Lipkin's Monster ME/CFS Study: Microbes, Immunity & Big Data
The Microbe Discovery Project outlines an ambitious new study by top researchers that has collected patient samples, but needs desperately funds to complete the work.
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Mitochondrial dysfunction in a family with psychosis and chronic fatigue syndrome

Discussion in 'Latest ME/CFS Research' started by Dolphin, Nov 1, 2016.

  1. Dolphin

    Dolphin Senior Member

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    http://www.sciencedirect.com/science/article/pii/S1567724916302215

     
  2. A.B.

    A.B. Senior Member

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    It's on sci-hub. Conclusions:

     
  3. A.B.

    A.B. Senior Member

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    Three people in my family. I need to find some researcher who wants to test us.
     
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  4. Hutan

    Hutan Senior Member

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    Have you, or others, considered getting a lactate monitor and checking for yourself? A monitor seems to cost around $300.

    There was the thread on lactate monitoring
    http://forums.phoenixrising.me/inde...-study-to-measure-blood-lactate-levels.40152/

    (I was thinking about getting a monitor at the time, then forgot about it.)
     
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  5. taniaaust1

    taniaaust1

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    Four people in my family with ME/CFS (my sister and two of my first cousins have too) and my father is on disability as he has had a schizophrenia diagnoses. We also have a lot of severe celiac disease (3-4 members) and also have Autism on that side of family too (3 with Aspergers) and also systemic mastocytosis (severe mast cell disorder).

    I think its great they are doing family studies. I'd like to see more of these done to try to figure out the genes involved.
     
    Last edited: Nov 1, 2016
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  6. Hip

    Hip Senior Member

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    The Myhill, Booth and McLaren-Howard explanation for the dramatic lactate build up soon after exercise that is found in ME/CFS is the following:

    Because of mitochondrial dysfunction in ME/CFS, there is not enough ATP supplied by the mitochondria. The cells try to make up for this lack of ATP by manufacturing ATP via the alternative route of glycolysis (glycolysis takes place in the cell cytosol, not in the mitochondria, so is not impacted by the mitochondrial dysfunction).

    However, glycolysis without the participation of the mitochondria results in the production of lactic acid (in glycolysis, the pyruvate produced is either sent to the mitochondria to be burnt, or is otherwise converted to lactic acid).

    So by making ATP in this way, you get a dramatic build up of lactic acid.
     
  7. alex3619

    alex3619 Senior Member

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    Logan, Queensland, Australia
    The lower mitochondrial DNA is interesting, as is the lower RNA. If RNA is lower then the proteins made using it may also be deficient. So its possible, but not proven, that the mitochondria might have a problem with many of its proteins, which would also include transporters. I would need to know details of the oxygen testing and enzymatic testing before I could comment. Its possible these are from other causes than intrinsic mitochondrial dysfunction. Indeed this is possibly not incompatible with the recent ideas that mitochondrial dysfunction is induced by non-mitochondrial factors.
     
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  8. anciendaze

    anciendaze Senior Member

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    If there is no difference in mtDNA or nuclear DNA used by mitochondria there is a real possibility of autoantibodies interfering with mitochondrial activity and replication. Possible autoimmunity makes me wonder about onset in case histories. Detailed information might identify the type of defect.

    The increase in mitochondrial mass and decrease in mtDNA and mtRNA sounds like a problem eliminating abnormal proteins, which slows mitochondrial replication. This fits the hypothesis of an autoimmune problem.

    The bright spot in this is that it should be possible to treat this without replacing genes.
     
  9. ash0787

    ash0787 Senior Member

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    So would this be the first study to assess these particular aspects of the mitochrondria ? im sure you can appreciate the issue with such a small sample size and them all being related to each other
     
  10. anciendaze

    anciendaze Senior Member

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    This is a case history ash, not a statistical study. These are very different ways of gaining understanding about a problem.

    As I learned repeatedly in my previous career, R.W. Hamming was right when he said "The purpose of computing is insight, not numbers."

    Sheer numerical evidence can give a spurious impression of objectivity and understanding, as happened when PACE applied their preferred therapies to cohorts apparently defined as "patients who say they are tired when we don't think they should."
     
  11. pattismith

    pattismith Senior Member

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    My opinion is that every single CFS/ME should be checked for his mitochondrial function (at least monitored for the blood lactates), and that every time an impaired mitochondrial function would be noticed, a genetic cause should be looked for.
    it would allow
    -to identify a subgroup of CFS/ME patients with mitoD
    -to improve the mitoD genetic science

    Then if no genetic cause could be identifyed, auto-antibodies should be looked for

    I would like to know the genes concerned by these variants...:thumbdown:
     

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