Concept: Obstructive sleep apnea
Background:Short sleep and weight gain are inversely related. Sleep deprivation acutely increases food intake but little is known about eating behavior in chronically sleep-deprived, obese individuals.Objective:To characterize the relationship between sleep, food intake and alcohol consumption under free-living conditions in obese, chronically sleep-deprived individuals.Design:Cross-sectional study of a cohort of obese men and premenopausal women.Subjects:A total of 118 obese subjects (age: 40.3±6.7 years; 91 females/27 males; body mass index 38.7±6.4 kg m(-2)).Measurements:Energy, macronutrient, alcohol and caffeine intake assessed by 3-day food records. Sleep duration estimated by actigraphy. Respiratory disturbance index assessed by a portable device.Results:Subjects slept 360.7±50.2 min per night and had a total energy intake of 2279.1±689 kcal per day. Sleep duration and energy intake were inversely related (r=-0.230, P=0.015). By extrapolation, each 30-min deficit per day in sleep duration would translate to an ∼83 kcal per day increase in energy intake. In addition, sleep apnea was associated with a shift from carbohydrate to fat intake. Alcohol intake in subjects consuming >3.5 g of alcohol per day (N=41) was inversely related to sleep duration (r=-0.472, P=0.002).Conclusions:Shorter sleep duration and obstructive sleep apnea are associated with higher energy, fat and alcohol intakes in obese individuals. The importance of this study relies on the population studied, obese subjects with chronic sleep deprivation. These novel findings apply to the large segment of the US population who are obese and sleep-deprived.
Background Obstructive sleep apnea is associated with an increased risk of cardiovascular events; whether treatment with continuous positive airway pressure (CPAP) prevents major cardiovascular events is uncertain. Methods After a 1-week run-in period during which the participants used sham CPAP, we randomly assigned 2717 eligible adults between 45 and 75 years of age who had moderate-to-severe obstructive sleep apnea and coronary or cerebrovascular disease to receive CPAP treatment plus usual care (CPAP group) or usual care alone (usual-care group). The primary composite end point was death from cardiovascular causes, myocardial infarction, stroke, or hospitalization for unstable angina, heart failure, or transient ischemic attack. Secondary end points included other cardiovascular outcomes, health-related quality of life, snoring symptoms, daytime sleepiness, and mood. Results Most of the participants were men who had moderate-to-severe obstructive sleep apnea and minimal sleepiness. In the CPAP group, the mean duration of adherence to CPAP therapy was 3.3 hours per night, and the mean apnea-hypopnea index (the number of apnea or hypopnea events per hour of recording) decreased from 29.0 events per hour at baseline to 3.7 events per hour during follow-up. After a mean follow-up of 3.7 years, a primary end-point event had occurred in 229 participants in the CPAP group (17.0%) and in 207 participants in the usual-care group (15.4%) (hazard ratio with CPAP, 1.10; 95% confidence interval, 0.91 to 1.32; P=0.34). No significant effect on any individual or other composite cardiovascular end point was observed. CPAP significantly reduced snoring and daytime sleepiness and improved health-related quality of life and mood. Conclusions Therapy with CPAP plus usual care, as compared with usual care alone, did not prevent cardiovascular events in patients with moderate-to-severe obstructive sleep apnea and established cardiovascular disease. (Funded by the National Health and Medical Research Council of Australia and others; SAVE ClinicalTrials.gov number, NCT00738179 ; Australian New Zealand Clinical Trials Registry number, ACTRN12608000409370 .).
Obstructive sleep apnea (OSA) has been reported to be a risk factor for cardiovascular (CV) disease. Although the apnea-hypopnea index (AHI) is the most commonly used measure of OSA, other less well studied OSA-related variables may be more pathophysiologically relevant and offer better prediction. The objective of this study was to evaluate the relationship between OSA-related variables and risk of CV events.
