International Consensus Statement on Obstructive Sleep Apnea

In the paper

“Occasional snoring (snoring on three or less nights per week) is almost universal in the population with a prevalence of 38%–76% in different populations.66–69”

What the sources say

• ?Not checked — no full text of the sourcecites [66] source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [67]
• Disputed

  The paper defines snoring on at least three nights per week as habitual, so it does not classify three-night-per-week snoring as occasional (introductory passage; page unavailable). Its Results report 16.6% moderate snorers and 59.9% non-snorers in the Saudi sample; the Discussion gives a 17–35% range for habitual snoring across populations, not the claimed 38–76% for occasional snoring. (LLM, conf=0.84)

  Checked by a reasoning model — may be wrong.

  cites [68] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [69] source

In the paper

“These mechanisms include a decrease in topo alpha mRNA and protein,878 changes in proteasome function,879 and small interfering RNA.880”

What the sources say

• ?Not checked — no full text of the sourcecites [878] source
• ?Not checked — no full text of the sourcecites [879] source
• Disputed

  Citation 880 is attached to the small-interfering-RNA portion of the sentence, not the topo alpha or proteasome claims. The Results and Discussion (page numbers not provided) describe HIF-1α-targeting siRNA as an intervention that prevents intermittent-hypoxia-associated resistance, rather than a mechanism that produces it. (LLM, conf=0.85)

  Checked by a reasoning model — may be wrong.

  cites [880] sourceExperimental — accuracy not yet measured

In the paper

“but has not demonstrated a significant, persistent change in AHI or improvement in sleep quality.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [895]
• ?Not checked — no full text of the sourcecites [896] source
• ?Not checked — no full text of the sourcecites [897] source
• ?Not checked — no full text of the sourcecites [899] source
• ?Not checked — no full text of the sourcecites [900] source
• ?Not checked — no full text of the sourcecites [901] source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [902]
• Disputed

  The Sleep apnoea severity results report a statistically significant reduction in AHI on the active-treatment night. The Sleep stage architecture results and Discussion report improved sleep architecture and subjective sleep quality. The study lasted only one night, so it cannot establish whether the AHI change persisted. (LLM, conf=0.89)

  Checked by a reasoning model — may be wrong.

  cites [903] sourceExperimental — accuracy not yet measured
• Partly supported

  The Results and Discussion (pages not provided) report no significant difference in AHI or measured sleep characteristics between the nasal dilator and placebo in nonobese patients with chronic rhinitis. The Trial protocol describes overnight testing of one dilator, not long-term follow-up or multiple treatments, so the paper cannot establish the broader or persistent-treatment claim. (LLM, conf=0.85)

  cites [904] sourceExperimental — accuracy not yet measured

In the paper

“While data from a total of 4563 individuals with OSA was included, the majority of the data came from a single study.1061”

What the sources say

• ?Not checked — no full text of the sourcecites [1060] source
• Disputed

  The Study Design and Data Source section identifies this paper as a prospective observational cohort study, not a meta-analysis. The Results report 2,311 patients analyzed from that cohort, rather than 4,563 individuals pooled across studies; no single-study contribution to a meta-analysis is reported. (LLM, conf=0.88)

  Checked by a reasoning model — may be wrong.

  cites [1061] sourceExperimental — accuracy not yet measured

In the paper

“The effect on BP appears to be sustained over time with continued use of CPAP and some evidence suggests that fixed CPAP devices may be better at decreasing BP than auto-titrating devices (APAP), although better tolerated APAP may be used for longer durations.39”

What the sources say

• Disputed

  Split into 2 atoms — 0 confirmed, 1 partially supported, 1 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  Checked by a reasoning model — may be wrong.

  cites [39] sourceExperimental — accuracy not yet measured

In the paper

“The group solely identified with use of the AASM definition had a high prevalence of hypertension as compared to the group classified using the more conservative 4% definition, supporting the importance of using more inclusive definitions for identifying individuals at risk for hypertension.17”

What the sources say

• Partly supported

  Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [17] sourceExperimental — accuracy not yet measured

In the paper

“This analysis highlighted that the largest differences in mean AHI occurred at lower OSA disease severity, with convergence at higher levels of disease severity, underscoring how different hypopnea definitions may reclassify individuals with mild to moderate OSA.”

What the sources say

• Supported

  Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [14] source

In the paper

“The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) standardized guidelines8 were used to inform the SRs.”

What the sources say

• Supported

  The citation identifies the PRISMA guidelines used by the citing authors, rather than asking this source to verify how the ICS:OSA reviews were conducted. The Abstract describes PRISMA as a reporting guideline for systematic reviews and meta-analyses, and Section 4 says it helps authors report such reviews. Page numbers are not provided in the supplied passages. (LLM, conf=0.91)

  cites [8] source

In the paper

“Several other classifications, based on pathophysiology,36 comorbid conditions,37 and clinical outcomes,38 have also been described.”

What the sources say

• Supported

  Citation 36 is attached to the pathophysiology-based classification, not the classifications based on comorbid conditions or clinical outcomes. In “The PALM Scale, Simplified Approaches, and Potential Novel Targets for Therapy,” the paper presents a scale that categorizes patients with OSA by anatomic and nonanatomic pathophysiologic traits. (LLM, conf=0.94)

  cites [36] source
• ?Not checked — no full text of the sourcecites [37] source
• ?Could not verify

  Citation 38 is attached to the claim about classifications based on clinical outcomes. The Outcomes and Follow-up section measures hypertension and cardiovascular events, while the Statistical Analysis section divides patients by disease severity and CPAP adherence; neither describes a classification based on clinical outcomes. I searched for outcome-based classification and risk stratification in our copy. (LLM, conf=0.76)

  cites [38] sourceExperimental — accuracy not yet measured

In the paper

“Both occasional and habitual snoring are more frequent in men than in women.66–68”

What the sources say

• ?Not checked — no full text of the sourcecites [66] source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [67]
• Supported

  The Discussion reports habitual snoring in 31.4% of men versus 16.2% of women. The Results report any snoring in 53% of men versus 28% of women; subtracting the habitual rates shows that non-habitual snoring was also more frequent in men in this Saudi sample. The Methods classify this less-frequent group as moderate snorers. (LLM, conf=0.88)

  cites [68] source

In the paper

“OSAS is recognized to be a heterogeneous syndrome.32”

What the sources say

• Supported

  The Introduction explicitly describes obstructive sleep apnea as an increasingly recognized complex and heterogeneous disorder. It also identifies heterogeneity in symptoms, physiology, comorbidities, and outcomes. (LLM, conf=0.95)

  cites [32] source

In the paper

“Current guidelines for the treatment of OSA typically take into account several factors including the AHI, presence or absence of symptoms, and associated comorbidities.39”

What the sources say

• Partly supported

  The PAP Therapy recommendations (page unavailable in our copy) consider symptoms such as excessive sleepiness and impaired sleep-related quality of life; the hypertension recommendation considers a comorbidity. The guideline does not establish AHI-based treatment recommendations: its discussion of hypertension says the evidence did not permit recommendations specific to OSA severity. Thus the cited guideline supports some, but not all, of the factors listed. (LLM, conf=0.87)

  cites [39] sourceExperimental — accuracy not yet measured

In the paper

“Habitual snoring, defined as snoring on most nights of the week, is present in as many as 12%–25% of the population.66–69”

What the sources say

• ?Not checked — no full text of the sourcecites [66] source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [67]
• Partly supported

  The Results report habitual snoring in 23.5% of the Saudi sample, which falls within the claimed range. But the paper defines it as loud snoring at least three nights per week, not necessarily most nights, and the Discussion gives a 17%–35% range across other populations rather than 12%–25%. No page numbers are available in our copy. (LLM, conf=0.88)

  cites [68] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [69] source

In the paper

“OSA is associated with a multitude of CV outcomes in observational studies, especially in studies utilizing the CMS definition of OSA, as most CV outcomes are thought to be associated with oxygen desaturation.111”

What the sources say

• Partly supported

  The Introduction (page unavailable) reports observational associations between OSA and cardiovascular morbidity and mortality, and describes intermittent hypoxia as one mechanism of adverse cardiovascular effects. It does not say these associations are especially strong in studies using the CMS definition of OSA, or that most cardiovascular outcomes are associated specifically with oxygen desaturation. (LLM, conf=0.88)

  cites [111] sourceExperimental — accuracy not yet measured

In the paper

“The prevalence of OHS in the general population is unknown, but conservative estimates range between 0.15% and 0.4% amongst adults in the US.82,83”

What the sources say

• ?Not checked — no full text of the sourcecites [82] source
• Partly supported

  The Epidemiology section says the general-population prevalence of OHS is unknown and gives a conservative estimate of approximately 0.4% among US adults. It does not give the claimed lower bound of 0.15%, so this source does not support the full range. (LLM, conf=0.88)

  cites [83] sourceExperimental — accuracy not yet measured

In the paper

“Using rates of obesity, race/ethnicity data, age, and regional prevalence data, it has been estimated that nearly one billion people have OSA worldwide, of which the vast majority is undiagnosed.98”

What the sources say

• Partly supported

  The Results estimate 936 million adults aged 30–69 with OSA worldwide, and Methods > Data collection and analysis describes using BMI, race, age, and geographic proximity to estimate prevalence where country data were unavailable. The Introduction says most cases remain undiagnosed even in developed countries, but the paper does not estimate the undiagnosed share of the global total or establish that it is a vast majority. (LLM, conf=0.85)

  cites [98] sourceExperimental — accuracy not yet measured

In the paper

“As BMI increases, the risk of OSA rises with an increase in prevalence of AHI ≥ 15 from 3.6% in normal weight to 56% in those with BMI ≥40 among men aged 50–70 years.95”

