Effect of CPAP on insulin resistance and HbA1c in men with obstructive sleep apnoea and type 2 diabetes Obstructive Sleep Apnea in Young Lean Men CPAP therapy for patients with sleep apnea and type 2 diabetes mellitus improves control of blood pressure Selective Activation of Inflammatory Pathways by Intermittent Hypoxia in Obstructive Sleep Apnea Syndrome Inflammation, Oxidative Stress, and Repair Capacity of the Vascular Endothelium in Obstructive Sleep Apnea CPAP therapy of obstructive sleep apnea in type 2 diabetics improves glycemic control during sleep. Effect of continuous positive airway pressure therapy on cardiovascular risk factors in patients with type 2 diabetes and obstructive sleep apnea. Sleep loss results in an elevation of cortisol levels the next evening. Effect of continuous positive airway pressure on the incidence of hypertension and cardiovascular events in nonsleepy patients with obstructive sleep apnea: a randomized controlled trial. Increased prevalence of sleep-disordered breathing in adults. Driving ability in sleep apnoea patients before and after CPAP treatment: evaluation on a road safety platform Influence of Marital Status and Employment Status on Long-Term Adherence with Continuous Positive Airway Pressure in Sleep Apnea Patients Longitudinal association of sleep-disordered breathing and nondipping of nocturnal blood pressure in the Wisconsin Sleep Cohort Study. Effect of Positive Airway Pressure on Cardiovascular Outcomes in Coronary Artery Disease Patients with Nonsleepy Obstructive Sleep Apnea. The RICCADSA Randomized Controlled Trial. The Effect of Treatment of Obstructive Sleep Apnea on Glycemic Control in Type 2 Diabetes. Prevalence and recognition of obstructive sleep apnea in Chinese patients with type 2 diabetes mellitus. Prospective study of the association between sleep-disordered breathing and hypertension. Effects of Obstructive Sleep Apnea and Obesity on Cardiac Remodeling: The Wisconsin Sleep Cohort Study. Obstructive Sleep Apnea and Cardiovascular Events After Percutaneous Coronary Intervention The effect of race and sleep-disordered breathing on nocturnal BP "dipping": analysis in an older population. CPAP for Prevention of Cardiovascular Events in Obstructive Sleep Apnea. Residual sleepiness in sleep apnea patients treated by continuous positive airway pressure. Brief Communication: Sleep Curtailment in Healthy Young Men Is Associated with Decreased Leptin Levels, Elevated Ghrelin Levels, and Increased Hunger and Appetite
Background : The effects of continuous positive airway pressure ( CPAP ) for obstructive sleep apnoea ( OSA ) on insulin resistance are not clear . Trials have found conflicting results and no appropriate control groups have been used . Methods : Forty-two men with known type 2 diabetes and newly diagnosed OSA ( > 10 dips/h in oxygen saturation of > 4 % ) were r and omised to receive therapeutic ( n = 20 ) or placebo CPAP ( n = 22 ) for 3 months . Baseline tests were performed and repeated after 3 months . The study was double blind . Results : Results are expressed as mean ( SD ) . CPAP  improved the Epworth sleepiness score significantly more in the therapeutic group than in the placebo group ( −6.6 ( 4.5 ) vs −2.6 ( 4.9 ) , p = 0.01 ) . The maintenance of wakefulness test improved significantly in the therapeutic group but not in the placebo group ( + 10.6 ( 13.9 ) vs −4.7 ( 11.8 ) min , p = 0.001 ) . Glycaemic control and insulin resistance did not significantly change in either the therapeutic or placebo groups : HbA1c ( −0.02 ( 1.5 ) vs + 0.1 ( 0.7 ) , p = 0.7 , 95 % CI −0.6 % to + 0.9 % ) , euglycaemic clamp ( M/I : + 1.7 ( 14.1 ) vs −5.7 ( 14.8 ) , p = 0.2 , 95 % CI −1.8 to + 0.3 l/kg/min1000 ) , HOMA-%S ( −1.5 ( 2.3 ) vs −1.1 ( 1.8 ) , p = 0.2 , 95 % CI −0.3 % to + 0.08 % ) and adiponectin ( −1.1 ( 1.2 ) vs −1.1 ( 1.3 ) , p = 0.2 , 95 % CI −0.7 to + 0.6 & mgr;g/ml ) . Body mass index , bioimpedance and anthropometric measurements were unchanged . Hours of CPAP use per night were 3.6 ( 2.8 ) in the treatment group and 3.3 ( 3.0 ) in the placebo group ( p = 0.8 ) . There was no correlation between CPAP use and the measures of glycaemic control or insulin resistance . Conclusion : Therapeutic CPAP does not significantly improve measures of glycaemic control or insulin resistance in men with type 2 diabetes and OSA OBJECTIVE To assess whether the presence of obstructive sleep apnea ( OSA ) affects glucose metabolism in young , lean individuals who are healthy and free of cardiometabolic disease . RESEARCH DESIGN AND METHODS In a prospect i ve design , 52 healthy men ( age 18–30 years ; BMI 18–25 kg/m2 ) underwent laboratory polysomnogram followed by a morning oral glucose tolerance test ( OGTT ) .  We stratified all subjects according to the presence or absence of ethnicity-based diabetes risk and family history of diabetes . We then used a frequency-matching approach and r and omly selected individuals without OSA , yielding a total of 20 control men without OSA and 12 men with OSA .  Indices of glucose tolerance , insulin sensitivity , and insulin secretion ( early phase and total ) were compared between men with OSA and control subjects . The incremental areas under the glucose ( incAUCglu ) and insulin ( incAUCins ) curves were calculated using the trapezoidal method from 0 to 120 min during the OGTT . RESULTS Men with OSA and control subjects were similar in terms of age , BMI , ethnicity-based diabetes risk , family history of diabetes , and level of exercise . Both groups had normal systolic and diastolic blood pressure and fasting lipid levels . After ingestion of a glucose load , men with OSA had 27 % lower insulin sensitivity ( estimated by Matsuda index ) and 37 % higher total insulin secretion ( incAUCins ) than the control subjects , despite comparable glucose levels ( incAUCglu ) . CONCLUSIONS In young , lean , and healthy men who are free of cardiometabolic disease , the presence of OSA is associated with insulin resistance and a compensatory rise in insulin secretion to maintain normal glucose tolerance . Thus , OSA may increase the risk of type 2 diabetes independently of traditional cardiometabolic risk factors Purpose Obstructive sleep apnea ( OSA ) is highly associated with type 2 diabetes mellitus ( DM ) , and treatment of OSA may have a positive impact on cardiometabolic profile . This study investigates the effects of continuous positive airway pressure ( CPAP ) treatment on glycemic control and