Here is a non-paywalled article by Dr. Bell where she discusses her olfactory-limbic model of multiple chemical sensitivity, with a lot of content overlap with the above paywalled article. 9/n
www.ncbi.nlm.nih.gov/books/NBK234...
@nataliezzz
Sharing info on the connection between sleep-disordered breathing/upper airway resistance syndrome (UARS) & ME/CFS & related disorders. Mostly following art accounts here to have a chill feed; don’t be offended if I don’t follow you. On Xitter @nataliezzz3
Here is a non-paywalled article by Dr. Bell where she discusses her olfactory-limbic model of multiple chemical sensitivity, with a lot of content overlap with the above paywalled article. 9/n
www.ncbi.nlm.nih.gov/books/NBK234...
Appreciate this discussion of how improvement of MCS w/ a psychological approach doesn't prove it's a psychological disorder, & I think it fits in nicely with my discussion of ME/CFS mind-body/"brain retraining" recoveries 🔽 (ppl report recovering from MCS this way too). 8/n
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7/n
One reason I find the olfactory nerve hypothesis of UARS compelling is that it is based on Dr. Bell's olfactory-limbic model of multiple chemical sensitivity (MCS), and a high % of ppl w/ ME/CFS (and fibro, GWI) appear to have (at least some degree of) MCS. 6/n
www.sciencedirect.com/science/arti...
Dr. Gold uses "snoring" to refer to both audible and inaudible IFL. During IFL (even when inaudible), there is actual "fluttering" (rapid opening and closing) of the pharyngeal airway, so in that sense (vibration of airway tissues), we are snoring, it may just be "silent snoring." 😄 5/n
Explanation of why this would be occurring more often in people with milder sleep-disordered breathing (SDB) than in those with more severe obstructive sleep apnea. FSS = functional somatic syndromes. "Snoring" can refer to inaudible inspiratory flow limitation (IFL) too. 4/n
I can't believe we've spent so much time/resources on CPET. Though physical exertion was always my #1 PEM trigger (so it was easier for me to think it was a metabolic problem), this isn't universal, and PEM clearly doesn't correspond simply to energy expenditure (a few examples from X/Reddit): 28/n
And thank you once again Dr. @renzpolster.bsky.social for saying what people (and ME/CFS researchers, specifically) need to hear about PEM! I think we’d be a lot further along with our understanding of ME/CFS and PEM if researchers designed their studies with these questions in mind: 27/n
That flow limitation predicts sleepiness was shown >25 yrs ago (snoring = flow limitation, tho many ppl have flow limitation w/out audible snoring); think how much further along we’d be if sleep medicine hadn’t ignored this! Oh well, at least we’re finally getting there. 5/
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Consider getting evaluated for sleep-disordered breathing, it’s 1 possible cause of migraines. Here’s a case report of a woman whose migraines were (mostly) cured w/ treatment of OSA. & consider checking out my content; I think you could help (I’m the old Emandal connection)
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To understand how flow limitation is causing sleepiness/fatigue (& countless other symptoms) in sleep-disordered breathing patients, see 🔽 It’s not the flow limitation itself but the brain’s response to it (just think of those ppl you know who snore and are asymptomatic!) 4/
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[i.e. how quickly one falls asleep, as measured by mean sleep latency on MSLT], and likely measures an uninterpretable mix of objective sleepiness and fatigue, but I'll get into that another time). Here is another study on flow limitation. More studies like these, please! 3/
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held true when accounting for age, sex, BMI, race/ethnicity, and average sleep duration." The referenced study 🔽 EDS = excessive daytime sleepiness (Epworth Sleepiness Scale [ESS] score ≥ 11 here; the ESS isn't a great measure of true objective sleepiness... 2/
www.atsjournals.org/doi/full/10....
Thank you American Thoracic Society @atscommunity.bsky.social for drawing attention to the importance of flow limitation! "Flow limitation was found to be a significant & independent risk factor for sleepiness in individuals w/ low AHI (<15/hr); this association... 1/
www.youtube.com/watch?v=pMw2...
