The Silent Epidemic: Upper Airway Resistance Syndrome in Women and Its Hidden Links to Chronic Fatigue, Fibromyalgia, and Dementia
There is a condition affecting millions of women that most doctors have never heard of. It does not show up on standard sleep studies. It does not fit the profile that most clinicians associate with disordered breathing. And yet, left unaddressed, it may be silently fueling some of the most debilitating and poorly understood conditions in medicine — chronic fatigue syndrome, fibromyalgia, and even dementia.
It is called Upper Airway Resistance Syndrome, or UARS.
If you are a woman struggling with crushing fatigue, widespread pain, brain fog, or non-restorative sleep — and you have been told your bloodwork is normal, your sleep study is “fine,” and maybe you should try to reduce your stress — this may be the missing piece no one has looked for.
What Is UARS, and Why Should Women Care?
Upper Airway Resistance Syndrome was first described in the early 1990s by Dr. Christian Guilleminault and his team at Stanford University. It sits on the spectrum of sleep-disordered breathing between simple snoring and obstructive sleep apnea (OSA), but it is a fundamentally different clinical picture.
In UARS, the airway does not fully collapse the way it does in sleep apnea. Instead, there is a subtle, repeated narrowing that increases the effort required to breathe during sleep. This increased effort triggers micro-arousals — brief awakenings the sleeper never remembers — that fragment sleep architecture and prevent the brain from reaching or sustaining deep, restorative sleep stages.
Here is what makes this especially relevant for women: UARS is more prevalent in women than in men. A large epidemiological study from São Paulo (the EPISONO study, published in Sleep Medicine in 2022) found a UARS prevalence of approximately 4.4% in women compared to 1.5% in men. UARS was most common among younger, non-obese women — a demographic that does not fit the typical sleep apnea profile that most clinicians screen for.
UARS has even been informally dubbed the “Young, Fit, Female Syndrome” because it so disproportionately affects women who appear healthy by conventional measures. These women are often of normal weight, physically active, and do not snore loudly — which means their breathing problems during sleep are virtually invisible to the standard medical evaluation.
Research also shows that postmenopausal women with chronic insomnia have strikingly high rates of sleep-disordered breathing. A 2002 study by Guilleminault and colleagues (PubMed ID: 12127179) found that 82.7% of postmenopausal women with chronic insomnia had either OSA or UARS. The most prevalent form of sleep-disordered breathing in postmenopausal women was partial upper airway obstruction — the hallmark of UARS — occurring approximately ten times more frequently than full-blown sleep apnea.
A 2022 clinical study published in the Journal of Clinical Sleep Medicine (Vizcarra-Escobar et al., PMC9059598) measured health-related quality of life in adults with UARS compared to those with OSA and the general population. The study found that UARS was associated with significantly impaired quality of life — despite low AHI scores and preserved oxygen saturation. This is a critical finding for women who have been told their sleep study numbers look “mild” or “normal”: the clinical impact of UARS on daily functioning is real and measurable, even when conventional metrics understate the severity.
A 2007 study by Guilleminault and colleagues (PubMed ID: 17552380), using a technique called cyclic alternating pattern analysis to quantify sleep instability, demonstrated that adults with UARS — including 15 women with UARS and 15 age- and sex-matched female controls — had measurably increased sleep instability that correlated directly with fatigue and sleepiness. This finding is important because it confirms that fatigue in UARS arises from sleep instability and fragmentation, not from oxygen desaturation. It is the repeated disruption of sleep architecture — not a drop in oxygen levels — that drives the debilitating tiredness these women experience.
As journalist and breathing researcher James Nestor writes in his bestselling book Breath: The New Science of a Lost Art, “no amount of snoring is normal.” Nestor, referencing the work of Dr. Guilleminault, identifies UARS as “a real problem that should be addressed” and notes that many primary care providers have not been trained to recognize sleep-disordered breathing symptoms — meaning they are “often misdiagnosed and treated in ways that do nothing for the core problem.”
The Hormonal Connection: Why Women’s Risk Changes Across a Lifetime
Female sex hormones play a direct role in airway stability during sleep, which helps explain why UARS risk shifts throughout a woman’s life.
