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In Brief: Muscles and the 'myalgia' in ME/CFS

Discussion in 'Phoenix Rising Articles' started by Phoenix Rising Team, Mar 11, 2014.

  1. Legendrew

    Legendrew Content team

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    I hope you don't mind me answering this, I'm sure Russ would give a not dissimilar answer.This is a very difficult question to answer simply because it is not yet clear what exactly is going on in ME/CFS. It is clear that the ME/CFS cohort is not a homogeneous one so it's likely that in under this umbrella like sub-heading there are people who suffer primarily with chronic infections in which case the infectious agent is quite likely to have a strong influence upon the symptomology. On the other hand one leading theory at the moment is that of ME/CFS as an autoimmune disease, in this case the triggering infection, stress or otherwise is unlikely to have much influence upon the symptoms outside of the initial few weeks/months at which point the infection is presumably cleared or under control by the immune system. The symptoms in this case are a by-product of the ongoing autoimmune response and is dependent upon which bodily organs, tissues or systems are targetted.
     
  2. Ren

    Ren Primum Non Nocere

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    Thanks, Legendrew. In regard to, "The symptoms in this case are a by-product of the ongoing autoimmune response and is dependent upon which bodily organs, tissues or systems are targetted." Meaning "dependent upon which bodily organs, tissues or systems are targetted" in each individual personal? And this could be dependent on a person's genes for example or perhaps previous injury? Like it's going to manifest in a way that refects that individual's weakest link, so to speak?
     
    Last edited: Mar 19, 2014
  3. Legendrew

    Legendrew Content team

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    Remembering this is all hypothesis at this point; if it is confirmed then there is either going to be a single primary target as is the case in autoimmune diseases such as graves disease, or there is the potential that it could affect a large number of bodily systems as is the case in systemic lupus - all of this being dependent upon what the autoantibodies are targeting. In both the aforementioned diseases there exists quite a degree of variation symptom wise for a variety of different reasons including the exact auto-antibody, the stage of the disease and as you mention genetics does appear play quite a prominent role.

    All of this is complex enough however, in addition, there is the possibility that ME/CFS, being the umbrella that it is, could encompass numerous autoimmune conditions which has the potential to explain the wide variation in symptoms.
     
    Ren likes this.
  4. August59

    August59 Daughters High School Graduation

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    It definitely helps with the cramps, but hasn't completely ridded myself of them. I'm taking 1200mgs a day.
     
  5. mtnbibliophile

    mtnbibliophile

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    Back to the original article: you state that Dr. Newton's research "suggests a potential pathological problem during the process of muscle contraction, namely a problem during the process of aerobic respiration causing anaerobic respiration to take place at much higher incidence than healthy individuals. . . .
    Everybody has experienced the build-up of lactate in the muscles following intense periods of exercise. This research however indicates the possibility that ME patients experience this at much lower levels of exercise intensity."
    "Possibility"? We have known for over a dozen years that ME/CFS patients switch to anaerobic respiration at a much lower level of exercise intensity: Dr. Cheney tested me for this as part of his standard CFS examination in 2002. Since lactic acid is produced by anaerobic respiration, of course we experience build-up of lactate at lower levels of exercise intensity.
    From what you've written, I don't see what is "new" about Dr. Newton's research conclusions. What am I missing?
     
  6. Legendrew

    Legendrew Content team

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    While this has been suggested and discussed in the past this is, as far as I'm aware, the first time that this has been studied and recognised 'in vitro'. By studying this outside of the body we remove a certain degree of influence from factors such as deconditioning and can state that there appears to be a fundamental abnormality present within the muscle tissue itself. Even if this has been studied before, replication and confirmation of this principle is an incredibly important part of the research process and helps to drive research forwards.
     
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  7. Simon

    Simon

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    First off, the evidence on anaerobic threshold for ME/CFS patients is inconsistent, esp compared with appropriately deconditioned controls - even the latest Snell study found the big difference was on Day 2 anaerobic threshold, rather than day 1. But assuming that the lower anaerobic threshold is robust, this new work by Newton and her team throw a lot more light on the situation, particularly at a molecular level.

    As @Legnedrew points out, the ability to replicate in cell culture (where patient and controls cells are exercised equally as they grow) adds weight to the finding and removes the possibility of deconditioning being a factor.

    Perhaps more importantly, you can do a lot of stuff to cultured cells that you wouldn't do to patients. Introducing acid nanosensors for a start, and also molecules like DCA that can be used to probe the molecular mechanism behind the respiration problems (DCA is toxic so couldn't be used on patients). For instance, the current evidence suggests that the problem is in the cytoplasm rather than the mitochondria, and an enzyme called AMP-activated-Kinase - which is something of a cell-sensor for energy levels - is involved. So Newton et al really are getting in to the molecular detail of what might be going wrong.

    Oh, one final thing. Although they found that DCA helps reverse the problem in cell culture, it's toxic - but they can use their cell culture system to test other drugs that might do the same thing while being safe for humans. Still early days but this is an approach with great potential.

    Here's Julia Newton talking about the work at AfME's AGM
     
    Last edited: Mar 20, 2014
  8. kisekishiawase

    kisekishiawase sad

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    heres one i can find:
    http://lactateplus.com/home.php
    thanks for the link i try to digest it. just hope i could find a doctor who would willing to consider and help to papers i read cause im overwhelmed by all these puzzles.
    you know i google about muscle problem and magnesium calcium connection i even got insulin and magnesium correlation.
    but im confused cause some pro magnesium and some pro calcium.
     
  9. Valentijn

    Valentijn Activity Level: 3

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    For ME patients, I've heard of magnesium helping many (it was even prescribed to me by an ME/CFS doctor who unfortunately then retired), but don't think calcium has been as beneficial? Though calcium supplements almost always have magnesium added, so maybe that's why it helps :p
     
  10. kisekishiawase

    kisekishiawase sad

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    maybe for some needs mag more but some other needs calcium more.
    its still confusing to me. which one is more needed in greater amount since taking the wrong one will cause more imbalance. let alone potassium. itd be better if i can measure intracellular magnesium.
    one of the resource that says calcium is needed than magnesium is here:
    http://www.acu-cell.com/dis-mus.html
    what can do is only try and see. but it doesnt work for me (also with other supplements) cause my health changes overtime by itself. so i cant identify which supplement helps or worsen.
     
  11. Leopardtail

    Leopardtail Senior Member

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    August, if you are getting such awful muscle cramping (I had it too) have your levels of 0,25 Vitamin D3 been assessed, or your levels of Dopamine? Either being too long cause this cramping as can very low levels of Magnesium or Potassium.
     

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