New Atmosphere, New Vision: Gibson and Whittemore Kick Off Invest in ME Conference 2016
Mark Berry reports on Dr. Gibson's introduction and Dr. Whittemore's keynote speech, at the 11th Invest in ME International ME Conference in London.
Discuss the article on the Forums.

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. pattismith

    pattismith Senior Member

    Messages:
    1,436
    Likes:
    2,139

    A model of the mitochondrial basis of bipolar disorder

    2017

    Highlights


    Bipolar disorder phenomenologically is a biphasic disorder of energy; increased in mania and decreased in depression.


    There is evidence of increased mitochondrial respiration and ATP production in bipolar mania contrasting with decreased mitochondrial function in patients in the euthymic or depressive phase of the illness.


    Consequently, the central thesis of this paper is that bipolar disorder is due to a phasic dysregulation of mitochondrial biogenergetics.
    ...
    Discussion
    There are many potential mediators of mitochondrial function which collectively are implicated in bipolar disorder. Levels of oxidative stress, pro-inflammatory cytokines and intracellular calcium ions are all higher in bipolar mania than in the euthymic and depressive phases of the illness. Increased levels of calcium ions can partly account for increased oxidative phosphorylation via well documented pathways such as the modulation of the F1–FO elements of ATP synthase."

    I have often wonder if my own CFS/ME was in fact a bipolar disorder lacking the mania episode...

    if high intracellular calcium increases OXPHOS and is linked to MANIA and if low intracellular calcium decreases OXPHOS and is linked to depressive phase of BP, it would be very similar to Sonya Marshall theory
     
  2. arboretum

    arboretum

    Messages:
    37
    Likes:
    50
    Those are two different lines of research that are both in their early stages. Also CFS is totally different in symptoms to the depressive episode of Bipolar. I just don't think it's possible to put two very different lines of research together like that because they both feature calcium ions.
     
    EsetIsadore and hixxy like this.
  3. Learner1

    Learner1 Forum Support Assistant

    Messages:
    2,268
    Likes:
    3,880
    Pacific Northwest
    Has anyone tried amlodipine?
     
  4. pattismith

    pattismith Senior Member

    Messages:
    1,436
    Likes:
    2,139
    if both intracellular calcium and energy pathway are impaired in BP depressive episodes and ME, it makes some common points, but they are not the only ones:

    Post activity exhaustion is also part of the BP clinical findings, and BP is often associated to FM (like ME can be often associated to FM as well)...
     
  5. alicec

    alicec Senior Member

    Messages:
    1,508
    Likes:
    2,850
    Australia
    The recent article is trying to conflate calcium changes with a study they have done showing differences in microRNAs (miRNA) between ME/CFS patients and controls, which they claim might be the basis for a diagnostic test.

    In this respect it is similar to the earlier report where the conflation was with TRPM3 receptors, but they are making new claims.

    I am tired of the exaggerated claims coming from this group and the incoherent press reports that bring the claims to us. There may be some problems with reporters incorrectly interpreting scientific information but they wouldn't have made up the statements - the researchers must have made the links which the journalists go on to report.

    In the case of the recent claims about miRNA's, even if the miRNA study does show a real statistical difference between the test and control patients

    which I doubt since in their original publication they specifically say they didn't correct for multiple comparisons -

    what on earth does this have to do with calcium in cells?

    Well nothing but by linking the two the researchers mislead us into thinking that a very small observational study has some causal link. It gives it more gravitas.

    Just for the record - the miRNA study which I linked above could conceivably form the basis for a way of discriminating between patients and controls, provided very large numbers of people are tested and the differences observed to date are shown to hold up with statistically robust analysis.

    There is no known biological link between this difference and the disease however - ie we have no idea what such a difference means, assuming that the difference is real. We do know a little bit about the particular miRNA's but nothing whatsoever about how they might be acting in ME/CFS.

    And there is no reason whatsoever to link this to calcium in cells.

    And as for changes in calcium being behind the disease, well they would need to do an enormous amount more work than they have so far published before I would give that claim any credence.

    Their claim to fame on the calcium front is a small in vitro study on isolated NK cells.

    All they showed was that in cells isolated from CFS/ME patients, there are fewer TRPM3 receptors (one type of calcium channel) on the surface of the minor sub-group of NK cells (about 10% of the total NK cell population), but the major group had normal numbers.

    When these two populations of NK cells were stimulated in a test tube with a natural ligand for the receptor, there were differences in intracellular calcium response, both between the two groups of NK cells from patients and between cells from patients and controls.

    That is as far as the study went. We don't even know if this effect happens in the body or if it is an in vitro artefact. Assuming it is real, we don't know where it fits in to the wider scheme of things. It could be causal or it could be a downstream consequence of some other problem.

