Action for ME Study Reports.

[Remy]

Action for M.E. reports on the studies they funded on their website:

https://www.actionforme.org.uk/research/research-we-fund/

Click under Recently Funded Projects to read the details.

Two Newcastle University research studies funded by Action for M.E. have concluded, having investigated immune responses and muscle dysfunction in people with M.E.

Each research team has provided a lay summary of their findings, which can be found via our page detailing the research we fund at https://www.actionforme.org.uk/research/research-we-fund/

Prof Stephen Todryk, Professor of Immunology, Department of Applied Sciences, Northumbria University, investigated the immune responses of people with M.E. in a £19,500 study joint-funded by Action for M.E. and the ME Association.

He found that those who were more severely affected had fewer natural killer cells and fewer bacteria-fighting antibodies, but more inflammatory interferon.

“The study of larger numbers of patients over a period of time will help to prove these associations, making these measurements useful for working out new and effective ways of diagnosing and treating CFS/M.E.,” says Prof Todryk in his lay summary.

Understanding muscle dysfunction in M.E.

In May 2012, Action for M.E. awarded £25,000 to Dr Phil Manning and Prof Julia Newton at Newcastle University for their study into muscle dysfunction.

The funding provided by Action for M.E. was matched by Newcastle University’s Faculty of Medical Sciences to establish the Action for M.E. PhD Studentship, awarded to top science graduate, Gina Rutherford.

“In this project, muscle samples were obtained from CFS/M.E. patients in an attempt to investigate muscle function in more detail,” explains Gina in her lay summary.

“This research project did not find any evidence of biochemical or metabolic dysfunction in muscle cell samples obtained from CFS/M.E. patients. This contrasts previous work that has reported muscle dysfunction in CFS/M.E. patients following exercise. Further investigations are required to determine the biological basis of fatigue in CFS/M.E. patients.”

 

[Cort]

Action for M.E. reports on the studies they funded on their website:

https://www.actionforme.org.uk/research/research-we-fund/

Click under Recently Funded Projects to read the details.

The Julia Newton study finding is not good news....If

This research project did not find any evidence of biochemical or metabolic dysfunction in muscle cell samples obtained from CFS/M.E. patients. This contrasts previous work that has reported muscle dysfunction in CFS/M.E. patients following exercise. Further investigations are required to determine the biological basis of fatigue in CFS/M.E. patients.”

In fact this study failed to replicate a bunch of what seemed to be important findings: no changes in pH, lactate plus no mitochondrial dysfunction or free radical generation

• Interestingly, there was no difference in pH when CFS/M.E. muscle samples were compared to healthy control sample, which contrasts previous work conducted when CFS/M.E. patients performed an exercise intervention .
• When specifically measuring glycolytic (anaerobic) activity there was no significant difference in lactate which is produced at a rate comparable to glycolysis or any of the glycolytic parameters measured.
• Thus, it can be determined that mitochondrial dysfunction is not the cause of muscle fatigue symptomology experienced by CFS/M.E. patients.
• However, the results demonstrated there to be no evidence of elevated free radical generation when compared to control samples. This would suggest that the muscle fatigue phenotype exhibited in CFS/M.E. patients is not related to elevated oxidative stress at the isolated muscle cell level.

WOW...those are a lot of negatives...

They're also funding

• an autonomic dysfunction feasability study at Newcastle University - YAH!
• a study looking at severe paedriatic M.E.
• a study comparing patterns of mitochondrial DNA variation in people with M.E. and healthy controls - I don't think they will find anything
• further development of the M.E. Disease Register at Buckingham New University.

 

[Cort]

In the end they stated they will have to look elsewhere.....that's really something!

 

[Phil Hayward]

The Julia Newton study finding is not good news....If

This research project did not find any evidence of biochemical or metabolic dysfunction in muscle cell samples obtained from CFS/M.E. patients. This contrasts previous work that has reported muscle dysfunction in CFS/M.E. patients following exercise. Further investigations are required to determine the biological basis of fatigue in CFS/M.E. patients.”

In fact this study failed to replicate a bunch of what seemed to be important findings: no changes in pH, lactate plus no mitochondrial dysfunction or free radical generation
WOW...those are a lot of negatives...

They're also funding

• an autonomic dysfunction feasability study at Newcastle University - YAH!
• a study looking at severe paedriatic M.E.
• a study comparing patterns of mitochondrial DNA variation in people with M.E. and healthy controls - I don't think they will find anything
• further development of the M.E. Disease Register at Buckingham New University.

Yeah, but that is a comparison immediately post-exercise, against "healthy controls". How about at one day later, or one week later?

Of course this was regarding ME/CFS, not FM. My experience with FM which I believe is typical, is that actual physical problems in the muscle tissue can be felt by massage therapists and hands-on practitioners, and differences with healthy controls relates to response to treatment - which is absent with FM sufferers. If there is not any difference with muscle chemistry, some other mechanism needs to be found, but my hypothesis about muscle lubrication has strong explanatory power. In fact Devin Starlanyl references studies on chemical changes in the myofascial ground substance, which looks to be responsible for a lot (becoming sticky and glue-like instead of slippery). Maybe the change is limited to the myofascial ground substance, and actual muscle fibre is the wrong place to be looking?