What the sources say

• Supported

  Table 3 (indexed under Discussion; no page supplied) gives model-based AHI ≥15 prevalence estimates for men aged 50–70 of 3.6% at BMI <25 and 56.0% at BMI ≥40. The Results also state that sleep-disordered breathing prevalence was higher at higher BMIs. (LLM, conf=0.95)

  cites [95] source

In the paper

“Among subjects with resistant hypertension, OSA is highly prevalent (up to 85% in one series) and the most common secondary cause of hypertension.113”

What the sources say

• Partly supported

  Section 2 reports OSA in 85% of subjects with resistant hypertension in one clinic-based study. It also reports OSA as the most common condition associated with resistant hypertension in a separate observational study, but does not establish it as the most common secondary cause of hypertension. (LLM, conf=0.86)

  cites [113] sourceExperimental — accuracy not yet measured

In the paper

“An updated estimate based on the Wisconsin data in 2013 indicated higher rates of OSA in 14% of men and 5% of women ages 30–70 in the US over time, attributed to changes in population levels of obesity.95”

What the sources say

• Supported

  The Discussion (p. 1009) estimates that 14% of men and 5% of women aged 30–70 have sleep-disordered breathing with daytime sleepiness, a definition the paper says meets Medicare criteria for an indication of obstructive sleep apnea. It reports that prevalence increased as US obesity rose; the Extrapolation section explains how Wisconsin data were applied to US population estimates. (LLM, conf=0.90)

  cites [95] source

In the paper

“The AASM definition of hypopneas for OSA classification (≥3% desaturation or arousal) is more inclusive and captures more variable sleep disruption phenotypes of OSA, seen in younger, nonobese, and women patients who tend not to desaturate as substantially.36”

What the sources say

• Partly supported

  Split into 2 atoms — 0 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 1 unverifiable. Expand the claim to see per-atom verdicts.

  cites [36] sourceExperimental — accuracy not yet measured

In the paper

“Minority populations have lower rates of clinical diagnosis of OSA despite a higher prevalence than white US populations and greater burden of obesity, diabetes, and CV disease.103,104”

What the sources say

• Partly supported

  The Results (SDB; page unavailable) report that only 1.3% of Hispanic/Latino participants had received a physician diagnosis of sleep apnea despite substantially higher measured SDB prevalence. The At a Glance Commentary describes a high prevalence of obesity, diabetes, and other cardiovascular risk factors in this population. The paper does not establish lower diagnosis rates or a greater burden of those conditions than in white U.S. populations; the Discussion says prior findings on ethnic differences in SDB prevalence were mixed. (LLM, conf=0.88)

  cites [103] sourceExperimental — accuracy not yet measured
• Partly supported

  The Introduction reports more sleep apnea syndrome among African Americans than non-Hispanic whites, and the Discussion reports that 95% of clinically significant OSA cases in the Jackson Heart Sleep Study were undiagnosed. The paper does not establish that clinical diagnosis rates are lower than in white populations, or that minority populations generally have a greater burden of obesity, diabetes, and cardiovascular disease. (LLM, conf=0.87)

  cites [104] sourceExperimental — accuracy not yet measured

In the paper

“Age and BMI are risk factors for OSA in both men and women, though the degrees of their impact vary between the sexes.147”

What the sources say

• Partly supported

  The Population characteristics passage reports higher average BMI among women diagnosed with OSA, and the Discussion calls adiposity a strong OSA risk factor. The paper also notes that OSA is more common in men and that incidence rises in women after menopause. It does not establish that age and BMI are risk factors in both sexes or compare the strength of their effects between men and women; its age-at-menopause analysis is not a comparison of chronological-age effects. (LLM, conf=0.84)

  cites [147] sourceExperimental — accuracy not yet measured

In the paper

“A number of CEA have evaluated the value of managing moderate to severe OSA from a payer perspective: the estimated cost per QALY over 5 years has varied considerably but generally support its value when compared to other accepted interventions (<$50,000 per QALY).140”

What the sources say

• Partly supported

  Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [140] sourceExperimental — accuracy not yet measured

In the paper

“Similarly, in the Outcomes of Sleep Disorders in Older Men (MrOS) study, among 1316 elderly men, mean annualized total healthcare costs were 11.6% higher in untreated subjects with moderate to severe SDB than in those without SDB.136”

What the sources say

• Partly supported

  The Results (Table 1, page not provided) report unadjusted mean annualized costs of $8,305 for men with moderate-to-severe SDB versus $7,441 for men without SDB—a descriptive difference of 11.6% in the 1,316-man cohort. The Additional analyses section says 72 men initiated sleep-apnea treatment during follow-up, so the reported comparison is not specifically for untreated men. The Results also say the adjusted cost difference was not statistically significant. (LLM, conf=0.87)

  cites [136] sourceExperimental — accuracy not yet measured

In the paper

“Weight loss trials show improvement in both diabetes outcomes and reduced sleep apnea severity.123”

What the sources say

• Partly supported

  The Results report that the weight-loss intervention produced greater reductions in sleep apnea severity than the control condition at years 1 and 4. The Methods identify participants as adults with type 2 diabetes, but the paper does not report improved diabetes outcomes; its HbA1c figures describe baseline characteristics only. (LLM, conf=0.88)

  cites [123] sourceExperimental — accuracy not yet measured

In the paper

“Loop gain and other measures of ventilatory control have been measured in men and women, and in post- and pre-menopausal women, with some evidence to suggest sex differences in respiratory control.177–182”

What the sources say

• ?Not checked — no full text of the sourcecites [177] source
• ?Not checked — no full text of the sourcecites [178] source
• ?Not checked — no full text of the sourcecites [179] source
• Supported

  The Abstract says the study measured loop gain in men and women with OSA. The Discussion reports that the women included both premenopausal and postmenopausal participants, and notes possible subtle sex differences in respiratory control despite finding no significant difference in measured loop gain. (LLM, conf=0.88)

  cites [180] source
• ?Not checked — no full text of the sourcecites [181] source
• ?Not checked — no full text of the sourcecites [182] source

In the paper

“OSA is prevalent in 44.6% of men and 13.5% of women aged 30–49 years with BMI of 30–39.9 kg/m2, compared to 7% of men and 1.4% of women whose BMI is less than 25 kg/m2.95”

What the sources say

• Partly supported

  Table 2 (indexed under Discussion; page not provided) gives all four cited estimates for adults aged 30–49 in the specified BMI groups. But it labels them as mild-to-severe sleep-disordered breathing (AHI ≥5), not OSA; the Discussion describes more restrictive criteria for a positive indication of OSA. The figures are supported, but their characterization as OSA prevalence is not. (LLM, conf=0.86)

  cites [95] sourceExperimental — accuracy not yet measured

In the paper

“However, this association with BMI decreases with age, and after age 60 years may be less significant.95”

What the sources say

• Partly supported

  The Results report that BMI was more strongly related to sleep-disordered breathing prevalence in the younger age stratum, supporting the age-related weakening of the association. The paper compares younger adults with a 50–70-year-old group; it does not establish a change specifically after age 60 or show that the association becomes statistically less significant then. The supplied Results passage has no page number. (LLM, conf=0.88)

  cites [95] sourceExperimental — accuracy not yet measured

In the paper

“Some studies suggest this is due to retropalatal fat deposition, while others suggest it is parapharyngeal fat or increased pharyngeal wall thickness that determines the development of OSA in obese individuals.200,202,205–208”

What the sources say

• ?Not checked — no full text of the sourcecites [200] source
• ?Not checked — no full text of the sourcecites [202] source
• ?Not checked — no full text of the sourcecites [205] source
• ?Not checked — no full text of the sourcecites [206] source
• ?Not checked — no full text of the sourcecites [207] source
• Partly supported

  The Discussion (page unavailable) reports studies linking enlarged parapharyngeal fat pads to airway narrowing, while also noting conflicting adjusted findings. It reports increased soft-palate fat in apneics, but does not establish retropalatal fat deposition as a cause of OSA or address increased pharyngeal wall thickness as a determinant. This paper's own findings concern tongue fat. (LLM, conf=0.85)

  cites [208] sourceExperimental — accuracy not yet measured

In the paper

“There are different pathways to disease, such that OSA is a heterogeneous disorder.”

What the sources say

• Partly supported

  The Discussion (p. 4) describes a wide spectrum of sleep-disordered breathing severity, and Risk Factors (p. 5) identifies sex and obesity as risk factors. These findings support variation in the disorder, but the paper does not establish different pathways to disease. (LLM, conf=0.85)

  cites [90] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [107] source
• ?Not checked — no full text of the sourcecites [250] source

In the paper

“Since obesity confers additional CV risk to OSA patients, weight loss directly benefits CV health.215”

What the sources say

• Supported

  The Discussion (page not provided) concludes that weight loss improves the cardiovascular risk-factor profile of patients with obesity and obstructive sleep apnea. It also suggests that obesity independently contributes to hypertension, supporting the claim that obesity adds cardiovascular risk in this population. (LLM, conf=0.86)

  cites [215] sourceExperimental — accuracy not yet measured

In the paper

“This increased airway resistance can narrow the pharyngeal lumen leading to more frequent obstructive events, as demonstrated by Fitzpatrick et al. who found worsening of OSA severity when mouth breathing compared to nose breathing.287”

What the sources say

• Partly supported

  The Results report substantially more obstructive events during oral than nasal breathing, and the summary reports higher upper-airway resistance during oral breathing. The Mouth opening section describes pharyngeal narrowing as a plausible cause of the increased resistance, not an established consequence of it; the claimed causal sequence is therefore not supported. (LLM, conf=0.86)

  cites [287] sourceExperimental — accuracy not yet measured

In the paper

“However, the variant in GPR83 was specific to Caribbean background and data were unavailable for replication.”

