But there is no agreed marker for PEM (2 day CPET proposed in past) no agreed identifying symptom (certain delay now promoted as key but that is just assertion). It is a disputable term as to what is entailed and sb who gets it after 14 hrs may be different from sb who gets it after7 or 24 in key aspects or not. We don't know. We don't know and defining PEM as unique by a specific descriptive feature e.g 24hr + delay is cart before horse if that means to deny commonalities with earlier onset post exertional malaises. 24 + PEM it may be researched separataely as e.g." Biomarkers in PEM with 24 hr + onset" but without any foregome conclusion re. the nature of those with earlier onset, though there must be some differences. presumably, but not necessarily key ones.
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Upper Airway Resistance Syndrome (UARS): a common underlying cause for all "chronic complex illnesses"? (ME/CFS, fibro, GWI, etc.)
- Thread starter nataliezzz
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Utsikt
Senior Member (Voting Rights)
I don’t think I’ve said anything about PEM needing a delay of 24 hours. I think I’ve only linked the factsheet that says «PEM usually starts hours or a day or two after it is triggered and can last for hours, days, weeks or longer.» And said something similar about how PEM is often/usually delayed.
If I’ve said something else, I’ll go back and edit it because that wasn’t my intention.
No worries I was just commenting generally on the uncertainties of PEM (or trying to). Sorry for any misunderstanding.
Utsikt
Senior Member (Voting Rights)
Ah, I see. No worries!
nataliezzz
Established Member (Voting Rights)
It's not a core symptom of ME/CFS, but some patients do experience excessive daytime sleepiness (and many patients experience excessive sleeping, like you said, of course). I had daytime sleepiness in addition to fatigue earlier on in my illness and the sleepiness went away.
Both sleepiness and fatigue are well recognized to be associated with UARS/OSAS; some people with these disorders complain of one more than the other. Other people with UARS/OSAS appear to have other complaints like insomnia as their primary complaint (chronic insomnia patients with excessive daytime sleepiness and other OSA signs & symptoms [obesity, witnessed apneas, etc.] were excluded in that study and 40/40 left were still diagnosed with OSA/UARS [90% OSA - the prevalence of OSA in the general population is ~20%]. Many experienced remission from chronic insomnia with PAP therapy). UARS/OSAS being able to cause chronic insomnia may not seem logical (aren't these patients supposed to be tired/sleepy?), but it fits with the stress response paradigm of sleep-disordered breathing: the brain reacting to sleep-disordered breathing as a stressor results in a state of somatic arousal -> chronic insomnia (I think it fits with the "tired but wired" feeling many of us know so well).
And I think the study and case reports I've cited support that for yet others, fibromyalgia/body pain may the dominant complaint. It seems the symptoms and combination of symptoms varies highly in different individuals with UARS/OSAS.
There is no universal pattern of how UARS (or OSAS) patients presents.
As I think I think I've convincingly argued above, a person with UARS/OSAS can present with sleepiness without insomnia, or insomnia without sleepiness, e.g.
No one knows if UARS could cause symptoms like PEM because no one has ever taken a group of people who meet strict criteria for ME/CFS, evaluated them for UARS, and treated those who may have it to see the effect on ME/CFS symptoms like PEM.
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nataliezzz
Established Member (Voting Rights)
Yes, I do want to do this at some point, the idea of it just sounds really exhausting at the moment, especially as I have already spent 10s of hours compiling it all into threads on Bluesky/etc. (but I know that's not an accessible option for people).
Yes, agreed.
No need to do everything at once. If there's a study that's central to the hypothesis, you can make a thread for just that one to start. Normally we don't add any color commentary in the first post either, just the abstract, so you don't have to add comments immediately either. Maybe others will make comments that you can later reply to if you want.
The thing is that if you fixed my frozen shoulder with an injection that took away the mobility issues and pain that meant it interrupted my sleep then
Insisted on not being incredibly careful what you were measuring and the time period.
