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

[Hoopoe]

The hypothalamic dysfunction makes sense. In my case symptoms were initially interpreted as indicating a pituitary, adrenal or thyroid disorder. There were some abnormalities, but not consistent with any specific diagnosis in this category. At the time the symptoms and abnormalities included unrefreshing sleep, mildly low blood pressure, initial orthostatic hypotension, episodes of mild hypoglycemia, fatigue, low stress tolerance, abnormal diurnal cortisol curve, a tendency to crash after trying to resume normal activity levels and responsibilities, poor thermoregulation. I also experienced symptoms that were more typical of a mood disorder like social withdrawal, depressive mood, and outbursts of anger but I view these more as reaction of an adolescent to the adverse situation represented by the illness itself and the experience of not being understood.

Also I have an empty sella which may be relevant. During an ACTH stimulation test I had a panic attack which indicates an abnormal reactivity of some kind. I read this can be either hypothalamic in origin or due to increased receptor sensitivity.

 

[Tom Hill]

Which might bring in age-dependent instability of hypothalamic co-ordination

But if this were the cause of why people tend to get me/cfs as adolescents or circa 40 (or, in another interpretation, why rates drop off after 40ish, rather than peak strictly speaking) then we’d see a lot more me/cfs onset from a much wider range of viruses, wouldn’t we? As they would all set up the hypothalamic reset challenge, I’d imagine. A specific set of neurotropic viruses seem in a class of their own in me/cfs onset.

 

[Mij]

It always just makes me think of the French énervé (annoyed) and ça m'énerve (that p****s me off, that drives me mad).

Exactly what I interpreted until I looked up enervate.

Comment calmer une sensation de malaise? oof

 

[Jonathan Edwards]

The members here who seem confident that studying the immune system further is a waste of resources

I think, to be fair, people are against studying aspects of immune responses that already look very likely to be blind alleys.

 

[V.R.T.]

I think, to be fair, people are against studying aspects of immune responses that already look very likely to be blind alleys.

I'm against that too! Although perhaps we might not all agree on what the blind alleys are likely to be...

 

[Jonathan Edwards]

we’d see a lot more me/cfs onset from a much wider range of viruses, wouldn’t we? As they would all set up the hypothalamic reset challenge, I’d imagine.

Maybe we do. Maybe the focus on EBV is heavily biased by how dramatic that can be and the fact that there is an antibody test (which doesn't discriminate very well between recent and old infection). It does seem likely that EBV is particularly prone to trigger ME/CFS but that might simply be because it produces very high and repeated fevers. It also leads to major CD8 cell recruitment directed at self B cells. The hypothalamus may well be susceptible to signals from those events. But it may also be susceptible to concussion, or other things.

 

[Tom Hill]

Maybe the focus on EBV is heavily biased by how dramatic that can be and the fact that there is an antibody test (which doesn't discriminate very well between recent and old infection). It does seem likely that EBV is particularly prone to trigger ME/CFS but that might simply be because it produces very high and repeated fevers.

That’s very interesting that EBV’s importance may be a mirage. But that’s a really big and powerful mirage given, for adolescents, the phrase “she/he’s not in school due to glandular fever” is essentially synonymous with “due to me/cfs/PVFS”.

And then there’s the big surge that’s come with COVID. Don’t think we’ve seen me/CFs surges during unusually bad flu seasons, for example.

I got dengue fever on field work once, and it had an unusually high fever sustained for an unusually long time. I could just be a random piece of data, of course, but it didn’t bring on me/cfs in my case, and I don’t think it’s been noted anywhere as a known me/cfs onset disease. Both my confirmed covid infections [the first of which brought on me/cfs] didn’t involve high fever.

 

[Mij]

Both my confirmed covid infections didn’t involve high fever

Incase you're interested, we have a thread on Lack of Fever during infections

I never had a fever during sudden-viral onset ME or Covid. During sudden-onset a viral infection attacked my thyroid, fever is a big symptom, but I didn't have fever at all.

 

[obeat]

I think a couple of members have alluded to drug/ alcohol addiction as triggers,?

@Tom Hill

Thread 'CFS/ME is associated with pandemic influenza infection, but not with an adjuvanted pandemic influenza vaccine, 2015, Magnus, Hornig, Lipkin et al'

Feb 24, 2020

Magnus P1, Gunnes N2, Tveito K3, Bakken IJ2, Ghaderi S2, Stoltenberg C2, Hornig M4, Lipkin WI4, Trogstad L2, Håberg SE2.

