Assessing cellular energy dysfunction in CFS/ME using a commercially available laboratory test, 2019, Morten, Newton et al

Tiabuf said:
I do think people have rather jumped the gun
for interest ACKNOWLEDGEMENTS MEA (not a great ME advocate but better than- Afme (supported PACE & controversial NICE Guidelines) & MRC - Medical Research Council - see Simon Wessely - "Wessely was a member of the scientific advisory board between 2002-2012. Funders that Wessely has professional links to include The Wellcome Trust, MRC, King’s College London, ESRC, Mental Health Foundation and the Mental Health Research Network."
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I am unimpressed that the Opathy Association funds and Julia Newton carries out studies into 'CFS/ME', an entity which lacks defintion or ICD classification.
 
Annamaria said:
I am unimpressed that the Opathy Association funds and Julia Newton carries out studies into 'CFS/ME', an entity which lacks defintion or ICD classification.
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I'm waiting for confirmation but I would be hugely surprised if this wasn't solely down to Julia Newton's seeming preference for CFS/ME over anything else.
 
If you look in the name bar on the MEA web site you will see 'Myalgic Encephalopathy Association'. None of us has 'Myalgic Encephalopathy' as it has no definition or classification.
 
Annamaria said:
I fear you may be right. If so, why would the Opathy Association fund her research?
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Her use of a term that I, and many others, dislike doesn't necessarily mean her work on this paper is without merit. I also have faith in the standard of work done by the other named authors. If you have doubts about the conclusions of this paper please explain what you think they should have done differently.

Michiel Tack said:
I think the ME Association once suggested to use the term Myalgic Encephalomyelopathy instead of Myalgic Encephalomyelitis because the evidence for inflammation is uncertain. They helped fund this study, so I'm guessing that Opathy Association refers to them.
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From an article from 2010
The MEA has not consulted with, or written to the WHO on this proposal and myalgic encephalopathy is not listed in WHO ICD10. But this does not prevent doctors, people with ME/CFS, or official/government bodies using the term if and wherever they want to . The MEA and myself use both encephalomyelitis and encephalopathy. For example, I normally use encephalomyelitis when doing media work and in joint initiatives with other ME/CFS charities but tend to use encephalopathy when speaking to doctors. There is no intention to try and force people or organisations to use this alternative name. It has just been put forward as a proposal for discussion and a way of allowing doctors to use the term ME when they would otherwise refuse to do so because of the term encephalomyelitis.. But everyone is free to make up their mind on whether and when it would be more helpful to use either option.

I remain open-minded about what may be happening in the central and peripheral nervous system in ME/CFS. However, I do not believe that there is any robust research evidence, at present, to confirm the use of the term encephalomyelitis – inferring significant and active inflammation involving the brain and spinal cord. I believe that encephalopathy, meaning a significant abnormality in various aspects of normal brain function, is a more appropriate name to use in our current state of knowledge regarding the neuroscience of ME/CFS.
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https://www.meassociation.org.uk/20...yalgic-encephalopathy-on-the-new-mea-website/

it seems a fair point to me.
 
Multiple names and definitions have contributed to the mess we are in. Why add another when your object is to help patients?

Charles Shepherd says above, "I do not believe that there is any robust research evidence, at present, to confirm the use of the term encephalomyelitis - inferring significant and active inflammation involving the brain and spinal cord...."

There is the evidence from autopsies of eg Sophia Mirza.
 
Andy said:
Her use of a term that I, and many others, dislike doesn't necessarily mean her work on this paper is without merit.
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There is lack of congruence between the stated use of the CCC which define 'ME/CFS', and the paper's use of the term 'CFS/ME'. Thinking as muddled as that on basic terminology does not give confidence in the rest of the paper, plus adds more confusion to the literature.
 
The topic of this thread is the evaluation of a mitochondrial function test.

Views have been expressed about the name used for the illness in the paper and by the MEA. Further posts on these issues in this thread will be regarded as off-topic.
 
Both my aunt and daughter had these tests.
The results both correlated to level of disability.
Findings re low glutathione, B3, sodases tie into other research.

Others whom I have known had the same experience which does suggest that further exploration may be warranted.
 
InitialConditions said:
this is the original paper: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2680051/

Could problems with storage and sample time really account for the original results, which show clear demarcation between HC and PWME, and also strong correlation between degree of disfunction and illness severity?
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Myhill et al 2009 said:
Seventy-one patients, 54 female of average age 47 (range 14 to 75) and 17 male of average age 52 (range 20 to 86), were selected from a total of 116 consecutive patients attending a private medical clinic specializing in CFS/ME.
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This, presumably, is Dr Myhill's clinic in Wales? So the blood samples would need to be sent by post, unless patients had the blood draw done separately at Biolab in London.

