nataliezzz
Established Member (Voting Rights)
Hi everyone,
Some of you may know me from X/Twitter as @PSSD_Info & more recently, @nataliezzz3 (thanks to those who follow me there, even if you don't directly engage with me it lets me know you see value in what I'm doing/saying
)
I think the evidence supports upper airway resistance syndrome (UARS) as a common underlying cause for many "chronic complex illnesses" (ME/CFS, fibromyalgia, Gulf War illness, etc.), as well as a causal/contributing factor to many cases of chronic insomnia/anxiety/depression/PTSD/etc. And I do think there is enough evidence to assert that UARS as a cause of (at least some cases of) fibromyalgia & Gulf War illness is a fact, not a theory. I'm linking threads I made on the subject on both Bluesky & X/Twitter (links to all of the relevant research are in the threads):
(linking towards the end of the thread as it is long & it doesn't automatically unroll the whole thing)
(very similar to the Bluesky one w/ a few additions)
https://xcancel.com/nataliezzz3/status/1924892171565494439 (this link will work for people without an X account - you can add "cancel" after the X to view any X/Twitter thread without an account)
https://xcancel.com/PSSD_Info/status/1906082129538093067 ("cancel" link for people w/out an account)
(this one is my longest thread - I'm linking towards the end where it has content that has not been added to the Bluesky thread yet including my own ME/CFS story and improvements with treating my UARS. I made this account on X to help raise awareness of PSSD [post-SSRI sexual dysfunction]; I probably should have made a new account for the UARS stuff back when I first started talking about it - oh well lol).
Upper airway resistance syndrome has been considered a sleep fragmentation disorder characterized by elevated respiratory effort related arousals (RERAs) in the absence of obstructive sleep apnea (OSA - apnea hypopnea index [AHI] ≥ 5), but it seems to be best understood as a stress response disorder driven by sensitization to inspiratory flow limitation (IFL - includes hypopnea, snoring & inaudible "fluttering" of the upper airway) during sleep. Dr. Avram Gold (the doctor who proposed this theory) believes that we had IFL during sleep before we became ill; then HPA axis activation by a stressor (infection, trauma, surgery, chemical/environmental exposure, etc.) sensitized the limbic system to perceive IFL as a noxious stimulus/stressor, and the stress response became ingrained, driving symptoms. He hypothesizes that the sensitization is occurring via the olfactory nerve, which senses nasal airflow/pressure and is directly connected to the limbic system. Here is a talk on the physiology/physics of what is occurring in IFL:
UARS & obstructive sleep apnea syndrome (OSAS) are not actually separate disorders (at least in many/most cases). It was shown 25 years ago that snoring (which almost always = IFL, though many people have IFL without audible snoring) is the factor most strongly associated with daytime sleepiness, not sleep fragmentation by (apnea/hypopnea/RERA-related) arousals. Sleep medicine ignored their own data that showed this, & thanks to that we have ended up in the situation we are now with millions of people being deprived of appropriate treatment simply because they have an AHI <5. It's kind of mind boggling how long this disaster has gone on for, considering how easily the sleep fragmentation paradigm of sleep-disordered breathing falls apart (if sleep fragmentation were the primary cause of symptoms in sleep-disordered breathing patients, why would we have OSA vs. OSA syndrome & >50% of people with OSA being asymptomatic?).
