Fibromyalgia in obstructive sleep apnea-hypopnea syndrome: a systematic review and meta-analysis, 2024, He et al.

[MrMagoo]

Hi, see below (and the UARS thread) for why it's not just correlation.

There definitely should be a CPAP mask out there for you (even if it's a pediatric one)! Not sure if you are able to go into your durable medical equipment provider's local office and try some different ones out.

The correlation (being overweight) is not necessarily causation for sleep apnoea or fibromyalgia. I still don’t meet the majority of the criteria (being male, neck size etc) however having FM, ME/CFS and OSA all untreated (save for GET CBT) can lead to weight gain.

No, you are not allowed to try a paediatric mask if you are an adult. They can only be prescribed by a paediatrician. The nearest charity which would allow trying a mask is 3 hours drive away. The NHS are content that they provided a mask which fits, despite the manufacturer confirming their smallest mask is too big according to their sizing scale. I sent in a PALS in March and have heard nothing back.

 

[Utsikt]

No, they didn't? They pointed out that we are not looking at the prevalence of fibromyalgia in all OSA patients here, the sample is more skewed towards OSA syndrome (OSAS - OSA + daytime sleepiness) patients (as they are more likely to be referred for sleep evaluations because they are sleepy), which I agreed with.

You said:

obviously people who are referred for sleep evaluations and ultimately diagnosed with OSA are more likely to be sleepy/fatigued (many people with OSA are asymptomatic but are unlikely to be referred for sleep evaluations unless their snoring is really bothersome to partners/etc.),

What I tried to convey is that people that sleep poorly have more pain, and because FM has become synonymous with «this patient has pain» for many doctors, any person with sleep issues is more likely to get an FM diagnosis.

If pwOSA that are given a diagnosis disproportionally are the minority of the pwOSA that also have sleep issues (which makes sense because why would an asymptomatic person go through these checks?), then that will by itself make OSA seem correlated with FM due to sleep issues being correlated with more pain.

Without your correction below that sleepiness != poor sleep, the above argument makes sense.

I pointed out that most OSAS patients are not sleepy because of traditional metrics of "poor sleep," (and provided evidence that sleepy and non-sleepy OSA patients do not differ on these metrics); thus "poor sleep" does not explain the elevated rates of fibromyalgia in OSA/S patients.

With this argument, assuming the data in the table you linked is correct, representative, and does not show sleep issues (is there norm data out there?), my explanation doesn’t hold up as well.

The reason OSAS patients are sleepy/fatigued is very likely to share a common underlying cause with the reason many of them have fibromyalgia.

This is the crux, isn’t it?

The reason I’m sceptical off the bat, is that we see hundreds of publication about ME/CFS, FM, LC, etc. every year by researcher and doctors that show some kind of correlation between two kinds of variables, and then try to make up an elaborate story about how they have to be connected somehow. Very few of them hold up under scrutiny.

I’m not saying you are wrong for that reason. But the default assumption has to be that there is no connection, and then it’s up to someone to disprove it and demonstrate that there actually is something there. Otherwise we’d spend all our time collectively chasing red herrings. That’s not to say that we don’t need people to have creative ideas and explore possible connections (we won’t get anywhere without it) - just that getting others to follow your particular path over something else will take some convincing.

Asking «how else would you explain this correlation» probably isn’t enough to make people think it’s worthwhile to invest time and energy into.

 

[nataliezzz]

The reason I’m sceptical off the bat, is that we see hundreds of publication about ME/CFS, FM, LC, etc. every year by researcher and doctors that show some kind of correlation between two kinds of variables, and then try to make up an elaborate story about how they have to be connected somehow. Very few of them hold up under scrutiny.

I’m not saying you are wrong for that reason. But the default assumption has to be that there is no connection, and then it’s up to someone to disprove it and demonstrate that there actually is something there. Otherwise we’d spend all our time collectively chasing red herrings. That’s not to say that we don’t need people to have creative ideas and explore possible connections (we won’t get anywhere without it) - just that getting others to follow your particular path over something else will take some convincing.

Asking «how else would you explain this correlation» probably isn’t enough to make people think it’s worthwhile to invest time and energy into.