Progesterone acts as a respiratory stimulant. It enhances the activity of the upper airway dilator muscles — the muscles that keep the airway open during sleep — and it stimulates breathing drive through central and peripheral chemoreceptors. During the luteal phase of the menstrual cycle, when progesterone peaks, upper airway muscle activity increases, leading to more stable breathing during sleep.
Estrogen receptors have been identified in the pharyngeal muscles. Experimental studies in animals have demonstrated that estradiol accentuates the contractility of the genioglossal muscle — the primary muscle responsible for keeping the tongue from falling back and obstructing the airway. Estrogen also plays a role in the sleep-wake cycle and in modulating neurotransmitters involved in sleep regulation.
A study by Mohsenin, published in Chest in 2001 (PubMed ID: 11713117), explored why women may have lower measured OSA prevalence despite comparable obesity risk by examining sex differences in upper airway dimensions, compliance, and pharyngeal muscle tone. The findings confirmed that women present with fundamentally different airway mechanics than men — differences in airway size, tissue properties, and neuromuscular control that result in different thresholds and different clinical expressions of sleep-disordered breathing. This is one of the reasons UARS so often goes undetected in women: the diagnostic criteria and clinical expectations were built around male physiology.
Here is the critical window: during perimenopause and menopause, levels of both progesterone and estrogen decline substantially. This decline reduces airway muscle tone, weakens the breathing drive, and shifts body fat distribution toward the android pattern — which can include fat deposition around the upper airway. It also disrupts the coordination between inspiratory muscles and pharyngeal dilator muscles in the central nervous system, a mechanism that may directly contribute to upper airway obstruction.
The result is that a woman who has breathed reasonably well during sleep for decades may begin to develop UARS — or have a mild, subclinical case become clinically significant — precisely during the years when she is also being told her fatigue, pain, and cognitive changes are “just menopause.”
Intriguingly, the hormonal influence on breathing may begin much earlier in life. A 2006 case study published in Fertility and Sterility (Ott et al., PubMed ID: 17027367) investigated whether premenstrual syndrome symptoms might be linked to luteal-phase hyperventilation. The researchers found a marked decline in end-tidal CO₂ during the luteal phase in women with PMS, suggesting that the hormonal shifts of the menstrual cycle may directly alter breathing chemistry — producing symptoms like anxiety, dizziness, and fatigue through hypocapnia rather than through purely psychological mechanisms. While this was a small study and should be interpreted cautiously, it suggests that the breathing-hormone connection in women may be relevant across the entire reproductive lifespan, not only at menopause.
Patrick McKeown, author of The Breathing Cure and founder of the Oxygen Advantage® method, identifies this hormonal transition as a critical vulnerability. His most recent book, The Breathing Cure for Better Sleep, explicitly targets the drivers of sleep-disordered breathing, including UARS and OSA, and addresses how breathing retraining can help improve menopause symptoms — including the sleep disruption, fatigue, and autonomic instability that accompany hormonal decline.
UARS and the Functional Somatic Syndromes: A Documented Connection
One of the most significant research findings in the UARS literature is its overlap with what medicine calls the functional somatic syndromes — conditions characterized by symptoms that cannot be fully explained by conventional diagnostic testing. These include chronic fatigue syndrome (ME/CFS), fibromyalgia, and irritable bowel syndrome, among others.
A landmark study by Gold and colleagues, published in CHEST in 2003, systematically compared the symptoms of UARS patients with those of patients with mild-to-moderate and moderate-to-severe obstructive sleep apnea. What they found was striking:
The proportion of women among patients with sleep-disordered breathing increased significantly as the severity of the condition decreased — meaning UARS had the highest percentage of female patients. And the symptoms of UARS closely resembled those of the functional somatic syndromes: sleep-onset insomnia, headaches, irritable bowel syndrome, and alpha-delta sleep (a specific EEG pattern associated with non-restorative sleep) were all significantly more prevalent in the UARS group.
The researchers concluded that the symptom profile of UARS more closely mirrors chronic fatigue and fibromyalgia than it does traditional sleep apnea.
UARS, Chronic Fatigue Syndrome, and Fibromyalgia: Shared Mechanisms
The overlap is not just symptomatic — it appears to be mechanistic.
