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Article Dec 23rd 2017: Aussie scientists discover CFS is real and may be treated with CCBlockers.

Discussion in 'General ME/CFS News' started by Countrygirl, Dec 23, 2017.

  1. Countrygirl

    Countrygirl Senior Member

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    http://www.couriermail.com.au/techn...t/news-story/2f62ddcf2d5a625b0c1f185fc649bbf0

    Australian scientists have, according to the article, discovered that CFS is real (again :lol: ) and the 'cure' may be calcium channel blockers. (Problem here is that some of us are already taking them when our orthostatic hypotension flipped into orthostatic hypertension, and still have ME.)

     
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  2. Hip

    Hip Senior Member

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    If you search for the above article via a Google search, you can avoid the paywall that you get by clicking on the direct link.

    The above article talks about Prof Sonya Marshall Gradisnik's finding that ME/CFS patients have lower calcium levels in their cells, and says this is the basis of ME/CFS.


    I don't think the above article is saying any more than this older March 2017 article covers.

    The older article explains that ME/CFS calcium abnormalities are found in natural killer (NK) cells, and that these abnormalities might be due to the lower number of TRPM3 calcium ion channel receptors found on NK cells in ME/CFS patients.

    So as I understand it, the lower calcium levels of ME/CFS only apply to NK cells.

    The older article says TRPM3 is activated by a wide variety of agents, from bacteria and viruses to temperature and environmental factors such as perfumes.

    It also says TRPM3 belongs to a class of receptors are known as "threat receptors", because they are up-regulated when the body is under any kind of threat, such as infection, trauma or even childbirth. So this perhaps links into Naviaux's danger response theory of ME/CFS.

    Although if TRPM3 gets up-regulated as part of a danger response, that's the opposite to what happens in ME/CFS patients' NK cells, where TRPM3 is found down-regulated.



    Griffith University scientists are looking at the calcium channel blocker nifedipine as a treatment for ME/CFS. One calcium channel blocker that has helped some ME/CFS patients is nimodipine.
     
  3. Gijs

    Gijs Senior Member

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    If we have lower calcium in our cells isn't a calcium BLOCKER then not be a paradox?
     
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  4. hixxy

    hixxy Senior Member

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    Straight from the article.
     
  5. E.man

    E.man Senior Member

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    So this 'new proof ' has been about since March.
    Why is it that it's researched in AU, printed in a major AU newspaper and even when I'm in Australia. .......nothing. No new diagnostics, no treatment, not a mention. Still the same old guessing game .
     
    pibee, Eneia, maybe some day and 2 others like this.
  6. Troyza

    Troyza

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    Theres a comment on the article:
    'This is not exactly new, as far as treatment goes:

    "Chronic Fatigue Syndrome: Possible Effective Treatment with Nifedipine", American Journal of Medicine, Dec. 1988. '
     
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  7. E.man

    E.man Senior Member

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    So it's been known for ages.
    Why has it not become widely known in medical circles.
    Invisible Epidemic.
     
    Troyza likes this.
  8. drewf2

    drewf2

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    Is there anyone on here that has tried calcium channel blockers and noticed any benefits? 15 people in the research group with CFS seems like a small amount to be conclusive that all CFS people will have low cellular calcium levels from a faulty gene but I guess it's the best evidence there is as far as current research goes so I would be interested in giving it a go. There are apparently natural calcium channel blockers, Magnesium and potassium, perhaps that could be of benefit over time rather than taking the medication?

    I'm in Australia also, I too find it crazy how big the gap is between all the good CFS research and breakthroughs being done in medicine here to the lack of any knowledge and understanding of CFS from most doctors.
     
  9. alex3619

    alex3619 Senior Member

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    I probably came close to death from a calcium channel blocker. I was progressively incapable of sleeping and at about the point I figured out why I was down to 42 minutes of sleep a day, broken into five and ten minute naps. It was also getting worse. At some point very low sleep quantity and quality can lead to immune failure and probably a host of other issues.

    It may or may not be beneficial to block calcium channels in immune cells such as NK cells, but its not clear that other cell types will benefit. This needs much more research, and probably a careful selection as to what types of calcium channel blockers are used.
     
  10. pattismith

    pattismith Senior Member

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    it looks so to me too! A calcium channel blocker to cure a calcium channelopathy ??:thumbdown:
     
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  11. alex3619

    alex3619 Senior Member

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    Doctors do not generally read original research. Even if they tried, for a doctor to keep up to date for every disease is flat impossible. The big issue here is not so much that doctors fail to keep up with ME and CFS research, though this is correct, its that they often think they do not need to. Even worse there is data that around 90% of doctors (look up Gigerenzer) do not have a sufficient grasp of science to really benefit from such reading.

