Ion Channel Problems Found in ME/CFS!

Discussion in 'Chronic Fatigue Syndrome (ME/CFS) Research' started by Cort, May 11, 2015.

  1. Cort

    Cort Founder of Health Rising and Phoenix Rising Staff Member

    We've been talking a lot about ion channel problems in chronic pain but the NCNED group in Australia just found ion channel problems in ME/CFS as well. An neurological ion channelopathy was actually conjectured to be present in ME/CFS by Chaudhuri and Behan, I think it was, about 15 years ago. The authors suggested the problems they found could affect nerve functioning.

    The ion channels measured mediate a variety of sensations like the sensations of pain, hotness, warmth or coldness, different kinds of tastes, pressure, and vision. Remarkably, nine of the polymorphisms more commonly found in ME/CFS take place in one ion channel - the TRPM ion channel. These channels regulate the flows of magnesium and calcium into the cells and have been implicated in inflammatory pain syndromes, rheumatoid
    arthritis, the secretion of proinflammatory cytokines, metabolic problems, pain and possibly glutamergic signaling.

    Exciting stuff. Ion channels are big in pain research now...Better techniques allow researchers to better understand them. It's definitely a growth field.

    I attached the paper.

  2. Issie

    Issie Well-Known Member

    Interesting. I just found out one of the meds I've been on for MCAS is a mild calcium channel blocker. I'm trying to come off it - very expensive. We will see what happens when that aid is not there. It had been one of my best POTS meds too.

  3. Issie

    Issie Well-Known Member

    Oh my doc won't let me supplement with magnesium (other than what is in my whole foods. As a vegan I get a lot of my minerals and vitamins that way ) it reinforces the biofilm that shields virus, bacteria and Protozoa. We want to break that down so the immune system can notice them and eradicate what it can/will.

    Last edited: May 13, 2015
  4. Cort

    Cort Founder of Health Rising and Phoenix Rising Staff Member

    Griffiths released this:

    New research findings may shed light on the potential cause of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME).
    Researchers from Griffith University’s National Centre for Neuroimmunology and Emerging Diseases (NCNED) – part of the new Menzies Health Institute Queensland – have uncovered significant factors contributing to the pathology of this illness.

    The results reveal genetic changes in important receptors associated with immunological and cellular function and contribute to the development of this complex illness.

    “These findings have been achieved through a team effort involving researchers, patients, funding bodies, clinicians and the support of Griffith University and the Queensland Government,” say chief investigators Professor Sonya Marshall-Gradisnik and Professor Donald Staines.
    Co-researcher and consultant immunologist Professor Pete Smith said that important signalling mechanisms are disrupted as a result of these genetic changes involving the detection and response to threats.

    “These are primitive genes that are involved in many cellular signals in the brain, gut, cardiovascular and immune systems, as well as in the mediation of pain.”

    These research findings coincide with International Neuroimmune Awareness week commencing Monday 11 May.'

    The Griffith Health Centre on the university’s Gold Coast campus is being lit up each evening from 10 -12 May to raise awareness of neurological conditions such as CFS/ME as well as other conditions such as Fibromyalgia and Gulf War Syndrome.

    “The lighting up of the Griffith Health Centre signifies Griffith’s commitment to the CFS patient community and our team approach to this research,” says Pro-Vice Chancellor (Health) Professor Allan Cripps.

    CFS/ME is a highly debilitating disorder characterised by profound fatigue, muscle and joint pain, cerebral symptoms of impaired memory and concentration, impaired cardiovascular function, gut disorder and sensory dysfunction such as noise intolerance and balance disturbance. Many cases can continue for months or years. It is believed to affect around 250,000 Australians.

    The research findings are to be presented at an international conference in London later this month.
    Issie likes this.
  5. Cort

    Cort Founder of Health Rising and Phoenix Rising Staff Member

  6. Remy

    Remy Administrator

    I think that it's a little shortsighted and simplistic to shun magnesium supplementation because it can reinforce biofilm formation. Basically all minerals, especially calcium, can contribute to biofilm formation yet no one is suggesting we not eat our leafy greens. Biofilms flourish in general in any sort of nutrient rich environment but depleting ourselves to starve biofilm seems counterproductive at best.

    We don't understand the complex subjects of biofilms and their formation well enough, in my opinion, to allow ourselves to become deficient in a mineral like magnesium that participates in so many important functions in the body. My LLMD is also of this mindset which also goes to show how many conflicting opinions there are on this and every other topic with relation to Lyme and co at this time.

    Hopefully future research will help to make this all more clear.
  7. Issie

    Issie Well-Known Member

    Wow. I've been saying I thought epigenetic changes is what triggered our immune systems into malfunctioning. Interesting info.
  8. Issie

    Issie Well-Known Member

    We get plenty of magnesium in our foods as vegans. It's the additional supplementation he doesn't want us to do. The goal is to have our bodies working and metabolizing so well we won't need hardly any supplements. Getting our minerals and vitamins in a whole food form that isn't so concentrated is a more balanced approach than individual supplementation. I used to be around and in the alternative supplement field. I can tell you what to take for what and what not to combine. Or what is counter indicated if you have this Or that illness. I've had years of experience with this. But my whole way of looking at supplementation has changed. I do still supplement. But not like I used to. I get it with my foods now.

  9. Remy

    Remy Administrator

    That's not the case for the vast majority of the people who might read your original post though and who could benefit from adequate supplementation, from increasing whole foods or from taking supplements.

    I wasn't saying that you *should* take magnesium, only that it's simplistic to tell people to avoid a crucial nutrient because it may contribute to biofilm formation in some complex and largely unknown way.
    Who Me? likes this.
  10. Issie

    Issie Well-Known Member

    Ok I made my post a little more clear. So hopefully it will be understood better.

  11. Remy

    Remy Administrator

    So these TRPs are pretty interesting even if it has taken me a whole year to get around to reading that article.

    Here's @Cort's post on ProHealth on this study (I couldn't find it elsewhere on the forum but let me know if I missed it):
    I'm still totally confused though and hoping you all can help me sort this out...

    I found this article on how probenecid is a TRPA1 agonist too and it made me think about how Lerner often prescribed probenecid to potentiate antiviral drugs. Could it have been that it was working on this channel also? But the title says that probenecid desensitizes channel responses...and the abstract says that it activates TRPA1. It also seems like probenecid might increase intracellular calcium which would of course not be good. But I feel like I'm missing something. Help!

    @Strike me lucky?

  12. Hip

    Hip Well-Known Member

    Does anyone know if these polymorphisms found in ME/CFS patients increase intracellular calcium?

    Because if these polymorphisms do increase the levels of calcium in cells, that may bring us back to the old RNase L cleavage story of ME/CFS.

    Recall that RNase L is released inside a cell in order to fight intracellular viral infections. The RNase L enzyme destroys viral RNA as well as human RNA in the cell (so RNase L can have both good and bad effects).

    However, it is known that in ME/CFS, the RNase L is chopped up (cleaved) into small fragments (called low molecular weight RNase L), and the degree of RNase L fragmentation in ME/CFS patients correlates with symptom severity.

    Elastase, calpain and cathepsin G are all able to cleave RNase L, but Rich Van Konynenburg argued that calpain is the likely culprit responsible for this cleaving.

    Now it just so happens that intracellular calcium activates calpain, so higher intracellular calcium means more activated calpain, which in turn may mean more chopped up RNase L.

    Thus if ME/CFS patients have polymorphisms that increase intracellular calcium, that could explain their fragmented RNase L.