That's why I also shared all of this:

It's definitely not just a random correlation considering the multiple case reports of fibromyalgia cures with treatment of OSA from different authors/countries (one with the objective finding of alpha-delta sleep [the only consistent objective finding associated with fibro] disappearing along with fibro symptoms), Dr. Gold's study showing that fibro patients had a more collapsible upper airway (and one fibro patient who was unemployed due to symptoms returned to full employment after getting on CPAP), other studies showing improvement in fibro symptoms with CPAP treatment over traditional medication therapy, etc... It's not just about one piece of evidence here, it's about all of it together (but apparently some people won't even consider it until there is a large RCT proving it; although at this point I think even if there were, most people might *still* ignore it lol)

Again, it's not just about one piece of data here, it's about the collective evidence (meta-analysis, small studies, case reports, etc.) and this clinical experience below from 2 sleep doctors not affiliated with Dr. Gold certainly doesn't hurt either:

However, most UARS patients do not have a primary complaint of sleepiness. Dr. Guilleminault (who was not affiliated with Dr. Gold, by the way; he passed away in 2019) said this in 2004: Today, the clinical picture of UARS is better defined. We have learned that patients usually seek treatment with a somatic functional syndrome rather than sleep-disordered breathing or even a disorder of excessive daytime sleepiness (Upper airway resistance syndrome--one decade later)

In addition, this from Dr. Denise Dewald (another sleep doctor not affiliated with Dr. Gold):

"I think of flow limitation as a really important thing to look at when you're looking at a PSG [polysomnogram] and deciding is this a normal study, or is it not? Spoiler alert: just about everyone who's referred for a sleep complaint does not have a normal study. After thousands of sleep studies, I have yet to see an actual normal study* in someone who was symptomatic. The only normal studies I've seen have been in people who are referred because they needed a sleep study for bariatric surgery or because they work in transportation. Oh, and there was one guy who was sent by his cardiologist because he developed atrial fibrillation, and so of course he needed a sleep study, but he had rheumatic valvular disease."

*i.e. no flow limitation during non-REM sleep; most people have some flow limitation during REM due to loss of muscle tone

Thank you for at least engaging with me on it. Though I remain skeptical that you have a serious intention to consider the evidence supporting this theory, at least you didn't flat out ignore it like many/most people.

 

[Utsikt]

That's why I also shared all of this:

I must have missed that.

Thank you for at least engaging with me on it. Though I remain skeptical that you have a serious intention to consider the evidence supporting this theory, at least you didn't flat out ignore it like many/most people.

If you want to help people follow along: don’t overwhelm them. To be honest, I struggle to understand the hypothesis you’re proposing because you’re presenting very much information all at once in various formats.

I think you’re more likely to get people to engage with you if you if you break it down and focus on one piece at the time, and don’t try to connect everything to a grand theory yet. You might think something is established as fact, but how would an outsider know that? Why would they take some other doctor’s word for it when they see so many truly terrible takes in publications every day from people that really should know better?

And everyone here has limited time and energy. So you have to find a way for them to justify spending time on your path, and not something else. You’re already facing an uphill battle there, because I think most perceive OSA etc. to at best be very tangentially connected to the main topic of interest here: ME/CFS. They are in their full right to decline participating if they don’t feel you’ve justified their attention - even though I understand that might be discouraging for you.

 

[Verity]

Natalie, most of us have seen dubious theories come and go a number of times. Usually there are some doctors promoting them, a small number of patients who claim to be majorly improved or cured, and (if you’re lucky) low-quality evidence or a small amount of evidence. I don’t see how this is different. You say people don’t want to consider your theory, but to be straight with you, why would anyone want to if there’s nothing setting it apart from 100 other theories? No one has the time to investigate all of those.

If there is something setting it apart, it’s getting lost for me because your posts are absolutely overwhelming. They really need much better structure and some ruthless editing. You’ve gotten that feedback multiple times, and the problem still hasn’t been resolved. That issue is seriously hurting your ability to communicate what you’re trying to communicate.

If you can majorly tighten up your posting style and then state clearly how this theory is different, you’ll get better engagement.

 

[nataliezzz]

If you want to help people follow along: don’t overwhelm them. To be honest, I struggle to understand the hypothesis you’re proposing because you’re presenting very much information all at once in various formats.

I've had a hard time finding the balance. When I present too little, people say "well, we can easily write this off since you haven't presented enough evidence"; when I try to present a lot of the evidence, people say they can't look into it because it's too much to read/process. I thought the AI summary was pretty good though.

I think you’re more likely to get people to engage with you if you if you break it down and focus on one piece at the time, and don’t try to connect everything to a grand theory yet.

I think this is actually the exact opposite of how it needs to be looked at. For ex, I did the "one piece at a a time" approach with this meta-analysis of prevalence of fibromyalgia in OSA and was getting "could be a random correlation" responses. This is why you need to look at the case reports of fibromyalgia cures with treatment of OSA, the other smaller studies, etc. along with the meta-analysis (and take into account Dr. Gold's theory of how sleep-disordered breathing could be causing fibromyalgia: as he states in his thesis in Sleep Medicine Reviews: One can demonstrate associations in cross-sectional studies and treatment effects in sham-controlled longitudinal studies, but if one cannot provide a rationale, a paradigm, connecting SDB [sleep-disordered breathing] to pain, diarrhea or anxiety, one will have a difficult time convincing anyone about the truth of the relationship.)