Abstract
BACKGROUND:
Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is associated to infections and it has been suggested that vaccination can trigger the disease. However, little is known about the specific association between clinically manifest influenza/influenza vaccine and CFS/ME. As part of a registry surveillance of adverse effects after mass...

• Hutan
• 2015 flu hornig lipkin magnus me/cfs norway paper vaccination
• Replies: 8
• Forum: ME/CFS research

• 

 

[leahcarn]

To bring the topic back around to the name, PCOS -> PMOS is one I can think of that has changed its name recently to reflect a better disease understanding.

What worked? What didn't? And do they get away with having more than two words by having a workable acronym?

 

[Peter T]

It may be just me, but in case anyone else struggles with acronyms:

Polyendocrine metabolic ovarian syndrome (PMOS) — formerly known as polycystic ovary syndrome (PCOS)

 

[N_Dina]

It may be just me, but in case anyone else struggles with acronyms:

Polyendocrine metabolic ovarian syndrome (PMOS) — formerly known as polycystic ovary syndrome (PCOS)

I slightly digress but I read an endocrinologist’s opinion, that this name seemed to be so confusing (for doctors, at least at first), as the first part resembles autoimmune polyendocrine syndrome. And from the patient’s perspective PMOS may also sound more intimidating in comparison to PCOS (but this is just personal opinion, although I am diagnosed with PCOS).

 

[Midnattsol]

To bring the topic back around to the name, PCOS -> PMOS is one I can think of that has changed its name recently to reflect a better disease understanding.

What worked? What didn't? And do they get away with having more than two words by having a workable acronym?

We don't know if it has worked yet. To take an older name change: diabetes is in Norway also known as "sugar disease". This is years and years ago, and the name change to diabetes has been wanted in part due to the stigma stemming from others believing you're sick because you ear too much sugar.

Type two diabetes was simply called "old man's sugar disease" because it was more common in the older population, while kids with diabetes had "children's diabetes" or more correctly type one/the autoimmune variant. When I say previously I mean this is what my mother was taught some 50+ years ago at nursing school.

Still today we have problems with adults with type one diabetes coming to hospital and being given the wrong treatment because hospital staff go "oh, an adult! Then it is diabetes two!", or kids with type two diabetes getting the wrong treatment because staff go "oh, a kid! Then it must be type one!". Not to mention the general public (and some literature used for teaching staff!) may still use the terms sugar disease, old man's diabetes and children's diabetes (though there are people who go about making authors aware if they find such terms used and seemingly making headway, I can't remember seeing them in my clinical learning material).

Stigma from misconceptions based on the name is still prevalent today. Patients with type one diabetes report more stigma from others, likely because they are more visibly ill. For example being in need of injections. Since the illness is caused by eating too much sugar, the people who are the most visibly ill are obviously those with the worst diet and it's their own bloody fault for being ill.

Name changes take time.

 

[Utsikt]

I fully agree that could be the case. I’m disinclined still to drop a potential immune system role in PEM onset because of 1) the sickness state just being so core across cases, and how it gets flicked on, fades, gets flicked back on etc;

That can all be explained by the brain.

2) people with PVF seem to go through what pwME/CfS go through, they just get over it within 6 months (which looks like a sustained immune response but which is then not retriggered);

Why can’t it just be a loop in the brain? If it exists for ME/CFS, it can be made use of for other diseases. Or PVF is just short-lived ME/CFS of sorts. Who knows. And why can’t we find very much evidence of a sustained immune response in LC?

3) the delayed onset characteristic of PEM might be easier to explain if there is a neuro-immune interaction, with, say, a neurological trigger acting on the immune system that then later causes the PEM onset;

Why can’t the delay happen in the brain and any immune interaction just follows the regular time course for that immune mechanism? And lots of the symptoms only exists in the brain, there’s no need for a detour to the rest of the body first.

4) signs there may be a kind of “combination lock” process needed to activate PEM, which might be why trigger mechanisms mysteriously vary from incident to incident, which sounds like the immune system and its need for multiple signals from several sources to get an activation.

That’s exactly how the brain works as well.