What the sources say

• Partly supported

  The Discussion reports an AHI association near GPR83 and says its lead SNPs were enriched in African reference populations, a point the authors considered particularly relevant to participants with Caribbean ancestry. It does not establish that the variant was specific to Caribbean background. The same passage says no independent Hispanic/Latino sample was available for replication, although smaller samples from other ancestry groups were examined; page numbers are unavailable in our copy. (LLM, conf=0.85)

  cites [263] sourceExperimental — accuracy not yet measured

In the paper

“However, candidate gene studies have been underpowered and largely have not been replicated.262”

What the sources say

• Supported

  The paper’s Measurements and Results passage reports that OSA genetic association studies were severely underpowered and that only four of 48 associations had been investigated in at least three studies. Its discussion also describes candidate-gene studies as susceptible to limited replication validity. Together, these support the citing sentence’s broad characterization. (LLM, conf=0.92)

  cites [262] source

In the paper

“Notably, local African ancestry was shown to have a protective effect on the AHI and associated with shorter duration events.”

What the sources say

• Partly supported

  The Admixture mapping section reports that local African ancestry at chromosome 2q37 was associated with lower AHI. It also reports an association between local African ancestry at chromosome 16q12-21 and event duration, but does not give its direction there; the shorter-event finding is stated for global African ancestry in Global ancestry associations. The paper describes a suggested protective association, not a demonstrated protective effect. (LLM, conf=0.84)

  cites [270] sourceExperimental — accuracy not yet measured

In the paper

“While there were several suggestive associations, only one reached genome-wide significance, that is, a variant in RAI1 with NREM AHI in males (but not females)”

What the sources say

• Supported

  The Sex-Combined and Sex-Stratified Analyses (p. 13) report several suggestive associations but only one significant locus: a chromosome 17 locus overlapping RAI1, associated with NREM AHI in men. The same passage says the association reflected results in men, not women. (LLM, conf=0.94)

  cites [265] source

In the paper

“Notably, significant sex by gene variants for sleep apnea was detected for multiple genes, supporting the importance of considering sex-specific genetic effects.”

What the sources say

• Supported

  The Gene-by-Sex Interaction section (p. 13) reports thirteen gene-by-sex interactions after Bonferroni correction and says the results suggest different genetic mechanisms for obstructive sleep apnea in women and men. The Discussion (p. 15) likewise describes multiple significant gene-by-sex interactions as evidence of distinct mechanisms, supporting the call to consider sex-specific genetic effects. (LLM, conf=0.94)

  cites [265] source

In the paper

“Other groups have studied the relationship between subjective (grade) or objective (volume/weight) tonsil evaluation and AHI and reported a trend toward significance328 or a significant association.318,329–334”

What the sources say

• ?Not checked — no full text of the sourcecites [318] source
• ?Not checked — no full text of the sourcecites [328] source
• ?Not checked — no full text of the sourcecites [329] source
• ?Could not verify

  The sleep-disordered breathing passage (section labeled CONCLUSIONS; page unavailable) describes how AHI was measured and used to offer treatment, but says nothing about tonsil evaluation. Searches for tonsil grade, volume, weight, and tonsillar hypertrophy found no passage assessing their association with AHI. (LLM, conf=0.76)

  cites [330] sourceExperimental — accuracy not yet measured
• Supported

  The Results report a significant positive correlation between objective tonsil volume and AHI (p = 0.04), supporting the significant-association part of the cited sentence. The same section notes that tonsil volume was not correlated with polysomnography in the multivariate analysis; the reported trend (p = 0.053) concerned OSA severity rank, not AHI. (LLM, conf=0.91)

  cites [331] source
• ?Not checked — no full text of the sourcecites [332] source
• ?Not checked — no full text of the sourcecites [333] source
• ?Not checked — no full text of the sourcecites [334] source

In the paper

“Several studies have shown an elevated loop gain in OSA compared to controls, although some debate is ongoing as to whether the observed abnormalities are a cause or effect of the disease.362”

What the sources say

• Supported

  In “Is loop gain inherently high in OSA?”, the paper reports that three studies found higher loop gain in OSA than in controls, while three found no difference. The same section says it remains unclear whether higher loop gain is inherent to OSA or induced by it. Page numbers are not provided in our copy. (LLM, conf=0.93)

  cites [362] source

In the paper

“In OSA, the contribution of loop gain to OSA pathogenesis is less clear, but many believe it plays an important role.345–347,360,361”

What the sources say

• ?Not checked — no full text of the sourcecites [345] source
• ?Not checked — no full text of the sourcecites [346] source
• Supported

  The sample-size discussion says elevated loop gain may be important in the development of sleep-related apnoeas in patients with OSA, supporting the claim's qualified statement about its possible role. The Discussion also reports low loop gain in a small elderly OSA subgroup, underscoring that its contribution is not settled across OSA patients. Page numbers are unavailable in our copy. (LLM, conf=0.85)

  cites [347] source
• ?Not checked — no full text of the sourcecites [360] source
• ?Not checked — no full text of the sourcecites [361] source

In the paper

“They also found that tonsil grade was more predictive of OSA than tonsil volume indicating that the actual tonsil volume may be less important than the proportion of space occupied within the OP.327”

What the sources say

• Supported

  The Conclusion states that tonsil grade was more strongly associated with OSA severity than tonsil volume and explains that grade measures the fraction of oropharyngeal space occupied. The Discussion likewise suggests that, in this U.S. adult cohort, the proportion of space occupied may matter more than actual tonsil volume. (LLM, conf=0.94)

  cites [327] source

In the paper

“High loop gain due to high plant gain is clinically less common, but situations in which the lung volume decreases (e.g., supine sleep)355 can increase overall loop gain.”

What the sources say

• Partly supported

  The Results report that supine lung volume was lower than lateral lung volume and that measured dynamic loop gain increased. The Discussion distinguishes this from steady-state loop gain, which it says is unchanged with body position. The cited paper therefore supports the claim for dynamic loop gain, but not an unqualified increase in loop gain overall. (LLM, conf=0.85)

  cites [355] sourceExperimental — accuracy not yet measured

In the paper

“Thus, the arousal threshold has become an important therapeutic target, but its manipulation is a double-edged sword: drugs (hypnotics, sedatives) which delay arousal may allow some stabilization of breathing but may also lead to severe hypoxemia prior to arousal.”

What the sources say

• Partly supported

  The Discussion (p. 5) says raising the arousal threshold could, in theory, stabilize ventilation in some OSA patients, but could instead prolong an apnoea when the airway is highly compromised. The paper describes worsening hypoxaemia during apnoeas (p. 3), but does not say that delaying arousal may cause severe hypoxemia before arousal. (LLM, conf=0.85)

  cites [399] sourceExperimental — accuracy not yet measured
• Supported

  The Introduction says raising the arousal threshold may benefit patients with a low threshold but may harm those with a high threshold if profound blood-gas disturbance occurs before arousal. The Abstract reports improved breathing with eszopiclone in selected patients, without worsening hypoxaemia. The claim describes a possible risk, not an outcome observed in this study. (LLM, conf=0.90)

  cites [400] source
• ?Not checked — no full text of the sourcecites [401] source

In the paper

“the tensor palatini which receives its output from the mandibular branch of the trigeminal nerve.”

What the sources say

• ?Not checked — no full text of the sourcecites [406] source
• ?Not checked — no full text of the sourcecites [407] source
• ?Not checked — no full text of the sourcecites [408] source
• ?Could not verify

  The Methods and Results passages describe the masseter muscles and trigeminal motor nucleus, not the tensor palatini’s innervation. Searches for the tensor palatini and the mandibular branch found no passage addressing the claimed connection; page numbers were not available. (LLM, conf=0.72)

  cites [409] sourceExperimental — accuracy not yet measured

In the paper

“The genioglossus is a large muscle comprising the substance of the tongue and maintains patency of the retroglossal airway.350,354,376”

What the sources say

• Partly supported

  The section “IV. Neurochemical Control of Upper Airway Patency” (page unavailable) calls the genioglossus a tongue muscle and the largest, most powerful upper-airway dilator. This supports its size and role in airway patency, but the copy does not say that it comprises the substance of the tongue or specifically maintains patency of the retroglossal airway. It also cautions that genioglossus activation alone may be insufficient to reduce pharyngeal collapsibility. (LLM, conf=0.84)

  cites [350] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [354] source
• ?Not checked — no full text of the sourcecites [376] source

In the paper

“These neurochemical targets may allow augmentation of hypoglossal motor output and effect genioglossus activity.”

What the sources say

• Supported

  The supplied passage labeled Abstract (no page provided) says that several neuromodulators excite pharyngeal motoneurons and that their inputs contribute to hypoglossal and genioglossus activity. It also identifies K+ channels as a possible shared mechanism, supporting the hedged claim that neurochemical targets may augment motor output and affect genioglossus activity. (LLM, conf=0.89)

  cites [375] source
• Supported

  In “Neural mechanisms in intact preparations,” applying serotonin directly to the hypoglossal motor nucleus increased genioglossus (GG) activity. The paper also notes that this effect varies with sleep state, consistent with the claim’s cautious wording. (LLM, conf=0.91)

  cites [403] source
• ?Not checked — no full text of the sourcecites [404] source
• Partly supported

  The future-treatments passage (section and page not supplied) says strategies to increase hypoglossal output might help patients with upper-airway muscle dysfunction. A separate passage identifies the genioglossus as a key airway dilator muscle, but the copy does not identify neurochemical targets as a means of increasing that output or directly state their effect on genioglossus activity. (LLM, conf=0.82)

  cites [405] sourceExperimental — accuracy not yet measured

In the paper

“The STOP-BANG is an 8-question survey including four subjective and four objective items with each positive item contributing 1 point for a maximum score of 8 points.”

