nataliezzz
Established Member (Voting Rights)
*This post is in the process of being updated. People have given me feedback that sharing the Bluesky/Twitter threads is not a preferred/accessible option, so I will be taking the time in the next week or so to try to convey all the relevant information from those threads here*
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 below (if you don't have an X/Twitter account, you can add "cancel" before the X in the URL to view full threads without an account).
Links to some of the studies mentioned in the threads:
Inspiratory Airflow Dynamics During Sleep in Women with Fibromyalgia
Inspiratory airflow dynamics during sleep in veterans with Gulf War illness: A controlled study
The effect of nasal continuous positive airway pressure on the symptoms of Gulf War illness
Obstructive sleep apnea syndrome as an uncommon cause of fibromyalgia: a case report
Resolution of fibromyalgia by controlling obstructive sleep apnea with a mandibular advancement device
The symptoms and signs of upper airway resistance syndrome: a link to the functional somatic syndromes
Sleep-disordered Breathing and Hypotension
Exploring the Abnormal Modulation of the Autonomic Systems during Nasal Flow Limitation in Upper Airway Resistance Syndrome by Hilbert–Huang Transform
Upper airway resistance syndrome has historically been considered a sleep fragmentation disorder characterized by elevated respiratory effort related arousals (RERAs) + daytime fatigue/sleepiness 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 due to narrowing/partial collapse) during sleep. Here is a talk by Dr. Denise Dewald on the physiology/physics of what is occurring in IFL. Dr. Avram Gold (the doctor who proposed this theory) believes that we had IFL during sleep before we became ill but our brains did not react to it as a stressor; 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 ongoing 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. There is already a known disorder - temporal lobe/limbic epilepsy - for which airflow input to the limbic system via the olfactory nerve is associated with pathological consequences: in patients with temporal lobe/limbic epilepsy, nasal hyperventilation increases the frequency of EEG abnormalities while oral hyperventilation suppresses them. Locally anesthetizing the olfactory nerve negates the effects of nasal hyperventilation in these individuals.
The inverse relationship that has been identified between AHI and the prevalence of "functional somatic syndrome" symptoms like sleep-onset insomnia, headaches and IBS in sleep-disordered breathing (SDB) patients could be explained by the fact that as frequency of apneas (complete cessation of airflow) increases, there is less exposure to IFL: While apnea isolates the nasal airway from the hypopharynx and results in nasal pressure that is equal to atmospheric pressure, hypopnea and, to a greater extent, snoring [or inaudible IFL] lead to prolonged decreases in nasal pressure. Gold postulates that SDB stimulates the HPA axis through the effect of subatmospheric pressure in the nasal airway on the olfactory nerve...the olfactory nerve portion of his paradigm is based on the mechanism by which multiple chemical sensitivity (MCS) is postulated to occur.
This theory could account for many aspects of ME/CFS: how it can be triggered by any kind of stressor (not just infection - I do not buy the suggestion that people with clear non-infectious triggers to their ME/CFS like surgery, childbirth, physical/psychological trauma, chemical exposure, etc. simultaneously acquired an asymptomatic infection which is the real trigger), gradual and rapid onsets, fluctuating severity levels, remissions and relapses, why people are more likely to recover early on, especially with rest/pacing (stress response less ingrained), and even the "brain retraining" recoveries (for some people, these types of nervous system regulation approaches may be enough to turn off the UARS stress response).
UARS and 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, and 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?).
So how could we have a person with high blood pressure and a primary complaint of sleepiness and a person with low blood pressure/orthostatic intolerance with a primary complaint of fatigue 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, for 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 [e.g. cold hands/feet without overt OI in my case] that were likely caused by UARS before we developed full-blown ME/CFS). Also many of us (myself included) who had a clearly defined rapid onset to our ME/CFS did not have PEM (the pathognomonic symptom of ME/CFS) when our symptoms began and only developed it later into the illness course (I highly doubt that I developed a different disorder when PEM emerged in addition to the fatigue and unrefreshing sleep I was previously experiencing). If UARS is indeed causing ME/CFS, I suspect that many of us likely have both:
Linking towards the end of the thread as it is long & it doesn't automatically unroll the whole thing:
Thread continued here; includes 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.