None of this rules out the immune system, but the dynamics do not require the immune system.

 

[bobbler]

I am saying that it is almost certain to have no effect if couched in term sof "ME" because that is an automatic off switch for everyone who might have the power to help. It would have been brilliant if instead of referring to ME it referred to ME/CFS and instead of the old stuff about complex neuroimmune disease and affecting lots of systems it said 'for which we now have major new evidence of biological origin within the nervous system' or something.

With that change in words people who sit on MRC committees or Royal COllege of Physician committees may just possibly thinkg "Oh, that's intriguing, maybe there is something to this after all'. Or their spouse or young medical daughter may say to them "Did you read that thing in the Times, mum, it made me think; what do you think".


It looks as if ME/CFS is neural. The immune bit looks uncertain. Even BTN2A1 may be a CNS marker. Yes, neuroimmune is sort of backed up, but as it stands 'neuroimmune' will be read by the committee member as the same old fairy story about ME, which was another disease in another century that never was and never had the neuro bits claimed. Without specific reference to the new completely different evidence for a neural basis there will be no connect. If the piece said why the genetics was so exciting and why Sequence is needed to build on Decode - in the very simplest terms - it could have hit the mark.

Nobody is denying that Beth's attempt to get attention for ME/CFS is brave and worthy. It is just a question of having some hope of it working.

And yes, ME/CFS is the least worst available, but it was not used.

I agree when put that way. It is a shame if there is such a conditioning/aversion issue that noone we might need to be behind changing the guard on gets past the first point where the name is listed ie 'a switch off issue'. People who might sit on ethics boards for whatever research we do or don't want signed off or be a bystander in a medical context we need to move from following the old herd to slowly another place. Or just those in training who think 'that doesn't apply to me' because they put it under 'functional medicine' etc.

I think if this is moved to another thread it should be one specific to the article (and applicable to future ones) and based on a term like marketing or communications of the condition planning/issues/topics discussion

That also sounds very smart from a 'getting those in the general public who might become allies' perspective too. Particularly if the level is got right so that we don't get the equivalent of people who switch off when someone mentions statistics methodology (the issue with how to mention the bps stuff). The odd person might look up one gene out of curiosity, but not if they see 5 and think it is a task beyond their capacity.

Because, particularly when times are hard for all and there is a lot of miserable stuff going on, there is a big difference between supporting something that is reporting good new developments. I think there are more people than we think who can spot generic blurb rather than intentional context that might be summarised or given in short.

And it also stops people who might well know nothing but still feel bombarded with 'yep we know, there's loads of em who are stuck in bed' to actually read the detail. If early on there is something slightly specific and different along these lines rather than phrases we might think sounds dramatic to others but whether they do or not is at best just telling them 'look at these sick people' and sadly a lot of readers don't necessarily have the response to it that you'd want, and there is the 'so what' factor even from those whose day has been ruined if they are that empathetic but can't actually do anything with it.

Plus there are the people who like being smart. And sounding smart. Who know generic descriptions are just terms used from a 'seeming politically correct' perspective, but firstly don't mean much to anyone and are not from a science perspective a conversation starter. Such developments might, for example, be interesting whether you care specifically about ME/CFS or not initially because of that bigger picture aspect of it being a finding and how does it fit etc.

Some people might look up 'who is this research group', others might look up who is this athlete or google to find out more about the illness (sadly the bit where we can't control all outlets with contradicting information - which is ironic, but)

DO we want a move forward, to know which people who we could get some significant change with that could make a difference, or an 'Aw' from others eating their toast, and what reactions and actions from whom are we looking for within all of these different communications that might come together as a complete strategy etc? Which will involve knowing the different audiences and how each thing will then operate with the different groups who might read it etc.

These are the questions people should be looking to think about and be on top of who are doing any advocacy, to ensure it is coordinated and doesn't contradict itself (harder in an illness with different severities and so many issues to unbundle etc without careful nuance that is planned out - so the mild person with a job needing adjustments isn't undermined by readers not understanding they are very capable within x limits at the thing they work in, but the severe person isn't understood and assumed to be 'making a meal of it' when they can't get to a dentist easily etc) but over multiple communications then is more than that whilst coherent (not just a repetition, but builds whilst making sure it makes sense of anything others might see as 'different to the last thing') so it can keep interesting people whilst pointing to similar directions.