What the sources say

• Partly supported

  The Introduction describes four subjective STOP items and four demographic Bang items; the scoring analysis uses scores up to 8. The paper does not explicitly say that each positive item contributes one point, so that scoring detail is not fully supported by our copy. (LLM, conf=0.82)

  cites [423] sourceExperimental — accuracy not yet measured

In the paper

“Clinical questionnaires validated to assess the risk of OSA include the Berlin,422 STOP-BANG,423 and NoSAS424–428 screening tools.”

What the sources say

• ?Not checked — no full text of the sourcecites [422] source
• Supported

  Citation 423 is attached to STOP-BANG, so this verdict concerns that questionnaire, not Berlin or NoSAS. The Discussion (page not supplied) states that STOP-Bang has been validated as an OSA screening tool and can identify patients at high risk. (LLM, conf=0.94)

  cites [423] source
• Supported

  This source is cited within the NoSAS group, not for the Berlin or STOP-BANG questionnaires. The Introduction describes NoSAS as a screening tool for identifying people at risk of OSA, and the Discussion reports its diagnostic ability across OSA severities (page numbers not provided). (LLM, conf=0.92)

  cites [424] source
• Supported

  The Discussion reports that this hospital-based study confirmed the clinical utility of NoSAS for screening patients at high risk of sleep-disordered breathing. In the citing sentence, this source is one of several citations attached to NoSAS, rather than to the Berlin or STOP-BANG tools. (LLM, conf=0.93)

  cites [425] source
• ?Not checked — no full text of the sourcecites [426] source
• Supported

  The citation is attached to NoSAS. The Methods describe evaluating it as a screening score in patients suspected of sleep-disordered breathing, and the Results report its predictive performance against polysomnography-based criteria. This supports identifying NoSAS as a clinically evaluated risk-screening tool. (LLM, conf=0.90)

  cites [427] source
• Supported

  The citation range 424–428 is attached to NoSAS, so this verdict concerns that tool rather than the separately cited Berlin and STOP-Bang questionnaires. The Introduction says NoSAS was developed and validated to identify people at high risk of sleep-disordered breathing, and the Discussion reports that this study evaluated its screening performance in a sleep clinic. (LLM, conf=0.90)

  cites [428] source

In the paper

“In one study, the FOSQ showed a larger improvement in scores in patients who used >4h of CPAP nightly while there was no difference in scores for the SAQLI.”

What the sources say

• Supported

  The Responsiveness section and Table 7 report a significantly larger FOSQ score improvement in the higher-CPAP-use group, but no significant difference between adherence groups in SAQLI score change. SAQLI scores did improve overall; the claim’s ‘no difference’ is supported as a comparison between CPAP-use groups. (LLM, conf=0.93)

  cites [437] sourceExperimental — accuracy not yet measured

In the paper

“The SAQLI includes 35 questions across four domains: daily functioning, social interactions, emotional functioning, and symptoms and can be combined with a fifth domain that assesses negative impacts of treatment.”

What the sources say

• Partly supported

  The Instruments section identifies the four claimed domains and says an additional subscale covers treatment-related symptoms for people receiving OSA treatment. But Internal Reliability reports 56 SAQLI items across the four domains, not 35; the first three domains alone account for 35 items, while symptoms accounts for 21. Page numbers are unavailable in our copy. (LLM, conf=0.90)

  cites [437] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [439] source
• Partly supported

  The SAQLI section (page not specified) describes a 35-item questionnaire with the four named core domains. Our copy does not describe an optional fifth domain assessing negative treatment impacts, so that part of the claim is unsupported. (LLM, conf=0.86)

  cites [440] sourceExperimental — accuracy not yet measured
• Partly supported

  The Methods section (Quality of Life Measures; page not provided) describes the SAQLI as a 35-item instrument covering the four named domains. It does not describe an optional fifth domain assessing negative treatment impacts, so that part of the claim is unsupported by our copy. (LLM, conf=0.88)

  cites [441] sourceExperimental — accuracy not yet measured

In the paper

“The SAQLI is a health-related QOL questionnaire that is diseasespecific and includes questions focused on evaluating functioning across daily aspects of life affected by poor sleep.”

What the sources say

• Supported

  The Introduction describes the SAQLI as a health-related quality-of-life instrument designed specifically for obstructive sleep apnea. The Instruments section says it evaluates sleep apnea’s effects on daily activities, emotional functioning, social interactions, and symptoms, supporting the description of functioning across daily life. (LLM, conf=0.93)

  cites [437] source
• ?Not checked — no full text of the sourcecites [439] source
• Supported

  The “Sleep Apnoea Quality of Life Index (SAQLI)” section describes the SAQLI as an OSA-specific questionnaire with domains covering daily functioning, social interactions, emotional functioning, and symptoms. This supports the description of a disease-specific quality-of-life questionnaire assessing aspects of life affected by sleep apnoea. (LLM, conf=0.92)

  cites [440] source
• Supported

  The Methods section (Quality of Life Measures) describes the SAQLI as a sleep-apnea-specific quality-of-life instrument. It says the questionnaire captures the adverse impact of sleep apnea on daily functioning, social interactions, emotional functioning, and symptoms, supporting the description of functioning across aspects of daily life affected by poor sleep. (LLM, conf=0.92)

  cites [441] source

In the paper

“The SAQLI and FOSQ both demonstrated the ability to detect change over time after treatment initiation.”

What the sources say

• Supported

  The Discussion states that both instruments were responsive to CPAP treatment over three months. The Sample section also reports significantly higher FOSQ and SAQLI subscores at three-month follow-up. (LLM, conf=0.94)

  cites [437] source
• ?Not checked — no full text of the sourcecites [438] source
• ?Not checked — no full text of the sourcecites [439] source
• Partly supported

  The Discussion reports that the SAQLI detected changes in quality of life over three months among patients receiving OSA-specific treatment. The Evaluative properties section compares the SAQLI with the SF-36, not the FOSQ; the retrieved passages do not support the FOSQ part of the claim. Page numbers were not supplied in our copy. (LLM, conf=0.90)

  cites [440] sourceExperimental — accuracy not yet measured

In the paper

“Both showed large effect sizes (d ≥ 0.8) after CPAP treatment in patients with OSA.”

What the sources say

• Supported

  The Responsiveness section reports large effect sizes after three months of CPAP therapy: 1.15 for FOSQ and 1.0 for SAQLI. Both exceed the claimed threshold of 0.8. (LLM, conf=0.95)

  cites [437] source
• ?Not checked — no full text of the sourcecites [439] source

In the paper

“The FOSQ has 30 questions in five domains: activity, vigilance, intimacy and sex, general productivity, and social outcome.”

What the sources say

• Supported

  The Instruments section describes the FOSQ as a 30-item questionnaire with five subscales: activity level, vigilance, intimacy, general productivity, and social outcome. The Construct Validity table labels the intimacy subscale “Sexual intimacy,” supporting the citing sentence’s wording. (LLM, conf=0.94)

  cites [437] source
• Supported

  The Methods section (Quality of Life Measures) describes the FOSQ as having 30 items and five subscales. Its subscale names match the citing sentence, with minor differences in wording. (LLM, conf=0.94)

  cites [441] source

In the paper

“The ASA checklist was validated in surgical population with a moderate sensitivity (72%–87%) which was comparable to both the STOP and Berlin questionnaires.”

What the sources say

• Supported

  The Discussion states that the study validated the ASA checklist for OSA screening in surgical patients and found its sensitivity similar to the STOP and Berlin questionnaires. Table 2 (under Postoperative Complications) reports ASA sensitivities of 72.1%, 78.6%, and 87.2% at the three AHI cutoffs, matching the rounded range in the claim. Page numbers are not available in the supplied passages. (LLM, conf=0.94)

  cites [489] source

In the paper

“However, they should not be used as a diagnostic tool without confirmatory sleep study testing given the low to moderate specificity and the potential for misdiagnosis.”

What the sources say

• ?Not checked — no full text of the sourcecites [446] source
• ?Not checked — no full text of the sourcecites [464] source
• Partly supported

  Section 2.2 (page unavailable) describes questionnaires as having modest accuracy and says screening can produce false positives and false negatives, supporting the concern about misdiagnosis. It recommends these tools to identify suspected OSA, but does not say that every positive screen requires a confirmatory sleep study; section 2.3 says evidence is insufficient to support delaying surgery for diagnostic sleep testing in most high-risk patients. (LLM, conf=0.85)

  cites [486] sourceExperimental — accuracy not yet measured

In the paper

“Data about postoperative mortality is mixed but generally shows no increased 30-day mortality, which is thought to be due to increased monitoring in this group of patients.”

What the sources say

• ?Not checked — no full text of the sourcecites [468] source
• ?Not checked — no full text of the sourcecites [472] source
• ?Not checked — no full text of the sourcecites [480] source
• Supported

  The Results (Mortality; page unavailable) report no significant difference in 30-day postoperative mortality by OSA risk or history. The Discussion suggests that targeted interventions might explain this finding, and Protocol and Design identifies continuous pulse oximetry and options for additional monitoring among those interventions. The paper presents monitoring as a possible explanation, not a demonstrated cause. (LLM, conf=0.86)

  cites [481] source
• Partly supported

  The Results (Subgroup Analyses) report lower adjusted odds of in-hospital death among surgical patients with OSA, and the Discussion suggests more vigilant care as one possible explanation. The study did not measure 30-day mortality, however, and the Discussion says systematic early recognition through monitoring was unlikely in its own cohort. It therefore does not establish increased monitoring as the explanation. (LLM, conf=0.87)

  cites [482] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [483] source
• Partly supported

  The Results (Adjusted comparisons; page unavailable) report lower in-hospital mortality among bariatric surgery patients with sleep-disordered breathing. The Discussion (page unavailable) reports that another study found no increase in 30-day mortality, but this paper did not measure 30-day mortality. It does not attribute the mortality finding to increased monitoring; it says the reason is unclear and suggests better postoperative care is unlikely. (LLM, conf=0.88)

  cites [484] sourceExperimental — accuracy not yet measured
• Partly supported

  The Results table reports two deaths in Group B and none in Groups A or C, with no statistically significant between-group difference; the study also reviewed deaths within 30 days. It does not characterize the broader mortality evidence as mixed or attribute the lack of a significant difference to increased monitoring. Page numbers are unavailable in our copy. (LLM, conf=0.84)

  cites [485] sourceExperimental — accuracy not yet measured

In the paper

“the Society of Anesthesia and Sleep Medicine Guidelines on preoperative screening and preparation of patients with OSA strongly recommends screening for OSA in the preoperative period.”