cardiometabolic parameters in patients with diabetes . Methods Diabetic patients , who were newly diagnosed of OSA with an apnea hypopnea index ( AHI ) ≥15 and HbA1c ≥7 % , were r and omly assigned to either CPAP treatment or no treatment ( control ) for 3 months . Measurements included HbA1c , blood pressure , fasting glucose and lipids , urinary albumin , and peripheral arterial tonometry ( to assess endothelial function ) . Results Sixty-four patients ( 52 men ) were r and omized , with mean ( ±SD ) age of 55.0 ± 9.6 years , body mass index of 29.9 ± 5.3 kg/m2 , HbA1c of 8.1 ± 1.1 % , and AHI of 45.3 ± 23.2 events/h . In the intention-to-treat analysis , no significant change in HbA1c but reduction of systolic ( 10 mmHg ( −18 to −2 ) , p < 0.05 ) and diastolic ( 6 mmHg ( −11 to −1 ) , p < 0.05 ) blood pressures were found in the CPAP group compared to the control group . Excluding those with medication changes or initiated dietary program during the study period and those who dropped out , CPAP treatment decreased HbA1c ( intervention group , n = 27 ; control group , n = 26 ) by 0.4 % ( −0.7 to −0.1 ) , p = 0.027 . Conclusions In patients with type 2 DM and moderate to severe OSA , 3 months of CPAP therapy did not decrease HbA1c but lowered systolic and diastolic blood pressures . In view of a potentially limited effect size of CPAP treatment on glycemic control , sample size estimation for future r and omized controlled studies must make adequate allowance for influence from external factors of medications/diet and CPAP use Background — Obstructive sleep apnea syndrome ( OSAS ) , characterized by intermittent hypoxia/reoxygenation ( IHR ) , is an independent risk factor for cardiovascular disease . We investigated the underlying molecular mechanisms of this association in a translational study . Methods and Results — In a novel in vitro model of IHR , we used HeLa cells transfected with reporter constructs and DNA binding assays for the master transcriptional regulators of the inflammatory and adaptive pathways ( NF&kgr;B and HIF-1 , respectively ) to investigate underlying transcriptional events initiated by repeated cell exposure to IHR . Furthermore , we prospect ively studied 19 male OSAS patients ( median apnea-hypopnea frequency , 48.5 episodes per hour ; interquartile range [ IQR ] , 28.5 to 72.9 ) and 17 matched normal control subjects . Circulating levels of the proinflammatory cytokine tumor necrosis factor-&agr ; and the adaptive factor erythropoietin were assayed in all subjects at baseline and again after 6 weeks of continuous positive airway pressure therapy in patients . Full blood count was measured as part of a detailed baseline evaluation . HeLa cells exposed to IHR demonstrated selective activation of the proinflammatory transcription factor NF&kgr;B ( P<0.001 by ANOVA ) , whereas the adaptive regulator HIF-1 was not activated , as demonstrated by luciferase reporter assays and DNA binding studies . Circulating tumor necrosis factor-&agr ; levels were higher in OSAS patients ( 2.56 pg/mL ; IQR , 2.01 to 3.42 pg/mL ) than in control subjects ( 1.25 pg/mL ; IQR , 0.94 to 1.87 ; P<0.001 ) but normalized with continuous positive airway pressure therapy ( 1.24 pg/mL ; IQR , 0.78 to 2.35 pg/mL ; P=0.002 ) . In contrast , erythropoietin levels were similar throughout . Furthermore , circulating neutrophil levels were higher in OSAS patients than in control subjects , whereas the hematocrit was unaltered . Conclusions — These data demonstrate selective activation of inflammatory over adaptive pathways in IHR and OSAS , which may be an important molecular mechanism of cardiovascular disease Background — Indirect evidence implicates endothelial dysfunction in the pathogenesis of vascular diseases associated with obstructive sleep apnea ( OSA ) . We investigated directly whether dysfunction and inflammation occur in vivo in the vascular endothelium of patients with OSA . The effects of continuous positive airway pressure ( CPAP ) therapy on endothelial function and repair capacity were assessed . Methods and Results — Thirty-two patients with newly diagnosed OSA and 15 control subjects were studied . Proteins that regulate basal endothelial nitric oxide ( NO ) production ( endothelial NO synthase [ eNOS ] and phosphorylated eNOS ) and inflammation ( cyclooxygenase-2 and inducible NOS ) and markers of oxidative stress ( nitrotyrosine ) were quantified by immunofluorescence in freshly harvested venous endothelial cells before and after 4 weeks of CPAP therapy . Vascular reactivity was measured by flow-mediated dilation . Circulating endothelial progenitor cell levels were quantified to assess endothelial repair capacity . Baseline endothelial expression of eNOS and phosphorylated eNOS was reduced by 59 % and 94 % , respectively , in patients with OSA compared with control subjects . Expression of both nitrotyrosine and cyclooxygenase-2 was 5-fold greater in patients with OSA than in control subjects , whereas inducible NOS expression was 56 % greater . Expression of eNOS and phosphorylated eNOS significantly increased , whereas expression of nitrotyrosine , cyclooxygenase-2 , and inducible NOS significantly decreased in patients who adhered to CPAP ≥4 hours daily . Baseline flow-mediated dilation and endothelial progenitor cell levels were lower in patients than in control subjects , and both significantly increased in patients who adhered to CPAP ≥4 hours daily . Conclusions — OSA directly affects the vascular endothelium by promoting inflammation and oxidative stress while decreasing NO availability and repair capacity . Effective CPAP therapy is associated with the reversal of these alterations BACKGROUND Type 2 diabetes and obstructive sleep apnea ( OSA ) are frequently comorbid conditions . OSA is associated with increased insulin resistance , but studies of continuous positive airway pressure ( CPAP ) have shown inconsistent effects on glycemic control . However , endpoints such as hemoglobin A1c and insulin sensitivity might not reflect short-term changes in glycemic control during sleep . METHODS We used a continuous glucose-monitoring system to measure interstitial glucose every 5 minutes during polysomnography in 20 patients with type 2 diabetes and newly diagnosed OSA . The measurements were repeated after an average of 41 days of CPAP ( range 26 - 96 days ) . All patients were on a stable diet and medications . Each 30-second epoch of the polysomnogram was matched with a continuous