Then of course not being troubled by the shoulder on top of my me/cfs would mean overall I was in less pain and exhaustion - but you wouldn’t have been treating my me/cfs other than what should be happening if there was a real medical otidsssion dealing with us of making sure we don’t have other treatable issues on top exacerbating it because it’s bad enough having that if you aren’t already ill, then add in what losing a nights sleep does to someone with me/cfs
But it’s down to research design etc , or just finding the others who also have frozen shoulders and claiming that’s a ‘sample of me/cfs’ rather than ‘your ten cherry-picked frozen shoulder people’ whether/what it says much about me/cfs ?
Eg taking careful research to find out what the me/cfs was like before the shoulder issue started (not using just before it was injected as the starting point) and how it might have indeed struggled whilst carrying that extra burden and maybe even after that shoulder is dealt with the me/cfs doesn’t even improve back to where it was before because eg months of bad shoulder and fixing it took its toll.
Because obviously if starting at the day the shoulder was eg injected and calling any improvement in exhaustion in me/cfs from that day where someone had a bad shoulder impacting their life up to that day was ‘improvement’ would be fine if you were just demonstrating not leaving something else untreated takes its toll but inaccurate if you say treating a shoulder improves the me/cfs and then think the shoulder might be part of the cause of me/cfs rather than a comorbidities that didn’t help?
… and this is why I have big issues with even the ActuonforME big survey using the ‘does x symptoms improve with y treatment that isn’t for me/cfs but to therapy for toe pain’ definition of me/cfs . Why just those aspects selected and not also frozen shoulders, UTIs and other things people commonly have that ‘don’t help their cfs’ if that’s the claim?
The taking it to this next level by claiming HPA axis stuff then feels obscure and in order to try and put some squaring of s circle that isn’t there - there is only a connection in that those he’s found/sought out who have this and that then also have x other illness apparently have both , not ‘the population’ which would involve a representative sample?
Or have I missed where he’s taken a representative sample of me/cfs or fibro or whatnot?
There are a few layers here to look into what has been done to demonstrate which claims in what illnesses vs the theory?
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Does UARS cause significant hypercapnia.? If so this may be worth a look and may be relevant to ME improving on rapamycin.
nataliezzz
Established Member (Voting Rights)
No, UARS doesn't cause hypercapnia. By definition, there is no significant oxygen desaturation in UARS. There can be hypercapnia in obstructive sleep apnea (OSA), but I don't think it's the primary driver of symptoms like fatigue, sleepiness and cognitive dysfunction in people with OSA syndrome either, though it may contribute for some.Does UARS cause significant hypercapnia.? If so this may be worth a look and may be relevant to ME improving on rapamycin.
nataliezzz
Established Member (Voting Rights)
I'm going to try to make some individual threads for Dr. Gold's fibro & Gulf War illness studies at some point where I can discuss the methodology of how the samples were recruited, so I can let you know once I have done that so you can take a look.
However, here is one study of what I believe is fair to say a pretty representative sample of fibromyalgia patients where 23/23 had obstructive sleep apnea (OSA) - of course it's possible that those with more disturbed sleep were more likely to agree to undergo polysomnography (but even if that were the case, it would be difficult to explain all 23 having OSA based on prevalence of OSA in the general population):
But here is a study (not from Dr. Gold) where a rheumatology clinic offered polysomnography to consecutive female (ACR criteria meeting) fibromyalgia patients who were not specifically complaining of sleep disturbances; 40% (23) agreed and all 23 had OSA, with 19/23 (83%) having an AHI >15. That does not happen by chance - the prevalence of OSA (AHI ≥ 5) in women in the general population based on epidemiological studies is ~15-20%.
Sleep-disordered breathing among women with fibromyalgia syndrome
Obstructive sleep apnea is a common disorder in the population—a review on the epidemiology of sleep apnea
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