What the sources say

• Partly supported

  Section 2.1 recommends identifying adults at risk for OSA before surgery and says practice groups should consider making screening part of standard preanesthetic evaluation. But it grades that recommendation “Weak for,” not strong. Section 2.2 gives a strong recommendation for the use of specified screening tools, which does not make the general screening recommendation strong. (LLM, conf=0.88)

  cites [486] sourceExperimental — accuracy not yet measured

In the paper

“The STOP-BANG questionnaire has a high sensitivity where a score of ≥3 score is associated with an increased risk of moderate-to-severe OSA,470,492,493 and a higher rate of perioperative complications.469,471,473,475–477,485,486,494–496”

What the sources say

• ?Not checked — no full text of the sourcecites [470] source
• Partly supported

  The Abstract and Discussion report high sensitivity for moderate-to-severe OSA at a STOP-Bang score of ≥3. They identify scores of 5–8, rather than the ≥3 cutoff, as indicating a high probability of moderate-to-severe OSA. The Discussion also reports that another study found more postoperative complications among patients classified as STOP-Bang high risk; this paper did not measure that outcome itself. (LLM, conf=0.87)

  cites [492] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [493] source

In the paper

“Despite being common in the general population, snoring or apneas may not be routinely screened for or reported in the primary care setting.509”

What the sources say

• Supported

  The introduction (included in passage [2]) describes sleep disorders as highly prevalent and gives general-population figures for OSA and symptoms suggesting OSA risk. The Results (passage [7]) report that 51 of 101 patients reported snoring on a questionnaire but only one was screened for it during the primary-care encounter; witnessed apnea was likewise reported more often on the questionnaire than documented by the clinician. (LLM, conf=0.88)

  cites [509] source

In the paper

“Among individuals diagnosed with OSA, 38%–80% report snoring, 10%–67% report witnessed apneas, and 32%–40% report excessive daytime sleepiness (ESS ≥ 11).”

What the sources say

• ?Not checked — no full text of the sourcecites [88] source
• Partly supported

  Table 1 (page not supplied) reports ESS ≥ 11 in 32% of participants with moderate-to-severe sleep-disordered breathing and 40% with severe sleep-disordered breathing. It reports witnessed breathing pauses in 38.9% and 66.9%, respectively, but not the claimed 10% lower bound. Its snoring figures are 55.9% and 69.6%, not the claimed 38%–80% range; the study also describes polysomnography-defined sleep-disordered breathing rather than a group explicitly diagnosed with OSA. (LLM, conf=0.90)

  cites [456] sourceExperimental — accuracy not yet measured
• Partly supported

  The Results (page not available in our copy) report that patients with OSA more often reported snoring and witnessed apneas than patients without OSA. The Introduction also discusses sleepiness as an OSA symptom, but the passages found do not give the claimed 38%–80%, 10%–67%, or 32%–40% ranges or an ESS ≥ 11 threshold. (LLM, conf=0.78)

  cites [505] sourceExperimental — accuracy not yet measured

In the paper

“Large community studies have demonstrated habitual snoring (occurring most nights of the week) in 34%–44% of the population, witnessed breathing pauses in 6%–29%, and daytime hypersomnolence in 18%–28% of individuals.”

What the sources say

• ?Not checked — no full text of the sourcecites [88] source
• ?Not checked — no full text of the sourcecites [145] source
• Partly supported

  Table 1 (indexed as Abstract; page unavailable) reports 44.1% snoring often or every day, 29.4% witnessed stopping of breathing, 19.3% tired or sleepy, and 28.0% with an Epworth Sleepiness Scale score of at least 11 in this community cohort. These figures support some values in the claimed ranges, but the paper does not establish the lower endpoints of 34%, 6%, and 18% or attribute the full ranges to multiple community studies. (LLM, conf=0.87)

  cites [456] sourceExperimental — accuracy not yet measured

In the paper

“Studies on patients with untreated OSA have demonstrated that increased caffeine intake is associated with less cognitive impairment523 thereby indicating a potential therapeutic effect of caffeine and evidence for self-treatment of OSA.”

What the sources say

• Partly supported

  The Results report that higher caffeine intake was associated with less cognitive impairment in untreated OSA patients, and the Discussion proposes further research into caffeine’s potential to improve neuropsychological function. The Introduction speculates that greater caffeine use among OSA patients may be an attempt to stay alert, but the study does not establish that patients were self-treating OSA or that caffeine had a therapeutic effect. (LLM, conf=0.82)

  cites [523] sourceExperimental — accuracy not yet measured

In the paper

“In comparison to patients with OSA without nocturia, mean SaO2, time spent in desaturation below 90%, and ODI were worse in OSA patients with nocturia.516”

What the sources say

• Supported

  The Discussion states that mean O2 saturation, T90 (time below 90% saturation), and ODI4 were worse in OSA patients with nocturia than in those without. The Results > Polysomnography section specifies that mean O2 saturation was lower and T90, ODI3, and ODI4 were higher in the nocturia group. (LLM, conf=0.94)

  cites [516] source

In the paper

“A large Canadian population study in 2009 found that 4.3% of the population reported awakening suddenly with gasping or choking rarely or sometimes, and 1.5% reported this symptom occurring once a week or more”

What the sources say

• Partly supported

  The Methods (section 2.1) identify a large Canadian survey conducted in 2009, and the Results (section 3) use the stated gasping-or-choking frequency categories. But our copy does not report that 4.3% answered “rarely or sometimes” or that 1.5% answered “once a week or more”; the Results give associations with diagnosed sleep apnea instead. Searches for both percentages and the frequency categories did not establish the claimed population rates. (LLM, conf=0.83)

  cites [508] sourceExperimental — accuracy not yet measured

In the paper

“of individuals diagnosed with OSA, 14.4% reported nocturnal choking or gasping episodes rarely or sometimes (OR 3.52, 95% CI 1.92–6.46), and 11.2% reported this symptom once a week or more (OR 7.92, 95% CI 3.74–16.74).”

What the sources say

• Partly supported

  The Results section reports that both “rarely or sometimes” and “once a week or more” awakenings with gasping or choking were significantly associated with diagnosed sleep apnea. The Discussion also describes a strong association. Our copy does not provide the claimed percentages, odds ratios, or confidence intervals in the retrieved passages, so those figures cannot be verified. (LLM, conf=0.82)

  cites [508] sourceExperimental — accuracy not yet measured

In the paper

“In addition, as disease severity increases, there is increased specificity and decreased sensitivity.”

What the sources say

• Supported

  The Interpretation explicitly describes a trade-off for level 3 portable devices: specificity increases and sensitivity decreases as disease severity increases. The Diagnostic accuracy of sleep tests section reports the same pattern in studies using multiple severity cut-offs. (LLM, conf=0.95)

  cites [583] source

In the paper

“Also sensitivity decreases and specificity increases when the AHI cut off was moved from 5 to 15 events/h.”

What the sources say

• Partly supported

  Table II (Between-Site Effects) shows sensitivity falling and specificity rising as the cutoff moves from 5 to 15 events/hour, both for all four sites and for the three-site reanalysis. However, the Statistical Analyses section identifies these as RDI thresholds, not AHI cutoffs. (LLM, conf=0.86)

  cites [584] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [585] source

In the paper

“The results showed that type III devices are both sensitive and specific for the diagnosis of OSA.”

What the sources say

• Supported

  The Interpretation section states that level 3 portable devices scored well for both sensitivity and specificity. The Conclusion limits their recommended diagnostic use to patients with a high pretest probability of moderate-to-severe OSA and no substantial comorbidities. (LLM, conf=0.93)

  cites [583] source

In the paper

“MC is associated with AHI but not among women.550”

What the sources say

• Supported

  The Results state that the Mallampati index was correlated with AHI overall (P < 0.05), but that the correlation was not significant among female patients (P > 0.05). This supports the claim if MC refers to Mallampati classification. (LLM, conf=0.92)

  cites [550] source

In the paper

“Home-based testing can broaden access to diagnostic services, in hopes to reduce the substantial economic burden related to OSA and provide consistent results signifying similar effectiveness.138”

What the sources say

• Partly supported

  The Discussion (page not available) reports similar clinical outcomes for high-risk OSA patients and lower costs for payers using the home-based pathway. It does not establish that home testing broadens access to diagnostic services, and its cost finding does not extend to providers, for whom the strategies had similar costs. (LLM, conf=0.86)

  cites [138] sourceExperimental — accuracy not yet measured

In the paper

“Older age and lower ESS were associated with OSA on the subsequent PSG.”

What the sources say

• Supported

  The Results report that, among patients undergoing PSG after a normal or technically inadequate home sleep test, older age was associated with higher odds of OSA and lower ESS scores were also associated with higher odds. Both associations were significant in the logistic regression model. (LLM, conf=0.95)

  cites [615] source

In the paper

“In a prospective single center cross-sectional study, Chernyshev et al. found HSAT was accurate for diagnosing OSA (accuracy 1.0 and 0.95 for AHI cutoff’s of 5 and 15).”

