The use of the labels ME, CFS, ME/CFS

Sasha said:
Sounds as though having a website front-end is in the pipeline but what Evergreen is suggesting sounds very much like a new factsheet which I would have thought could be knocked out quite quickly (by you, anyway!).
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I’m thinking more of a community FAQ than a factsheet. It could be broken up into more manageable bitsize bits, making it easier to produce as well as consume.
Sasha said:
Once your factsheet for health professionals is ready, I'm hoping that that will be a very clarifying and helpful set of information for PwME that we can disseminate widely - especially if charities take it up and spread it themselves.
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Agree we also need that and am looking forward to it and being a le to share it.
 
Jonathan Edwards said:
I think that is uncalled for Adrian.
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[edit] Ok my working was unfair. But I think you have made your views clear on including people with lived experience in research and that you are against it. I think you have stated that a number of times.

Jonathan Edwards said:
The 'lived experience' people seem to feel we should just sit and listen to their stories. There is a place for that in moral support but it has nothing to do with research. The problem with ME/CFS is not that clinicians have not listened. The problem is that they have misinterpreted what they heard. And the reason we did not have good research is not because we did not take the 'lived experience' as hard evidence. God forbid that we should use it as evidence of causal relation - which is always what is implied in these contexts. We need proper trials, not PACE on naltrexone with n=1.
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That is the point about having PwME involved so that wrong impressions can be corrected as part of the research process (also so that poor processes aren't designed - for example ensuring trials are physically accessible to patients). No one is suggesting using things patients say as evidence of causal relationships - or no one that I have heard - I think that is an interpretation you are placing on it.


Equally no one is suggesting that LDN with n=1 is evidence - those pushing for the repurposing of drugs trials are pushing hard for well run trials (and with mechanistic components). They are also saying that they could be very challenging given the difficulty of subtyping and that LDN is likely only to work for a (potentially small subgroup).

Jonathan Edwards said:
The Showcase meeting was, I had thought, about bringing in new researchers, as you have always emphasised. It turns out that NIHR and MRC had no intention of telling anyone about it other than the usual ME/CFS cronies who wanted to feel they were being listened to.
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I think the showcase event was about the MRC saying they were doing something - and it was all they would do - even then they left it up to the NIHR. It was an opportunity to bring other people in but the NIHR organized it and I don't think they achieved that - but I don't know as I wasn't able to attend in person and they wouldn't share the invite list.
I suspect it was a lost opportunity as you suggest - If it were up to me I would have run a very different event. I do think starting with patient experiences is useful - especially with new people as they don't know the level of suffering or the symptoms (and I think PEM particularly makes ME interesting) - I would see that as a backdrop to why it is an important area and an interesting area to study. For example, Ian Bruce did run a workshop on PEM and I think the patient experience at the beginning really did set the scene as to the problem (followed by some interesting talks).
 
I've just happened to look at the ME Association's article 'LONG COVID AND ME/CFS: Are they the same condition?'

it's full of stuff about mitochondrial dysfunction, dysregulation of the HPA axis, microclots, persistent viruses, and so on. I don't know how patients are supposed to know that these ideas aren't watertight (and will result in clinicians believing they should be shunned) when the major patient charity is publishing them.
 
Eleanor said:
I've just happened to look at the ME Association's article 'LONG COVID AND ME/CFS: Are they the same condition?'

it's full of stuff about mitochondrial dysfunction, dysregulation of the HPA axis, microclots, persistent viruses, and so on. I don't know how patients are supposed to know that these ideas aren't watertight (and will result in clinicians believing they should be shunned) when the major patient charity is publishing them.
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They also recommend pacing up:
The aim of pacing is to find a stable baseline of activity and avoid ‘doing too much’ on one day and then feeling unable to do anything the next, due to increased levels of fatigue and other symptoms. Once the situation has stabilised any increase in physical or mental activity needs to be gradual and flexible and allow for the fact that progress is still likely to be erratic.
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That publication is one of the things that contributed to me continuing to do far too much with my post-covid ME/CFS because I was «stable» at a very high symptom baseline (from constantly triggering PEM).
 
Eleanor said:
I've just happened to look at the ME Association's article 'LONG COVID AND ME/CFS: Are they the same condition?'

it's full of stuff about mitochondrial dysfunction, dysregulation of the HPA axis, microclots, persistent viruses, and so on. I don't know how patients are supposed to know that these ideas aren't watertight (and will result in clinicians believing they should be shunned) when the major patient charity is publishing them.
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Mentioning these ideas may get patients shunned by some clinicians, but in my experience, the clinicians are more likely to be the ones advancing these ideas and patients more likely to be shunned for questioning or refuting them.
 
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