Alpha-delta sleep intrusion is a hallmark finding in both UARS and fibromyalgia. This is the abnormal intrusion of alpha-frequency brainwave activity (8–13 Hz, normally associated with relaxed wakefulness) into delta-frequency activity (1–4 Hz, the signature of deep, restorative slow-wave sleep). Research published in the Journal of Neurophysiology (2015) explored the thalamic mechanisms underlying this pattern and found evidence suggesting that in fibromyalgia patients, the irregularities in sleep may actually cause the muscle and tissue pain that characterizes the disorder — not the other way around.
Critically, although resolution of alpha-delta sleep intrusion has never been described in fibromyalgia or CFS patients through conventional treatments, it has been observed in UARS patients when their sleep quality improves following treatment that overcomes upper airway resistance — such as rapid palatal expansion or nasal CPAP therapy.
This suggests a directional relationship: address the breathing dysfunction, and the sleep pathology that drives the pain and fatigue may resolve.
A pivotal study by Gold et al., published in Sleep in 2004 (PubMed ID: 15164899), tested this hypothesis directly. Researchers at Stony Brook University studied 28 women with rheumatologist-diagnosed fibromyalgia and compared their sleep breathing patterns to those of 11 women with confirmed UARS, matched for age and body weight. The results were striking: 27 of the 28 women with fibromyalgia had sleep-disordered breathing — 26 with the inspiratory airflow limitation pattern characteristic of UARS, and one with obstructive sleep apnea. Only a single patient showed no breathing abnormality during sleep. The pharyngeal critical pressure measurements in the fibromyalgia group were statistically indistinguishable from the UARS group. When 14 of these fibromyalgia patients were treated with nasal CPAP — a treatment that directly overcomes upper airway resistance — their functional symptoms improved by 23% to 47%, as measured by a validated questionnaire. The researchers concluded that inspiratory flow limitation during sleep may play a direct role in the development of functional somatic syndromes.
This study is especially important because these were women who had been diagnosed with fibromyalgia by rheumatologists — not patients presenting to a sleep clinic. Their breathing dysfunction had gone entirely unrecognized.
A 2024 study by Jonsson and colleagues, published in the Scandinavian Journal of Pain (PubMed ID: 38907689), provided further direct evidence of this connection. The researchers compared arterial blood gas measurements in 36 women with fibromyalgia against 36 age- and sex-matched healthy controls, examining CO₂, oxygen, bicarbonate, pH, and lactate levels to identify hypocapnia and acid-base disturbances consistent with chronic hyperventilation. This study is significant because it moves beyond symptom questionnaires to objective physiological measurement — directly testing whether women with fibromyalgia show the blood-gas signature of dysfunctional breathing. The findings provide high-quality recent evidence connecting fibromyalgia, hypocapnia, and breathing physiology in an all-female cohort.
And this pattern of misdiagnosis appears to be the norm, not the exception. A 2018 study published in Clinical Otolaryngology using drug-induced sleep endoscopy noted that patients with UARS “are often misdiagnosed as having chronic fatigue syndrome, fibromyalgia, or psychiatric disorders,” causing significant delays in appropriate treatment.
In one additional study examining patients with sleep-disordered breathing, approximately half of the women and 6% of the men were also found to have fibromyalgia. Fibromyalgia affects women six to nine times more frequently than men, with prevalence increasing from roughly 4% at age 20 to 8% by age 70 — a pattern that parallels both the demographics of UARS and the hormonal trajectory of declining progesterone and estrogen.
Autonomic Dysfunction: The Common Thread
A 2017 study from Stanford, co-authored by Dr. Guilleminault himself (published in Frontiers in Neuroscience, PMC5625011), examined the autonomic nervous system changes in UARS patients during sleep. All subjects reported daytime tiredness and fatigue (100%), unrefreshing sleep (100%), and difficulty concentrating (100%). Many also reported light-headedness and dizziness upon standing — symptoms of orthostatic intolerance that overlap directly with chronic fatigue syndrome. The researchers found measurable autonomic disturbances associated with inspiratory flow limitation during sleep, reinforcing the connection between subtle breathing dysfunction and whole-body autonomic dysregulation.