What the sources say

• Partly supported

  The PSG studies section identifies the device as Embletta X100, and Figure 2 reports values of 1.0 and 0.95 at AHI cutoffs of 5 and 15 in acute ischemic stroke patients. Those values are AUROC measures, however, not diagnostic accuracy rates as the citing sentence calls them. (LLM, conf=0.86)

  cites [614] sourceExperimental — accuracy not yet measured

In the paper

“The study by Sharma et al., 2017, was a prospective single center, controlled trial of 105 inpatients with acute CHF, where simultaneous HSAT with ApneaLink and a high-resolution pulse oximetry (HRPO) was performed for a single night.619 The HSAT-derived REI was compared to the HRPO-derived ODI using 30% drop in flow with 4% oxygen desaturations. The receiver operating curve (ROC) analysis showed”

What the sources say

• Partly supported

  The Methods describe same-night ApneaLink portable monitoring and HRPO in hospitalized patients with CHF, and the Results report 105 analyzable patients, an AUC of 0.89 at the REI 5-events/hour threshold, and 88% correct classification of moderate-severe REI. The Methods specify hospitalized CHF and testing after stabilization, but do not establish that all 105 patients had acute CHF. (LLM, conf=0.84)

  cites [619] sourceExperimental — accuracy not yet measured

In the paper

“Both HSAT and PSG events were scored according to the 4% desaturation criteria.”

What the sources say

• Supported

  The Diagnosis of sleep apnea section says respiratory events from both PSG and OCST were scored under the same scoring manual and that the 4% oxygen-desaturation hypopnea rule was used. The 4% requirement is specified for hypopneas, rather than for every type of respiratory event. (LLM, conf=0.93)

  cites [614] sourceExperimental — accuracy not yet measured

In the paper

“However, of note, this later study required only a 50% drop in airflow (no associated desaturation) to define a respiratory event on the PSG.”

What the sources say

• Partly supported

  The Protocol (page unavailable) says PSG was scored using Chicago criteria, and the Discussion (page unavailable) contrasts those criteria with defining hypopneas solely by 4% desaturation. Our copy does not specify a 50% airflow-drop threshold or say that an airflow drop alone defined every PSG respiratory event. (LLM, conf=0.82)

  cites [612] sourceExperimental — accuracy not yet measured

In the paper

“The study by Andrés-Blanco et al., a level 1b study, was a prospective single center in 193 COPD patients, where supervised portable oximetry was compared simultaneously to in-hospital PSG as well as to unsupervised portable oximetry at home.625 A control group of 100 non-COPD patients was also included. An ODI4% cutoff was used for the oximeter. There were no significant differences between COPD”

What the sources say

• Partly supported

  The Results (page unavailable) report no significant difference between COPD and non-COPD groups in oximetry screening performance at the studied cutoffs, including the severe-OSAS cutoff, in both hospital and home settings. But the reported sample sizes do not match the claim: 193 patients formed a training group regardless of COPD status; the test groups comprised 68 COPD and 110 non-COPD patients. The Discussion also states that home oximetry and PSG were performed on different nights, not simultaneously. (LLM, conf=0.90)

  cites [625] sourceExperimental — accuracy not yet measured

In the paper

“A small (N = 33) prospective single center cross-sectional study of patients with stable Gold II and III COPD and symptoms of OSA compared an HSAT (WatchPAT) to in lab PSG and found good sensitivity (92%–96%) with moderate specificities (55%–65%), and a concordance of 79% between the tests for an AHI > 15.”

What the sources say

• Partly supported

  The Abstract and Table 4 report sensitivity of 95.8% and 92.3% and specificity of 55.6% and 65.0% at AHI cut-offs of 5 and 15, respectively. The Results report 78.8% agreement in 33 subjects, but the Data analysis section defines that agreement as either both AHI values exceeding 15 or the values being within 10 events/hour—not simply concordance for AHI >15. The Subjects and Discussion sections describe an unselected, stable COPD cohort with GOLD stage 2 or higher, not a cohort restricted to GOLD II–III patients with OSA symptoms. Page numbers were not available in our copy. (LLM, conf=0.90)

  cites [612] sourceExperimental — accuracy not yet measured

In the paper

“OSA is highly prevalent in the general population and in individuals with CV disease.”

What the sources say

• ?Not checked — no full text of the sourcecites [632] source
• Supported

  The Introduction reports OSA prevalence of 7–10% in the general adult population and explicitly says it is highly prevalent in patients with hypertension, coronary artery disease, stroke, and atrial fibrillation. These passages support the statement about the general population and people with cardiovascular disease. (LLM, conf=0.93)

  cites [633] source
• Partly supported

  The Results (page unavailable) report that 46% of this community-dwelling cohort of older men had an obstructive apnea–hypopnea index of at least 15. The paper also states that sleep apnea is highly prevalent among people with heart failure, but it does not establish OSA prevalence in the general population or across people with cardiovascular disease more broadly. (LLM, conf=0.86)

  cites [634] sourceExperimental — accuracy not yet measured
• Partly supported

  The Background states that OSA is highly prevalent in patients with cardiovascular diseases and reports a 38%–65% prevalence in patients with coronary artery disease. It compares that prevalence with the general population but does not say OSA is highly prevalent in the general population. No page number is provided in our copy. (LLM, conf=0.85)

  cites [635] sourceExperimental — accuracy not yet measured

In the paper

“For example, in a study by Pataka et al., utilizing a 4% desaturation definition, there was good correlation between the ODI4% and the PSG ODI (r = 0.95), and for AHI > 15, ODI4% had a sensitivity, a specificity and an AUC of 82%, 94%, and 90%.616”

What the sources say

• Supported

  Materials and methods defines ODI using desaturations of at least 4% and sets the oximetry cutoff at ODI ≥15. Results reports a correlation of r = 0.95 between oximetry ODI and PSG ODI; Table 1 gives 82% sensitivity, 94% specificity, and AUC 0.90 for ODI ≥15 against AHI >15. (LLM, conf=0.93)

  cites [616] source

In the paper

“However, a number of these studies were downgraded for using the oximetry off the PSG as the comparison to the PSG derived AHI,617,618 or for using highly selective populations.619”

What the sources say

• ?Not checked — no full text of the sourcecites [617] source
• Supported

  Citation 619 is attached to the point about highly selective populations, not the preceding point about oximetry performed off the PSG. In Study limitations (page unavailable), the paper describes recruitment from a tertiary referral hospital’s outpatients with suspected OSA and reports that only 11.69% of the analyzed patients were classified as normal. These details support the citing authors’ reason for downgrading this study. (LLM, conf=0.90)

  cites [618] source
• Supported

  Citation 619 is attached to the point about a highly selective population, not the separate point about oximetry compared with PSG-derived AHI. The Methods section limits enrollment to hospitalized adults with CHF and lists further exclusions; the discussion explicitly says the population was limited to people with CHF and that validity needs confirmation in a more general setting. The decision to downgrade the study is the citing authors’ assessment, not a finding attributed to this paper. (LLM, conf=0.93)

  cites [619] source

In the paper

“The SleepMinder had an area under the curve (AUC) of 0.85 but misclassified 19% of patients using an AHI cutoff of 15 to define SDB and was unable to distinguish obstructive versus central events.”

What the sources say

• Supported

  The Results (AHI algorithm performance) report an AUC of 85.8% at AHI ≥15/h and say SleepMinder misclassified 9 of 47 patients (19%) at that threshold. The Discussion describes distinguishing obstructive from central events as a future enhancement, supporting the stated limitation. The cited AUC of 0.85 is an approximate rendering of 0.858. (LLM, conf=0.92)

  cites [610] source

In the paper

“OSA has been associated with coronary artery calcification,664 plaque instability,665 and vulnerability.644”

What the sources say

• ?Not checked — no full text of the sourcecites [664] source
• Supported

  Citation 665 is attached to “plaque instability,” not to calcification or vulnerability. The Conclusion states that OFDI analysis suggests an association between OSA and plaque instability in patients with coronary artery disease. (LLM, conf=0.93)

  cites [665] source
• ?Not checked — no full text of the sourcecites [644] source

In the paper

“However, another analysis of the full SHHS cohort has shown severe OSA to be an independent predictor of death, and in particular death related to CAD. While this relationship was again strongest in men under 70 years of age (adjusted HR 2.09; 95% CI: 1.31–3.33), it was nonetheless seen across all patients with severe OSA in the study population (adjusted HR 1.46; 95% CI: 1.14–1.86).642”

What the sources say

• Partly supported

  Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [642] sourceExperimental — accuracy not yet measured

In the paper

“Patients who have had prior STEMI are more likely than the general population to have OSA, and have worse event free survival compared to STEMI patients without OSA.666,670”

What the sources say

• Partly supported

  The Abstract says OSA prevalence is 2- to 3-fold higher in patients with a history of myocardial infarction, but it does not specify STEMI. The Results and Conclusions examine the time of MI onset, not event-free survival; the paper does not support the claimed survival comparison. Page numbers are not provided for these passages. (LLM, conf=0.88)

  cites [666] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [670] source

In the paper

“OSA and hypertension (HTN) are highly prevalent conditions in the general population.95,97,677”

What the sources say

• Partly supported

  The Discussion (p. 1009) estimates substantial prevalence of sleep-disordered breathing among US adults aged 30–70 and says the measured definitions meet criteria for an indication of OSA. The paper mentions hypertension as a possible long-term consequence of sleep-disordered breathing, but does not establish that hypertension is highly prevalent in the general population. (LLM, conf=0.88)

  cites [95] sourceExperimental — accuracy not yet measured
• Partly supported

  The Findings report a high prevalence of moderate-to-severe sleep-disordered breathing in the population-based cohort: 23.4% of women and 49.7% of men. The paper examines hypertension as an associated condition, but the cited passages do not establish that hypertension itself is highly prevalent in the general population. (LLM, conf=0.84)

  cites [97] sourceExperimental — accuracy not yet measured
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [677]

In the paper

“OSA is characterized by repeated episodes of UA collapse during sleep, resulting in intermittent hypoxemia and arousals.632–635”