    Note there is no reason to think this applies particularly to NK cells. They just chose to study isolated NK cells. The receptors are present on many cell types.

    In a similar attempt to give a tiny observational study more gravitas, publicity at the time (in the earlier link above) tried to link this observation with their SNP studies on TRPM3, ie tried to imply the changes were the result of a defect in an ion channel. The waters were made even murkier at the time with the first round of claims about a new test to detect CFS hinting that it might be based on these SNP differences.

    Yet they themselves went on to do a study on SNPs where they finally did what everyone criticised them for not doing in the first place, namely correct for multiple comparisons, and actually showed the SNP differences in TRPM3 didn't exist. To try to salvage something they tried to fudge a difference in one other SNP but really this doesn't exist either.

    This didn't stop them from continuing to claim in publicity that they have discovered a defect in a cell surface receptor involved in calcium signalling, even though they know this is not true. It leads us to believe the observed differences in calcium have some causal significance however - REALLY DISHONEST in my book.

    They flit from tiny observational study to tiny observational study. Some of these are interesting but we will only know if they mean something when this group does in depth follow-up studies that convince other scientists that here is something here that is worth trying to replicate and examine further.

    So far there doesn't seem to be any evidence of substantial studies of underlying mechanisms coming from the group, surely a hallmark of serious research. Instead there is periodic and vigorous beating of the publicity drum to make us think these studies mean something, but it's no substitute for the real thing.
     
  6. CCC

    CCC Senior Member

    Messages:
    398
    Likes:
    502
    Just look at the timing. It'll all have to do with funding application rounds.

    That's not a criticism of the scientists, by the way. It's a very harsh criticism of the way science is now funded in Australia thanks to the introduction of competitive grants (replacing appropriation funding) back in the early 1990s. You have to position yourself every round. My take is that these guys probably do good work given limited resources, but they haven't got a schmooze agent working for them where it matters.
     
    MastBCrazy, anni66 and Mel9 like this.
  7. alicec

    alicec Senior Member

    Messages:
    1,508
    Likes:
    2,850
    Australia
    Possibly such publicity might have some influence on small private funding bodies or individuals.

    It would have no effect on major government funding bodies such as NHMRC and ARC. Indeed scientists involved in peer review for these granting bodies may well be adversely influenced by the publicity.
     
  8. knackers323

    knackers323 Senior Member

    Messages:
    1,379
    Likes:
    404
    Anyone had an appointment with people connected to Griffith uni?
    I seen someone who has or had cfs recommend that anyone who can, to see a professor Pete smith in qld who is part of the Griffith uni cfs team.
    The person who made the recommendation wouldn’t elaborate on why they made the recommendation though
     
  9. hixxy

    hixxy Senior Member

    Messages:
    1,166
    Likes:
    1,349
    Australia
    There's no reason to consult Dr Smith unless you have a mast cell disorder, allergies, etc. He's an allergist immunologist specialising in these disorders and doesn't actually specialise in ME/CFS. For MCAS he might even be the best doctor in Australia.
     
  10. mariovitali

    mariovitali Senior Member

    Messages:
    953
    Likes:
    861
    @EsetIsadore

    Is it possible to check your Liver enzymes? whether you took Channel Blocker or not, what you took may be responsible for hepatotoxicity. If the "Liver Theory" is correct you simply took something that further added strain on your Liver.


    https://livertox.nih.gov/Verapamil.htm
     
    EsetIsadore likes this.
  11. EsetIsadore

    EsetIsadore

    Messages:
    45
    Likes:
    53
    @mariovitali

    Thanks. I will make sure to have them checked ASAP. I stopped it over a month ago now, though. Since it says in all known cases, liver recovery has stopped at cessation, I’d assume all is now hopefully righted, even if it had gone awry.
     
    mariovitali likes this.
  12. mariovitali

    mariovitali Senior Member

    Messages:
    953
    Likes:
    861
    @EsetIsadore

    I forgot to add : Please note that you might have an active Liver inflammation or even severe Liver problems but despite that, Liver enzymes may be entire normal.

    It seems to me that Researchers have ruled out that the Liver is not involved in ME/CFS making this false assumption. The only way to completely rule out Liver Disease is by performing Liver Biopsy from multiple sites with second best option having a Fibroscan to rule out Liver Fibrosis.
     
    Last edited: Jan 10, 2018
    EsetIsadore likes this.
  13. EsetIsadore

    EsetIsadore

    Messages:
    45
    Likes:
    53
    In ultrasounds my own liver has looked gorgeous, other than a small calcified cyst likely caused by the malaria I had or another parasite along the way. I’ve not done the other testing. My own instinct for myself is that the liver isn’t where it’s at for me. I will certainly keep it in mind, though, and appreciate your thinking!
     
    mariovitali likes this.

See more popular forum discussions.

Share This Page