And everyone here has limited time and energy. So you have to find a way for them to justify spending time on your path, and not something else. You’re already facing an uphill battle there, because I think most perceive OSA etc. to at best be very tangentially connected to the main topic of interest here: ME/CFS. They are in their full right to decline participating if they don’t feel you’ve justified their attention - even though I understand that might be discouraging for you.

That's why I'm focusing on fibromyalgia and not ME/CFS now, because that's where most of the evidence is. Many people on this forum seem to be interested in discussions of fibromyalgia (and other related disorders that are not ME/CFS) when it comes to other topics. But yes, as you stated, anyone is in their full right to decline participating.

 

[nataliezzz]

If there is something setting it apart, it’s getting lost for me because your posts are absolutely overwhelming. They really need much better structure and some ruthless editing. You’ve gotten that feedback multiple times, and the problem still hasn’t been resolved. That issue is seriously hurting your ability to communicate what you’re trying to communicate.

If you can majorly tighten up your posting style and then state clearly how this theory is different, you’ll get better engagement.

Hi Verity, thanks for your feedback. See my reply to @Utsikt above about finding the balance between providing too much/too little information.

And here is the AI summary of the UARS theory. One thing that didn't make it into that summary that I think is compelling is that it provides a very simple explanation for why people with hypermobility/EDS (many of whom had no significant issues other than occasional dislocating joints prior to an infection/other stressor) are more likely to develop ME/CFS, fibromyalgia, and other related disorders (more lax connective tissue = more collapsible upper airway). A meta-analysis (see below) found that "When directly compared to the general population, patients with EDS/MFS [Marfan syndrome] were on average six times more likely to have a diagnosis of OSA [obstructive sleep apnea]"

Prevalence of Obstructive Sleep Apnea in Joint Hypermobility Syndrome: A Systematic Review and Meta-Analysis

 

[Verity]

Hi Verity, thanks for your feedback. See my reply to @Utsikt above about finding the balance between providing too much/too little information.

Striking a balance between too much and too little information isn’t the problem. The issue is that you’re not presenting the necessary information efficiently or clearly. It is possible to present as much information as people need to understand your point in a way that is structured and not overwhelming.

What you need to do is write up a post and then ruthlessly cut it down to as few words as possible. Show no mercy to any extra words or sentences. Right now you simply have way more words than you actually need. You can also consider using bolded subheadings if you’re addressing more than one subject in a single post—that would help make your structure clearer.

 

[Utsikt]

I think this is actually the exact opposite of how it needs to be looked at. For ex, I did the "one piece at a a time" approach with this meta-analysis of prevalence of fibromyalgia in OSA and was getting "could be a random correlation" responses.

No, you did not do this one piece at a time. In the second post in this thread there are six different links to various sources, where you’re trying to tie it all together.

I’m suggesting that you focus on a singular piece of data at once, let people scrutinise it, and then move on to the next. If people ask about the relevance of it, or how it ties into something else, you’ve already got another thread for that.

I’m wondering what your intention is. What do you want other people to contribute with when you’re asking them to engange? If you want them to take in your entire theory, I can tell you right now that it’s not going to happen - it’s far too much to ask of anyone.

The best you can hope for is help to assess individual pieces, and there are no guarantees of getting engagement. You’ll have to accept that people might disagree with you on how good it is, how biologically plausible it is, or what you can reasonably infer from the data. Best case, all of us might learn something in the end.

 

[Sean]

What you need to do is write up a post and then ruthlessly cut it down to as few words as possible. Show no mercy to any extra words or sentences.

This.

I would also suggest not posting a comment immediately after writing it. Leave it overnight, or for a day or a week, and revisit it before posting.

 

[SNT Gatchaman]

I'd love to hear from other people who haven't weighed in on UARS yet like @Sean, @Andy @rvallee, @Nightsong @SNT Gatchaman etc. and @ME/CFS Science Blog

And here is the AI summary of the UARS theory.

The AI summary concludes:

This hypothesis provides a unifying framework that can explain many puzzling aspects of ME/CFS and related illnesses.