This matters because autonomic dysfunction is now recognized as a core feature of both CFS and fibromyalgia, not merely a secondary symptom. A 2025 study published in Frontiers in Medicine confirmed that dysfunctional breathing and hyperventilation are frequently observed in patients with ME/CFS, and that both patterns are associated with increased sympathetic tone and decreased parasympathetic tone, leading to hypocapnia (low CO₂), reduced cerebral blood flow, and symptoms including dizziness, fatigue, and mental fog. A separate 2025 study in the Journal of Clinical Medicine (PMC11818862) demonstrated significant autonomic nervous system dysfunction in CFS patients, including reduced baroreceptor sensitivity and impaired heart rate variability.
The Dementia Connection: How Disordered Breathing May Steal Cognitive Function
Perhaps the most alarming downstream consequence of untreated sleep-disordered breathing in women is its potential link to cognitive decline and dementia.
A prospective study led by Dr. Kristine Yaffe at UCSF, published in the Journal of the American Medical Association in 2011 (PubMed ID: 21828324), followed 298 older women without dementia over approximately five years. The study found that women with sleep-disordered breathing were nearly twice as likely to develop mild cognitive impairment or dementia compared to women without disordered breathing. Among the women with sleep-disordered breathing, 44.8% developed cognitive impairment, compared to 31.1% of those without it.
The critical finding was that the key driver of cognitive decline was intermittent hypoxia — repeated episodes of oxygen deprivation — rather than sleep fragmentation or sleep duration alone. Women who spent a greater proportion of their sleep time in a state of low oxygen were significantly more likely to develop cognitive problems.
The Glymphatic System: Your Brain’s Night Shift
The mechanism connecting disordered breathing to neurodegeneration has become clearer with the discovery of the glymphatic system — a brain-wide waste-clearance pathway first described in 2012–2013. During deep sleep, this system clears metabolic waste products from the brain by flushing cerebrospinal fluid through the interstitial space. Among the waste products it clears are amyloid-beta and tau protein — the same proteins that form the plaques and tangles characteristic of Alzheimer’s disease.
Research has shown that the glymphatic system is dramatically more active during sleep, clearing metabolites approximately twice as fast compared to wakefulness. The extracellular space of the brain expands by roughly 60% during sleep to facilitate this clearance.
Here is where UARS and sleep-disordered breathing become directly relevant: any condition that fragments sleep, prevents sustained deep sleep, or creates intermittent oxygen deprivation can impair glymphatic function. Research published in Frontiers in Neurology (2025, PMC11835678) confirmed that in humans, sleep deprivation impairs CSF-to-blood clearance of amyloid-beta and tau. OSA has been associated with increased amyloid burden over follow-up periods in cognitively normal adults. And the sympathetic nervous system activation caused by repeated breathing arousals directly inhibits the glymphatic clearance that depends on deep, uninterrupted slow-wave sleep.
Nasal obstruction — from a deviated septum, chronic mucosal inflammation, turbinate hypertrophy, or habitual mouth breathing — changes the way a person breathes during sleep and can initiate a cascade from fragmented sleep to glymphatic impairment to neuroinflammatory accumulation. This may be experienced as brain fog, cognitive difficulty, and fatigue long before any formal diagnosis of cognitive decline is made.
The Nasal Breathing Factor: Nitric Oxide and Autonomic Regulation
Underlying many of these connections is a physiological reality that the Oxygen Advantage® method addresses directly: the nose is not merely a passive air hole — it is a sophisticated air-treatment system and a nitric oxide production facility.
The paranasal sinuses continuously produce nitric oxide (NO), a molecule that serves as a vasodilator, bronchodilator, and antimicrobial agent. When you breathe through your nose, nitric oxide is carried into the lungs with each breath, where it improves pulmonary blood flow and enhances oxygen uptake. Mouth breathing bypasses this entirely.
Research published in the American Journal of Physiology has demonstrated that nasal breathing lowers diastolic blood pressure and increases parasympathetic contributions to heart rate variability compared to oral breathing. Nasal breathing activates diaphragmatic movement and reduces the recruitment of accessory inspiratory muscles. It promotes the parasympathetic “rest-and-digest” state that is essential for restorative sleep, efficient digestion, and calm cognitive function.
Chronic mouth breathing does the opposite. It tends to be faster and shallower, it activates the sympathetic nervous system even in the absence of an external threat, and it deprives the body of the nitric oxide that supports vascular health, immune function, and oxygen delivery. A recent randomized controlled trial (2025) studying women aged 35–45 with dysfunctional breathing found that a six-week breathing intervention combined with nocturnal mouth taping produced significant improvements in the high-frequency component of heart rate variability — a direct marker of parasympathetic function and autonomic regulation.