glucose-monitoring system reading , and the sleeping glucose level was calculated as the average for all epochs scored as sleeping . RESULTS The mean sleeping glucose decreased from untreated ( 122.0 + /- 61.7 mg/dL ) to treated ( 102.9 + /- 39.4 mg/dL ; p = 0.03 by Wilcoxon paired rank test ) . The sleeping glucose was more stable after treatment , with the median SD decreasing from 20.0 to 13.0 mg/dL ( p = 0.005 ) and the mean difference between maximum and minimum values decreasing from 88 to 57 mg/dL ( p= 0.003 ) . The change in the mean hemoglobin A1c from 7.1 % to 7.2 % was not significant . CONCLUSIONS Our study is limited by the lack of a control group , but the results suggest that sleeping glucose levels decrease and are more stable after patients with type 2 diabetes and OSA are treated with CPAP CONTEXT Few prospect i ve intervention studies have examined the effect of continuous positive airway pressure ( CPAP ) therapy on cardiovascular disease ( CVD ) risk factors in diabetes . OBJECTIVE Our objective was to determine whether CPAP improves CVD risk factors in patients with type 2 diabetes and obstructive sleep apnea ( OSA ) . DESIGN AND SETTING This was a r and omized parallel group intervention trial in an urban Australian community . PATIENTS Fifty-nine participants of the Fremantle Diabetes Study Phase II at high risk for OSA consented to confirmatory polysomnography followed by r and omization to a 3-month CPAP intervention initiated early ( < 1 wk ) or late ( 1 - 2 months ) . MAIN OUTCOME MEASURES Patients were assessed before and 1 and 3 months after CPAP started . Tests for repeated measures were used to compare variables of interest over time . RESULTS Forty-four patients ( 75 % ) completed the study . Their mean ± sd age was 66.1 ± 8.8 yr , and 61.4 % were male . Completers and noncompleters had similar age , sex , diabetes duration , apnea-hypopnea index , and Epworth Sleepiness Scale ( P ≥ 0.29 ) . There were no differences in outcome between early and late r and omization , and the data were pooled . The Epworth Sleepiness Scale decreased between entry and 1 month [ -4.8 ( -6.5 to -3.1 ) , P < 0.001 ] . Blood pressure improved between entry and 3 months ( from 149 ± 23/80 ± 12 to 140 ± 18/73 ± 13 mm Hg ; P ≤ 0.007 ) . Pulse rate declined within the first month [ -6 ( -10 to -2 ) beats/min , P = 0.002 ] . Glycemic control and serum lipids , which were mostly within recommended target ranges at entry , did not change . CONCLUSIONS Three months of CPAP  in community-based people with type 2 diabetes  significantly decreased blood pressure and pulse rate but did not influence metabolic control Sleep curtailment constitutes an increasingly common condition in industrialized societies and is thought to affect mood and performance rather than physiological functions . There is no evidence for prolonged or delayed effects of sleep loss on the hypothalamo-pituitary-adrenal ( HPA ) axis . We evaluated the effects of acute partial or total sleep deprivation on the nighttime and daytime profile of cortisol levels . Plasma cortisol profiles were determined during a 32-hour period ( from 1800 hours on day 1 until 0200 hours on day 3 ) in normal young men su bmi tted to three different protocol s : normal sleep schedule ( 2300 - 0700 hours ) , partial sleep deprivation ( 0400 - 0800 hours ) , and total sleep deprivation .  Alterations in cortisol levels could only be demonstrated in the evening following the night of sleep deprivation . After normal sleep , plasma cortisol levels over the 1800 - 2300-hour period were similar on days 1 and 2 . After partial and total sleep deprivation , plasma cortisol levels over the 1800 - 2300-hour period were higher on day 2 than on day 1 ( 37 and 45 % increases , p = 0.03 and 0.003 , respectively ) , and the onset of the quiescent period of cortisol secretion was delayed by at least 1 hour . We conclude that even partial acute sleep loss delays the recovery of the HPA from early morning circadian stimulation and is thus likely to involve an alteration in negative glucocorticoid feedback regulation . Sleep loss could thus affect the resiliency of the stress response and may accelerate the development of metabolic and cognitive consequences of glucocorticoid excess CONTEXT Continuous positive airway pressure ( CPAP ) is the first-line treatment for patients with symptomatic obstructive sleep apnea ( OSA ) . However , its indication for all patients with sleep-disordered breathing , regardless of daytime symptoms , is unclear . OBJECTIVE To evaluate the effect of CPAP treatment on the incidence of hypertension or cardiovascular events in a cohort of nonsleepy patients with OSA . DESIGN , SETTING , AND PATIENTS Multicenter , parallel-group , r and omized controlled trial in 14 teaching hospitals in Spain . Between May 2004 and May 2006 , 725 consecutive patients were enrolled who had an apnea-hypopnea index of 20 h(-1 ) or greater and an Epworth Sleepiness Scale score of 10 or less ( scores range from 0 - 24 , with values < 10 suggesting no daytime sleepiness ) . Exclusion criteria were previous cardiovascular event , physical or psychological incapacity , chronic disease , or drug or alcohol addiction . Follow-up ended in May 2009 . INTERVENTION Patients were allocated to receive CPAP treatment or no active intervention . All participants received dietary counseling and sleep hygiene advice . MAIN OUTCOME MEASURES Incidence of either systemic hypertension ( taking antihypertensive medication or blood pressure greater than 140/90 mm Hg ) or cardiovascular event ( nonfatal myocardial infa rct ion , nonfatal stroke , transient ischemic attack , hospitalization for unstable angina or arrhythmia , heart failure , or cardiovascular death ) . RESULTS Seven hundred twenty-three patients underwent follow-up for a median of 4 ( interquartile range , 2.7 - 4.4 ) years ( 1 patient from each group did not receive allocated treatment ) ; 357 in the CPAP group and 366 in the control group were included in the analysis . In the CPAP group there were 68 patients with new hypertension  and 28 cardiovascular events ( 17 unstable angina or arrhythmia , 3 nonfatal stroke , 3 heart failure , 2 nonfatal myocardial infa rct ion , 2 transient ischemic attack , 1 cardiovascular death ) . In the control group there were 79 patients with new hypertension and 31 cardiovascular events ( 11 unstable angina or arrhythmia , 8 nonfatal myocardial infa rct ion , 5 transient ischemic