I also understand of course there are issues for those doing advocacy that one of the audience which is more or less important vs other audiences for different advocates is the internal one. And that breaks down into eg pwme who care about the name and those who also feel squeamish about ME or CFS (but might accept ME/CFS better? - there is another issue about the guideline being under that term we need to be pointing people to look up) I'm aware so it will be a harder balance for some if they get patients who don't read the rest but write about the name used in the comments.

That [bit that I have not yet gone into, but waived at] would be the part that is for another thread (because of a larger discussion, not because this won't be one article relevant to that). I can see why within its limitations this bit is here on this one now.

I also think this is the time to discuss because it is very good to see different advocates co-ordinating - which means these issues across all the advocates probably do need to be hashed out to make the next time simpler regarding what it takes to find something that works across all.

I would also appreciate another thread that other people with strategic marketing experience (or other areas similar - just not at the 'just come up with a tagline' stage side of things) might also get into where we could discuss these different audiences and start picturing out the job to do. To get the over-arching 'messaging' discussed in these terms (who likes what and is turned off by what etc) so we can understand how a line great for one audience actually can backfire when read by another or used in a context not intended.

The science and cure and action and new development part is the bit that is great for us because it steps us around the part that risks inadvertently causing own goals for ourselves/patients by just being about attention for 'look at this person... discuss' which I'll be honest we need to be careful is actually helpful and not also risky for those sick and profiled and others similar to them. People don't need to be that expert to find it interesting that there are breakthroughs or changes in something eg how it is seen/what it turns out the issue might be.

Obviously I think we are both saying this in the context of improving further things, not criticising the good of which there is a lot in this - I hope we get to the point where others accept that goes without saying - and we don't have to say it. The technical feedback stage is part of moving forward not tearing down. And in an area like ours with often very short notice for things it is useful to be discussing this so those 'same page' things are at the ready as a starting point (and every new development will feed into that, so it is something that would be constantly updated to keep it from getting dated).

Really good stuff does need the input of all these different 'reads' and takes a lot, hence why from the outside the job some assume it look simpler so is (then perceive things as criticism) than what's behind getting marketing/PR etc really effective and has these constant conversations that want and use insight (it's seen as the help it is intended as, and to be debated over so that expertise from different angles is weighed to a collaboration above a 'compromise' end-point because each are hearing the pros and cons, rather than 'conflict' in the bad sense).

 

[Tom Hill]

That can all be explained by the brain.

Why can’t it just be a loop in the brain? If it exists for ME/CFS, it can be made use of for other diseases. Or PVF is just short-lived ME/CFS of sorts. Who knows. And why can’t we find very much evidence of a sustained immune response in LC?

Why can’t the delay happen in the brain and any immune interaction just follows the regular time course for that immune mechanism? And lots of the symptoms only exists in the brain, there’s no need for a detour to the rest of the body first.

That’s exactly how the brain works as well.

None of this rules out the immune system, but the dynamics do not require the immune system.

So my first sentence was that we can’t rule out it all being CNS only and I agree it might be, so i’m already in agreement with you. But I put all this together and I’m inclined to keep a very open mind about an immune system role.

Doesn’t mean I don’t want to see the fully fleshed out neurons only theory. Would like to see it very much.

 

[Tom Hill]

Or PVF is just short-lived ME/CFS of sorts

This speculation, and its implications, are why I really REALLY want to see the data contrasting the genetics of people with ME/CFS and those of people who walk away within 6 months with PVF only.

 

[Sean]

Perhaps! Except, it only applies after certain viruses, not just any old virus. PwME/CFS, before they got ME/CFS, seemed to have no problem with this reset when they got sick from flu etc prior to that.

Good point. I certainly bounced back normally after all the usual infections humans are subject to, before getting ME/CFS.

 

[V.R.T.]

Doesn’t mean I don’t want to see the fully fleshed out neurons only theory. Would like to see it very much.

Here is a thread about precicely that!

I wanted to make a thread to discuss the theory that ME/CFS is a signaling problem, located in the synapses of neurons in the brain. I think it fits and would help explain the few findings and observations that we have about the illness.

