The MEA Ramsay Research Fund is funding, or has been funding, four separate research studies into the role of mitochondrial dysfunction in ME/CFS and how it should be assessed - including the expensive commercial test you refer to
MEA funded research into the commercial mitochondrial function test:
http://www.meassociation.org.uk/201...-further-mitochondrial-research-20-july-2015/
The main problem here is that this expensive commercial test has not been validated by other independent researchers - which is why it is not used (and is normally dismissed) by NHS doctors who specialise in muscle and mitochondrial disease
The results from the research we have funded are now being analysed, along with some further laboratory work which has been done on this commercial test by two other independent researchers. The results will then be submitted for publication. Once the results have been published, the MEA will be making a further statement on this commercial test.
In our present state of knowledge, there is insufficient evidence to conclude that any of these commercial mitochondrial function test results are a reliable indicator of muscle or mitochondrial involvement or function in ME/CFS
And if mitochondrial function needs to be investigated, especially to rule out primary mitochondrial disease - which can be misdiagnosed as ME/CFS, then there are 'Gold Standard' NHS tests available (muscle biopsy, MRS etc)
So this is NOT a test that we can currently recommend or endorse
MEA funded studies into mitochondrial dysfunction:
www.meassociation.org.uk/2016/03/me-association-to-fund-fourth-study-into-the-role-of-the-mitochondria-in-mecfs-10-march-2016/
I would add that I have a deep personal interest in mitochondrial dysfunction having used my own skeletal muscle in the first research studies (which took place in the 1980s) to demonstrate evidence of mitochondrial dysfunction in ME/CFS. The first research, which I did with Professor George Radda et al at Oxford, and involved magneruc resonance spectroscopy, was published in The Lancet. The second, which involved electron microscopy of mitochondria from biopsy specimens, was carried out by Professor Mina Behan et al in Glasgow.
Dr Charles Shepherd
Hon Medical Adviser, MEA
Abstract from Lancet paper:
1984 Jun 23;1(8391):1367-9.
Excessive intracellular acidosis of skeletal muscle on exercise in a patient with a post-viral exhaustion/fatigue syndrome. A 31P nuclear magnetic resonance study.
Abstract
A patient with prolonged post-viral exhaustion and excessive fatigue (CS) was examined by 31P nuclear magnetic resonance. During exercise, muscles of the forearm demonstrated abnormally early intracellular acidosis for the exercise performed. This was out of proportion to the associated changes in high-energy phosphates. This may represent excessive lactic acid formation resulting from a disorder of metabolic regulation. The metabolic abnormality in this patient could not have been demonstrated by traditional diagnostic techniques.
Acta neuropathologica electron microscopy paper abstract:
Behan, W.M.H., More, I.A.R. & Behan, P.O. Acta Neuropathol (1991) 83: 61. doi:10.1007/BF00
Summary
We have examined the muscle biopsies of 50 patients who had postviral fatigue syndrome (PFS) for from 1 to 17 years. We found mild to severe atrophy of type II fibres in 39 biopsies, with a mild to moderate excess of lipid. On ultrastructural examination, 35 of these specimens showed branching and fusion of mitochondrial cristae. Mitochondrial degeneration was obvious in 40 of the biopsies with swelling, vacuolation, myelin figures and secondary lysosomes. These abnormalities were in obvious contrast to control biopsies, where even mild changes were rarely detected. The findings described here provide the first evidence that PFS may be due to a mitochondrial disorder precipitated by a virus infection.
