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Obstructive sleep apnea (OSA) worsens nocturnal asthma, but its potential impact on daytime asthma remains largely unassessed. We investigated whether the sleep disorder is associated with daytime, in addition to nighttime asthma symptoms.
Asthma patients at tertiary-care centers completed the Sleep Apnea scale of the Sleep Disorders Questionnaire (SA-SDQ), and an asthma control questionnaire. SA-SDQ scores ≥36 for men and ≥32 for females defined high OSA risk. Medical records were reviewed for established diagnosis of OSA and continuous positive airway pressure (CPAP) use.
Among 752 asthma patients, high OSA risk was associated similarly with persistent daytime and nighttime asthma symptoms (p<0.0001 for each). A diagnosis of OSA was robustly associated with persistent daytime (p<0.0001), in addition to nighttime (p=0.0008) asthma symptoms. In regression models that included obesity and other known asthma aggravators, high OSA risk retained associations with persistent daytime (odds ratio =1.96 [95% confidence interval 1.31–2.94]) and nighttime asthma symptoms (1.97 [1.32–2.94]). Diagnosed OSA retained an association with persistent daytime (2.08 [1.13–3.82]) but not with nighttime (1.48 [0.82–2.69]) asthma symptoms. CPAP use was associated with lower likelihood of persistent daytime symptoms (0.46 [0.23–0.94]).
Questionnaire-defined OSA risk and historical diagnosis were each associated with persistent daytime asthma symptoms, to an extent that matched or exceeded associations with nighttime asthma symptoms. Unrecognized OSA may be a reason for persistent asthma symptoms during the day as well as the night.
Asthma and obstructive sleep apnea (OSA) are both common disorders [1, 2]. Recent cross-sectional [3–6] and longitudinal  studies found an association of asthma with both OSA symptoms [4, 5, 7] and polysomnography (PSG)-established diagnoses [3, 6]. Bidirectional influences probably exist between the two conditions, and OSA appears to affect asthma control. Continuous positive airway pressure (CPAP) treatment for comorbid OSA improves asthma outcomes such as symptoms [8–10], rescue bronchodilator use , peak expiratory flow rates (PEFR) , and disease-specific quality of life . OSA was found to be a risk factor for frequent exacerbations during the prior year in a large population of difficult-to-control asthma patients . Additionally, in a cross-sectional manner, OSA risk is associated with poorly controlled asthma, as assessed on validated questionnaires .
However, the relationship between the nocturnal sleep disorder and asthma symptoms that occur specifically during daytime hours remains largely unstudied. The above interventional studies [8–10] focused on small numbers of patients enrolled for predominantly nocturnal asthma symptoms, and our previous study could not distinguish between daytime and nocturnal asthma control . Some of the mechanisms that may link OSA with asthma include increased parasympathetic tone during apnea, hypoxemia-related reflex bronchoconstriction, irritation of upper airway (UAW) neural receptors, altered nocturnal neurohormonal secretion, and increased inflammatory mediators . These mechanisms would be expected to affect daytime and nocturnal asthma manifestations differently. Neurally-mediated effects might have mainly nocturnal influence whereas other effects, from local airway and systemic inflammation for example, might have more daytime influence. Information on whether nocturnal OSA is also associated with daytime asthma symptoms could give important insight into mechanisms underlying this relationship.
In this context, we have assembled one of the largest existing cohorts of asthma patients, recruited at two tertiary care centers, to test for separate associations of OSA with daytime and nighttime asthma symptoms. Risk for OSA was assessed prospectively by a symptom inventory. Historical diagnosis of OSA and CPAP use for its treatment were ascertained from medical records. We hypothesized that OSA is associated with both daytime and nighttime asthma symptoms. Preliminary results of this analysis were presented at the May 2009 American Thoracic Society (ATS) meeting and published in abstract form . This study expands on our previous work [4, 13, 16] with a dataset enhanced by subjects enrolled at an additional center, and focuses on relationships between OSA and timing of asthma symptoms that could not have been examined previously .