• Diverse Triggers: It accounts for how any type of severe stressor—not just infections—can trigger an identical syndrome by focusing on HPA axis activation as the common pathway to sensitization.
• Post-Exertional Malaise (PEM): PEM can be understood as a manifestation of a dysfunctional CNS stress response. Exertion (physical, cognitive, or emotional) acts as an additional stressor on an already over-taxed system, leading to a crash. This aligns with observations that CNS depressants (e.g., benzodiazepines) can sometimes prevent or reduce PEM.
• Partial Efficacy of Treatment: It explains why treatments like CPAP/BiPAP often provide significant (~35-50%) but incomplete relief. While these therapies reduce IFL, the device itself (pressure, mask) can act as a new stressor on a highly sensitized nervous system, preventing full recovery. More curative treatments may involve surgery or, for some, nervous system regulation techniques that aim to desensitize the stress response itself.

The hypothesis depends on central sensitisation and we have too much evidence implicating peripheral pathology that needs investigating, before even needing to consider central sensitisation. The proposed treatment is brain/limbic/amygdala retraining, with extra steps.

Looking at GWI, how might this mechanism help explain the one third of deployed personnel in 1991 being affected not repeating in subsequent conflicts. The Gulf War was a short and "easy" conflict for Coalition forces. Afghanistan and Iraq were long, bloody, horrific and incredibly stressful. The evidence indicates GWI was due to our own forces blowing up enemy ammo dumps and dispersing organophosphate nerve gas over a wide area, at low level.

From my perspective I don't have any evidence of IFL - I've never snored and slept like the proverbial before becoming sick. I didn't have a stress event to blame when I did. In fact I initially got sick on an idyllic summer sailing cruise, drifting around in paradise with not a care in the world. I had no idea what was suddenly happening to me.

Spoiler: Example of a personal physical and emotional stress event involving death

Four years prior I responded to a close-by coastal Mayday for a cardiac arrest. I had to jump off our boat, swim across to the distressed vessel in 18 knots of wind and do CPR for 40 minutes till the helicopter arrived. The diver (my age, ex-military) died under my hands.

… I'm sure my HPA axis was quite activated - shouldn't I have developed this illness then?

 

[nataliezzz]

The hypothesis depends on central sensitisation and we have too much evidence implicating peripheral pathology that needs investigating, before even needing to consider central sensitisation. The proposed treatment is brain/limbic/amygdala retraining, with extra steps.

Well yes, that could be one approach to recovering from UARS (although I've never suggested everyone can recover this way); I've always focused my efforts on raising awareness on the sleep-disordered breathing treatment piece. I don't think a theory is bad simply because one proposed treatment approach for it is unpalatable to people.

Re: peripheral pathology, don't think UARS is incompatible with high rates of SFN, for ex. (SFN could be downstream of chronic ANS dysfunction/hypoperfusion caused by UARS).

Looking at GWI, how might this mechanism help explain the one third of deployed personnel in 1991 being affected not repeating in subsequent conflicts. The Gulf War was a short and "easy" conflict for Coalition forces. Afghanistan and Iraq were long, bloody, horrific and incredibly stressful. The evidence indicates GWI was due to our own forces blowing up enemy ammo dumps and dispersing organophosphate nerve gas over a wide area, at low level.

There's actually plenty of people coming back from other conflicts with "war-related illness" too. Although GWI may be more than one thing, the clinical presentation of GWI is often identical to ME/CFS and does not fit with the clinical picture of a toxic chemical injury (e.g. symptoms fluctuating by the day/hour, post-exertional malaise, etc.)

From my perspective I don't have any evidence of IFL - I've never snored and slept like the proverbial before becoming sick.

Many people with UARS do not audibly snore. You can't possibly know whether or not you have IFL unless you have a sleep study with pressure transducers used (thermistors don't cut it).

I didn't have a stress event to blame when I did. In fact I initially got sick on an idyllic summer sailing cruise, drifting around in paradise with not a care in the world. I had no idea what was suddenly happening to me.

Interesting that you had no apparent stressor as a trigger. Glad to hear from another non-infectious onset person (although maybe you suspect an asymptomatic infection?) I get pretty tired of the whole IACC/PAIS/etc. narrative when many of us had clear non-infectious triggers (and more rarely, as in your case, no apparent trigger at all; although many people with no clear trigger will report that they were going through some kind of period of increased stress of one kind or another when their illness started - obviously not the case for you though).

… I'm sure my HPA axis was quite activated - shouldn't I have developed this illness then?

We can ask the same question about why people can get a bunch of infections (including the same one that ultimately triggers their ME/CFS) without any problems; shouldn't the person have developed ME/CFS the 1st/2nd/3rd/etc. time they had the flu/COVID/etc.?

The trigger for my ME/CFS was a day of intense physical activity (and ongoing undiagnosed celiac disease with GI symptoms for >1.5 years was probably part of the picture too). Several months prior to that I had worked on a trail crew for a few months swinging pickaxes and sledgehammers for hours a day and did not develop ME/CFS. Why was the one day of intense physical activity months later the ultimate trigger? Who knows.