The clinical picture
First of all, there is no clear pathology in ME/CFS. No signs of inflammation (CPR and cytokines show no differences), no traces of ongoing infection, no deformities or neural damage, no notable increases in antibodies, no mitochondrial dysfunction, no organ damage, etc. I think this is the first important characteristic about the illness: not what we see, but what we don’t see.

The second point is that the disability and symptoms in ME/CFS are often greater than those in other chronic diseases, where there is clear pathology. Studies have compared ME/CFS patients to those with multiple sclerosis, rheumatoid arthritis, congestive heart failure, and renal disease and found that ME/CFS patients generally report more disability and impairment. Even terminal cancer patients can do much more than ME/CFS patients.

So, this poses a conundrum. Perhaps there is some pathology that we cannot yet detect: a hidden reservoir for the virus, antibodies that we don’t see, etc. The question, however, is: why would this ‘hidden’ pathology cause much more disabling symptoms than diseases where the pathology is all over the place? Why would it result in greater disability than in cases where we know there are tumors, inflammation, antibody responses, organ failure, etc? To me, the most plausible explanation is that ME/CFS pathology is in the signaling of symptoms itself.

Evolutionary, one can see symptoms as a response of the body to pathology. The organism retracts and avoids energy expenditure so that its focus can be on healing the disease. I think this explains why fatigue and malaise are part of almost all chronic illnesses. It’s simplistic, I know, but let’s call this the ‘symptom signal’. The hypothesis I’m exploring is that ME/CFS is mainly a pathology of this signal.

New illnesses are often studied by focusing on their most extreme manifestations, and only later is it found that milder and more subtle cases (forme frustre) exist. Let’s apply this and focus on (very) severe ME/CFS for a moment. These patients are so disabled by symptoms that they look like locked-in syndrome patients. They are bedbound, almost totally isolated from the outside world, and can hardly communicate or move. Yet from what we hear and the limited data that we get, there are still no clear signs of pathology. Blood work is largely normal. If we assume a different pathology, like a virus, an antibody, or blood flow problems, then in its severe form, this would, in some cases get out of control, show itself or cause tissue damage. If blood cloths, for example, are part of the pathology, we would perhaps expect to see more thrombosis. Blood flow problems would mean we are more likely to have brain or organ damage, etc. For most pathologies, this would again be a challenge to explain: the symptom/disability keeps increasing to a maximum while biological dysregulation remains elusive. For the signal theory, this is what we would expect with increasing severity: the volume knob for symptoms has been turned to 11, but the rest of the body seems relatively fine and functioning.

Let’s move on to symptoms. I’ll discuss PEM in the next section. The other characteristic ME/CFS symptoms, such as fatigue, malaise, pain, unrefreshing sleep, cognitive dysfunction, light and sound sensitivity, all clearly point to a neurological problem. But it’s not the kind of neurological problem that suggests brain damage. This forum is a good example that there is no retardation in ME/CFS, and specific memory loss has not been picked up in various cognitive tests. The main cognitive problems are brain fog, difficulty concentrating, slower reaction times, etc. Similarly, the sleep problem that is most reported is waking up unrefreshed. So, I would say these fit the ‘symptom signaling’ theory well and do no suggest other problems that require further explanation.

Orthostatic intolerance (needing to lie down, not POT or hypotension) and gut problems (not tolerating certain foods, poorer digestion) could also be viewed/explained from a neurological angle. So, the theory not only fits the most characteristic ME/CFS symptoms well but might also better account for the broad range of symptoms reported. Other theories have more difficulty with this. If you start with endothelial dysfunction or connective tissue, you have to make a lot more connections to come out to photophobia. I think that’s why so many documents say that ME/CFS is a complex multisystem disease. Theories often need to assume multiple pathologies in different body systems and complex connections between them to account for the many symptoms seen. I think this can be more easily explained by ME/CFS being a neurological problem of symptom perception.

Next: post-exertional malaise (PEM). A key observation is that patients can exceed their limit but then get payback and deterioration in symptoms afterwards. This means there is no hard physiological limit that stops patients, like in muscle or mitochondrial pathologies. ME/CFS patients don’t fall during CPET because their muscles stop working or they don’t quit because they can’t breathe enough. They are usually able to finish the test relatively ok but get much more ill afterwards. What stops them is the severity of symptoms, not a biological dysregulation. The mechanisms seem central (in the brain) rather than peripheral (in the muscle). Various studies have tested patients during PEM (e.g., after an exercise test), but overall, these show no clearer signs of pathology than before it. There is e.g., no clear buildup of lactate or detectable immune response during PEM. So, this is another tricky phenomenon to fit into a theory. Why would exertion make things worse?