attack , 5 heart failure , 2 nonfatal stroke ) . The hypertension or cardiovascular event incidence density rate was 9.20 per 100 person-years ( 95 % CI , 7.36 - 11.04 ) in the CPAP group and 11.02 per 100 person-years ( 95 % CI , 8.96 - 13.08 ) in the control group . The incidence density ratio was 0.83 ( 95 % CI , 0.63 - 1.1 ; P = .20 ) . CONCLUSIONS In patients with OSA without daytime sleepiness , the prescription of CPAP compared with usual care did not result in a statistically significant reduction in the incidence of hypertension or cardiovascular events . However , the study may have had limited power to detect a significant difference . TRIAL REGISTRATION clinical trials.gov Identifier : NCT00127348 Sleep-disordered breathing is a common disorder with a range of harmful sequelae . Obesity is a strong causal factor for sleep-disordered breathing , and because of the ongoing obesity epidemic , previous estimates of sleep-disordered breathing prevalence require updating . We estimated the prevalence of sleep-disordered breathing in the United States for the periods of 1988 - 1994 and 2007 - 2010 using data from the Wisconsin Sleep Cohort Study , an ongoing community-based study that was established in 1988 with participants r and omly selected from an employed population of Wisconsin adults . A total of 1,520 participants who were 30 - 70 years of age had baseline polysomnography studies to assess the presence of sleep-disordered breathing . Participants were invited for repeat studies at 4-year intervals . The prevalence of sleep-disordered breathing was modeled as a function of age , sex , and body mass index , and estimates were extrapolated to US body mass index distributions estimated using data from the National Health and Nutrition Examination Survey . The current prevalence estimates of moderate to severe sleep-disordered breathing ( apnea-hypopnea index , measured as events/hour , ≥15 ) are 10 % ( 95 % confidence interval ( CI ) : 7 , 12 ) among 30 - 49-year-old men ; 17 % ( 95 % CI : 15 , 21 ) among 50 - 70-year-old men ; 3 % ( 95 % CI : 2 , 4 ) among 30 - 49-year-old women ; and 9 % ( 95 % CI : 7 , 11 ) among 50 - 70 year-old women . These estimated prevalence rates represent substantial increases over the last 2 decades ( relative increases of between 14 % and 55 % depending on the subgroup ) Sleepiness is considered to be the major cause of increased traffic accidents in patients with obstructive sleep apnoea syndrome ( OSAS ) . Until now , OSAS patients ′ driving ability has been assessed using driving simulators , but no assessment in a more natural driving environment has been carried out to date . The aim of the present study was to evaluate driving parameters in OSAS and in controls on a road safety platform , and to compare them with attentional in-laboratory measures before and after continuous positive airway pressure treatment . The parameters measured were : reaction time ; distance to stop and number of collisions on the platform ; maintenance of wakefulness ; and sustained , selective and divided attention in laboratory . Patients exhibited much longer reaction times than controls , leading to a lengthening of the vehicle′s stopping distance of 8.8 m at 40 km·h-1 and to twice the number of collisions . Patients did not demonstrate objective sleepiness or selective and sustained attention deficits . Divided attention deficits were found . However , they did not allow the prediction of real driving impairment . After CPAP treatment , there was no longer any difference between patients and controls regarding driving and attention performances . Driving abilities are significantly impaired in  obstructive sleep apnoea syndrome . After continuous positive airway pressure treatment , deficits were normalised . This stresses the importance of evaluating attentional parameters in apnoeic patients and of offering continuous positive airway pressure treatment even to non-sleepy subjects Background Long-term adherence is a major issue in patients receiving home continuous positive airway pressure ( CPAP ) therapy for obstructive sleep apnea-hypopnea syndrome ( OSAHS ) . In a multicenter prospect i ve cohort ( the Institut de Recherche en Santé Respiratoire des Pays de la Loire [ IRSR ] sleep cohort ) of consecutive OSAHS patients in whom CPAP had been prescribed for at least 90 days , we studied the impact on long-term treatment adherence of socioeconomic factors , patients and disease characteristics prior to CPAP initiation . Methods and Principal Findings Among 1,141 patients in whom CPAP had been prescribed for an average of 504±251 days ( range : 91 to 1035 ) , 674 ( 59 % ) were adherent with a mean daily use of CPAP≥4 h ( mean : 6.42±1.35 h ) . Stepwise regression analysis identified 4 independent factors of CPAP adherence including apnea-hypopnea index ( AHI ) ( OR : 1.549 , 95%CI 1.163 to 2.062 for AHI≥30 vs. AHI<30 ; p = 0.003 ) , body mass index ( BMI ) ( OR : 1.786 , 95%CI 1.131 to 2.822 for BMI ≥25 and < 30 kg/m2 , p = 0.01 ; OR : 1.768 , 95%CI 1.145–2.731 for BMI ≥30 kg/m2 , p = 0.01 vs. BMI < 25 kg/m2 ) , employment status ( OR : 1.414 , 95%CI 1.097–1.821 for retired vs. employed ; p = 0.007 ) and marital status ( OR : 1.482 , 95%CI 1.088–2.019 for married or living as a couple vs. living alone ; p = 0.01 ) . Age , gender , Epworth sleepiness scale , depressive syndrome , associated cardiovascular morbidities , educational attainment and occupation category did not influence CPAP adherence . Conclusions Marital status and employment status are independent factors of CPAP adherence in addition to BMI and disease severity . Patients living alone and /or working patients are at greater risk of non-adherence , whereas adherence is higher in married and retired patients . These findings suggest that the social context of daily life should be taken into account in risk screening for CPAP non-adherence . Future interventional studies targeting at-risk patients should be design ed to address social motivating factors and work-related barriers to CPAP adherence STUDY OBJECTIVES The association of sleep-disordered  breathing ( SDB ) and blunting of normal nocturnal lowering of blood pressure ( BP ) ( nondipping ) has only been examined cross-sectionally . The purpose of this study is to investigate whether SDB is prospect ively associated with nondipping . METHODS The longitudinal association between SDB and incident nondipping was examined in a sub sample of 328 adults