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
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
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 below (if you don't have an X/Twitter account, you can add "cancel" before the X in the URL to view full threads without an account).
Links to some of the studies mentioned in the threads:
Inspiratory Airflow Dynamics During Sleep in Women with Fibromyalgia
Inspiratory airflow dynamics during sleep in veterans with Gulf War illness: A controlled study
The effect of nasal continuous positive airway pressure on the symptoms of Gulf War illness
Obstructive sleep apnea syndrome as an uncommon cause of fibromyalgia: a case report
Resolution of fibromyalgia by controlling obstructive sleep apnea with a mandibular advancement device
The symptoms and signs of upper airway resistance syndrome: a link to the functional somatic syndromes
Sleep-disordered Breathing and Hypotension
Exploring the Abnormal Modulation of the Autonomic Systems during Nasal Flow Limitation in Upper Airway Resistance Syndrome by Hilbert–Huang Transform
Upper airway resistance syndrome has historically been considered a sleep fragmentation disorder characterized by elevated respiratory effort related arousals (RERAs) + daytime fatigue/sleepiness 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 due to narrowing/partial collapse) during sleep. Here is a talk by Dr. Denise Dewald on the physiology/physics of what is occurring in IFL. Dr. Avram Gold (the doctor who proposed this theory) believes that we had IFL during sleep before we became ill but our brains did not react to it as a stressor; 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 ongoing 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. There is already a known disorder - temporal lobe/limbic epilepsy - for which airflow input to the limbic system via the olfactory nerve is associated with pathological consequences: in patients with temporal lobe/limbic epilepsy, nasal hyperventilation increases the frequency of EEG abnormalities while oral hyperventilation suppresses them. Locally anesthetizing the olfactory nerve negates the effects of nasal hyperventilation in these individuals.
The inverse relationship that has been identified between AHI and the prevalence of "functional somatic syndrome" symptoms like sleep-onset insomnia, headaches and IBS in sleep-disordered breathing (SDB) patients could be explained by the fact that as frequency of apneas (complete cessation of airflow) increases, there is less exposure to IFL: While apnea isolates the nasal airway from the hypopharynx and results in nasal pressure that is equal to atmospheric pressure, hypopnea and, to a greater extent, snoring [or inaudible IFL] lead to prolonged decreases in nasal pressure. Gold postulates that SDB stimulates the HPA axis through the effect of subatmospheric pressure in the nasal airway on the olfactory nerve...the olfactory nerve portion of his paradigm is based on the mechanism by which multiple chemical sensitivity (MCS) is postulated to occur.
This theory could account for many aspects of ME/CFS: how it can be triggered by any kind of stressor (not just infection - I do not buy the suggestion that people with clear non-infectious triggers to their ME/CFS like surgery, childbirth, physical/psychological trauma, chemical exposure, etc. simultaneously acquired an asymptomatic infection which is the real trigger), gradual and rapid onsets, fluctuating severity levels, remissions and relapses, why people are more likely to recover early on, especially with rest/pacing (stress response less ingrained), and even the "brain retraining" recoveries (for some people, these types of nervous system regulation approaches may be enough to turn off the UARS stress response).
UARS and 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, and 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?).
So how could we have a person with high blood pressure and a primary complaint of sleepiness and a person with low blood pressure/orthostatic intolerance with a primary complaint of fatigue 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, for 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 [e.g. cold hands/feet without overt OI in my case] that were likely caused by UARS before we developed full-blown ME/CFS). Also many of us (myself included) who had a clearly defined rapid onset to our ME/CFS did not have PEM (the pathognomonic symptom of ME/CFS) when our symptoms began and only developed it later into the illness course (I highly doubt that I developed a different disorder when PEM emerged in addition to the fatigue and unrefreshing sleep I was previously experiencing). 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
Linking towards the end of the thread as it is long & it doesn't automatically unroll the whole thing:
Thread continued here; includes 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.
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
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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