The study population included asthma patients seen in routine follow-up at the Allergy and Pulmonary subspecialty clinics at the University of Michigan (UM)- Ann Arbor (May 2004 – April 2006) and the University of Wisconsin (UW)- Madison (July 2007– March 2009). Subjects were enrolled in an ongoing study of the relationship between OSA and asthma, which was approved by The University of Michigan Medical School Institutional Review Board for Human Subject Research and The University of Wisconsin Health Sciences Institutional Review Board. Written informed consent was obtained from each subject. Participants were 18–75 years old and had asthma diagnosed (based on ATS criteria ) and managed by an academic specialist. During visits, patients underwent history, physical examination, spirometry and asthma control assessment. Patients seen for urgent asthma visits and pregnant women were excluded.
Study assistants handed out and collected the questionnaires. The survey included two self-administered questionnaires and items regarding demographics.
The first instrument, the Sleep Apnea scale of the Sleep Disorders Questionnaire (SA-SDQ), assessed OSA risk . Its eight symptom-items asked about loud snoring disruptive to the bed partner, pauses in breathing during sleep, sudden gasping arousals from sleep, worsening of snoring while supine or after alcohol, nocturnal sweating and nasal congestion, and history of hypertension. Responses were on a 5-point Likert scale (“never” to “always”). Data on weight, age, smoking, and body mass index (BMI) were rated on a 1 to 5 scale. The SA-SDQ has been validated with PSG in a large sample of sleep patients . Scores range from 12–60, with cut-points of ≥36 for men and ≥32 for females used to define high OSA risk .
The second instrument asked about frequency of daytime and nighttime asthma symptoms following the National Asthma Education and Prevention Program (NAEPP) classification of asthma severity based on clinical features . This allowed separation of daytime from nighttime asthma symptoms. There were four categories of daytime symptom frequency: ≤2 days/week, 3–6 days/ week, daily, and continuously. Similarly, nighttime symptom frequency included: ≤2 nights/ month, 3–4 nights/month, ≥5 nights/month (or > 1 night/week), and frequently. Asthma symptoms occurring >2 days /week defined persistent daytime symptoms and those occurring >2 nights /month defined persistent nighttime symptoms.
Study physicians reviewed medical records for diagnosed comorbid lung diseases (such as allergic bronchopulmonary aspergillosis, chronic obstructive pulmonary disease and interstitial lung diseases), OSA diagnosis (which had been confirmed by polysomnography), and whether or not the patients were using CPAP— as documented in the clinic visit notes at the time of our survey. Data in regard to polysomnography indices or objective CPAP use were not collected in this study. Also noted from charts were established diagnoses of comorbidities known to worsen asthma (rhinitis, chronic sinusitis, nasal polyposis, gastroesophageal reflux disease [GERD], and psychiatric disease specifically depression, anxiety, panic or bipolar disorders) , and current asthma medications.
Obesity was defined by BMI≥30 kg/m2, following Centers for Disease Control guidelines. Given the Caucasian predominance of our sample, African-Americans — a group with particular susceptibility for worse asthma  — were compared to Caucasians and all other races combined. From the SA-SDQ, habitual snoring was identified by scores of 4 or 5 (“usually” or “always”). SAS statistical software Version 9.2 (SAS Institute, Cary, NC) was used for analyses. Two-sample t-tests and chi-squared tests were used to analyze group differences in continuous and categorical variables, respectively.