    What doctors sometimes read is review articles. There are almost no quality review articles of ME or CFS in existence that are of clinical relevance. I am also not sure about my use of the qualifier "almost". Since there are no broadly effective treatments for ME right now, though some do benefit from treatments like Ampligen, a review article could only be written about diagnostic protocols and complicated decisions in patient care without actually having effective treatments. I am not sure how such a document could be published. These documents can be published outside of mainstream journals, much as the IOM report was, but most doctors will not ever see them.

    The doctors education conundrum is one of the things we are working toward dealing with. As the medical science finds more answer I expect to see change. This happened with MS after tests became available. It happened with gastric ulcers after antibiotics were proven to be effective.
     
  12. alex3619

    alex3619 Senior Member

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    This would only be the case if a particular calcium channel blocker blocked calcium channels both into and out of a cell, and in different cell types had different calcium blocking functions, or were to block different calcium channels in different ways. It would be in the details, and we have not seen those details.
     
  13. GreenBlanket

    GreenBlanket

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    Last edited: Dec 24, 2017
  14. dreampop

    dreampop Senior Member

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    I think it's a little confusing, I could be wrong, but I think TRPM3 was reduced in unstimulated (I think w/o ligand present) CFS patient's NK cell vs controls. But when stimulated, CFS cells' TRPM3 influxed more calcium than controls.

    Now in another type of NK cell, TRPM3 was the same as controls unstimulated. Stimulated, they expressed more TRPM3, but influxed the same amount of calcium. And I think when primed with a ligand specific to TRPM3, this CFS NK cell increased effectiveness relative to controls.

    So, it's almost as if the receptor is over-reacting when stimulated. It looks to someone who doesn't know what he's talking about, that it could be some minor sensitization-like finding (this is obviously different from central sensitization since were talking about NK cells), that the receptor is reduced to match low levels of ligands on a 'normal' basis, and the overreacts when it encounters a lot of it's ligand at one time. Or it could be some signal to the NK cells to produce these receptors is reduced normally, but when more interaction with the lignad-receptor occurs, TRPM3 receptor expression is pumped up.

    TRP receptors could be really interesting in CFS, on the surface level they make a lot of sense. But, afai gene expression in them hasn't come up before, except Light's TRPV1 post- exercise. And so it's hard to reconcile that with the claims from this Australian group. Either this only happens in NK cells, or everyone else missed it? I don't know. I also noticed the CFS group is almost 10 years older, and that seems pretty high.

    I think nifepidine just happens to be an agonist, I don't think it's like all calcium channel blockers.
     
    Last edited: Dec 26, 2017
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  15. HowToEscape?

    HowToEscape? Senior Member

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    2017-1956 = 61 years For a reporter, that's a quick study. **

    **1956 Melvin Ramsay identifies M.E
     
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  16. EsetIsadore

    EsetIsadore

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    I haven’t studied the various CCBs to know their different mechanisms of action. And right now my cognitive function is low, so I ask your forgiveness in advance...

    Very recently, I did a multi-week trial on a custom-compounded low-dose (titrated up to 40mg thrice daily) Verapamil because I have Hemiplegic Migraines (as well as ME). Suffice it to say, my HM worsened precipitously with badly lingering symptoms (severe aphasia, apraxia, dysarthria, ataxia, etc.) in the rare windows between them. My ME further worsened as well - and I was in no position to afford that decline.

    That’s the very short summary. It may or may not be applicable to this thread or to anyone other than myself. Nonetheless, it’s evident that, if anything, I’d need an agonist rather than antagonist!
     
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  17. wastwater

    wastwater Senior Member

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    Is the blood in urine considered important I did have that intermittently maybe still do (microscopic)
    That would be easy test
     
    Last edited: Jan 1, 2018
  18. hixxy

    hixxy Senior Member

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    This is the first time I've ever heard of it. I guess it could be a part of interstitial cystitis that some people have as a secondary diagnosis.
     
  19. wastwater

    wastwater Senior Member

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    The explanation I got was athletic overtraining but I’m mostly bed bound
    With me/cfs you maybe in a state of althletic overtraining even at rest
     
  20. arboretum

    arboretum

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    I don't think their study(s) have been replicated, so I wouldn't jump to any conclusions about the veracity of their claims
     

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