When chronic mouth breathing and hyperventilation become habitual, the result is a self-reinforcing cycle: sympathetic dominance leads to shallow, rapid breathing, which leads to hypocapnia (low CO₂), which leads to further sympathetic arousal, which leads to vasoconstriction, reduced cerebral blood flow, and the symptoms of fatigue, brain fog, pain sensitivity, and poor sleep that characterize CFS, fibromyalgia, and UARS alike.
McKeown’s The Breathing Cure addresses these mechanisms directly, detailing how breathing techniques can improve conditions including PMS, high blood pressure, and sleep disruption, and how nasal breathing supports deeper sleep and improved autonomic balance. His Atomic Focus extends these principles to cognitive performance, exploring how breathing pattern optimization supports sustained attention, stress resilience, and mental clarity — functions that are directly impaired by the autonomic dysregulation and sleep fragmentation described throughout this article.
Do You Recognize These Signs?
One of the most important things to understand about UARS and dysfunctional breathing is that how you breathe during the day carries directly into how you breathe at night. The mouth breathing, upper chest breathing, sighing, and over-breathing patterns that have become habitual during waking hours do not switch off when you fall asleep. They shape airway stability, breathing effort, and nervous system state throughout the night — and their effects accumulate over years.
The clinical picture of UARS and breathing dysfunction in women is rarely a single dramatic symptom. It is more often a constellation of signs that, taken together, paint a recognizable pattern. You may want to consider whether breathing dysfunction is playing a role if you experience several of the following:
• Waking unrefreshed despite spending adequate time in bed
• Chronic fatigue, brain fog, poor concentration, or reduced resilience to stress
• Insomnia, frequent waking, or feeling “tired but wired” at bedtime
• Morning headaches, jaw tension, teeth clenching or grinding (bruxism)
• Dry mouth upon waking — a reliable indicator of mouth breathing during sleep
• Habitual mouth breathing, audible breathing, or upper chest breathing during the day
• Poor nasal airflow, chronic nasal congestion, or frequent sighing and yawning
• Anxiety-like symptoms, heart pounding, or breathlessness that may partly reflect a dysregulated breathing pattern rather than a psychological disorder
• Worsening symptoms before menstruation, or a sharp decline in sleep quality during perimenopause
• Widespread pain, light-headedness upon standing, or dizziness that has been attributed to stress or anxiety
If several of these resonate, it does not mean you have UARS — but it does mean that your breathing mechanics deserve a closer look, both during the day and during sleep.
Putting It Together: The Chain from Breathing Dysfunction to Disease
When we step back and look at the full picture, a pattern emerges that is both sobering and empowering:
Dysfunctional breathing (mouth breathing, hyperventilation, upper chest breathing) → increased upper airway resistance during sleep → micro-arousals and sleep fragmentation → loss of deep slow-wave sleep → impaired glymphatic clearance → accumulation of neuroinflammatory waste → alpha-delta sleep intrusion → widespread pain, fatigue, and cognitive dysfunction → chronic sympathetic dominance → further breathing dysfunction.
This is a vicious cycle. And at every stage, women are disproportionately affected — by hormonal fluctuations that alter airway stability, by medical screening criteria that were designed around male presentations, by diagnostic tools that may miss the subtle airflow limitations of UARS, and by a medical culture that has historically attributed unexplained symptoms in women to stress, anxiety, or psychosomatic causes.
What Can Be Done: The Role of Breathing Retraining
The encouraging part of this research is that the entry point into this cycle — breathing pattern — is modifiable. Unlike genetics or age-related hormonal decline, breathing is a behavior. It can be assessed, retrained, and optimized.
As an Oxygen Advantage® Instructor, I work with clients to restore functional breathing through several evidence-supported strategies:
Restoring nasal breathing — both during waking hours and during sleep — re-engages the nitric oxide pathway, supports parasympathetic tone, and reduces upper airway resistance. The evidence shows that nasal breathing improves oxygen uptake, enhances autonomic regulation, and promotes the kind of calm, diaphragmatic breathing pattern that supports deep sleep.
Addressing chronic hyperventilation — by normalizing breathing volume and restoring healthy CO₂ tolerance — counteracts the hypocapnia, cerebral vasoconstriction, and sympathetic dominance that drive many of the symptoms associated with CFS, fibromyalgia, and UARS.