In the symptom signaling theory, it would make sense. The main problem is that neurons get info that something is horribly wrong in the body, so the organisms must be told to rest and retract. If we do activities, these might give a different signal telling the nervous system that the organism isn’t listening. There might be signs of high energy expenditure that it cannot afford at this time, such as muscle breakdown or a stress response. When the neurons get this info, they interpret this as the body being naughty so the volume of the symptom signal is increased to induce the appropriate response (feeling awful and not doing anything anymore). The delay in PEM would then be explained by the various signals coming through, communicating, and finding the right response.

 

[bobbler]

We don't know if it has worked yet. To take an older name change: diabetes is in Norway also known as "sugar disease". This is years and years ago, and the name change to diabetes has been wanted in part due to the stigma stemming from others believing you're sick because you ear too much sugar.

Type two diabetes was simply called "old man's sugar disease" because it was more common in the older population, while kids with diabetes had "children's diabetes" or more correctly type one/the autoimmune variant. When I say previously I mean this is what my mother was taught some 50+ years ago at nursing school.

Still today we have problems with adults with type one diabetes coming to hospital and being given the wrong treatment because hospital staff go "oh, an adult! Then it is diabetes two!", or kids with type two diabetes getting the wrong treatment because staff go "oh, a kid! Then it must be type one!". Not to mention the general public (and some literature used for teaching staff!) may still use the terms sugar disease, old man's diabetes and children's diabetes (though there are people who go about making authors aware if they find such terms used and seemingly making headway, I can't remember seeing them in my clinical learning material).

Stigma from misconceptions based on the name is still prevalent today. Patients with type one diabetes report more stigma from others, likely because they are more visibly ill. For example being in need of injections. Since the illness is caused by eating too much sugar, the people who are the most visibly ill are obviously those with the worst diet and it's their own bloody fault for being ill.

Name changes take time.

I think that is a really pertinent example. People who use lazy heuristics have to be dealt with by any name/term rather than someone assuming they can be ignored or will somehow change with training. And by dealt with I mean that type tends to have a very quick 'I already know' excuse, because they don't want to change.

Tho I'm imagining sadly even with the right terms for diabetes older type 1s get that a lot, and anyone could on a bad day find they make the mistake simply because of % likelihoods etc.

The sugar bit is fascinating to see how the logic works for many. Goes to show what a problem the literal names can be - I remember an assembly as a kid had diabetes 1. I assume most understand it in UK at least to the extent of having to be careful with sugars but I don't know. Diabetes 2 wasn't as common/need to know when I was learning that so.

There's a lot of second-guessing to be done here, and then to work out what to scrap as second-guessing that doesn't matter vs what does. I've definitely been interested in watching how people are over many decades with these things, so some of it is interesting to me to just think out.

I might think I like hypothalamus for example being introduced because even though I was obviously thoroughly exhausted I was even more so 'able to push through and much less capable than myself but fitter than others' for so many years when caught between PEM with a lot of caffeine and grit (and that was me in performance mode, noone knew how smart or whatever I used to be other than in myself) and then bedbound and out of it and when woken might struggle to lift an arm, and ill in so many other ways.

I'll be honest I never sought out POTS type anything but knew of it because I had more OI type stuff - the 'lie flat' was such a relief to see when it came on here when it did. Battling with OI type permanent eyeing up things to rest my head on has been so constant to have to ignore and develop tricks to stay upright and hide (like moving, caffeine, adrenaline etc helps short term), ignoring deep aches etc. I now wonder whether coming round after an op and the drugs from that General Anesthetic wearing off meant I experienced in those minutes a new 'frame of reference' of how bad my body is vs when it is all not there by it all coming back from not being there so quickly (vs the boiling frog over decades, with new tricks and equipment and measures added in to compensate) my head being supported right was the worst thing.