He also began having pleasant dreams, which had previously been rare. Re: his daytime PTSD symptoms, in addition to decreased startle response, he was also able to "shake off" flashbacks when exposed to stimuli like the smell of diesel fuel that would previously trigger them. 67/n
Now to PTSD. Let's start with a case report: 42 y/o male PTSD patient with daily nightmares was unsuccessfully treated w/ doxepin/hypnotics. CPAP for severe OSA resulted in dramatic improvement in PTSD sx, nightmare intensity & frequency (daily ▶️ monthly). 66/n
www.sciencedirect.com/science/arti...
This paper included 3 case reports: with CPAP for OSA, 1) 45 y/o male: resolution of day & nighttime panic attacks 2) 55 y/o male: resolution of PM panic attacks & daytime anxiety 3) 32 y/o male: resolution of PM panic attacks & marked decreased in anxiety. 65/n
www.sciencedirect.com/science/arti...
Case report: 43 y/o female with 4-year history of daytime panic attacks with agoraphobic avoidance (& 1.5-year history of "nocturnal panic attacks") with only modest response to CBT experienced full remission of her panic disorder w/ CPAP treatment for OSA. 64/n
www.sciencedirect.com/science/arti...
In this study, 12 OSA patients (w/ AHI ≥ 20) & daytime panic disorder (none with sleep panic attacks) experienced sign. reduction in frequency of panic attacks, Panic Disorder Severity Scale (PDSS) scores, & alprazolam use on therapeutic CPAP vs. sham CPAP. 63/n
www.sciencedirect.com/science/arti...
Patients weren't divided into OSA vs. central SA due to coding (but a previous population-based study by the authors found that >99% of SA patients had OSA). SA was associated w/ 🔼 panic disorder (PD) independent of comorbidities, & it was noted the actual prevalence of PD in SA pts may higher. 62/n
In this study, sleep apnea (SA) patients were compared to controls w/out SA (matched for age/sex/income/urbanization; 4 controls per SA patient); over a mean 3.92 year follow-up period, 1.34% of the SA patients developed panic disorder vs. 0.42% of controls. 61/n
pmc.ncbi.nlm.nih.gov/articles/PMC...
PSG findings suggested UARS. Upon treatment with CPAP, "his complaints resolved dramatically." The authors concluded: "This case seemed interesting in showing that UARS may clinically present as symptoms of chronic fatigue, anxiety and depression in young, non-obese people." 60/n
Case report: 17-year old male with complaints of chronic fatigue, insomnia, social and academic problems was unsuccessfully treated for anxiety, depression and insomnia with hypnotics, sedatives and antidepressants. He was referred for PSG for insomnia eval; 59/n
www.researchgate.net/publication/...
Here's a follow-up study of 94 UARS patients 4.5 years after they were diagnosed with UARS. Insurance refused to provide CPAP for 90/94 patients. When will doctors help fix this disaster? (I don't blame any individual dr. btw, but individual drs. can help!) 58/n
www.sciencedirect.com/science/arti...
people who are both highly sensitized to IFL (who likely often have innately sensitive nervous systems) and have mild SDB (high % IFL with little/no time spent in apnea), you get people with the most severe presentations of UARS (likely includes many ME/CFS patients). 57/n
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Two factors likely determine UARS severity: 1) % IFL 2) how sensitized one is to IFL. So is there a % IFL threshold below which one is not at risk for UARS? This study attempted to provide an answer, but we don't actually know. Here's Dr. Gold's take on it 🔽 20/n
pmc.ncbi.nlm.nih.gov/articles/PMC...
asymptomatic Gulf War vets) have OSA, and others would meet traditional UARS criteria based on RDI (AHI + RERA index). In the GWI patients, AHI/RDI varies greatly, but they all have high % IFL. Some controls have fairly high % IFL too; they may be at risk of developing some degree of UARS. 19/n
Back to inspiratory flow limitation (IFL). Here's the data from Dr. Gold's Gulf War illness (GWI) study; you can see that arousals (RERAs/AHI - most apneas/hypopneas terminate in an arousal) are not the relevant factor: IFL is! Some controls (age/BMI-matched 18/n
www.researchgate.net/publication/...
No one has ever been able to explain why ppl w/ a genetic disorder affecting collagen (who often had no previous issues other than occasional dislocating joints prior to an infection/other stressor) are more likely to develop ME/CFS, fibro, etc. Well, UARS/OSAS explains it!
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