OBJECTIVE We tested the hypothesis of an independent cross-sectional association between obstructive sleep apnea (OSA) severity and glycated hemoglobin (HbA(1c)) in adults without known diabetes. RESEARCH DESIGN AND METHODS HbA(1c) was measured in whole-blood samples from 2,139 patients undergoing nocturnal recording for suspected OSA. Participants with self-reported diabetes, use of diabetes medication, or HbA(1c) value ≥6.5% were excluded from this study. Our final sample size comprised 1,599 patients. RESULTS A dose-response relationship was observed between apnea-hypopnea index (AHI) and the percentage of patients with HbA(1c) >6.0%, ranging from 10.8% for AHI <5 to 34.2% for AHI ≥50. After adjustment for age, sex, smoking habits, BMI, waist circumference, cardiovascular morbidity, daytime sleepiness, depression, insomnia, sleep duration, and study site, odds ratios (95% CIs) for HbA(1c) >6.0% were 1 (reference), 1.40 (0.84-2.32), 1.80 (1.19-2.72), 2.02 (1.31-3.14), and 2.96 (1.58-5.54) for AHI values <5, 5 to <15, 15 to <30, 30 to <50, and ≥50, respectively. Increasing hypoxemia during sleep was also independently associated with the odds of HbA(1c) >6.0%. CONCLUSIONS Among adults without known diabetes, increasing OSA severity is independently associated with impaired glucose metabolism, as assessed by higher HbA(1c) values, which may expose them to higher risks of diabetes and cardiovascular disease.
Insufficient sleep duration and obstructive sleep apnea, two common causes of sleep deficiency in adults, can result in excessive sleepiness, a well-recognized cause of motor vehicle crashes, although their contribution to crash risk in the general population remains uncertain. The objective of this study was to evaluate the relation of sleep apnea, sleep duration, and excessive sleepiness to crash risk in a community-dwelling population.
Comparative Effectiveness of Maxillomandibular Advancement and Uvulopalatopharyngoplasty for the Treatment of Moderate to Severe Obstructive Sleep Apnea
- Journal of oral and maxillofacial surgery : official journal of the American Association of Oral and Maxillofacial Surgeons
- Published over 5 years ago
PURPOSE: To directly compare the clinical effectiveness of maxillomandibular advancement (MMA) and uvulopalatopharyngoplasty (UPPP)-performed alone and in combination-for the treatment of moderate to severe obstructive sleep apnea (OSA). PATIENTS AND METHODS: The investigators designed and implemented a retrospective cohort study composed of patients with moderate to severe OSA (baseline AHI >15). The predictor variable was operative treatment and included MMA, UPPP, and MMA followed by UPPP (UPPP/MMA). The primary outcome variable was the apnea-hypopnea index (AHI) measured preoperatively and 3 months to 6 months postoperatively. Other variables were grouped into the following categories: demographic, respiratory, and sleep parameters. Descriptive and bivariate statistics were computed. RESULTS: The sample was composed of 106 patients grouped as follows: MMA (n = 37), UPPP (n = 34), and UPPP/MMA (n = 35) for treatment of OSA. There were no significant differences between the 3 groups for the study variables at baseline, except for AHI. Surgical treatment resulted in a significant decrease in AHI in each group: MMA (baseline AHI, 56.3 ± 22.6 vs AHI after MMA, 11.4 ± 9.8; P < .0001), UPPP/MMA (baseline AHI, 55.7 ± 49.2 vs AHI after UPPP/MMA, 11.6 ± 10.7; P < .0001), and UPPP (baseline AHI, 41.8 ± 28.0 vs AHI after UPPP, 30.1 ± 27.5; P = .0057). After adjusting for differences in baseline AHI, the estimated mean change in AHI was significantly larger for MMA compared with UPPP (MMA AHI, -40.5 vs UPPP AHI, -19.4; P = < .0001). UPPP/MMA was no more effective than MMA (P = .684). CONCLUSION: The results of this study suggest that MMA should be the surgical treatment option of choice for most patients with moderate to severe OSA who are unable to adequately adhere to CPAP.