Yet it's moving away from just that 'fatigue' issue I crave because people would then think I was a terrible person because I couldn't sleep at the right time, did so deeply for days at the wrong time, even if I went to work having not slept for 3 days 3 days in a row and then set my alarm 4hrs early to try and force my body to work enough to 'presenteeism' on the 4th be seen as someone who was either too lazy or too disorganised and stupid to have 'sorted myself out' to 'get out of bed in the morning' or 'learn to manage myself'.

People who kindly advocate for me/cfs by just using the term 'pacing' and who slept normal hours really did not do me any favours. That word needs to be banned because it was never trained-in with the right nuance and specificity. I still don't know if they have something different to me or were just fortunate enough to not know what it was like to never have lived in a world where the environment and things I couldn't avoid have always been more exertion than the envelope, but whilst it might be better than not having more if it is a haywire hypothalamus too me I mean it never was 'trainable'.

But 'pacing's' most understood meaning has been really harmful to me and I assume countless others. Particularly as other patients will say it (even if they mean something different re: themselves not having too much exerting them instead of what I got levied at me 'not sleeping because you hype yourself up or something'). I can see how it can be made to look like 'well done the others who don't have what you do' as if they can train it.

Pacing was also horrendously problematic because there are so many these days who believe 'they get it' and 'got the skills' to whatever heuristic of theirs to do with 'training' other people in that informal sense of the term by being coercive in their own behaviour and effectively name-calling by assuming eg it's 'like my kids get emotional when they don't have an early enough bed time' or 'just need to force em to know they can't get up late so they'll go to sleep early when their body needs it if there's no leeway on that'. Or just it's OK for them to be selfish and cause noise and vibrations as long as it stops when they themselves want to sleep at night time so that other person can just be coerced to live on their routine, when the over-exertion takes that whole time to start un-exerting from and never gets to sleep.

Still not a single person who said that or wrecked my health by doing counterproductive things to me telling themselves they were either training me or 'showing me' (as if I deserved it) has apologised and realised what their behaviour and wilful ignorance did to my health at the time and led to now - not me and my managing it. I walked the only lines of bartering survival for today, and never really got any options of survival for tomorrow or next year.

Anyway my point is having the term fatigue in anything makes people be sympathetic or not sympathetic to those who look slow and fatigued, as long as they get out of bed and are there at the right time and look sufficiently disabled in the right way.

That's not what the illness looks like to me until I'm now severe (and it still isn't what it looks like because now it is both combined, ie it is still the former just with a lot more constant disability on top).

The biggest thing which means we can't 'manage our illness' as the awful people suggest is that if the things we can't control (and indeed they've been incited to do things to us that undermine that stability and acceptance we need to make the most of what we have) mean what is on our plate doesn't give us options to cut it to near our cloth... well we don't have reliability. So those 2hrs a week someone migth have that they are 'OK' to do something small might land at 4-5am Tues, 3.30-4pm Sat and 20mins at 1am on Sun. And we only know that when we can move and stay awake.

Oh and unkind onlookers assume that because they forced the person to wake up and get out of bed on Thurs even though their head and balance system couldn't work and they were on adrenaline and then couldn't sleep for 4 days before starting the PEM cycle of recovery from scratch again meant even those tiny windows disappeared for two weeks or more.

And no we weren't insane or 'emotional' cause when they did that force awake and so no it isn't 'mental health' because someone should be able to be awake on Wed at 9am. But that person will never study someone left to do their natural thing, firstly because they'll refuse to watch or let info in that contradicts what they choose to believe, but also because it wouldn't be safe to have them near the person so would wreck that being able to sleep as body needs etc.


Problem is that those wrong-headed people will just invent what the issue with the hypothalamus is. They aren't interested in learning. They are interested in their narrative and being right and bast***ising fact and truth into it.

They definitely are likely to want to take the term dysfunction and use it to justify to what to me on the ground ends up with receiving brutality and tropism dressed up as if it is 'understanding' or 'help' - to them the fairy story that actually I believe began with adrenaline being looked into but warped into them thinking they understood cortisol and the entire HPA cos they could recite simplified fight or flight stories which had been then changed for anxiety = enough for them to give an answer on pretending to know what the hypothalamus is. So learning mode switched off.

We also have an issue between the visual and what is really going on and I don't even mean scientifically just if people can see you 'look fine' they don't understand why you are slurring your words and falling asleep and suddenly needing to recline. In fact they jump sometimes to the most unkind unflattering conclusions.