The 12th Invest in ME Conference, Part 1
OverTheHills presents the first article in a series of three about the recent 12th Invest In ME international Conference (IIMEC12) in London.
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Dr. Myhill/ Mitochondria Hypothesis

Discussion in 'General Treatment' started by cman89, Nov 4, 2014.

  1. cman89

    cman89 Senior Member

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    I have not been up on the research of mitochondrial damage in general illness, and certainly not on this topic as it pertains to ME. Dr. Myhill has good info on her site, but I still have questions. If we consider mito dysfunction to be part of the ME spectrum of "malfunctions" , is it such that the mito DNA damage is that of an accelerated aging process? In other words, if we were able to address the healing of mitochondria and put ourselves in recovery in a simple manner, would there still be the effects of damage in the DNA? Or could this theoretically be rolled back also. I ask this because I am 24 years old, and I often feel like I am 70 or so. I do not have full blown ME, but I do struggle with faitigue quite a bit. i'm holding out hope for some sort of recovery/solution, but I fear that the damage done is to the core, at the genetic level. Anyone familiar open to helping me out here?
     
  2. *GG*

    *GG* Senior Member

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    Just broke this up to make it easier for me to read. Sorry, have nothing to offer, but hopefully someone will jump in!

    44 YO who definitely feel years beyond my age also, and I have no children to take care of!
     
  3. ahmo

    ahmo Senior Member

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  4. Esther12

    Esther12 Senior Member

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    I think that Myhill uses some unvalidated testing, and is on the experimental/dodgy side of things. I would not assume that the claims she makes about the role of mitochondria in CFS are supported by any good evidence.

    I expect that lots of different conditions end up being lumped together under ME and CFS, and some of them are unlikely to see effective treatments any time soon, while some likely will. Personally, I think that the uncertainty around these matters just needs to be accepted for the moment, however irritating that may be.
     
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  5. dannybex

    dannybex Senior Member

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    @Esther12 , I guess you've been ignoring the work of RichVank, Neil Nathan, Ben Lynch, and others, as it seems like you dismiss anything that isn't a drug as "dodgy". You're certainly entitled to your opinion. Anyway, here's another paper linking ME to mitochondrial dysfunction.


    http://link.springer.com/article/10.1007/s11011-013-9435-x
     
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  6. JPV

    JPV ɹǝqɯǝɯ ɹoıuǝs

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    There seems to be a lot of that going on around this forum lately.
     
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  7. cman89

    cman89 Senior Member

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    I am aware of the shortcomings of her approach. It is far too one size fits all for me to accept fully. There are good ideas coming from that approach though
     
  8. Esther12

    Esther12 Senior Member

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    I think that the way lots of drugs are promoted for ME is dodgy too. I'm not familiar with a lot of those names (but I am bad with names... I used to always get Michael Sharpe and Peter White mixed up). Really, I've got a problem with anyone making claims to patients that are not supported by good evidence, especially when they fail to make clear how speculative and unsupported their claims are. Unfortunately there are too many people like this for me to look in to them all or be as critical as I'd like.
     
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  9. Jonathan Edwards

    Jonathan Edwards Senior Member

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    I don't think DNA damage can come into it. Each cell, or each mitochondrion has its own DNA so it is hard to think of a process that would damage the DNA in all mitochondria in the same way. Usually the effect of DNA damage to an individual cell or organelle would be drop out of that cell or organelle and replacement by a healthy one. Rarely, the DNA damage will allow uncontrolled growth and malignancy but that is a local effect on one cell, not a general effect. There are some exceptions to this maybe but this would be the simple story.

    There are rare mitochondrial diseases which produce progressive disability over time through a complicated mechanism that I forget but somebody else may remember. I do not think this is progressive DNA damage but it might be 'ageing' analogous to the premature ageing that occurs with abnormalities of telomeres in ordinary DNA. You start off with abnormal mitochondrial DNA in the first place.

    I was not aware that Dr Myhill was suggesting that DNA damage was involved in ME. Was there an indication of this on her website?
     
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  10. Marco

    Marco Grrrrrrr!

