Ron Davis: Preliminary data shows problems with energy metabolism

alex3619

alex3619

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aimossy said:
Would be interesting to see what happens to metabolomics results and microbiome after exercise as well. There are so many measure points in different aspects that could happen in that scenario.
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That is an obvious next step in testing the metabolome of ME patients. What happens when they over-exert? The Lights have done some of this, Workwell has done some more, but a full metabolomic result could give us a blood test.
 
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Groggy Doggy

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The issue is not damaged mitochondria. It is instead the role that mitochondria plays in cell metabolism. A friend of mine recently attended the American Diabetes Association conference and told me "there was a major interest in the role of mitochondria as a foundation of the orchestration of metabolic organization of behavioral and physical phenotype. The data presented confirmed the modeling of biology that can be applied to ME/CFS and suggested several potential targets for treatment at the systemic and cellular levels of organization. In particular the role of heat as a cellular level signal was addressed."
 
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duncan

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Although I am as enthused as can be about the work Davis is doing, and the results he is yielding about demonstrable and, likely, replicable mito issues...And the prospects of using these findings as they gel into biomarkers, and generating a diagnostic...I can't help but worry this energy depletion explanation and explaining the dysfunction of the mito and its role, are nevertheless ultimately explaining a downstream effect.

This concern does not undo the significance of what Davis and Crew are finding and doing.
 
Ben H

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duncan said:
Although I am as enthused as can be about the work Davis is doing, and the results he is yielding about demonstrable and, likely, replicable mito issues...And the prospects of using these findings as they gel into biomarkers, and generating a diagnostic...I can't help but worry this energy depletion explanation and explaining the dysfunction of the mito and its role, are nevertheless ultimately explaining a downstream effect.

This concern does not undo the significance of what Davis and Crew are finding and doing.
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The CDR response which has been implicated by Davis and OMF as causing this 'hypo metabolism' is a consequence of various things, such as viruses, bacteria, parasites, trauma etc.

So it doesn't happen out of nowhere per se. I should say that Davis is optimistic for not only biomarker(s), but a cure too.

The mitochondria not being regulated properly, or working as they should, can explain almost everything in this illness. Initial stressor>maintained CDR>resulting systemic issues.


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duncan

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Ben Howell said:
The CDR response which has been implicated by Davis and OMF as causing this 'hypo metabolism' is a consequence of various things, such as viruses, bacteria, parasites, trauma etc.

So it doesn't happen out of nowhere per se. I should say that Davis is optimistic for not only biomarker(s), but a cure too.

The mitochondria not being regulated properly, or working as they should, can explain almost everything in this illness. Initial stressor>maintained CDR>resulting systemic issues.
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Right. But I am not talking about trigger mechanisms for ME, which I think you are @Ben Howell when you mention viruses and bacteria, etc. In effect, the mito disruption IS ME/CFS, if I understand correctly -as opposed to being a byproduct of ME/CFS.

Perhaps that is the case. But I fear the emphasis seems still to be on explaining away insufficient energy. I think this is certainly an essential component, perhaps even the most important. Is it ME/CFS in its entirety, though? Or is it an important ramification of the disease? If, for example, EBV throws the mito off, or disrupts its functioning, what perpetuates the condition?

I think that has yet to be determined.

But hey! I'm a fan of reverse engineering, or follow the clues. Especially when they validate the disease and lead to diagnostics.
 
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Ben H

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duncan said:
Right. But I am not talking about trigger mechanisms for ME, which I think you are @Ben Howell when you mention viruses and bacteria, etc. In effect, the mito disruption IS ME/CFS, if I understand correctly -as opposed to being a byproduct of ME/CFS.

Perhaps that is the case. But I fear the emphasis seems still to be on explaining away insufficient energy. I think this is certainly an essential component, perhaps even the most important. Is it ME/CFS in its entirety, though?

I think that has yet to be determined.
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I was just pointing out that what Davis is proposing fits with a downstream effect. I'm guessing you mean that you fear M.E is something else entirely? Would you care to elaborate?