enrolled in the Wisconsin Sleep Cohort Study who completed 2 or more 24-hour ambulatory BP studies over an average of 7.2 years of follow-up . SDB identified by baseline in-laboratory polysomnography was defined by apnea-hypopnea index ( AHI ) categories . Systolic and diastolic nondipping was defined by systolic and diastolic sleep-wake BP ratios > 0.9 . All models were adjusted for age , sex , body mass index at baseline and follow-up , smoking , alcohol consumption , hypertension , sleep time , length of follow-up time , and antihypertensive medication use . RESULTS There was a dose-response increased odds of developing systolic nondipping in participants with SDB . The adjusted odds ratios ( 95 % confidence interval ) of incident systolic nondipping for baseline AHI 5 to < 15 and AHI > or = 15 , versus AHI < 5 , were 3.1 ( 1.3 - 7.7 ) and 4.4 ( 1.2 - 16.3 ) , respectively ( P trend = 0.006 ) . The adjusted odds ratios ( 95 % confidence interval ) of incident diastolic nondipping for corresponding SDB categories were not statistically significant : 2.0 ( 0.8 - 5.6 ) and 1.3 ( 0.2 - 7.1 ) . CONCLUSIONS Our longitudinal findings of a dose-response increase in development of systolic nondipping of BP with severity of SDB at baseline in a population -based sample provide evidence consistent with a causal link . Nocturnal systolic nondipping may be a mechanism by which SDB contributes to increased cardiovascular disease RATIONALE Obstructive sleep apnea ( OSA ) is common in patients with coronary artery disease ( CAD ) , many of whom do not report daytime sleepiness . First-line treatment for symptomatic OSA is continuous positive airway pressure ( CPAP ) , but its value in patients without daytime sleepiness is uncertain . OBJECTIVES To determine the effects of CPAP on long-term adverse cardiovascular outcome risk in patients with CAD with nonsleepy OSA . METHODS This single-center , prospect i ve , r and omized , controlled , open-label , blinded evaluation trial was conducted between December 2005 and November 2010 . Consecutive patients with newly revascularized CAD and OSA ( apnea-hypopnea index ≥15/h ) without daytime sleepiness ( Epworth Sleepiness Scale score < 10 ) were r and omized to auto-titrating CPAP ( n = 122 ) or no positive airway pressure ( n = 122 ) . MEASUREMENTS AND MAIN RESULTS The primary endpoint was the first event of repeat revascularization , myocardial infa rct ion , stroke , or cardiovascular mortality . Median follow-up was 57 months . The incidence of the primary endpoint did not differ significantly in patients who did versus did not receive CPAP ( 18.1 % vs. 22.1 % ; hazard ratio , 0.80 ; 95 % confidence interval , 0.46 - 1.41 ; P = 0.449 ) . Adjusted on-treatment analysis showed a significant cardiovascular risk reduction in those who used CPAP for ≥4 versus < 4 hours per night or did not receive treatment ( hazard ratio , 0.29 ; 95 % confidence interval , 0.10 - 0.86 ; P = 0.026 ) . CONCLUSIONS Routine prescription of CPAP to patients with CAD with nonsleepy OSA did not significantly reduce long-term adverse cardiovascular outcomes in the intention-to-treat population . There was a significant reduction after adjustment for baseline comorbidities and compliance with the treatment . Clinical trial registered with www . clinical trials.gov ( NCT 00519597 ) RATIONALE There is uncertainty about the effects of treating obstructive sleep apnea on glycemic control in patients with type 2 diabetes . OBJECTIVES To determine whether treatment of  obstructive sleep apnea in patients with type 2 diabetes improves glycemic control . METHODS In this trial , we r and omized patients with type 2 diabetes and no previous diagnosis of obstructive sleep apnea , with a glycated hemoglobin level of 6.5 - 8.5 % , and an oxygen desaturation index of 15 or more events per hour to positive airway pressure therapy or to usual care .  MEASUREMENTS AND MAIN RESULTS A total of 416 patients met the entry criteria as determined by each site and were r and omized . Of the 298 participants who met central ly adjudicated entry criteria , no differences between the study groups were seen for change in glycated hemoglobin . Furthermore , there were no between-group differences when analyses were restricted to those with poorer baseline glycemic control , those with more severe sleep apnea , or those who were adherent to therapy . A greater fall in diastolic blood pressure occurred in the positive airway pressure group than in the usual care group ( -3.5 mm Hg vs. -1.5 mm Hg ; P = 0.07 ) . This difference was significant in those who were adherent to positive airway pressure therapy ( -4.4 mm Hg vs. -1.6 mm Hg ; P = 0.02 ) . There was a significant reduction in sleepiness in the positive airway pressure therapy group ( P < 0.0001 ) . Quality of life assessment revealed improvements in vitality , mental health , and mental component summary scores in the positive airway pressure therapy group . CONCLUSIONS This trial showed no effect of positive airway pressure therapy on glycemic control in patients with relatively well-controlled type 2 diabetes and obstructive sleep apnea . Clinical trial registered with www . clinical trials.gov ( NCT00509223 ) BACKGROUND  Obstructive sleep apnea ( OSA )  is associated with disorders of glucose metabolism . Previous studies revealed a high prevalence of OSA among subjects with type 2 diabetes mellitus ( DM ) . The aims of this study were to determine the prevalence of OSA and associated clinical factors in Chinese patients with DM . METHODS All records of the DM clinic at a teaching hospital in Hong Kong were screened between January 2007 and June 2008 . Inclusion criteria for patients were Chinese , aged 18 to 75 years , with type 2 DM . Patients with unstable medical illnesses , gestational diabetes , or on renal replacement therapy were excluded . RESULTS Of 3,489 records screened , 1,859 subjects were eligible . A r and om sample of 663 ( mean age , 58.2 ± 10.8 ; mean BMI , 26.0 ± 4.6 ) , except six with known OSA , were invited for polysomnography ( PSG ) . Of 165 subjects on which PSG was performed , OSA was diagnosed ( apnea-hypopnea index [ AHI ] ≥ 5.0/h ) in 89 subjects ( 53.9 % , median Epworth Sleepiness Scale , 6 [ interquartile range 3 , 10 ] ) . Fifty-four ( 32.7 % ) had moderate/severe OSA ( AHI ≥ 15/h ) . The estimated OSA prevalence in this diabetic cohort was 17.5 % ( 24.7 % in men , 10.3 % in women ) . Regression analysis identified that AHI was