MEA Summary Review: The Role of Mitochondria in ME/CFS | 13 July 2019

MEA Summary Review: The Role of Mitochondria in ME/CFS | 13 July 2019

https://www.meassociation.org.uk/20...-role-of-mitochondria-in-me-cfs-13-july-2019/

Charlotte Stephens, Research Correspondent, ME Association.

Introduction

For many years, a leading theory of causation in ME/CFS has been problems with the mitochondria (the part of the cell responsible for generating energy).

However, researchers are now suggesting that this is less likely and that we should be looking for something that is impacting the mitochondria’s ability to function properly – rather than at the mitochondria themselves.

In light of this, we have created an overview of mitochondrial research to date; explaining what mitochondria are, exploring the possibility of mitochondrial dysfunction as the cause of ME/CFS and offering other possible explanations if the mitochondria are not to blame…

 

And here I was thinking all this time that doctors and researchers were already thinking it was a functional mitochondrial problem rather than inherently damaged or malformed mitochondria.

 

@Eagles That was an interesting read, thanks.

 

This summary was inspired by the published article discussed here, https://www.s4me.info/threads/artic...-cfs-a-perspective-2019-tomas-and-elson.8367/

 

I shared this recently. Somebody sent me this.

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Thanks for sharing this important report.

I think the central thesis that mitochondria are unlikely to be both the cause and victim is overstated as few people used "mitochondrial problems" in that way colloquially. Just as cardiovascular disease often means the heart is, or could be, damaged due to downstream effects of things like atherosclerosis I think most people use "mitochondrial problems" to mean something else was causing an inhibition, or malfunction, of mitochondria either all the time or in the state of exertion. With the something else, likely, being upstream. (the mitochondria are downstream as it gets when it comes to energy production)

Overall, it looks like a useful summary of recent research in this area and hopefully people will share it.

There are a few mistakes–iirc the relevant biochemistry.

Gluconeogenesis is distinct from fatty acid oxidation.

The creatine pathway doesn't damage muscle.

However the enzyme creatine kinase in the blood is used as an index of muscle damage due to the logic that if it is leaking into the blood the muscle cells must be damaged.

I share this in the spirit of collaboration (the correct description of the metabolic pathways will render it more credible to doctors and public officials.)

Sincerely