The main analysis was conducted on data from subjects without OSA and those with diagnosed OSA but not on CPAP treatment at the time of survey. Logistic regression models were constructed to test for univariate associations of persistent daytime or nighttime asthma symptoms with high OSA risk or diagnosed and untreated OSA, demographics, and other factors known to influence asthma control . The same technique was then applied to explore associations of high OSA risk or diagnosed OSA with persistent asthma symptoms among subsets of subjects, ie those with sole persistent daytime, sole persistent nighttime and lastly, those with both daytime and nighttime persistent symptoms. Each of these subsets was compared to the subset of subjects without persistent asthma symptoms in any time period. In multivariate logistic regression models, persistent daytime or nighttime asthma symptoms were each regressed on high OSA risk or diagnosed OSA, while controlling for the above covariates and study site.
Data from subjects with diagnosed OSA were separately tested in logistic regression models for associations of CPAP use with persistent asthma symptoms. Due to the small sample size of CPAP users, multivariate models adjusted only for obesity. Two-sided p-values<0.05 indicated statistical significance.
Among the 938 subjects approached, 873 (93%) agreed to complete the survey. However, 46 were excluded because of comorbid lung diseases including COPD. Among the remaining 828 subjects, 136 (16%) had an established diagnosis of OSA, and among these, 75 were on CPAP treatment at the time of survey and excluded from the main analysis, yielding a sample of n=752 subjects (80% of those approached). Among them, 244 were recruited at the UM and 508 at the UW.
Demographic, physiologic and clinical characteristics of this sample (n=752) are presented in Table 1. Subjects at UM had increased representation of African-Americans (11% vs. 3%, p<0.0001), were more obese (51% vs. 32%, p<0.0001), had worse lung physiology (FEV1%: 88±20 vs. 94±18, p<0.0001; FEV1/FVC: 72±10 vs. 77±9, p<0.0001 and FEF25-75%: 63±30 vs. 70±30, p=0.005), more frequent history of GERD (55% vs. 43%, p=0.002) and psychopathology (30% vs. 24%, p=0.04). They tended to use ICS more frequently (82% vs. 75%, p=0.05), and were more often on LABA (66% vs. 56%, p=0.008) and leukotriene modifiers (45% vs. 19%, p<0.0001).
Table 2 shows the prevalence of daytime and nighttime asthma symptoms: 260 (35%) of the subjects reported persistent daytime symptoms, 283 (38%) reported persistent nighttime asthma symptoms, and 210 (27%) reported both (persistent asthma symptoms daytime and nighttime subset). Among those with persistent daytime symptoms, 50 (19%) did not report nighttime symptoms (persistent asthma symptoms daytime only subset). Conversely, among those with persistent nighttime symptoms, 73 (26%) did not report daytime symptoms (persistent asthma symptoms nighttime only subset). As expected, when compared to subjects without, those with persistent daytime symptoms had worse lung physiology (mean±standard deviation [s.d.]: FEV1% predicted 87±21 vs. 95±18, FEV1/FVC 74±10 vs. 77±9, FEF25-75% predicted 61±29 vs. 71±31, all p<0.0001), as did those with persistent nighttime symptoms (FEV1% predicted 87±21 vs. 94±18, p<0.0001; FEV1/FVC 75±10 vs. 77±9, p=0.0009; FEF25-75% predicted 63±30 vs. 70±31, p=0.003).
Among self-reported OSA symptoms, snoring and witnessed apnea (with any frequency) were endorsed by 581 (77%) and 204 (27%) of the subjects, respectively, while habitual snoring was reported by 200 (27%). The mean (±s.d.) SA-SDQ score was 28±7, and 212 (28%) of the subjects met high OSA risk. In this sample, 60 subjects (8%) had diagnosed and untreated OSA, and their SA-SDQ scores were significantly worse on average than those of other subjects in the sample (37±6 vs. 28±7, p<0.0001).
The prevalence of persistent daytime and nighttime asthma symptoms were similar among subjects with high OSA risk, and both higher among these subjects than among those with lower OSA risk (p<0.0001 for each) (Figure 1). Likewise, among subjects with diagnosed and untreated OSA, the prevalence of persistent daytime and nighttime asthma symptoms were comparable, and each was significantly higher than it was among subjects without an established OSA diagnosis (p<0.0001 and p=0.0006, respectively) (Figure 2).
