenixrising.me/inde...-understanding-of-me-part-4-lactic-acid.2186/

    Spoiler alert - things I try to explain: PEM episodes, Metabolic findings, effects of mTOR inhibitors (hence why I need your help).
     
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  5. msf

    msf Senior Member

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    Having thought some more about the delayed onset of PEM, I am not sure if the main mechanism is an secondary surge of lactic acid through the TNF-a-PDK-PDC pathway that the second study I quoted in my blog proposed, or whether the symptoms are primarily caused by some other mechanism (I was thinking about doing intense exercise before I fell ill, and how my muscles would be sore but didn´t have the heavy feeling of lactic acid buildup the next day, and I wasn´t sure whether this was qualitively or just quantitatively different from PEM). Perhaps two (or more) mechanisms are key to the awfulness of PEM (here I´m referring to the feeling in the muscles, I am sure there are other mechanisms at work elsewhere in the body).
     
  6. Manganus

    Manganus Senior Member

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    Canary islands
    Well put!

    A good request for discussion, i mean! :star::star::star:

    Yes, that might be a good idea.

    It's almost unfathomable, that a disturbance in (relatively few) white blood cells might have such a strong effect on blood lactate levels, that it then influences all other cells and creates metabolic changes in all cells, ...or in many of them.
     
  7. msf

    msf Senior Member

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    Yes, it was a bit surprising to me too, but that seems to be one possibility that would account for the blood lactate level increases seen in sepsis (the muscles have pretty much been ruled out as a source). One paper I read said that there was evidence that in sepsis, the lactate is mainly produced in the lungs, but whether the immune cells are being activated there or in the blood, or whether most of the lactate is produced by some other mechanism, is apparently still to be proven.
     
    Last edited: Jun 26, 2017
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