Optimizing breathing during sleep — through techniques including mouth taping (where appropriate and under guidance), lateral sleeping position, and pre-sleep breathing exercises — can reduce the airway resistance events that fragment sleep and impair the glymphatic system’s ability to clear the brain.
Building CO₂ tolerance and improving the BOLT score — the foundational assessment used in the Oxygen Advantage® method — provides a measurable, trackable indicator of breathing efficiency that correlates with autonomic balance, exercise tolerance, and sleep quality.
Restoring proper tongue posture — the nose, tongue, diaphragm, and nervous system work together as a functional unit. When nasal breathing is lost and the tongue no longer rests on the palate, the upper airway loses a critical source of structural and muscular support — especially during sleep, when muscle tone naturally decreases. Re-establishing a resting tongue position on the roof of the mouth, combined with consistent lip seal, helps maintain the airway architecture that resists collapse and narrowing.
Breathing retraining is most effective when it is part of an integrative approach. Depending on the individual, complementary interventions may include myofunctional therapy — which retrains the muscles of the tongue, lips, and face to support proper oral posture and swallowing patterns — and oral appliance therapy, which physically repositions the jaw to improve airway dimensions during sleep. For some women, orthodontic intervention or palatal expansion may also be appropriate. The most effective path is rarely a single modality; it is proper diagnosis, airway-aware care, and consistent retraining of daily breathing habits working together.
The evidence for breathing retraining is not limited to clinical observation. A randomized controlled trial by Thomas and colleagues, published in Thorax in 2003 (PubMed ID: 12554890, PMC1746567), tested breathing retraining against standard asthma education in adults with dysfunctional breathing. The retraining group showed significant improvements in quality of life and symptom scores compared to controls. While this trial was conducted in asthma patients rather than UARS patients, it provides Level 1 evidence that breathing-pattern retraining produces measurable clinical benefit in people with dysfunctional breathing — the same biochemical and biomechanical patterns that overlap with UARS.
For athletes and high performers, breathing dysfunction is not limited to sedentary or deconditioned populations. A 2023 study by Shimozawa and colleagues, published in the Journal of Strength and Conditioning Research (PubMed ID: 35612946), found that biomechanical dysfunctional breathing patterns are prevalent even among competitive athletes. This has direct relevance to athletes who may present with unexplained exertional breathlessness, poor recovery, or sleep disruption — symptoms often attributed to overtraining or fitness when breathing mechanics may be a contributing factor.
When to Seek Professional Evaluation
Breathing retraining can meaningfully support airway function, autonomic regulation, and sleep quality — but it is not a substitute for medical diagnosis. Because UARS is a sleep-breathing disorder with measurable physiological consequences, women with persistent symptoms should be encouraged to seek evaluation from a sleep medicine professional who understands respiratory effort-related arousals and inspiratory flow limitation — not only the apnea-hypopnea index (AHI) used in standard sleep studies, which may miss UARS entirely.
If your sleep study came back “normal” but your symptoms persist, ask whether flow limitation and respiratory effort-related arousals were specifically scored. Many standard polysomnography reports do not include these measures. A 2024 study by Mann and colleagues, published in the Annals of the American Thoracic Society (PubMed ID: 38530665, PMC11298983), demonstrated that flow limitation is associated with excessive daytime sleepiness even in individuals whose AHI falls below the moderate-to-severe threshold. In other words, the standard metric used to decide whether your sleep-disordered breathing is “significant” may be systematically missing the very pattern that is making you tired. A sleep specialist experienced with the full spectrum of sleep-disordered breathing — including UARS and flow limitation — can provide a more complete evaluation.
As a breathing educator, my role is to assess and retrain breathing patterns, optimize nasal function, and support nervous system regulation. When the clinical picture suggests a structural or medical component beyond the scope of breathing retraining, I refer to sleep physicians, ENTs, airway-focused dentists, and myofunctional therapists. The best outcomes happen when these disciplines work together.
A Note on What We Know and What We Don’t
I want to be transparent about the state of the science, because honesty matters more than a tidy narrative.