Univariate analyses (Table 3) showed similar relationships of high OSA risk with persistent daytime and nighttime asthma symptoms, with nearly overlapping confidence intervals. These associations were more robust when using the clinical diagnosis of OSA, particularly in relation to daytime symptoms.
Subjects with asthma symptoms that were persistent during both day and night, in comparison to those without any persistent symptoms, showed the strongest association between persistent asthma and high OSA risk or diagnosed OSA (Table 4), as opposed to subjects whose asthma symptoms persistent just during one of the time periods. Among subjects who had persistent asthma symptoms only during the daytime, as compared to subjects with no persistent symptoms, asthma symptoms were associated with diagnosed OSA and showed a trend toward association with high OSA risk. Among subjects whose asthma symptoms persisted only during the nighttime, as compared to those without persistent symptoms, no significant associations emerged between high OSA risk or diagnosed OSA and persistent asthma symptoms.
In multivariate regression models (Table 5), high OSA risk was significantly associated with higher odds for both persistent daytime and nighttime asthma symptoms. These relationships again showed similar magnitudes: independent of the covariates, a high OSA risk predicted on average 96% higher odds for persistent daytime asthma symptoms (odds ratio=1.96 [95% confidence interval 1.31–2.94]) and a nearly identical 97% higher odds for persistent nighttime asthma symptoms (1.97 [1.32–2.94]). Analogous models with the diagnosed and untreated OSA as the predictor (Table 6), rather than OSA risk, showed a similar association with persistent daytime symptoms: a history of OSA was associated on average with 108% higher odds for persistent daytime asthma symptoms (2.08 [1.13–3.82]). However, the association with persistent nighttime symptoms was attenuated (1.48 (0.82–2.69).
Of these 136 subjects, 75 were using CPAP at the time of survey, as documented in their asthma clinic visit notes. CPAP users and non-users were of similar age (54±11 vs. 52±10, p=0.27), and had similar female gender (57% vs. 62%, p=0.55) and African-American race (44% vs. 45%, p=0.97) predominance; however, their prevalence of obesity may have been slightly higher (83% vs. 72%, p=0.14). In univariate analyses CPAP use was associated with lower odds for persistent daytime asthma symptoms (0.50 [0.25–1.00], p=0.049) and but not nighttime symptoms (0.62 [0.31–1.22], p=0.16). These relationships seemed to strengthen when adjusted for obesity (Table 7), such that CPAP users were on average 54% less likely to report persistent daytime symptoms (0.46 [0.23–0.94]).
Data from this large sample of asthma patients show that symptoms indicative of high OSA risk or diagnosed and untreated OSA are each associated with persistent asthma symptoms during the daytime. These associations were at least as strong as those found between OSA symptoms or history and persistent asthma symptoms at night, and were most robust among subjects who had both persistent daytime and nighttime symptoms. These relationships emerged independently of obesity and other contributors to poor asthma control. Furthermore, CPAP use attenuated the likelihood of persistent daytime symptoms. Although this cross-sectional study cannot prove causal relationships, our data strengthen available evidence for the relationship between OSA and asthma – specifically implicating a role for OSA in daytime asthma control – in a manner analogous to previously reported effects of this same nocturnal sleep disorder on daytime hypertension . These results suggest that OSA may have carry-over effects during the day, possibly through inflammatory pathways that exacerbate asthma, and that CPAP treatment for OSA may improve asthma around the clock.
By testing associations of OSA separately with daytime and nighttime symptoms that could not be separated previously  and in a large sample of patients, the current findings represent a key advance which builds on knowledge generated by earlier reports  that used the Asthma Control Questionnaire (ACQ).The ACQ was validated to assess overall asthma control , and not to discriminate between daytime and nighttime asthma control, as most of its symptom-items do not specify timing. In this large sample of patients, we found significant independent associations of high OSA risk or diagnosed OSA with persistent daytime asthma symptoms that were at least as strong as those found with persistent nighttime symptoms (Table 5 and and66).