OBJETIVE: To evaluate the effectiveness of adenotonsillectomy for the treatment of obstructive sleep apnea hypopnea syndrome (OSAHS) in children by respiratory polygraphy (RP). MATERIAL AND METHODS: Prospective study was conducted on children referred with clinical suspicion of OSAHS. A clinical history was taken and a general physical and ENT examination was performed on all patients. RP was performed before adenotonsillectomy and six months afterwards. Patients with craniofacial syndromes, neuromuscular disorders, and severe concomitant disease were excluded. RESULTS: We studied 150 children (67. 8% male), with a mean age of 3.74±1.80 years and a BMI of 41.70±31.75. A diagnosis of OSAHS was made if the total number of respiratory events, apneas and hypopneas, divided by the total study time (RDI) was > 4.6, using RP before undergoing adenotonsillectomy. The mean respiratory disturbance index (RDI) was 15.18±11.11, with 58.7% (88) of with severe OSAHS (RDI>10). There was a significant improvement in all clinical and polygraphic variables six months after adenotonsillectomy. The residual OSAHS was 14%. The preoperative RDI was significantly associated with persistent disease (P=.042). CONCLUSIONS: Respiratory polygraphy is useful for monitoring the efficacy of surgical treatment by adenotonsillectomy in children with OSAHS.
macronutrient intake has been found to affect sleep parameters including obstructive sleep apnoea (OSA) in experimental studies, but there is uncertainty at the population level in adults.
Modern lifestyle has profoundly modified human sleep habits. Sleep duration has shortened over recent decades from 8 to 6.5 hours resulting in chronic sleep deprivation. Additionally, irregular sleep, shift work and travelling across time zones lead to disruption of circadian rhythms and asynchrony between the master hypothalamic clock and pacemakers in peripheral tissues. Furthermore, obstructive sleep apnea syndrome (OSA), which affects 4 - 15% of the population, is not only characterized by impaired sleep architecture but also by repetitive hemoglobin desaturations during sleep. Epidemiological studies have identified impaired sleep as an independent risk factor for all cause of-, as well as for cardiovascular, mortality/morbidity. More recently, sleep abnormalities were causally linked to impairments in glucose homeostasis, metabolic syndrome and Type 2 Diabetes Mellitus (T2DM). This review summarized current knowledge on the metabolic alterations associated with the most prevalent sleep disturbances, i.e. short sleep duration, shift work and OSA. We have focused on various endocrine and molecular mechanisms underlying the associations between inadequate sleep quality, quantity and timing with impaired glucose tolerance, insulin resistance and pancreatic β-cell dysfunction. Of these mechanisms, the role of the hypothalamic-pituitary-adrenal axis, circadian pacemakers in peripheral tissues, adipose tissue metabolism, sympathetic nervous system activation, oxidative stress and whole-body inflammation are discussed. Additionally, the impact of intermittent hypoxia and sleep fragmentation (key components of OSA) on intracellular signaling and metabolism in muscle, liver, fat and pancreas are also examined. In summary, this review provides endocrine and molecular explanations for the associations between common sleep disturbances and the pathogenesis of T2DM.
Pediatric OSA is associated with cognitive risk. Since adult OSA manifests MRI evidence of brain injury, and animal models lead to regional neuronal losses, pediatric OSA patients may also be affected. We assessed the presence of neuronal injury, measured as regional grey matter volume, in 16 OSA children (8 male, 8.1 ± 2.2 years, AHI:11.1 ± 5.9 events/hr), and 200 control subjects (84 male, 8.2 ± 2.0 years), 191 of whom were from the NIH-Pediatric MRI database. High resolution T1-weighted whole-brain images were assessed between groups with voxel-based morphometry, using ANCOVA (covariates, age and gender; family-wise error correction, P < 0.01). Significant grey matter volume reductions appeared in OSA throughout areas of the superior frontal and prefrontal, and superior and lateral parietal cortices. Other affected sites included the brainstem, ventral medial prefrontal cortex, and superior temporal lobe, mostly on the left side. Thus, pediatric OSA subjects show extensive regionally-demarcated grey matter volume reductions in areas that control cognition and mood functions, even if such losses are apparently independent of cognitive deficits. Since OSA disease duration in our subjects is unknown, these findings may result from either delayed neuronal development, neuronal damaging processes, or a combination thereof, and could either reflect neuronal atrophy or reductions in cellular volume (neurons and glia).