Thread on this: https://bsky.app/profile/nataliezzz.bsky.social/post/3lqg2gmyop22q
So how could we have a person with high BP and a primary complaint of sleepiness and a person with ME/CFS with low BP/OI e.g. actually having (differing presentations of) the same underlying disorder? I think the reasons there are such hugely varying presentations of UARS/OSAS are:
1) People's brains/bodies react very differently to the stress IFL induces; some may have sleepiness > fatigue while others have fatigue > sleepiness, or some the primary complaint may be pain/insomnia/headaches/IBS/etc. without dramatic fatigue or sleepiness. I just see ME/CFS as the most severe presentation of UARS (& many of us, myself included, had milder symptoms/issues that were likely caused by UARS before we developed full-blown ME/CFS). If UARS is indeed causing ME/CFS, I suspect that many of us likely have both:
Thread with more info on the UARS/OSAS - fibromyalgia connection, including 2 case reports of dramatic resolution of fibromyalgia symptoms from treating OSA. I think there was enough evidence to say UARS/OSAS could cause fibromyalgia without these, but they seal the deal (esp. because they are not coming from Dr. Gold); alpha-delta sleep is an objective finding associated with fibromyalgia (& UARS) and if it disappears along with fibromyalgia symptoms with treatment of UARS/OSAS, I think it's fair to conclude that UARS/OSAS is the cause of (that person's) fibromyalgia:
https://bsky.app/profile/nataliezzz.bsky.social/post/3ltwu7f27jc2u (I have some more studies on prevalence of OSA in fibromyalgia & vice versa I'll be adding to this thread soon)
These are linked in my long thread on the @PSSD_Info X account, but I'll link them here too for convenience (add the "cancel" after the X to view without an account):
https://x.com/PSSD_Info/status/1917661692785483973
Thread on why I think UARS can explain PEM & why I think PEM is best explained as a CNS problem (including discussion of how benzodiazepines alleviate/reduce PEM symptoms for many patients, as well as preventing/reducing PEM when taken ahead of exertion - and the same is true for other CNS depressants/sedatives like dextromethorphan)
https://x.com/PSSD_Info/status/1924352017792737568
Thread on why CPAP/BiPAP is not typically a cure for ME/CFS/fibro/etc. patients (basically, it also seems to be acting as a stressor on a sensitized nervous system).
Also, to help put some of the findings of the studies in my thread in context:
https://pmc.ncbi.nlm.nih.gov/articles/PMC4561280/ Prevalence of OSA (AHI ≥5) in the general population in 11 published epidemiological studies: mean of 22% (range, 9-37%) in men and 17% (range, 4-50%) in women
https://www.sciencedirect.com/science/article/abs/pii/S1389945722000478 Attempted UARS prevalence study from the São Paulo Epidemiologic Sleep Study data found a 3.1% prevalence with 4.4% in females and 1.5% in males (UARS criteria was IFL time ≥5% of total sleep time, minimum SpO2 ≥92%, AHI < 5, and symptoms of excessive daytime sleepiness or fatigue) - I am not sure if people with diagnoses like ME/CFS were excluded as I couldn't access the full paper.
I look forward to (hopefully) hearing from people and getting the conversation started. If my experience on X/Twitter is any indication, many people will likely ignore it, but I suspect there are some people here who will engage!
-Natalie
Some of you may know me from X/Twitter as @PSSD_Info & more recently, @nataliezzz3 (thanks to those who follow me there, even if you don't directly engage with me it lets me know you see value in what I'm doing/saying
)I think the evidence supports upper airway resistance syndrome (UARS) as a common underlying cause for many "chronic complex illnesses" (ME/CFS, fibromyalgia, Gulf War illness, etc.), as well as a causal/contributing factor to many cases of chronic insomnia/anxiety/depression/PTSD/etc. And I do think there is enough evidence to assert that UARS as a cause of (at least some cases of) fibromyalgia & Gulf War illness is a fact, not a theory. I'm linking threads I made on the subject on both Bluesky & X/Twitter (links to all of the relevant research are in the threads):
(linking towards the end of the thread as it is long & it doesn't automatically unroll the whole thing)
(very similar to the Bluesky one w/ a few additions)
https://xcancel.com/nataliezzz3/status/1924892171565494439 (this link will work for people without an X account - you can add "cancel" after the X to view any X/Twitter thread without an account)
https://xcancel.com/PSSD_Info/status/1906082129538093067 ("cancel" link for people w/out an account)
(this one is my longest thread - I'm linking towards the end where it has content that has not been added to the Bluesky thread yet including my own ME/CFS story and improvements with treating my UARS. I made this account on X to help raise awareness of PSSD [post-SSRI sexual dysfunction]; I probably should have made a new account for the UARS stuff back when I first started talking about it - oh well lol).