associated independently with higher BMI , advanced age , male sex , and higher diastolic BP ( R(2 ) = 29.6 % ) . The adjusted OR of requiring three or more antihypertensive drugs in moderate/severe OSA was 2.48 ( 95 % CI , 1.05 - 5.87 ) . No association between glycemic control ( HbA1c ) and sleep was identified . CONCLUSIONS In conclusion , OSA is more prevalent in Chinese adults with DM than in the general population . A high index of suspicion for OSA in patients with DM is warranted , because they may not have overt daytime sleepiness BACKGROUND Sleep-disordered breathing is prevalent in the general population and has been linked to chronically elevated blood pressure in cross-sectional epidemiologic studies . We performed a prospect i ve , population -based study of the association between objective ly measured sleep-disordered breathing and hypertension ( defined as a laboratory-measured blood pressure of at least 140/90 mm Hg or the use of antihypertensive medications ) . METHODS We analyzed data on sleep-disordered breathing , blood pressure , habitus , and health history at base line and after four years of follow-up in 709 participants of the Wisconsin Sleep Cohort Study ( and after eight years of follow-up in the case of 184 of these participants ) . Participants were assessed overnight by 18-channel polysomnography for sleep-disordered breathing , as defined by the apnea-hypopnea index ( the number of episodes of apnea and hypopnea per hour of sleep ) . The odds ratios for the presence of hypertension at the four-year follow-up study according to the apnea-hypopnea index at base line were estimated after adjustment for base-line hypertension status , body-mass index , neck and waist circumference , age , sex , and weekly use of alcohol and cigarettes . RESULTS Relative to the reference category of an apnea-hypopnea index of 0 events per hour at base line , the odds ratios for the presence of hypertension at follow-up were 1.42 ( 95 percent confidence interval , 1.13 to 1.78 ) with an apnea-hypopnea index of 0.1 to 4.9 events per hour at base line as compared with none , 2.03 ( 95 percent confidence interval , 1.29 to 3.17 ) with an apnea-hypopnea index of 5.0 to 14.9 events per hour , and 2.89 ( 95 percent confidence interval , 1.46 to 5.64 ) with an apnea-hypopnea index of 15.0 or more events per hour . CONCLUSIONS We found a dose-response association between sleep-disordered breathing at base line and the presence of hypertension four years later that was independent of known confounding factors . The findings suggest that sleep-disordered breathing is likely to be a risk factor for hypertension and consequent cardiovascular morbidity in the general population STUDY OBJECTIVES To characterize the prospect i ve associations of obstructive sleep apnea ( OSA ) with future echocardiographic measures of adverse cardiac remodeling . METHODS This was a prospect i ve long-term observational study . Participants had overnight polysomnography followed by transthoracic echocardiography a mean ( st and ard deviation ) of 18.0 ( 3.7 ) y later . OSA was characterized by the apnea-hypopnea index ( AHI , events/hour ) . Echocardiography was used to assess left ventricular ( LV ) systolic and diastolic function and mass , left atrial volume and pressure , cardiac output , systemic vascular resistance , and right ventricular ( RV ) systolic function , size , and hemodynamics . Multivariate regression models estimated associations between log10(AHI+1 ) and future echocardiographic findings . A secondary analysis looked at oxygen desaturation indices and future echocardiographic findings . RESULTS At entry , the 601 participants were mean ( st and ard deviation ) 47 ( 8) y old ( 47 % female ) . After adjustment for age , sex , and body mass index , baseline log10(AHI+1 ) was associated significantly with future reduced LV ejection fraction and tricuspid annular plane systolic excursion ( TAPSE ) ≤ 15 mm . After further adjustment for cardiovascular risk factors , participants with higher baseline log10(AHI+1 ) had lower future LV ejection fraction ( β = -1.35 [ st and ard error = 0.6]/log10(AHI+1 ) , P = 0.03 ) and higher odds of TAPSE ≤ 15 mm ( odds ratio = 6.3/log10(AHI+1 ) , 95 % confidence interval = 1.3 - 30.5 , P = 0.02 ) . SaO2 desaturation indices were associated independently with LV mass , LV wall thickness , and RV area ( all P < 0.03 ) . CONCLUSIONS OSA is associated independently with decreasing LV systolic function and with reduced RV function . Echocardiographic measures of adverse cardiac remodeling are strongly associated with OSA but are confounded by obesity . Hypoxia may be a stimulus for hypertrophy in individuals with OSA Background — There is a paucity of data from large cohort studies examining the prognostic significance of  obstructive sleep apnea ( OSA ) in patients with coronary artery disease . We hypothesized that OSA predicts subsequent major adverse cardiac and cerebrovascular events ( MACCEs ) in patients undergoing percutaneous coronary intervention . Methods and Results — The Sleep and Stent Study was a prospect i ve , multicenter registry of patients successfully treated with percutaneous coronary intervention in 5 countries . Between December 2011 and April 2014 , 1748 eligible patients were prospect ively enrolled . The 1311 patients who completed a sleep study within 7 days of percutaneous coronary intervention formed the cohort for this analysis . Drug-eluting stents were used in 80.1 % and bioresorbable vascular scaffolds in 6.3 % of the patients , and OSA , defined as an apnea-hypopnea index of ≥15 events per hour , was found in 45.3 % . MACCEs , a composite of cardiovascular mortality , nonfatal myocardial infa rct ion , nonfatal stroke , and unplanned revascularization , occurred in 141 patients during the median follow-up of 1.9 years ( interquartile range , 0.8 years ) . The crude incidence of an MACCEs was higher in the OSA than the non-OSA group ( 3-year estimate , 18.9 % versus 14.0 % ; p=0.001 ) . Multivariate Cox regression analysis indicated that OSA was a predictor of MACCEs , with an adjusted hazard ratio of 1.57 ( 95 % confidence interval , 1.10–2.24 ; P=0.013 ) , independently of age , sex , ethnicity , body mass index , diabetes mellitus , and hypertension . Conclusions — OSA is independently associated with subsequent MACCEs in patients undergoing percutaneous coronary intervention . Evaluation of therapeutic approaches to mitigate OSA-associated risk