How research directions and patient experiences connect to the terms ME, CFS and future names

[Jonathan Edwards]

I raised the issue of ME terminology for a specific reason. It will mean that the people who can change things - funding authorities and service providers - will take no notice. They might not take notice anyway but I think a few could have had their interest piqued by some unexpected science - which we have on offer.

The reason why physicians will take no interest is because they know that "ME" was resurrected to sound scientific when in reality it was the opposite. We read regularly of young women who cannot barely cope with their tiredness due to Ehlers Danlos syndrome to such an extent that they can barely manage to compete in three day equestrian events. The press can do a huge disservice in this line, by feeding the public all the folklore stories, which any reasonably competent doctor know are nonsense. The tragedy is that someone like Beth should get caught up in this. Things are not black and white here.They are very messy.

I just can't understand why doctors would care so much about this. It comes across, frankly, as petulant. I would have thought everyone would care more about the patient's quality of life than what sounds accurate in a textbook.

My previous comment was open to misreading. This is not the situation. Doctors could not care less about names. It is the patients who care because they want something to cling on to. Doctors will care about a patient's quality of life irrespective of the diagnostic name. With ME/CFS it all hinges on whether they believe what the patient says. Some do, some don't. What doctors react negatively is the use of the ME name as a disease concept - because it is seen as a label used to appeal to bogus science to justify attention. Which it has been.

The arguments around folklore don't work either because all of that applies equally to the hybrid term ME/CFS.

I think they do. "ME" is entirely folklore. It is an artificial construct resurrected for political purposes. There is no scinetific literature on it. The literature on ME/CFS has become heavily tainted by that folklore but ME/CFS is also the preferred term for scientists now producing excellent work.

Do doctors reject DecodeME too because of its name?

I have not met a single doctor who rejects or even shows lack of interest in DecodeME but everyone is clear that the ME at the end is just a logo for a research project. This is not a serious argument for going back to ME.

As long as it is spelled out clearly in communication we are referring to the CCC/IoM syndrome referred to both as ME and CFS I feel like any sensible person clinician or otherwise ought to be open to listening.

But there is the world of difference between IOM and ICC. IOM is what we are studying. ICC is a bizarre pseudoscientific rationalisation with no legitimate. basis that was clearly part of the political push to 'scientise' ME. It may be the key source to the persisting ME folklore and biobabble.

 

[Jonathan Edwards]

I am also thinking we need a new term and that it is a pity that SEID was not so well constructed.

ME/CFS is hard to say and hard for patients to understand the rationale for. Cutting it to ME just as systemic lupus erythematosus is cut to lupus isn't a good option, much as as the lupus move would not have been good in the days when ordinary lupus (TB) was prevalent.

I ambeginning to think that we have enough evidence from Dinan, and maybe from Felipe here, to focus on the hypothalamic disturbance in ME/CFS and make it the core concept. Immune triggering, and perhaps continuing, events are important but they may be generic - we think lots of infections can trigger. In Reiter's syndrome the triggering agent is separated off from the syndrome itself. For narcolepsy everything changed with nailing the orexin cell defect. If we can nail. something similar in ME/CFS, even if it does not cover the immune preamble, we can give it a name.

 

[Jonathan Edwards]

A simple point is that a disturbance in hypothalamic pathways connecting to thalamus, sensory tracts and maybe things like nucleus accumbens would explain all the features of ME/CFS at one stroke. As some immunologists and psychiatrists in 2000 probably had worked out. They just did not think quite far enough out of their boxes,

 

[Jonathan Edwards]

The final practical point, which we have had before but is relevant here, is that the more people call for special ME services the more the NHS kneejerk will snap back to community-based BPS mutidisciplinary rehab. People with ME/CFS should be. seen in the same clinics as people with other sorts of fatigue, if only because until they have been seen nobody will know the right diagnosis.

 

[Sasha]

I am also thinking we need a new term and that it is a pity that SEID was not so well constructed.

ME/CFS is hard to say and hard for patients to understand the rationale for. Cutting it to ME just as systemic lupus erythematosus is cut to lupus isn't a good option, much as as the lupus move would not have been good in the days when ordinary lupus (TB) was prevalent.

I ambeginning to think that we have enough evidence from Dinan, and maybe from Felipe here, to focus on the hypothalamic disturbance in ME/CFS and make it the core concept. Immune triggering, and perhaps continuing, events are important but they may be generic - we think lots of infections can trigger. In Reiter's syndrome the triggering agent is separated off from the syndrome itself. For narcolepsy everything changed with nailing the orexin cell defect. If we can nail. something similar in ME/CFS, even if it does not cover the immune preamble, we can give it a name.

This is very exciting, because the name, whether it's ME, CFS, ME/CFS, has been a millstone around our necks for decades.