The research linking UARS to functional somatic syndromes is compelling but still evolving. UARS itself remains a subject of debate in sleep medicine — some researchers consider it a distinct syndrome, while others view it as part of the obstructive sleep apnea spectrum. The JAMA study on sleep-disordered breathing and dementia in women studied women with more severe sleep apnea (AHI ≥ 15), not specifically UARS, so the direct link between UARS and dementia is an inference drawn from the shared mechanism of sleep disruption and intermittent hypoxia rather than a directly proven relationship.
What is well established is that sleep fragmentation, loss of deep sleep, chronic hypoxia, sympathetic dominance, and impaired glymphatic function are harmful — and that all of these are consequences of disordered breathing during sleep, whether that breathing disorder meets the threshold for an OSA diagnosis or not.
The takeaway is not that UARS causes dementia, or that breathing retraining cures fibromyalgia. The takeaway is that breathing dysfunction is a modifiable upstream factor that influences sleep quality, autonomic balance, oxygen delivery, and brain health — and that women are both the most affected population and the most underserved by current diagnostic and treatment models.
If you recognize yourself in any part of this article — the unexplained fatigue, the pain that no one can explain, the sleep that never refreshes, the brain fog that steals your sharpness — consider whether anyone has ever assessed the way you breathe.
It may be the question no one thought to ask.
References and Key Studies Cited
1. Tufik S, Pires GN, Palombini L, Andersen ML. "Prevalence of upper airway resistance syndrome in the São Paulo Epidemiologic Sleep Study." Sleep Medicine, 2022.
2. Gold AR, Dipalo F, Gold MS, O’Hearn DJ. "The symptoms and signs of upper airway resistance syndrome: a link to the functional somatic syndromes." CHEST, 2003.
3. Gold AR, Dipalo F, Gold MS, Broderick J. "Inspiratory airflow dynamics during sleep in women with fibromyalgia." Sleep, 2004; 27(3):459-66. PubMed ID: 15164899.
4. Yaffe K, Laffan AM, Harrison SL, et al. "Sleep-disordered breathing, hypoxia, and risk of mild cognitive impairment and dementia in older women." JAMA, 2011; 306(6):613-9. PubMed ID: 21828324.
5. Vijayan S, et al. "Thalamic mechanisms underlying alpha-delta sleep with implications for fibromyalgia." Journal of Neurophysiology, 2015. PMC4575971.
6. Xie L, Kang H, Xu Q, et al. "Sleep drives metabolite clearance from the adult brain." Science, 2013.
7. Guilleminault C, Stoohs R, Clerk A, Cetel M, Maistros P. "A cause of excessive daytime sleepiness: the upper airway resistance syndrome." CHEST, 1993.
8. Lin Y-N, Lo Y-L, Guilleminault C. "Exploring the abnormal modulation of the autonomic systems during nasal flow limitation in UARS." Frontiers in Neuroscience, 2017. PMC5625011.
9. Shahar E, Redline S, Young T, et al. "Hormone replacement therapy and sleep-disordered breathing." American Journal of Respiratory and Critical Care Medicine, 2003.
10. Driver HS, McLean H, Kumar DV, et al. "The influence of the menstrual cycle on upper airway resistance and breathing during sleep." Sleep, 2005.
11. Cassol CM, Martinez D, et al. "Fibromyalgia and sleep-disordered breathing: the missing link." Arthritis Research & Therapy, 2009. PMC2656224.
12. Bing-Canar H, et al. "Abnormal breathing patterns and hyperventilation in patients with chronic fatigue syndrome." Frontiers in Medicine, 2025.
13. Palombini L, et al. "Treatment of upper airway resistance syndrome in adults: Where do we stand?" Sleep Science, 2015. PMC4608900.
14. Milovanovic B, et al. "Assessment of autonomic nervous system function in patients with CFS." Journal of Clinical Medicine, 2025. PMC11818862.
15. Frontiers in Neurology. "Glymphatic system in neurological disorders and implications for brain health." 2025. PMC11835678.
16. Cheng CY, et al. "Impaired glymphatic system actions in obstructive sleep apnea adults." Frontiers in Neuroscience, 2022. PMC9120580.
17. American Journal of Physiology. "Acute nasal breathing lowers diastolic blood pressure and increases parasympathetic contributions to heart rate variability." 2023.