is warranted . Clinical Trial Registration — URL : http://www . clinical trials.gov . Unique identifier : NCT01306526 STUDY OBJECTIVES BP normally drops ( or " dips " ) by approximately 10 % at nighttime ; however , in a number of illnesses there is an increased amount of " nondipping " of nocturnal BP . This study examined whether nondipping in older African Americans and older white subjects is related to the presence of sleep-disordered breathing ( SDB ) and hypertension . DESIGN Prospect i ve study with a convenience sample . SETTING All data were collected in the subjects ' homes . PARTICIPANTS Seventy self-defined African Americans with complaints of snoring or excessive daytime sleepiness , and 70 age-matched and gender-matched white subjects . MEASUREMENTS AND RESULTS  Sleep  was recorded for 2 nights , with 1 night of oximetry . BP  was recorded on a separate 24-h period . African Americans had higher dipping ratios than white subjects even after accounting for covariates such as respiratory disturbance index ( RDI ) , oxygen desaturation index ( ODI ) , body mass index , and average 24-h mean arterial pressure ( p = 0.025 ) . Higher values of RDI ( R(2 ) = 0.0686 , p = 0.021 ) and ODI ( R(2 ) = 0.042 , p < 0.03 ) were correlated with higher dipping ratios in both African Americans and white subjects . However , there was a three-way interaction such that higher RDIs were correlated primarily with nondipping in African Americans receiving antihypertensive medication ( R(2 ) = 0.0373 , p = 0.022 ) . CONCLUSIONS These results demonstrated that African Americans tend to be " nondippers , " while white subjects tended to be " dippers . " This nondipping was not a result of weight , gender , or of having SDB . The analyses also confirmed that , in both races , the dipping ratio was greatest in those with SDB and hypertension . The third hypothesis , that RDI would be greatest in the nondipping hypertensive subjects , was true only for the African Americans 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 r and omly 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 infa rct ion , 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 Clinical Trials.gov number , NCT00738179 ; Australian New Zeal and Clinical Trials Registry number , ACTRN12608000409370 . ) Hypoxic brain damage might explain persistent sleepiness in some continuous positive airway pressure-compliant obstructive sleep apnea called residual excessive sleepiness . Although continuous positive airway pressure may not be fully efficient in treating this symptom , wake-promoting drug prescription in residual excessive sleepiness is no longer allowed by the European Medicines Agency . The aim of this study is to describe residual excessive sleepiness phenotypes in a large prospect i ve sample of patients with obstructive sleep apnea . Residual excessive sleepiness was defined by an Epworth Sleepiness Scale score ≥ 11 . Eligible patients from the French National Sleep Registry attending follow-up continuous positive airway pressure visits numbered 1047 . Patients using continuous positive airway pressure < 3 h ( n = 275 ) , with residual apnea-hypopnea index > 15 h⁻¹ ( n = 31 ) or with major depression were excluded ( n = 150 ) . Residual excessive sleepiness prevalence in continuous positive airway pressure-treated obstructive sleep apnea was 13 % ( 18 % for those with an initial Epworth Sleepiness Scale score > 11 ) , and significantly decreased with continuous positive airway pressure use ( 9 % in ≥ 6 h night⁻¹ continuous positive airway pressure users , P < 0.005 ) . At the time of diagnosis , patients with residual excessive sleepiness had worse subjective appreciation of their disease ( general health scale , Epworth Sleepiness Scale and fatigue score ) , and complained more frequently of continuous positive airway pressure side-effects . Residual excessive sleepiness prevalence was lower in severe obstructive sleep apnea than in moderate obstructive sleep apnea ( 11 % when AHI > 30 h⁻¹ versus 18 % when AHI 15 - 30 , P < 0.005 ) . There was no relationship between residual excessive sleepiness and body mass index , cardiovascular co-morbidities or diabetes . Continuous positive airway pressure improved symptoms in the whole population , but to a lower extent in patients with residual excessive sleepiness ( fatigue scale : -5.2 versus -2.7 in residual excessive sleepiness- and residual excessive sleepiness+ patients , respectively , P < 0.001 ) . Residual excessive sleepiness prevalence decreased with continuous positive airway pressure compliance . Hypoxic insult is unlikely to explain residual excessive sleepiness as obstructive sleep apnea severity does not seem to be critical . Residual symptoms are not limited to sleepiness , suggesting a true ' continuous positive airway pressure-resistant syndrome ' , which may justify treatment by wake-promoting drugs Context Studies in animals and humans suggest that sleep duration is an important regulator of metabolism . Contribution In this study , 12 young , healthy , normal-weight men exhibited reductions in the satiety hormone leptin , increases in the hunger hormone ghrelin , and increases in hunger after 2 nights of only 4 hours of sleep compared with after 2 nights of 10 hours of sleep . Implication s Inadequate sleep seems to influence the hormones that regulate satiety and hunger in a way that could promote excess eating . The Editors Sleep plays an important role in energy balance . In rodents , food shortage or starvation results in decreased sleep ( 1 ) , and , conversely , total sleep deprivation leads to marked hyperphagia ( 2 ) . Leptin and ghrelin are peripheral signals that contribute to the central regulation of food intake . Leptin , a hormone released by the adipocytes , provides information about energy status to hypothalamic regulatory centers ( 3 ) . In humans , circulating leptin levels rapidly decrease or increase in response to acute caloric shortage or surplus , respectively ( 4 ) . These changes in leptin levels have been associated with reciprocal changes in hunger ( 4 ) . Ghrelin , a peptide produced predominantly by the stomach , is also involved in energy balance regulation , but , in contrast to the anorexigenic effects of leptin , ghrelin stimulates appetite ( 5 ) . It has been proposed that leptin and ghrelin represent the yinyang of one regulatory system that has developed to inform the brain about the current energy balance state ( 6 ) . Over