Additionally, we observed a reduced likelihood for persistent daytime asthma symptoms (Table 7) with CPAP use among previously diagnosed OSA patients. Previous interventional studies of CPAP therapy for OSA in asthma report improved outcomes, such as asthma symptoms [8–10], rescue bronchodilator use , PEFR , and disease-specific quality of life measured on validated questionnaires ; however, these studies have focused on patients with predominant nocturnal symptoms. In the only study which examined daytime and nighttime asthma symptoms separately in relation to OSA, Chan et al found that two weeks of CPAP in 9 subjects with OSA significantly improved asthma not only during the night but also during the day, and also improved morning and evening pre/postbronchodilator PEFR . Cessation of CPAP returned the PEFR to pre-CPAP levels . Our findings (Table 7) now add to this evidence and together suggest that treatment for OSA in patients with asthma could improve asthma symptoms day and night
The mechanisms through which OSA worsens asthma still remain largely unstudied. Shared features or common comorbid conditions, such as obesity  and GERD , may link OSA with asthma. However, when we controlled for these variables in the multivariate models (Table 5 and and6),6), the associations of interest persisted, as another recent study has also found , suggesting that other links exist. Several mechanisms by which the events of airway obstruction in OSA might lead to immediate, but short lived effects on asthma symptoms have also been proposed. Increased nocturnal bronchial reactivity  could be caused by vagal neural receptor activation that accompany the Muller maneuvers of obstructive events . Hypoxia stimulates the carotid body, and enhances vagal activity and bronchial reactivity . Additionally, short exposure to sustained hypoxia impairs defenses particularly important to asthmatics at night, such as cough  and arousal thresholds to resistive loading , and suppresses perception of asthma symptoms . These effects are short lived in most cases and thus would be expected to affect primarily nighttime asthma.
In contrast, our observed associations of high OSA risk and diagnosed OSA with persistent daytime symptoms (Tables 5 and and6)6) and the “protective” association with CPAP use (Table 7), do suggest that nocturnal OSA events may have carryover effects on asthma during the daytime. Inflammatory changes present in the UAW of OSA patients (reviewed in ) may also be present in the lower airways. Compared with controls, OSA patients have elevated numbers of neutrophils, and higher concentrations of bradykinin and vasoactive intestinal peptide in nasal lavage fluid. Subepithelial edema, mucous gland hypertrophy, reduction of connective tissue and inflammatory cell infiltration were present on histology of surgical specimens from uvulopalatopharyngoplasty and tonsillectomy. In the uvula for example, although with a different cellular profile in each structural layer, this leukocyte-predominant inflammation is present at levels as deep as the musculature and may contribute to the UAW dysfunction. The snoring-related mechanical stress, and local and systemic effects of intermittent hypoxia have been implicated in the occurrence of UAW inflammation [31, 32]. These OSA features may have similar effects on the lower airways. Induced sputum, an established method to evaluate lower airway inflammation  confirms a neutrophilic profile in OSA patients [34, 35] and polymorphonuclear neutrophil cell numbers correlate with AHI . Moreover, preliminary work in animal models shows neutrophilic lung inflammation arising from both apnea-related strenuous respiratory efforts and intermittent hypoxia [36, 37]. Additionally, one established feature of OSA is a sustained state of systemic inflammation, implicated in the associated cardiovascular morbidity , which also shares similarities with asthma-related systemic inflammation . Thus OSA, through direct airway or systemic effects, may exacerbate a neutrophilic phenotype, one that is poorly characterized but increasingly recognized among subsets of asthmatics . CPAP may have multiple beneficial effects on the mechanical and neuromechanical properties of the lower airway, it may ameliorate gastroesophageal reflux and also the systemic and local inflammation [41, 42]. It is also possible that CPAP, through sleep restoration, may help improve asthma control around the clock, as recent studies indicate that proper sleep is an important factor in the control of disease and quality of life of asthma patients [43, 44]. A robust univariate relationship of diagnosed and untreated OSA with persistent nocturnal asthma symptoms was noted (Table 4). Attenuation of this association in the final multivariate model (Table 6) does not negate its existence. Our subset of diagnosed but untreated OSA subjects was small (n=60), relative to much larger subsets of the other covariates included in the model, ie rhinitis (n=674), GERD (n=351), obesity (n=285). The small sample size limited statistical power to test for this specific association. Nevertheless, as our questionnaire suggests, there is likely a substantial burden of unrecognized and untreated OSA among asthmatics, a population which, as our data also put forth, could realize considerable benefit [8–11] by having their sleep disorder addressed.