Upper airway resistance syndrome has been considered a sleep fragmentation disorder characterized by elevated respiratory effort related arousals (RERAs) in the absence of obstructive sleep apnea (OSA - apnea hypopnea index [AHI] ≥ 5), but it seems to be best understood as a stress response disorder driven by sensitization to inspiratory flow limitation (IFL - includes hypopnea, snoring & inaudible "fluttering" of the upper airway) during sleep. Dr. Avram Gold (the doctor who proposed this theory) believes that we had IFL during sleep before we became ill; then HPA axis activation by a stressor (infection, trauma, surgery, chemical/environmental exposure, etc.) sensitized the limbic system to perceive IFL as a noxious stimulus/stressor, and the stress response became ingrained, driving symptoms. He hypothesizes that the sensitization is occurring via the olfactory nerve, which senses nasal airflow/pressure and is directly connected to the limbic system. Here is a talk on the physiology/physics of what is occurring in IFL:
UARS & obstructive sleep apnea syndrome (OSAS) are not actually separate disorders (at least in many/most cases). It was shown 25 years ago that snoring (which almost always = IFL, though many people have IFL without audible snoring) is the factor most strongly associated with daytime sleepiness, not sleep fragmentation by (apnea/hypopnea/RERA-related) arousals. Sleep medicine ignored their own data that showed this, & thanks to that we have ended up in the situation we are now with millions of people being deprived of appropriate treatment simply because they have an AHI <5. It's kind of mind boggling how long this disaster has gone on for, considering how easily the sleep fragmentation paradigm of sleep-disordered breathing falls apart (if sleep fragmentation were the primary cause of symptoms in sleep-disordered breathing patients, why would we have OSA vs. OSA syndrome & >50% of people with OSA being asymptomatic?).
Thread on this: https://bsky.app/profile/nataliezzz.bsky.social/post/3lqg2gmyop22q
So how could we have a person with high BP and a primary complaint of sleepiness and a person with ME/CFS with low BP/OI e.g. actually having (differing presentations of) the same underlying disorder? I think the reasons there are such hugely varying presentations of UARS/OSAS are:
1) People's brains/bodies react very differently to the stress IFL induces; some may have sleepiness > fatigue while others have fatigue > sleepiness, or some the primary complaint may be pain/insomnia/headaches/IBS/etc. without dramatic fatigue or sleepiness. I just see ME/CFS as the most severe presentation of UARS (& many of us, myself included, had milder symptoms/issues that were likely caused by UARS before we developed full-blown ME/CFS). If UARS is indeed causing ME/CFS, I suspect that many of us likely have both:
- Mild sleep-disordered breathing (high % IFL with little/no time spent in apnea to balance it out)
- Highly sensitized to IFL.
Thread with more info on the UARS/OSAS - fibromyalgia connection, including 2 case reports of dramatic resolution of fibromyalgia symptoms from treating OSA. I think there was enough evidence to say UARS/OSAS could cause fibromyalgia without these, but they seal the deal (esp. because they are not coming from Dr. Gold); alpha-delta sleep is an objective finding associated with fibromyalgia (& UARS) and if it disappears along with fibromyalgia symptoms with treatment of UARS/OSAS, I think it's fair to conclude that UARS/OSAS is the cause of (that person's) fibromyalgia:
https://bsky.app/profile/nataliezzz.bsky.social/post/3ltwu7f27jc2u (I have some more studies on prevalence of OSA in fibromyalgia & vice versa I'll be adding to this thread soon)
These are linked in my long thread on the @PSSD_Info X account, but I'll link them here too for convenience (add the "cancel" after the X to view without an account):
https://x.com/PSSD_Info/status/1917661692785483973
Thread on why I think UARS can explain PEM & why I think PEM is best explained as a CNS problem (including discussion of how benzodiazepines alleviate/reduce PEM symptoms for many patients, as well as preventing/reducing PEM when taken ahead of exertion - and the same is true for other CNS depressants/sedatives like dextromethorphan)
https://x.com/PSSD_Info/status/1924352017792737568
Thread on why CPAP/BiPAP is not typically a cure for ME/CFS/fibro/etc. patients (basically, it also seems to be acting as a stressor on a sensitized nervous system).
Also, to help put some of the findings of the studies in my thread in context:
https://pmc.ncbi.nlm.nih.gov/articles/PMC4561280/ Prevalence of OSA (AHI ≥5) in the general population in 11 published epidemiological studies: mean of 22% (range, 9-37%) in men and 17% (range, 4-50%) in women
https://www.sciencedirect.com/science/article/abs/pii/S1389945722000478 Attempted UARS prevalence study from the São Paulo Epidemiologic Sleep Study data found a 3.1% prevalence with 4.4% in females and 1.5% in males (UARS criteria was IFL time ≥5% of total sleep time, minimum SpO2 ≥92%, AHI < 5, and symptoms of excessive daytime sleepiness or fatigue) - I am not sure if people with diagnoses like ME/CFS were excluded as I couldn't access the full paper.
I look forward to (hopefully) hearing from people and getting the conversation started. If my experience on X/Twitter is any indication, many people will likely ignore it, but I suspect there are some people here who will engage!
-Natalie
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