What the sources say

• ?Not checked — no full text of the sourcecites [632] source
• Partly supported

  The Introduction describes repeated complete or partial upper-airway obstruction during sleep. The Discussion links OSA to intermittent hypoxia, but our copy does not say that these episodes cause arousals. (LLM, conf=0.87)

  cites [633] sourceExperimental — accuracy not yet measured
• Partly supported

  The PSG Exposures section defines obstructive apneas and hypopneas in association with oxygen desaturation, and What This Study Adds to the… links sleep apnea with hypoxemia and fragmented sleep (page numbers unavailable). Our copy does not explicitly describe repeated upper-airway collapse or state that it causes arousals, so it supports only part of the attributed characterization. (LLM, conf=0.80)

  cites [634] sourceExperimental — accuracy not yet measured
• Partly supported

  The Discussion says CPAP reverses upper-airway obstruction and hypoxemia, supporting those features of OSA. Our copy does not state that the obstruction occurs in repeated episodes during sleep or that it causes arousals; searches for those terms found no supporting passage. No page number is available in the indexed copy. (LLM, conf=0.85)

  cites [635] sourceExperimental — accuracy not yet measured

In the paper

“The inevitable meta-analyses suggest that OSA confers an increased risk of incident clinically overt CAD in men, with an apparent weaker relationship between OSA and CAD in women.633,635,639”

What the sources say

• ?Could not verify

  The Methods and Results assess cardiovascular and all-cause mortality, not incident coronary artery disease (CAD). The Discussion reports cardiovascular-mortality estimates for women and men but says the evidence was insufficient for a gender subgroup analysis. Searches for incident CAD and coronary heart disease found no passage establishing the claimed sex difference in CAD incidence. (LLM, conf=0.76)

  cites [633] sourceExperimental — accuracy not yet measured
• ?Could not verify

  The Background discusses subsequent cardiovascular events in patients who already have CAD, and the Discussion describes CPAP as secondary prevention. Neither addresses incident CAD risk in men versus women; searches for incident CAD and sex differences found no supporting passage. No page numbers were provided in our copy. (LLM, conf=0.78)

  cites [635] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [639] source

In the paper

“Furthermore, the effects of OSA on BP seem to be more pronounced in subjects with subjective and objective daytime sleepiness686,687; these individuals may have a greater degree of desaturation and higher diastolic BP following SDB events.688”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [686]
• ?Not checked — no full text of the sourcecites [687] source
• Partly supported

  Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [688] sourceExperimental — accuracy not yet measured

In the paper

“A recent study demonstrated a two-fold increase in risk of resistant HTN in African-Americans with severe OSA, and it is notable that the burden of undiagnosed OSA is high in this population.702”

What the sources say

• Partly supported

  The Abstract Results report approximately twofold higher *odds* of resistant hypertension for participants with moderate or severe OSA, and the Discussion states that OSA was largely undiagnosed. For severe OSA alone, however, the Results report adjusted odds of 3.58 relative to no OSA, not a twofold increase; the study reports odds rather than risk. (LLM, conf=0.91)

  cites [702] sourceExperimental — accuracy not yet measured

In the paper

“Despite these limitations, studies that systematically evaluated AF patients using home or laboratory sleep testing report a prevalence of OSA (AHI ≥ 5) of 43%–85%, with prevalence >75% in most studies.704–710”

What the sources say

• Partly supported

  The Results (§3.2; page not available) report OSA in 85% of AF patients, using the AHI ≥5 definition and home sleep testing described in §2.2. This supports the upper end of the cited range, but this paper does not establish the 43% lower end or that prevalence exceeded 75% in most studies. (LLM, conf=0.87)

  cites [704] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [705] source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [706]
• ?Not checked — no full text of the sourcecites [707] source
• ?Not checked — no full text of the sourcecites [708] source
• Supported

  The Methods describe systematic portable sleep testing of patients admitted for AF ablation and define OSA as AHI ≥5. The Results report OSA in 115 of 251 patients (45.8%), within the cited 43%–85% range. This paper serves as one study in the cited group; the sentence does not say that every study found prevalence above 75%. (LLM, conf=0.91)

  cites [709] source
• Partly supported

  The Methods (Ambulatory sleep testing) describe two nights of home testing, and the Results (Prevalence and severity of SA) report sleep apnea at AHI ≥5 in 82.7% of patients with paroxysmal AF, predominantly obstructive. The Discussion also reports an 85% OSA prevalence in a Canadian study. This paper does not establish the claimed 43%–85% range or that prevalence exceeded 75% in most studies; it describes earlier studies as varying from 21% to 62%. (LLM, conf=0.86)

  cites [710] sourceExperimental — accuracy not yet measured

In the paper

“While studies using administrative claims data721 or patientreported diagnosis of OSA722 suggest an association of OSA with incident AF, these studies have a high risk of bias.”

What the sources say

• Supported

  The Methods (p. 2) describe linked insurance-claims data, and the results (p. 1) report a higher incidence of new-onset AF among patients diagnosed with sleep-disordered breathing. The paper studies sleep-disordered breathing rather than verified OSA specifically, but its Study Limitations (p. 5) note that most such patients referred for polysomnography had the obstructive type. The citing authors’ assessment of high risk of bias is not presented as a finding of this source. (LLM, conf=0.87)

  cites [721] source
• ?Not checked — no full text of the sourcecites [722] source

In the paper

“In one, patients with AHI ≥ 5 were twice as likely to develop AF as those with AHI < 5, an effect that was limited to those under age 65; however, adjusting for age, sex, BMI, and prevalent CV disease, mean nocturnal SaO2 but not AHI was an independent predictor of incident AF.414”

What the sources say

• Partly supported

  Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [414] sourceExperimental — accuracy not yet measured

In the paper

“An MA was conducted of 12 prospective cohort studies that followed a total of 25,760 participants for major CV events, fatal and nonfatal stroke, coronary heart disease, and all-cause mortality. It was found that severe OSA is independently associated with an increased risk of stroke, CV disease, and all-cause mortality.”

What the sources say

• Supported

  The Abstract reports 12 prospective cohort studies involving 25,760 participants and lists CVD, coronary heart disease, stroke, and all-cause mortality outcomes. The Discussion states that severe OSA was significantly and independently associated with increased risk of CVD, stroke, and all-cause mortality. The Statistical analyses section says the pooled analysis used the most fully adjusted risk estimates available. (LLM, conf=0.95)

  cites [757] source

In the paper

“OSA is more common in the hFrEF population, with prevalence estimates varying between 12% and 53%.738”

What the sources say

• Supported

  The section “Prevalence of Obstructive Sleep Apnea in Heart Failure with Reduced Ejection Fraction” reports OSA prevalence of 12%–53% in HFrEF patients and says it is higher than in the general population. (LLM, conf=0.95)

  cites [738] source

In the paper

“with greater prevalence in male patients, patients with recurrent strokes, and patients with strokes of unknown etiology.”

What the sources say

• Supported

  The Abstract Results report higher sleep-disordered breathing prevalence in men than women (65% vs 48%), in patients with recurrent versus initial strokes (74% vs 57%), and in patients with strokes of unknown versus other etiologies. The Discussion says the breathing disorder was primarily obstructive and explicitly identifies obstructive sleep apnea as more common in the recurrent-stroke and unknown-etiology groups. (LLM, conf=0.92)

  cites [613] source

In the paper

“Patil et al. performed an MA of five RCTs measuring LVEF by echocardiography or radionuclide ventriculography to compare the efficacy of CPAP against control conditions in patients with hFrEF. While some studies showed modest improvements in the absolute value of LVEF associated with CPAP, most reported changes (typically less than 5%) that would not be considered clinically significant.39”

What the sources say

• ?Could not verify

  Split into 2 atoms — 0 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 2 unverifiable. Expand the claim to see per-atom verdicts.

  cites [39] sourceExperimental — accuracy not yet measured

In the paper

“which ultimately prolongs the hospitalization stay and compromises rehabilitation participation.”

What the sources say

• ?Not checked — no full text of the sourcecites [760] source
• Partly supported

  The Introduction (page unavailable) says stroke patients with obstructive sleep apnea have longer hospitalization and rehabilitation stays and worse functional outcomes than those without it. It does not say that the symptoms themselves prolong hospitalization or compromise participation in rehabilitation. (LLM, conf=0.85)

  cites [761] sourceExperimental — accuracy not yet measured

In the paper

“CPAP adherence has not been associated with weight loss and may even lead to weight gain.”

What the sources say

• Supported

  The Discussion reports no systematic weight change with PAP therapy overall, but finds that higher PAP compliance was associated with weight gain. Section 4.2 specifies that the adherence-related gain was seen in non-obese patients, so the finding does not imply that every adherent patient gains weight. (LLM, conf=0.91)

  cites [791] source
• Supported

  The correlation table reports no association between CPAP use and BMI change (r = 0.02, p = 0.94). The Sleep parameters and CPAP compliance section reports that participants gained an average of 1.6 kg after CPAP treatment, and the Discussion suggests CPAP alone may not reduce body weight. The study is limited to obese patients with obstructive sleep apnea and does not establish that CPAP caused the gain; page numbers are unavailable in our copy. (LLM, conf=0.90)

  cites [792] source
• Supported

  The Abstract reports that most CPAP-treated OSAS patients had no significant weight change and that high adherence did not prevent continued weight gain in 10% of patients. The Discussion also suggests that a CPAP-related decrease in nocturnal energy expenditure might lead to weight gain under certain conditions. This supports the claim’s cautious wording, not a conclusion that adherence causes weight gain. (LLM, conf=0.87)

  cites [793] source
• Supported

  The Discussion states that adherence to CPAP was not associated with weight loss and that subjects with very good adherence had a larger increase in BMI. The Results likewise report a significant BMI increase among subjects meeting the stricter adherence threshold compared with controls. (LLM, conf=0.94)

  cites [794] source

In the paper

“A study by Minic et al. showed that SDB (OSA, CSA, hypoventilation) was present in the majority of patients with PAH, with more than half of patients having significant nocturnal hypoxemia.”

