I had hoped you were here to debate the science behind these issues.
I am. And that was my primary intention starting out, but I'm not really sure many people here are interested in that? I don't think I've ever not responded to an actual question/critique from someone here on the subject. If you want to see the debate that followed the updated/edited AI summary on the theory and my responses to criticisms by
@Trish,
see here. If you want to see an actual discussion with
@forestglip that occurred on one of the threads on the subject,
see here. Part of me trying up to build up a more comprehensive picture of what is driving the symptoms in OSA syndrome - which is why I've been adding studies that may seem unrelated (and I'm going to stop adding individual threads for so many of them and just link the URLs in the future) - was because I was going to try to tie them all together into a thread/post about "What is causing symptoms in OSA?" and the two possible OSA "phenotypes," so the kind of discussion I had with
@forestglip on that thread re: "If most of these GWI patients just had OSA and improved on CPAP, isn't that just showing that people with OSA improve on CPAP?" can unfold in a more productive way, or so when people say things like this...
The idea that partial relief of GWI, FM and ME/CFS symptoms after using CPAP shows a connection is flawed too. All that may be happening is reduction in some symptoms due to sleeping better, it may have no connection with the underlying illness.
...people can think about: what does "sleeping better" actually mean in the context of OSA syndrome (especially given that a high % of OSA patients are asymptomatic)? And how might partial improvement on CPAP in GWI/fibro patients connect to the broader phenomenon of CPAP generally not being a cure for many UARS/OSAS patients?
It strikes me there is a potentially interesting phenomenon, namely the suggested association between obstructive sleep apnea and various conditions including ME/CFS, which obviously is of prime interest to our members and visitors.
Thank you! I know there's no evidence specifically on people meeting strict criteria for ME/CFS, but there is a lot of evidence related to conditions that many people with ME/CFS have like chronic insomnia and fibromyalgia. I made a thread specifically to discuss the evidence on UARS/OSA and chronic insomnia (since there are multiple supporting studies) - I was planning on doing something similar for fibromyalgia and orthostatic intolerance as well.
Sleep-disordered breathing (UARS/OSA) and chronic insomnia
No one responded to it. So I can't say I agree with "obviously of prime interest to our members."
But I will say engaging with everyone here was my initial goal, but I've realized that it's quite helpful to be able to link the summary of the theory on here to people outside of S4ME - like ME/CFS, fibro, and sleep doctors/researchers on Twitter - because like I said, people find the Twitter thread format cumbersome. So even if there is very little engagement here, it still has value.
In relation to the current study I worry that their defining a range of conditions/symptoms in relation to a particular set of assumptions and then looking at their relationship to questionnaire responses, when those questionnaires were devised using the same assumptions risks being circular and may end up telling us more about the researchers preconceptions than any underlying physiology or neurophysiology.
The current study taken by itself is not particularly strong evidence of anything, it's just showing an association between elevated BSQ scores and prevalence of self-reported "somatic syndromes." But as one piece of evidence in the larger framework - including
the study using the same data set that showed reduction in BSQ and Fatigue Severity Scale scores on CPAP - and the evidence on OSA and fibromyalgia, it is important.
And I brought in the restless legs syndrome (RLS) studies and case report because I figured people would probably be thinking "What the heck does RLS have to do with these other 'somatic syndromes'?" and "Yeah, people with RLS are going to have higher BSQ scores because of the symptoms of RLS, but is there any evidence that RLS actually has anything to do with OSA/improves with treatment of OSA?" - yes, there is, and prevalence of RLS is elevated in disorders like fibromyalgia and IBS, so you can start to see how all of this may be related.
If stress mechanisms are being postulated we need objective physiological measures if we are going to escape the traps of such as the BPS research into ME/CFS and their unhelpful lumping of everything under a functional heading without any independent objective criteria.
Yes. I just talked to a radiologist who has UARS a couple days ago and he said he thought the experiment below was feasible (sleeping in an MRI machine poses challenges but is not impossible), and that if there is actually activation of the limbic system in response to IFL that it would likely be visible on fMRI (and he's done a lot of education/advocacy in the medical community related to UARS, so I'm optimistic he might actually have the connections to make it happen at some point in the future):
The crucial unperformed experiment
The olfactory-limbic-HPA hypothesis is supported by strong convergent evidence but has not been directly demonstrated in sleeping humans. The key experiment would measure limbic activation during IFL in symptomatic vs. asymptomatic sleep-disordered breathing patients — or, where direct limbic measurement is impractical, downstream markers like CAP and K-complexes — and show reduction of these findings with CPAP and abolition with more curative interventions such as oral appliance or surgery. This experimental design could also help elucidate a clinically familiar but poorly understood observation: that CPAP produces only partial improvement in many symptomatic sleep-disordered breathing patients. The olfactory-limbic framework suggests one reason: pressurized airflow delivers a different nasal pressure and flow input than normal unobstructed breathing, potentially continuing to drive olfactory – limbic stress responses in a sensitized system even as it eliminates IFL. A complementary experiment could test the effects of nasal anesthesia on limbic activation and its downstream markers, directly probing the olfactory nerve's role.
Cyclic alternating pattern (CAP) and K-complexes are two things mentioned there that can already be measured - and in the case of K-complexes, have already been shown to be directly induced by inspiratory flow limitation (IFL) (using a suboptimal CPAP design to induce IFL) and associated with an objective finding - increased psychomotor vigilance task (PVT) lapses - which when you put it together with the study that showed that increased IFL predicts PVT lapses, already paints a compelling picture - even if we haven't directly measured the hypothesized limbic stress response, we can measure something in the brain that is happening in response to IFL that is associated with an objective finding. The referenced studies:
When we suggested
@nataliezzz that you present the individual studies behind Gold’s theory of a stress response to obstructive sleep apnea causing various conditions, it was because we wished to understand the rationale behind the theory and evaluate how robust the underpinning evidence is. Sheer volume of papers alone does not do that.
Sorry, I'm going to try to stop posting so many abstracts for papers and just link the papers themselves in my posts unless they are essential to the theory / more directly related to topics typically discussed on this forum. But I did have an actual goal behind posting all of the studies related to the two OSA "phenotypes" (which showed that objective - but not subjective - sleepiness is associated with inflammatory markers, hypertension, etc. - see below). I do think people need to have a broader understanding of UARS/OSAS and what the evidence suggests about what is (and is not) causing symptoms in different OSA patients in order to be able to discuss/debate the connection to disorders like fibromyalgia, GWI, etc., so I was going to make a post/thread discussing the evidence on the OSA "phenotypes" and tying it into the larger evidence base on sleep-disordered breathing and Dr. Gold's theory (give me a week or so to finish that - it's not just going to be a rehash of what I've already written on Dr. Gold's theory, don't worry).
Re: the pathophysiology of objective excessive daytime sleepiness (EDS) (
"OSA Phenotype 1") vs. subjective EDS / fatigue (
"OSA Phenotype 2"):
In recent years, a series of studies in patients with OSA have considered whether the presence of objective EDS (MSLT) and subjective EDS (ESS) correlated with the following parameters:
• inflammation – levels of IL-6 and cortisol [6].
• sympathetic activation – urinary norepinephrine and blood pressure measurements [7].
• glucose metabolism - blood glucose, insulin, HOMA-IR, serum metabolomics, fecal microbiota [8].
• all cause and...
