ME Association’s contributions towards mitochondrial muscle research in ME/CFS | 17 May 2016

May 17, 2016

MEA OMEGA talk May 10th copy

The ME Association is heavily involved in medical research that is exploring whether there are faults in mitochondrial muscle function that can be linked exclusively to ME/CFS.

Following our joint meeting last week at the John Radcliffe Hospital in Oxford last week with the Oxfordshire ME Group for Action (OMEGA), where there was a talk by Dr Karl Morten on his current research into the subject, you can find a YouTube video of Dr Morten's presentation by clicking on this link:

[Before watching this video, turn the volume up fairly high to listen to it comfortably.]

And his slide show can be downloaded HERE.

The talk discusses in easy to understand language what the mitochondria actually get up to, and the new research study into mitochondrial dysfunction in ME/CFS that is being funded there by the MEA Ramsay Research Fund.

Link to paper on viral infection and mitochondrial dysfunction that was referred to by Dr Morten:

From the abstract:

“Furthermore, we demonstrate that herpesviruses induce mtDNA stress, which enhances antiviral signalling and type I interferon responses during infection. Our results further demonstrate that mitochondria are central participants in innate immunity, identify mtDNA stress as a cell-intrinsic trigger of antiviral signalling and suggest that cellular monitoring of mtDNA homeostasis cooperates with canonical virus sensing mechanisms to fully engage antiviral innate immunity.”

This meeting – which also included the film ‘Forgotten Plague'– was organised and paid for during ME Awareness Week by the ME Association and OMEGA (Oxfordshire ME Group for Action)

The MEA Ramsay Research Fund is the major funder of mitochondrial function research and is funding/has been funding the following three further studies into mitochondrial dysfunction:


Employing new technology, this research aims to demonstrate that skeletal muscle mitochondria are dysfunctional and cause the muscle fatigue experienced in ME/CFS:

‘The dysfunctional mitochondria then activate a process which leads to a chronic, low grade inflammation, commonly reported in patients with CFS, which in turn results in further mitochondrial abnormalities and the establishment of a vicious circle of events. Understanding the processes by which muscle fatigue occurs will lead to optimal interventions that break this vicious circle and improve muscle function and wellbeing of individuals.’

Extract taken from: Medical Research Council CFS/ME Current Projects

Preliminary results from the study were published in a recent paper: ‘The Role of Cytokines in Muscle Fatigue in Patients with Chronic Fatigue Syndrome’, The FASEB Journal, April 2015.

The authors recruited 100 untreated patients with CFS and 100 age and sex matched healthy controls, and concluded:

‘…a sub-group of patients with CFS may have low-level inflammation and analyses are underway to further characterise other inflammatory markers in serum and muscle of these patients and to determine whether such changes could affect indices of muscle function or central fatigue.’

Lead researcher: Professor Anne McArdle

This research is being jointly funded with the Medical Research Council

Investment by the MEA Ramsay research Fund = £30,000


This study will be comparing the results of a commercial blood test for mitochondrial function that has been developed by Dr Sarah Myhill and colleagues with the results from an international and widely accepted test of mitochondrial function which has a long and successful track record in clinical diagnosis and research of muscle disease particularly in the UK.

The aim is to determine the efficacy of each set of tests in relation to ME/CFS. In the exciting case that a synergy between the two diagnostic approaches exists, it is hoped that this preliminary study will promote an investigation into a more inclusive and highly resolved analytical technique for metabolic testing of people with ME/CFS.

Lead researcher: Dr Sarah Jayne Boulton

MEA Ramsay Research Fund investment = £21,305

MEA website information HERE


This is an 18-month study that began in May 2014 and seeks to determine if patterns of mitochondrial DNA variation in ME/CFS are different than in healthy controls.

At the launch of the initiative, Dr Joanna Elson commented:

“Mitochondria are the powerhouses of the cell, and mitochondrial DNA provides the codes for proteins that are essential for energy production. We want to see if patients with ME/CFS have different patterns of mitochondrial DNA variation that could affect a person’s chances of succumbing to ME/CFS, or act as a barrier to recovery.”

Lead researcher: Dr Joanna Elson

This research is being funded by Action for M.E.

Donation from the MEA Ramsay Research Fund = £5,000

Dr Charles Shepherd
Hon Medical Adviser, ME Association

4 thoughts on “ME Association’s contributions towards mitochondrial muscle research in ME/CFS | 17 May 2016”

  1. It’s good to see that Norman Booth’s long-running efforts to drive this strand of research forward and to get other researchers involved, are now starting to bear fruit.

  2. I am so glad to see this vital research funded by MEA. Thank you. Many years ago, in the 1980’s, a time when so many of us long-term pwME were getting sick, Professor Behan found mitochondrial abnormalities in patients.
    Then, of course, as we know all too well, some rather vocal little psychs, some cost-cutting governments and some private medical insurance companies concocted a long-running soup of obfuscation as regards to all things ME, and so much promising biomedical research of the 80’s and early 90’s seemed to disappear into the ether.
    Such a huge relief to see research like this latest mitochondrial work go ahead. If the government had funded this instead of £5m being woefully squandered on PACE, a lot of very ill people might have had the chance of getting their lives back.
    As a patient of Dr Sarah Myhill, and having taken the test she uses (it showed malfunctioning mitochondria), I am particuarly interested in these new studies.

  3. As inorganic Red Cell Phosphate levels are also routinely elevated in ME patients, this suggests that glycolysis is also affected in this disorder.

    Please note:
    Red blood cells have no mitochondria and if there is an increase in red cell phosphate (which is readily demonstrable), then the intracellular combining of inorganic phosphate with ADP to form ATP must be defective via, and only via, an intrinsic defect in glycolysis in such cells.

    Dr John L Whiting
    Brisbane, Australia

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