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    I have to admit to being somewhat unconvinced by Dr MyHill's theories, nevertheless this might suggest that gradual changes in mitochondrial integrity may cause 'step changes' resulting in disease states :

    Steadily rising increases in mitochondrial DNA mutations cause abrupt shifts in disease

    "By showing that subtle changes in the cellular proportion of the same mitochondrial DNA mutation can result in a wide range of different clinical manifestations, these findings challenge the traditional model that a single mutation causes a single disease,"

    http://medicalxpress.com/news/2014-10-steadily-mitochondrial-dna-mutations-abrupt.html
     
  11. Jonathan Edwards

    Jonathan Edwards Senior Member

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    Yes, this is part of this strange story of progressive, or maybe stepwise, deterioration in mitochondrial disease. As I understand it, it all starts with a mutation in the DNA of mitochondria in a small proportion of cells - maybe derived from a single cell during embryo development. For some reason the cells with 'bad' mitochondria gradually come to 'compete out' those with 'good' mitochondria. No new DNA damage occurs, it is just that the damaged copy gradually takes over organs like muscle. I would not rule out the possibility that ME/CFS in some cases is a manifestation of this sort of disease but there are various features that seem anomalous. One would not expect remissions much and sensory sensitivity would seem hard to explain - but maybe in some cases it is relevant. What I think vanishingly unlikely is that most ME/CFS is this sort of mitochondrial disease.
     
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  12. A.B.

    A.B. Senior Member

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    Mitochondrial problems as per Dr Myhill is an interesting topic! There is no definitive evidence but it fits observations made by patients very well and I think means one should seriously consider the possibility that a lot of what she says on this page may be right: http://www.drmyhill.co.uk/wiki/CFS_-_The_Central_Cause:_Mitochondrial_Failure

    Pacing is exactly what one would do if they had this sort of problem. Aerobic exercise and pushing one's limits is exactly what would be harmful. The CPET studies also support the notion of impaired aerobic metabolism.

    There was a fatigue thread here on this forum where many patients agreed that there is some sort of "low battery" component to their condition.
     
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  13. Marco

    Marco Grrrrrrr!

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    I'm not being too serious in suggesting this but a great deal of brain activity (energy dependent) is inhibitory. As some folks seem to be discussing 'near death' experiences on another thread, some time ago someone (a Doctor incidentally) sent me a paper that suggested that at the point of (near) death it's the brain's inhibitory circuits that keel over - hence the 'whole life flashed before me'/'spiritual' experience.

    Who knows. 'Sensory overload' seems to be discussed a little on mito disease on-line fora but not in the scientific literature.
     
  14. Marco

    Marco Grrrrrrr!

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    Actually in confirmed mitochondrial diseases exercise is a first line treatment on the basis that exercise increases mitochondrial biogenesis (via the PPAR pathway if I recall correctly) on the rationale that its better to have more even compromised mitochondria than less.

    Not that the PACE trial provided objective proof of anything but it's interesting that on some measures the GET only arm produced better results than the CBT only arm which must have come as a little kick in the whatevers to the CBT industry.
     
  15. NK17

    NK17 Senior Member

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    This might be of interest to @Jonathan Edwards and seems pertinent to this thread.

    I think it was a poster presentation by Dr. Rajeevan from the CDC at this year IACFS/ME conference in San Francisco, titled Telomere Shortening in ME/CFS.
     
  16. Helen

    Helen Senior Member

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    cman89 and A.B. like this.
  17. A.B.

    A.B. Senior Member

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    Thanks, that is an interesting study. The completion date is september 2014 so we should hopefully hear about the results soon (or were they published already somewhere?).

    Some info for the curious:

    http://clinicaltrials.gov/ct2/show/NCT01471652?term=chronic fatigue syndrome&rank=12
     
  18. adreno

    adreno PR activist

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    I am not convinced that mitochondrial dysfunction is the cause of ME/CFS. However, it seems to be the case that we have heightened levels of oxidative stress, and mitochondria are especially vulnerable to this. For this reason, I believe it is important to protect the mitochondria, and certain supplements (as suggested by Myhill et al.) can help with that.
     
  19. cman89

    cman89 Senior Member

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    I agree, isnt te above more relevant to the so called "mitochondrial diseases", the ones that cause a rather quick deterioration in ability levels? In other words, the MELAS, MERFF, etc... I can see the effect of oxidative stress damaged Mitochonria in CFS, but would there be a DNA spread effect? And how long would it take for oxidative stress-damaged DNA to become the new norm in mito cells?
     
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  20. cman89

    cman89 Senior Member

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    No, that is my additional question. the Myhill site talks more about defective Mito as structural damage, at least as I read it. I am just interested in the idea of how DNA is damaged by external sources and then propagates, both mito and cellular. Seems to be target that could address many varying ailments
     

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