Limitations of our study include use of a questionnaire-based approach (SA-SDQ) to evaluate OSA symptoms prospectively, in a large number of patients, and also reliance on established clinical diagnoses in only a small number of subjects. However, prospective polysomnography on all subjects would have been prohibitively expensive for this study. Additionally, in a large sample of sleep patients, the SA-SDQ demonstrated high internal validity, and good sensitivity and specificity . This instrument has high diagnostic value in comparison to other sleep apnea screening instruments . Although the SA-SDQ has not been validated specifically in asthma patients, the scale does predict PSG-diagnosed OSA well in other samples [46, 47]. Our observation that the subset of subjects with diagnosed OSA had SA-SDQ scores nearly 10 points higher on average (37±6 vs. 28±7, p<0.0001) suggests that this instrument does have good utility in these patients; however, further studies aimed at its validation in asthmatics are needed.
The possibility of an overlap between OSA symptoms and nighttime asthma may also be raised. However, the symptoms included in the SA-SDQ primarily concern loud snoring and witnessed apneas specifically during sleep, and their worsening when supine or with alcohol. These sleep-related symptoms should be specific to upper rather than lower airway compromise. Further studies are necessary to validate the SA-SDQ specifically in patients with asthma.
Although asthma may contribute to OSA pathogenesis , the cross-sectional design of this study precludes conclusions about causality. In the context of data from interventional studies [8–11] and readily conceived underlying mechanisms as discussed above, our findings are suggestive of an effect of OSA on both daytime and nighttime asthma symptom control. Clearly, research on OSA and asthma is often complicated by shared comorbidities and potential for multidirectional causal pathways. For example, we cannot be certain whether obesity, GERD and psychopathology are more closely tied, etiologically, to asthma or OSA, or some may be intermediary variables in causal pathways between asthma and OSA. Finally, conducting this study in specialty-based clinic populations may have underestimated the true relationships of interest. The main breathing route during sleep is through the nose, and nasal congestion is a recognized risk factor for OSA . The high prevalence of rhinitis corroborated with its “protective” association with asthma symptoms (most likely a treatment effect), may have attenuated the true OSA risk, because nasal steroid treatment improves nasal breathing and reduces AHI in patients with rhinitis . This in turn may have attenuated the association of high OSA risk with asthma symptoms.
In summary, this sizeable study shows associations of at least equal magnitude between OSA, as assessed by symptoms or history, and both daytime and nighttime asthma symptoms. These associations occurred independently of obesity and traditional contributors to poor asthma control. Additionally, CPAP appeared to attenuate the likelihood of persistent daytime asthma symptoms. Our observations suggest that nocturnal OSA could contribute to daytime asthma control. Clinicians should consider OSA as a potential reason for poor asthma control, even in patients with daytime symptoms. Additionally, our data have important implications for local and systemic inflammatory pathways by which these diseases may be associated. Prospective studies with objective sleep and airway assessments of these putative mechanistic links are needed, to better understand and find means to intervene in the relationship of OSA with asthma.