18. StatPearls (NCBI Bookshelf). "Upper Airway Resistance Syndrome." NBK564402. Updated 2025.
19. Shah MA, Feinberg S, Krishnan E. "Sleep-disordered breathing among women with fibromyalgia syndrome." Journal of Clinical Rheumatology, 2006; 12:277-281.
20. Branco J, Atalaia A, Paiva T. "Sleep cycles and alpha-delta sleep in fibromyalgia syndrome." Journal of Rheumatology, 1994; 21:1113-1117. PubMed ID: 7932424.
21. McKeown P, O’Connor-Reina C, Plaza G. "Breathing Re-Education and Phenotypes of Sleep Apnea: A Review." Journal of Clinical Medicine, 2021. PubMed ID: 33530621. PMC7865730.
22. Nestor J. Breath: The New Science of a Lost Art. Riverhead Books, 2020.
23. McKeown P. The Breathing Cure. OxyAt Books, 2021.
24. McKeown P. The Breathing Cure for Better Sleep. OxyAt Books.
25. McKeown P. Atomic Focus. OxyAt Books, 2021.
26. Vizcarra-Escobar D, et al. "Quality of life in upper airway resistance syndrome." JCSM, 2022. PMC9059598.
27. Guilleminault C, et al. "The cyclic alternating pattern demonstrates increased sleep instability and correlates with fatigue and sleepiness in adults with UARS." Sleep, 2007. PubMed ID: 17552380.
28. Mohsenin V. "Gender differences in the expression of sleep-disordered breathing: role of upper airway dimensions." Chest, 2001. PubMed ID: 11713117.
29. Ott HW, et al. "Symptoms of premenstrual syndrome may be caused by hyperventilation." Fertility and Sterility, 2006. PubMed ID: 17027367.
30. Jonsson K, et al. "Hypocapnia in women with fibromyalgia." Scandinavian Journal of Pain, 2024. PubMed ID: 38907689.
31. Mann DL, et al. "Flow Limitation Is Associated with Excessive Daytime Sleepiness in Individuals without Moderate or Severe OSA." Annals of the American Thoracic Society, 2024. PMC11298983.
32. Thomas M, et al. "Breathing retraining for dysfunctional breathing in asthma: a randomised controlled trial." Thorax, 2003. PMC1746567.
33. Shimozawa Y, et al. "Point Prevalence of the Biomechanical Dimension of Dysfunctional Breathing Patterns Among Competitive Athletes." J Strength Cond Res, 2023. PubMed ID: 35612946.
34. Guilleminault C, et al. "Chronic insomnia, postmenopausal women, and sleep disordered breathing: part 1." J Psychosomatic Research, 2002. PubMed ID: 12127179.
35. Guilleminault C, et al. "From obstructive sleep apnea syndrome to upper airway resistance syndrome: consistency of daytime sleepiness." Sleep, 1992. PubMed ID: 1470801.
This blog reflects the best available scientific evidence as of mid-2026. I encourage readers to verify specific claims with their healthcare providers and to consult the original studies where possible. Science evolves, and so should our understanding.
ABOUT THE AUTHOR
Somatic Movement Educator | Oxygen Advantage® Instructor | Developer of the Functional Living Method™
Nicole Tavernier is a somatic movement educator and Oxygen Advantage® Instructor specializing in the intersection of breathing science, nervous system regulation, and chronic illness recovery. As the developer of the Functional Living Method™ at Tantien Integrative Medicine in Branford, Connecticut, she works with clients locally across the Connecticut Shoreline and Greater New Haven area as well as with clients worldwide — including athletes, physicians, and other high achievers who demand precision from their bodies and their health.
Nicole’s approach is grounded in peer-reviewed research and clinical reasoning. She bridges the gap between what the science shows and what the medical system often overlooks — helping her clients identify and address the breathing dysfunctions, autonomic imbalances, and movement patterns that may be quietly driving their symptoms. Whether working with a woman navigating unexplained fatigue and the complex health transitions of perimenopause, or with a competitive athlete optimizing sleep and recovery, her work integrates Oxygen Advantage® breathing protocols, somatic movement education, and individualized functional assessment to restore the foundational systems that support sleep, cognition, resilience, and quality of life.
If you recognize yourself in this article and want to explore whether breathing dysfunction may be contributing to your symptoms, Nicole offers consultations and programs both in-person and remotely through Tantien Integrative Medicine.
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