CFSME ATLAS site
- Thread starter Dolphin
- Start date
No worries!
Utsikt
Senior Member (Voting Rights)
Velkommen! I hope you join us.
I think that having a searchable repository of ME/CFS research that’s tagged according to inclusion criteria, topic and so on is valuable no matter what.
The thing that might do more harm than good is when claims made in papers are presented as fact when they very often don’t hold up under scrutiny. Even lots of established truths are simply false.
With LLM specifically, there’s also the issue of hallucinations etc. that might end up spreading (slightly) wrong information that requires lots of effort to catch and correct.
Me too. I've split it in the thread title.
I agree. Looking back, I was testing things and chose the name a bit too quickly. I may be able to change it later if people seem to find the site genuinely useful.
I am paying for it myself. I can manage that, but probably not for long if the site is not good enough to justify it. Still, I think we are not far from a point where systems like this will be able to do this extremely well with the right setup.
For now, I see this as version 0.1. Perhaps the right setup could eventually be developed in a group like this. I would be happy to build it.
I could share the setup I have today here, if that would be useful, and people could then give their input. It may be that this version is good enough to refine and harden, or it may be that a fresh start would be better.
Felis Catus
Senior Member (Voting Rights)
Why CFS/ME and not ME/CFS? Is it like that in Norwegian?
Yes..
Agree.. was reading MEAT, and MECFSAtlas would be better!
Good to see the effort and welcome to forum! Best of luck w the project..
rvallee
Senior Member (Voting Rights)
Hi and welcome. Don't be put off by the criticism, it's what we do here, and it's all meant in a constructive way. Brief and direct aren't meant to be rude, some of us struggle a lot with brain fog and sometimes that gets confused as a bit mean. As you have noticed over the years, the literature on ME/CFS is a mess and so with that comes a lot of repetitive criticism. It's not always easy but we have seen a lot, and always try to make other people's projects better for it if they are willing.
I think this project is something that could be useful, and opinions vary among forum members on the usefulness of AI to achieve this, but what matters most here is that AI is not a fixed thing, it will get better, and having a strong foundation for this can become very useful over time.
I hope you stick around. This forum has many goals, from simply being a support community (no medical advice, though) to being hopelessly annoyed at the low quality of research and the lost opportunity that LC has represented. There isn't a more rigorous community dedicated to improving the science of ME/CFS out there, at least not that we are aware of.
rvallee
Senior Member (Voting Rights)
By the way, there are several threads relevant to Norway, if you haven't found them yet. Several things going on right now, with a guidelines project that isn't doing great, a disability law case that rendered a verdict recently involving, somehow, the head of Norwegian medical research, and quite a lot going back years.
Many of them can be found by searching for Norway, and we have regional threads that sum up things happening in either one or a few country, lumped up in Scandinavia here: https://www.s4me.info/threads/news-from-scandinavia.647/.
Jonathan Edwards
Senior Member (Voting Rights)
Norway has actually produced much of the best innovative science in ME/CFS - epidemiology and Fluge and Mella's work. The Norway Health Institute is 'behind' the UK NICE guidelines maybe but our College of Physicians takes much the same view as the Norway Institution under Signe Flottorp. So the 'establishment view' is pretty behind everywhere.
You might think that Norway is behind the USA but I don't think the sort of view espoused by the Bateman Horne Centre and by high profile science Twitterati in the US is 'ahead'. If anything it is seriously out of date and misleading. This is the stuff i think you need to be wary of. CPET does not 'measure PEM' and the evidence for neuroinflammation is essentially zilch. The immunology is confused and hyped. This stuff is in a sense just as much of a problem as the psychiatric stuff because it distracts everyone from finding the real problem.
Yes, I know about the good work, but it's quite divided. Media is dominated by a small and loud group of psychosomatic believers, and has been for the last 15 years or so. They are also at the table of governmental decision making.
Utsikt
Senior Member (Voting Rights)
No, it isn’t. Check the recent guideline draft or the publications from Haukeland. ME/CFS is the standard in Norway today. The only ones using CFS/ME are the psychosomatics.
Edit: most Norwegian patients use ME, but they are slowly transitioning to ME/CFS.