The authors are grateful to the study subjects for their participation. As well, to Carolyn M. Senger, BS, Ashley S. Holland, MPH, Radu C. Nistor, Jesica M. Pedroza, BS, Stephanie V. Hall, BS, Whitney Stalsberg, BS, Roman Aydiko, BS and Padau Yang, BS for assistance with administration of screening questionnaires in clinics and data entry. We recognize the help from the providers and staff at the Pulmonary Clinics and Briarwood Asthma-Airways Center at the University of Michigan- Ann Arbor, and Allergy and Pulmonary Clinics at the University of Wisconsin -Madison in recruiting subjects for this study.
Funding support: National Institutes of Health [T32 NS007222, MO1 RR00042, 1UL1RR025011]; the University of Wisconsin School of Medicine and Public Health, Medical Education and Research Committee - New Investigator Award; the University of Wisconsin School of Medicine and Public Health Department of Medicine; additional resources from the William S. Middleton Memorial Veterans Hospital, Madison, Wisconsin.
Declaration of interest Funding support for this study was from: the University of Michigan Department of Neurology Training Grant [T32 NS007222] and General Clinical Research Center [MO1 RR00042]; the University of Wisconsin School of Medicine and Public Health, Medical Education and Research Committee - New Investigator Award, Department of Medicine, and 1UL1RR025011 from the Clinical and Translational Science Award (CTSA) program of the National Center for Research Resources, National Institutes of Health; and the William S. Middleton Memorial Veterans Hospital, Madison, Wisconsin.
Dr. Mihaela Teodorescu received funding support from the University of Michigan Department of Neurology Training Grant [T32 NS007222] and General Clinical Research Center [MO1 RR00042]; University of Wisconsin School of Medicine and Public Health, Department of Medicine and Medical Education and Research Committee- New Investigator Award, and 1UL1RR025011 from the Clinical and Translational Science Award (CTSA) program of the National Center for Research Resources, National Institutes of Health for asthma-sleep apnea research. She received additional support from and uses facilities at the William S. Middleton Memorial Veterans Hospital, Madison, Wisconsin.
Drs. DA Polomis, MC Teodorescu, RE Gangnon, FB Consens and Ms. AG Peterson have no relationships to disclose.
Dr. RD Chervin has received research support from the National Institutes of Health and Fox Foundation; has served on advisory boards for Pavad Medical, not-for-profit Sweet Dreamzzz, and the NHLBI (Sleep Disorders Research Advisory Board); is a section editor for UpToDate, Inc.; received support for educational purposes from Philips Respironics, Inc. and Fisher Paykel, Inc.; has consulted for Arena Pharmaceuticals, Proctor & Gamble, and Zansors; serves on boards of directors for the American Academy of Sleep Medicine and the International Pediatric Sleep Association; and is named in University of Michigan patents for algorithms and devices to facilitate diagnosis and treatment of sleep disorders.
Dr. NN Jarjour receives funding support from the National Institutes of Health, GlaxoSmithKline and Bristol Meyer Squib; he received honorarium <$5,000 from the Saudi Thoracic Society for a GSK-supported continuing medical education program.
Conception and design: M. Teodorescu, D.A. Polomis
Data collection: M. Teodorescu, D.A. Polomis, M.C. Teodorescu and A.G. Peterson
Data analysis: M. Teodorescu, R.E. Gangnon
Interpretation of the data: M. Teodorescu, D.A. Polomis, R.E. Gangnon, R.D. Chervin, F.B.
Consens, M.C. Teodorescu, A.G. Peterson, N.N. Jarjour
Drafting of the article: M. Teodorescu, D.A. Polomis
Critical revision of the article for important intellectual content: D.A. Polomis, R.D. Chervin, R.E. Gangnon, M.C. Teodorescu, F.B. Consens, N.N. Jarjour
No scientific writing assistance was used for this article.
The contents of this article do not represent the views of the Department of Veterans Affairs or the United States Government.