A simple point is that a disturbance in hypothalamic pathways connecting to thalamus, sensory tracts and maybe things like nucleus accumbens would explain all the features of ME/CFS at one stroke. As some immunologists and psychiatrists in 2000 probably had worked out. They just did not think quite far enough out of their boxes,

Even more exciting! What do you think it would take for us to get a name-change, and how far might we be away from that?

 

[Sasha]

A simple point is that a disturbance in hypothalamic pathways connecting to thalamus, sensory tracts and maybe things like nucleus accumbens would explain all the features of ME/CFS at one stroke. As some immunologists and psychiatrists in 2000 probably had worked out. They just did not think quite far enough out of their boxes,

Sorry if I've missed discussion of this but would it account for the two age peaks?

 

[Kitty]

Sorry if I've missed discussion of this but would it account for the two age peaks?

It might not have to, if the age peaks are about susceptibility to trigger infections?

 

[Sasha]

It might not have to, if the age peaks are about susceptibility to trigger infections?

I might well have missed a discussion of that, too! Do we think that there are two age peaks in trigger infections? If there were, wouldn't we see these two age peaks in infections in the general population too - for example, with Covid?

 

[neophyte32]

A simple point is that a disturbance in hypothalamic pathways connecting to thalamus, sensory tracts and maybe things like nucleus accumbens would explain all the features of ME/CFS at one stroke. As some immunologists and psychiatrists in 2000 probably had worked out. They just did not think quite far enough out of their boxes,

I really enjoy exploring broader hypotheses, and I think it would be interesting to start a discussion dedicated to this one, which strikes me as one of the most reasonable hypotheses at the moment.

We could bring together the findings from the buspirone challenge test, the work of Felipe Correa da Silva, whose results of course still need to be confirmed, as well as the data from DecodeME, while also awaiting the results from SequencEM.

I'd also really like to see you develop this hypothesis in a bit more detail. I think it would be particularly interesting for those of us who don't necessarily have your ability to synthesize information and draw connections between such different lines of research.

 

[Mij]

I think no one in the US knew anything about ME back then. I had never heard of ME when I started on this project. I think pretty much no one in the US ever used ME until the more recent period. It was always CFS, except for the early '90s when for a while it was branded as CFIDS.

I live in Canada and the ME specialist I saw in 1992 who co-authored the the Canadian Consensus Criteria gave me a diagnosis of CFS. He sometimes used ME and CFS interchangeably, the health code here was under "CFS", and my diagnosis still remains CFS today. I had no issues using CFS as a dx in the earlier years during appointments with specialists. It might be different today though because pwME/CFS want to avoid CFS like the plague.

 

[Jonathan Edwards]

Sorry if I've missed discussion of this but would it account for the two age peaks?

Peak infection exposure is a possible factor but I continue to think that the first peak is too early to based purely on EBV contact.

The hypothalamic model could account for the two age 'peaks' on its own, though. The adolescent period from 12-18, when the first peak occurs, is a time when the hypothalamus is endergoing major shifts in function. Puberty is one, with prolactin, FSH, LH and oxytocin all being relevant to pregnancy. Growth hormone stops driving continuing growth at this time and becomes an exertion response hormone. There is also a major shift in interaction with environment. Prolactin is said to confer child rearing behaviour in both sexes. I suspect what that means is that it is part of the shift from the child state of passivity and freedom from responsibility to an adult state of vigilant action and responsibility. I don't see that as directly relevant but it is further evidence for a re-wiring 'metamorphosis' of the hypothalamus which may make it susceptible to disordered function. A further observation is that sleep patterns go all over the place in adolescence and sleep control is closely linked to hypothalamus. Teenage years are almost like a chrysalis phase when everything is changing but the preference is sometimes for wrapping up in a cocoon. Again, I don't think that relates to ME/CFS directly but is another indicator that this may be a period of susceptibility to disordered control.

The second peak probably isn't really a peak. It would be consistent with an underlying tendency for disordered signalling to arise following a. disturbance, or spontaneously that can involve an accumulation of shifts over time but which isless likely to occur after 40 simply because by then the system is less open to new tricks and new mistakes.

 

[rvallee]

I'd say this is likely a UK-centric perspective. Don't think this necessarily applies across the board to doctors in the US--at least, if so, I haven't come across it.

Yes and it pretty much makes the point about how the whole ME thing is irrelevant. It only applies to the UK, no other country has this odd conflict over the history of how it was named ME, then not. And every country has the same complete disregard and negligence, whatever name they use for it. Some don't even have a name for it, or have completely folded the concept within their own preferred version of it.

In Canada very few physicians would even think of using any other term than chronic fatigue, wouldn't even bother adding syndrome. We don't have fatigue clinics or anything like that. No history of anything. Exact same situation: FUBAR. And I do mean exact, there is no difference whatsoever in how pwME are treated in Canada vs the UK, Australia, Norway or Japan. We are all abandoned, for the same reasons. The excuses and rationalizations might change, but that's all they are.