Thanks, just a quick followup. What do you think the real underlying mechanism is more specifically? When you say CPET does not measure PEM, do you mean it has no real value at all, or that it only captures part of it? And when you say the evidence for neuroinflammation is basically zilch, what standard of evidence are you using there, and which studies do you think are most often overinterpreted?
Jonathan Edwards
Senior Member (Voting Rights)
I wish I knew but I have a rough idea of what sort of thing it might be. The link to viral infection suggests to me that immune signals such as cytokines are being generated as part of an immune response and that for some reason these persist. My work in the past was on autoimmune diseases and we have a reasonably good idea how persistent signalling can be set up for those, but involving specific autoantibody. We also know that persistent signalling can occur in autoinflammatory disease like psoriasis without involving antibody.
There are likely to be other possible mechanisms for aberrant eprsistence of immune signals. But they do not need to involve inflammation. Lots of autoimmune diseases are not primarily inflammatory. Moreover, if signals are very local and act perhaps directly on nociceptor nerve endings there would be nothing to find in blood and markers of circulating cytokines like CRP would not go up.
I have put together one potential model which we published in the open access journal Qeios - invoking gamma interferon. it was just an example. Another member here is keen on type I interferon signls (alpha or beta). Either seem plausible.
I also think we have to accept that some long term shift can occur in central nervous signalling - that might be in eresponse to interferons initially and fail to switch off. Again, there is no need to invoke inflammmation. Cytokines and neural signals can produce symptoms without generating inflammation.
The shift on the second day CPET seen in some people with ME/CFS is not measuring PEM as such because PEM is defined as an increase in a set of symptoms. If someone has PEM from day 1 they will feel dreadful before trying another CPET. (I find it hard to see how anyone with significant PEM could even try the second CPET.) The second CPET measures a shift in physiology that may reflect the existence of worse symptoms but it is unclear what it shows us. One possibility that seems likely is that if you feel awful you are less efficient trying to do work with muscles because the nociceptor signals block you from using muscle efficiently. So maybe the second CPET just relfects what we already know - that some people are feeling rotten.
This is fairly easy because if you have even very mild inflammation in the brain you tend to be comatose or appear to have a stroke. The brain does not tolerate inflammation at all well. The term 'neuroinflammation' is new and nobody really knows what they mean by it. It is mostly used by people with no training in tissue pathology who like buzzwords. In very simple terms we know that there is noovert inflammation in the ME/CFS brain because a simple MRI fails to show increased water content of tissue - which is the hallmark of even mild inflammation.
Sometimes neuroinflammation is used to imply microglial activation. That can occur without other aspects of inflammation like increased water content. But in most cases it accompanies other pathologies probably as a a repair response - in things like Alzheimer's or Parkinson's. It is misleading to talk of those as neuroinflammatory. In ME/CFS there was a study by Nakatomi that was reported as indicating microglial activation. When I saw the pictures my impression was that it was likely a claibration shift than any real biological result but I was prepared to accept that it might mean something. Subsequently, however, studies have not replicated Nakatomi's finding. Another recent study initially reported as showing inflammation actually seems to show the reverse - as members here worked out by carefully looking at the data.
Other people like Younger and Van Elzakker constantly talk about neuroinflammation but I don't think we have actually seen any results from them that show that.
So in summary there is no evidence for neuroinflammation. You might ask why so many people say there is. I think this simply reflects the continuoing confusion with "myalgic encephalomyelitis" which was a term coined to describe an acute epidemic illness that seemed to have signs of local brain damage, like weakness or loss of sensation in an arm or leg. That then got confused with a persisting illness that seemed to follow in some of these cases which Ramsay called 'chronic M.E.'. But chronic ME did not have the signs of local brain infalmmamtion. The whole history is one of garbled confusions that got perpetuated and re-invented by the 'International Consensus Criteria' for 'ME'. We have long discussion threads about these things here.
ME/CFS is a very real illness but has nothing to do with encephalomyelitis as far as we know, other than perhaps one of the infections it can follow was misdiagnosed as en encephalomyelitis in the 1950s.
Thanks for such a detailed and thorough reply. Very interesting, and intuitively a lot of it seems quite reasonable to me.
I think the distinction you make between persistent immune signalling and actual inflammation is especially useful, and also the point that very local signalling could still produce major symptoms without obvious blood markers.