If the mitochondria in the immune system are affected by the CDR response, that could cause huge issues. Same with the brain. The mitochondria are everywhere, in varying quantities. So mitochondria, though energy mechanisms by their very nature, could theoretically cause immune issues, gut issues, cognitive issues etc. So it potentially goes far beyond just 'insufficient energy'.

Its all yet to be determined, we have been given some very interesting clues however. I believe Davis feels it is fundamentally a mitochondrial issue, via regulation. I'm inclined to think that makes a heck of a lot of sense. I am yearning for the research paper!


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Ben H

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duncan said:
I am suggesting the mito dysfunction may be a component or byproduct of ME/CFS. Can I say what ME/CFS is? No.

Davis may be right. I hope he is. I am a fan. I am routing for him.
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Okay. Have you read the CDR paper by Naviaux? It theoretically explains your concerns about EBV and what perpetuates the condition. In short, a (sustained) CDR could perpetuate the condition. The mitochondria may well be the basis for M.E in its entirety.

I don't have the answers either ofcourse, but I feel Davis is onto them. We need to wait and see what's published.

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duncan

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Ben Howell said:
kay. Have you read the CDR paper by Naviaux? It theoretically explains your concerns about EBV and what perpetuates the condition. In short, a (sustained) CDR could perpetuate the condition. The mitochondria may well be the basis for M.E in its entirety.

I don't have the answers either ofcourse, but I feel Davis is onto them. We need to wait and see what's published.
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I hope he is onto them. He seems to be onto something that many of us have long suspected contributed to our woes. Only he is coming at it with solid and impressive science.

I have no concerns about EBV per se. I just tossed it in as an example of a trigger. There are many such examples.

I am familiar with Naviaux and I've read about him and I've read his stuff. I need to reread him, though, to be honest.

What causes the chronic CDR?
 
Ben H

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duncan said:
I hope he is onto them. He seems to be onto something that many of us have long suspected contributed to our woes. Only he is coming at it with solid and impressive science.

I have no concerns about EBV per se. I just tossed it in as an example of a trigger. There are many such examples.

I am familiar with Naviaux and I've read about him and I've read his stuff. I need to reread him, though, to be honest.

What causes the sustained CDR?
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http://www.sciencedirect.com/science/article/pii/S1567724913002390

CDR is maintained by purigenic signalling.


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duncan

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Ben Howell said:
CDR is maintained by purigenic signalling.
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This is a somewhat vague concept that I think even Naviaux admitted might be problematic back in 2014 when he addressed autism. He suggests the purine signal gets stuck in the on position, but I don't believe he adequately explains how.

But it sounds good to me.
 
Ben H

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paul80 said:
Can someone explain the CDR stuff in simple terms. I tried reading the document by Naviaux but couldn't understand it.
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CDR= Cell danger response.

CDR is an evolutionary metabolic response to stressors that exceed the threshold for homeostasis. Be it viral, bacterial, psychological etc. Anything that could kill the cell.

It's a totally normal response. It releases metabolic intermediates ATP and ADP, Krebs cycle intermediates, oxygen, and reactive oxygen species.

This is proposed to be a short lived event and is reversed by regenerative pathways once the danger has been dealt with.

If this persists abnormally, whole body metabolism and normal energy production, gut microbiome are disturbed.


The main point is that a continued CDR is not a normal event, and could have dramatic consequences.



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Ben H

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duncan said:
This is a somewhat vague concept that I think even Naviaux admitted might be problematic back in 2014 when he addressed autism. He suggests the purine signal gets stuck in the on position, but I don't believe he adequately explains how.

But it sounds good to me.
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I think it's vague because it's so new and not fully understood. Or wasn't at time of publication. I'm presuming for Davis, Naviaux and OMF to have stated it is implicated in M.E. they must have a lot more information than that paper.

If you have a reference to Naviaux admitting that, I'd love to see it (genuinely).



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Ben H

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duncan

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This is his theory, @Ben Howell , his hypothesis. You will note in the autism piece that treatment which conformed to this theory only was effective for a while.

But it is a GOOD theory, and he may be right.

ETA: We cross-posted, and we seem to both agree he is just theorizing.
 
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