What the sources say

• Supported

  The Characteristics of Subjects section reports SDB in 71% of the studied PAH cohort and nocturnal oxygen desaturation in 60%, defined as more than 10% of sleep time below 90% oxygen saturation. The introduction defines SDB to include OSA, CSA, and sleep-related hypoventilation, although the cohort's reported SDB prevalence comprises OSA and CSA. (LLM, conf=0.93)

  cites [775] source

In the paper

“Untreated OSA can cause impaired cognitive function, decreased concentration, and excessive daytime sleepiness”

What the sources say

• ?Not checked — no full text of the sourcecites [760] source
• Partly supported

  The Discussion (page not available) links OSA with lower cognitive status in stroke rehabilitation patients and notes that patients with OSA outside the stroke setting experience more daytime sleepiness. It does not address decreased concentration, and its findings do not establish that untreated OSA causes all three effects. (LLM, conf=0.84)

  cites [761] sourceExperimental — accuracy not yet measured

In the paper

“Although the mechanism behind PH associated with OSA is not entirely understood, it is postulated to be due to a combination of factors including pulmonary arteriolar remodeling, susceptibility to hypoxia, and underlying left heart disease.”

What the sources say

• Supported

  The “Pulmonary Hypertension and Sleep Apnea” section describes several possible mechanisms rather than a settled explanation. It specifically discusses intermittent hypoxia, direct pulmonary-artery remodeling, and sleep apnea’s contribution to left-sided heart failure and increased pulmonary pressures. The supplied passages do not include page numbers. (LLM, conf=0.92)

  cites [773] source

In the paper

“similar to PAP, the therapeutic effect and likelihood of achieving successful therapy are decreased in obesity.”

What the sources say

• ?Not checked — no full text of the sourcecites [808] source
• Partly supported

  The passage on patient factors (indexed as Abstract; page unavailable) suggests that lower BMI and neck circumference indicate a greater likelihood of oral-appliance treatment success. It does not establish that obesity decreases the therapeutic effect itself, and it cautions that overweight patients can achieve complete resolution of OSA. (LLM, conf=0.85)

  cites [810] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [811] source

In the paper

“A linear correlation between OSA severity and insulin resistance has been documented with greater severity at diagnosis predicting the risk of incident diabetes.”

What the sources say

• Partly supported

  The Results and Discussion report a significant linear correlation between OSA severity, measured by AHI, and insulin resistance, measured by HOMA–IR. The study was cross-sectional and excluded patients with diabetes; it does not show that severity at diagnosis predicts incident diabetes. (LLM, conf=0.90)

  cites [821] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [822] source

In the paper

“Several authors have outlined a role for episodic hypoxia during apneic events promoting increased adipose lipolysis and levels of free fatty acids systemically which have a pro-inflammatory effects leading to dysregulated glucose homeostasis and reduced insulin sensitivity.”

What the sources say

• Partly supported

  The Introduction and Discussion link intermittent hypoxia to adipose lipolysis, elevated circulating free fatty acids, impaired glucose homeostasis and insulin resistance. The Discussion also proposes that fatty-acid release might induce an adipose-tissue pro-inflammatory state, but it does not establish inflammation as the pathway leading to the glucose and insulin effects; it separately proposes lipid accumulation as a way to impair insulin signalling. No page numbers are available in our copy. (LLM, conf=0.85)

  cites [817] sourceExperimental — accuracy not yet measured

In the paper

“An MA by Iftikhar et al. evaluated 16 case–controlled studies to evaluate the association between OSA and insulin resistance. This study found a significant relationship for increasing HOMA-IR with baseline BMI, but not with age, AHI, or gender.”

What the sources say

• Supported

  The 'Meta-Analysis and Meta-Regression of Studies for the Association of Sleep Apnea and Insulin Resistance' section reports 16 case-control studies and an association of increasing HOMA-IR with baseline BMI, but not age, AHI, or gender composition. Table 5 supports the significance distinction (BMI p = 0.003; the other p values are 0.54–0.92). (LLM, conf=0.95)

  cites [656] source

In the paper

“In humans, OSA was associated with increased spontaneous lipolysis that correlated with the severity of OSA as well as insulin resistance and impaired insulin secretion in patients with type 2 DM.”

What the sources say

• Partly supported

  The Results section reports that OSA severity correlated with spontaneous lipolysis and that spontaneous lipolysis correlated with insulin resistance. It links impaired insulin secretion, measured by the disposition index, to epinephrine-stimulated lipolysis—not specifically to spontaneous lipolysis. The Discussion describes augmented lipolysis more broadly as associated with impaired insulin secretion. (LLM, conf=0.88)

  cites [817] sourceExperimental — accuracy not yet measured

In the paper

“fat deposits around the thorax and abdomen reduce chest wall compliance and diminish functional residual capacity, which both increases oxygen demand and contributes to greater nocturnal hypoxia, especially among apneic patients.”

What the sources say

• Partly supported

  The Discussion (page unavailable) links excess body weight to reduced functional residual capacity and greater oxygen desaturation during apnea and hypopnea. It also describes possible effects of abdominal and chest-wall fat on breathing. It does not state that fat reduces chest-wall compliance or that reduced compliance and lung capacity themselves increase oxygen demand; it describes greater oxygen demand as a possible factor that accentuates desaturation. (LLM, conf=0.85)

  cites [802] sourceExperimental — accuracy not yet measured

In the paper

“In MCI patients, the association is less clear, with a highly variable prevalence of OSA (11%–71%) based on OSA diagnostic methods and patient recruitment locations”

What the sources say

• Supported

  The Results section (“Prevalence of OSA in MCI”; page not available) reports OSA prevalence of 11–71% in MCI and shows that rates differ by diagnostic method and recruitment setting. The Results section (“Risk of OSA in MCI”) finds increased risk relative to controls in one study but no difference in the others, supporting the description of the association as less clear. (LLM, conf=0.94)

  cites [834] source

In the paper

“Interestingly, adherence rates are not lower among those with obesity, with some studies even demonstrating superior adherence in this population.”

What the sources say

• Partly supported

  The Adherence to CPAP Treatment section (page not provided) reports that patients using CPAP for more than eight hours daily were more obese than the rest of the cohort, and that higher baseline BMI predicted increasing adherence. This supports an association between greater obesity and better adherence in this cohort, but does not establish the broader claim that adherence rates are not lower among patients with obesity than among patients without obesity. (LLM, conf=0.85)

  cites [793] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [806] source

In the paper

“Evidence shows that OAs are more efficacious and have a greater responder rate among those with lower BMIs.”

What the sources say

• ?Not checked — no full text of the sourcecites [808] source
• Partly supported

  The paper’s discussion of patient factors (indexed as Abstract; page unavailable) says lower BMI is suggested as an indicator of oral-appliance treatment success, supporting a higher likelihood of response. The citing sentence states greater efficacy and responder rates as established facts, whereas the review presents BMI as a suggested, non-universal predictor and does not give a BMI-stratified responder rate. (LLM, conf=0.82)

  cites [810] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [811] source

In the paper

“Higher OSA severity as measured by PSG, specifically those related to an increased hypoxic burden (e.g., T90), has been associated with melanoma aggressiveness,866 pancreatic cancer progression,867 lung cancer prevalence,868 and cancer mortality.869”

What the sources say

• ?Not checked — no full text of the sourcecites [866] source
• Partly supported

  The Results and Discussion associate an OSA diagnosis with differences in pancreatic cancer pathology that the authors interpret as relevant to progression. But the Discussion says OSA severity was not established for all cases; the study does not show an association between PSG-measured hypoxic burden, such as T90, and pancreatic cancer progression. In fact, OSA cases had less nodal involvement and lower average tumor stage than non-OSA cases. (LLM, conf=0.86)

  cites [867] sourceExperimental — accuracy not yet measured
• Supported

  Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [868] source
• ?Not checked — no full text of the sourcecites [869] source

In the paper

“These include increased cancer incidence853 and increased cancer mortality in patients <65 years old with severe OSA854”

What the sources say

• ?Not checked — no full text of the sourcecites [853] source
• Supported

  Citation 854 is attached to the cancer-mortality finding, not the separately cited incidence finding. The Discussion reports that patients aged <65 with higher OSA severity had greater adjusted cancer-mortality risk, and the Abstract concludes that the association was particularly evident in this age group. (LLM, conf=0.93)

  cites [854] source

In the paper

“when epidemiological studies assessed an association of OSA and specific cancers, results were heterogeneous but support a higher incidence of breast cancer,858 primary central nervous system cancers,860 nasal and prostate cancer,861 colorectal cancer,862 and melanoma, kidney, breast, and uterine cancer.863”

What the sources say

• ?Not checked — no full text of the sourcecites [858] source
• ?Not checked — no full text of the sourcecites [860] source
• Supported

  The citation to this paper is attached to the nasal and prostate cancer portion of the sentence, not the other cancer types. The Results report significantly higher risks of both cancers among patients with OSA than in the comparison group. (LLM, conf=0.94)

  cites [861] source
• ?Not checked — no full text of the sourcecites [862] source
• Supported

  Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [863] source

In the paper

“Lastly, CIH may increase expression of genes associated with metastases,881 and cancer cell migration.882”

What the sources say

• ?Not checked — no full text of the sourcecites [881] source
• Supported

  Citation 882 is attached to the cancer-cell-migration part of the sentence. The Results report that intermittent hypoxia increased migration of human breast cancer MDA-MB-231 cells, with the effect varying by the number of hypoxia–reoxygenation cycles. The separate claim about expression of metastasis-associated genes is attached to citation 881, not this source. (LLM, conf=0.92)

  cites [882] source