Excuses are not the same thing as reasons. There are no reasons anywhere for any of this, only excuses.

 

[Jonathan Edwards]

Moderation note: for context, this post (along with pages 1-9 of this thread) were split off from the thread
UK: Beth Dobbin -- BBC: The Olympic sprinter now bedbound for 22 hours a day

Yes and it pretty much makes the point about how the whole ME thing is irrelevant.

But it is no way irrelevant to this thread. This is a thread about an article in a UK newspaper in which a UK citizen is calling for the UK government to fund UK research intoME/CFS, which is currently the best there is but could be way better with another £15M. She is also calling for better care in the UK from this government.

And the people who the government will turn to, to generate a response, will not take a blind bit of notice of anything labelled "ME". Except of course the rehab people who are only too happy to expand their empires.

 

[neophyte32]

Personally, I completely understand the debate around the name of our illness, because it's an additional burden in itself, at least here in France.

I've repeatedly noticed that doctors struggle to take us seriously as soon as we mention chronic fatigue syndrome or myalgic encephalomyelitis. More than once, I've been told: "But you don't have encephalomyelitis or myalgia!" And to be fair, it's difficult to blame them for pointing out the inconsistency.

I really think changing the name of this disease is essential. We simply cannot continue calling such a debilitating illness by names that reflect neither its clinical reality nor the severity of its symptoms.

In France, I even get the impression that doctors would rather use the term Long Covid, which has become much more familiar, than myalgic encephalomyelitis, a name they often consider medically unjustified. As for "chronic fatigue syndrome", it's probably one of the most damaging names imaginable. It reduces a potentially devastating disease to mere tiredness and contributes to the lack of credibility we face, particularly in the media and among the general public.

So how are we supposed to move forward? We're stuck in a vicious circle: the disease is poorly understood, its name reinforces that misunderstanding, and that misunderstanding in turn prevents it from gaining proper recognition.

In short, we're going round in circles, and meanwhile, patients continue to pay the price.

 

[Jonathan Edwards]

What about:

Syndrome of Exertion Intolerance with Hypothalamic Dysregulation
SEIHD

You cannot say that doesn't sound scientific and serious and it is based on documented fact.

I tend not to like dysregulation when it is used just to dress abnormal some abnormal measurements. But in this case it is a valid description because the experiments show abnormal responses in regulatory hormones to defined stimuli.

It might be jumping the gun a bit but it is the best I can do this afternoon.

 

[neophyte32]

Hypothalamic Exertion Intolerance Syndrome (HEIS)
Emphasizes the possible role of hypothalamic dysfunction in the body's inability to tolerate physical and cognitive exertion.

Hypothalamic Post-Exertional Dysregulation Syndrome (HPEDS)
Focuses on the hypothesis that hypothalamic dysregulation contributes to post-exertional malaise (PEM) and the body's abnormal response to stimulation.

 

[Sasha]

What about:

Syndrome of Exertion Intolerance with Hypothalamic Dysregulation
SEIHD

You cannot say that doesn't sound scientific and serious and it is based on documented fact.

I tend not to like dysregulation when it is used just to dress abnormal some abnormal measurements. But in this case it is a valid description because the experiments show abnormal responses in regulatory hormones to defined stimuli.

It might be jumping the gun a bit but it is the best I can do this afternoon.

I like it, or the variants that @neophyte32 suggests but how do name-changes come about for diseases? What hoops have to be jumped through, and are we in a position yet to jump through them?

 

[ScoutB]

Sorry if I've missed discussion of this but would it account for the two age peaks?

I don’t think we know enough about the hypothalamus yet to really say, but maybe a point in this direction is that narcolepsy (with its loss of Orexin in the hypothalamus) may have two age peaks as well.

 

[neophyte32]

I like it, or the variants that @neophyte32 suggests but how do name-changes come about for diseases? What hoops have to be jumped through, and are we in a position yet to jump through them?

I'm not a scientist, and I don't have much experience in this field, but I think the only thing that will really lead to a change in the name of our disease is solid, reproducible scientific evidence that is difficult to dispute.

We'll probably have to wait another two years or so to see whether Da Silva's findings are replicated, whether DecodeME's analyses reveal anything significant, and whether SequencEM starts providing some promising leads. We could also add the research involving the buspirone challenge test. Who knows, perhaps all these findings will eventually point in the same direction?

But without sufficiently robust scientific evidence, I find it hard to imagine a new name being officially recognized and widely adopted by the medical community.

 

[Robert 1973]

I’m hopeful that within the time it would take to change the name we will have enough understanding of the mechanisms to call it something more precise. In the meantime I think we should make do with ME/CFS.