The laboratory carrying out the tests (Biolab Medical Unit, www.biolab.co.uk) was blinded to the Ability associated with any blood sample.
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Blood samples from fifty-three normal, healthy volunteers were obtained by one of us (JMH) as Laboratory Director of Biolab until retirement from that position in 2007.
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So, JMH was "blinded to the *Ability*" (a mutually agreed number on the Bell Ability Scale, between patient and SM), but, surely, if the samples have been obtained in different ways and at different times, some by himself and others by the private medical clinic, he would know what was what. This wasn't a blinded study.

Can we assume control subjects attended Biolab in London, in person? Or might they have sent samples by post?

The samples from the patient group and the normal (control) group were processed in the same way.
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Hmm, I'm not sure about this... Were is the information on storage time, for patient samples vs controls?

The control group consisted of 40 females of average age 36 (range 18 to 63) and 13 males of average age 35 (range 18 to 65).
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Just adding that info for completeness.
 
I dont think Canadian Consensus Criteria are reliable but I have had this test a few times and feel I ought to speak about my experience to provide information for others to consider even if it is just another anecdotal account.

The first thing I ought to do is declare my interest which is that I depend on Dr Myhill's diagnosis to provide medical evidence for benefits assessment i.e. PIP and ESA. I don't know of another doctor in the UK who will provide a diagnosis as evidence and back it up with written statements as she has done for me, for which I am grateful. Other doctors I saw before finding Dr Myhill, who had diagnosed aspects of my condition had turned me down flat when it came to providing evidence for benefits assessment. This is my financially and politically influenced medical reality and an example of how the medical establishment closes ranks against ME patients in the face of uncertainty, with the exception of a few brave souls like Dr Myhill who has paid a price for nonconformity. So in my view she is a hero even if the mito test is an uncertain quantity. What is science about if not investigating the uncertain?

I had these mitochondrial tests (ATP translocation) from Dr Myhill and Drs McLaren Howard which provided evidence at one point along with cell free DNA tests for benefits assessment. To be honest at the time they provided really good value for money as they meant I could win the "card game" with the DWP who have twice now tried to unfairly and improperly disallow my claim and drop me in the meat grinder of coerced activity, which would be very counterproductive for me indeed as I have the real deal with PEM which can get very nasty for me.

However to be honest, the mito tests while at first consistent, later provided conflicting results after I gave up eating nightshades (as they caused mouth ulcers) since the mito test normalised while the cell free DNA test improved but was still outside normal ranges. However my ME CFIDS did not improve, in particular, I still had recurring virus and PEM (post exertion malaise) but the neutrophil mito test did not show abnormality any more.

This might be related to the fact my virus attacks were cyclical and I was just catching the cycle at the wrong time with the blood test; but its also possible nightshade vegetables contain toxins which can interfere with mito function. These are solanines, which can interfere with mitochondrial membrane function by opening the inner mitochondrial membrane pore, decoupling the mitochondria, releasing calcium and inducing apoptosis (see previous posts for more discussion of this at https://boolyblog.blogspot.com/). Once I stopped eating nightshades the mito tests normalised and the constant mouth ulcers induced by eating nightshades stopped. I also needed a lot more calcium in my diet to prevent muscle pain but apoptosis remained abnormally high and my CFIDS with PEM continued.

Yet I did have empirical photographic evidence of ongoing CFIDS. Since for purposes of full disclosure and open discussion, I had felt I needed empirical evidence for my doctors (including Dr Myhill and my GP too) and assessors because I was used to facing disbelief and a "turn down culture" of the DWP despite continual raging CFIDS. All I could provide to back up the high cell free DNA test and claims of CFIDS was dated (via newspaper headers) photographic evidence of my recurring virus, which is HSV2 in the context of prior severe EBV, to show that it still recurred 30 years after infection, which historically coincided with ME onset plus neurological plus TH2 shift symptoms i.e. classic MEA type London criteria viral onset. The evidence unequivocally showed an abnormally high frequency of viral episodes (imaging 10 of 13p/a) demonstrating I still had immune dysfunction symptomatic of CFIDS.

My feeling is the mito function test did record something which was abnormal and related to CFIDS but not causal of CFIDS but possibly secondary to it and alleviated by a nightshade free diet.

My comment would be that we need a reliable test for ME CFIDS and CCC aside, for the reasons given above IMHO we don't have one.
 
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