the past 40 years ,  sleep duration in the U.S. population has decreased by 1 to 2 hours ( 7 - 10 ) . The proportion of young  adults sleeping fewer than 7 hours per night has more than doubled between 1960 and 20012002 ( from 15.6 % to 37.1 % ) ( 7 - 10 ) . The effect of sleep curtailment on the control of appetite and food intake is not known . Because of the well-documented associations between sleep and food intake ( 1 , 2 ) , we sought to determine whether sleep duration influences the daytime profiles of leptin and ghrelin . Methods Participants Twelve healthy men(mean age [ SD ] , 22 2 years ] ; mean body mass index [ SD ] , 23.6 2.0 kg/m2 ) who did not smoke or take any medications participated in the study . All of the men were within 10 % of ideal body weight and had regular nocturnal time in bed of 7 to 9 hours . We excluded persons who had traveled across time zones less than 4 weeks before the study . Experimental Protocol The Institutional Review Board of the University of Chicago approved the protocol , and we obtained written informed consent from all participants . During the week preceding each study , we asked participants not to deviate from a fixed time in bed ( 11:00 p.m. to 7:00 a.m. ) by more than 30 minutes . Naps were not allowed . The men participated in 2 studies that were conducted in a r and omized order , were spaced at least 6 weeks apart , and were performed in the Clinical Research Center at the University of Chicago , Chicago , Illinois . Six of the 12 men first performed the study with  restricted time in bed , and the remaining 6 men first performed the study  with extended time in bed .  Average weight did not change over the time period separating the 2 study conditions ( 75.2 kg in the sleep restriction condition vs. 75.4 kg in the sleep extension condition ; P > 0.2 ) . We obtained blood sample s at 20-minute intervals from 8:00 a.m. to 9:00 p.m. after 2 consecutive nights of 10 hours in bed ( 10:00 p.m. to 8:00 a.m. ; sleep extension ) and after 2 consecutive nights of 4 hours in bed ( 1:00 a.m. to 5:00 a.m. ; sleep restriction ) . Sleep was recorded every night . For both extension and restriction conditions , each overnight stay began at 7:00 p.m. with a st and ard hospital dinner , and the first overnight stay ended after breakfast , which was served at 8:00 a.m. We instructed the participants not to deviate from their usual eating habits between breakfast and dinner , but caloric intake was not otherwise monitored . Participants were readmitted in the early evening and , after receiving a st and ard hospital dinner at 7:00 p.m. , remained at bed rest . At 8:00 a.m. after the second night , the participants ' caloric intake was kept constant to avoid meal-related fluctuations of hunger and satiety and consisted of an intravenous glucose infusion at a constant rate of 5 g/kg of body weight every 24 hours . There was no other source of calories . Every hour from 9:00 a.m. to 9:00 p.m. , the men completed vali date d visual analogue scales ( 0 to 10 cm ) for hunger ( 11 ) and appetite for various food categories ( 12 ) . To assess hunger , we asked participants to mark their response to the question How hungry do you feel right now ? on a 10-cm scale ( with not at all hungry on the left and extremely hungry on the right ) . To assess appetite , we asked participants to mark their response to how much they would enjoy eating foods from 7 different food categories on a 10-cm scale ( with not at all on the left and very much on the right ) . They were asked to provide a score based only on their appetite at the moment , without concern for calories , fat , or a healthy diet . The food categories were sweets ( such as cake , c and y , cookies , ice cream , and pastry ) ; salty foods ( such as chips , salted nuts , pickles , and olives ) ; starchy foods ( such as bread , pasta , cereal , and potatoes ) ; fruits and fruit juices ; vegetables ; meat , poultry , fish , and eggs ; and dairy products ( such as milk , cheese , and yogurt ) . Assays We measured serum leptin levels in all sample s by using a human leptin radioimmunoassay kit ( Linco Research , St. Charles , Missouri ) with a sensitivity of 0.5 ng/mL and an intra-assay coefficient of variation of 8.3 % . In 9 of the 12 participants , we also measured total ghrelin levels at hourly intervals by radioimmunoassay ( Linco Research ) with a sensitivity of 0.5 ng/mL and an intra-assay coefficient of variation of 7.9 % . Statistical Analysis We performed paired comparisons by using the Wilcoxon matched-pairs signed-rank test . We calculated correlations by using the Spearman coefficient . The mean relative changes in leptin , ghrelin , hunger , and appetite between extended sleep ( the reference category ) and restricted sleep were calculated by using the ratios of the corresponding individual data and then deriving the mean across all individuals . Role of the Funding Sources This work was partially supported by grants from the National Institutes of Health , the European Sleep Research Society , the Belgian Fonds de la Recherche Scientifique Mdicale , the University of Chicago Diabetes Research and Training Grant , and The University of Chicago General Clinical Research Center . The funding sources had no role in the design , conduct , and reporting of the study or in the decision to su bmi t the manuscript for publication . Results Leptin levels were stable across the daytime period under both sleep conditions , which was consistent with the fact that calories were exclusively delivered in the form of a constant glucose infusion . Average total sleep time was 9 hours and 8 minutes when the men spent 10 hours in bed and 3 hours and 53 minutes when the men spent 4 hours in bed ( P < 0.01 ) . When spending 4 hours in bed , the participants had mean leptin levels that were 18 % lower ( 2.1 ng/mL vs. 2.6 ng/mL ; P= 0.04 ) ( Figure 1 , part A ) and mean ghrelin levels that were 28 % higher ( 3.3 ng/mL vs. 2.6 ng/mL ; P= 0.04 ) ( Figure 1 , part B ) than when the participants spent 10 hours in bed . The ratio of the concentrations of orexigenic ghrelin to anorexigenic leptin increased by 71 % ( CI , 7 % to 135 % ) with 4 hours in bed compared with 10 hours in bed . Sleep restriction relative to sleep extension was associated with a 24 % increase in hunger ratings on the 10-cm visual analogue scale ( P < 0.01 ) and a 23 % increase in appetite ratings for all food categories combined ( P= 0.01 ) ( Figure 1 , parts C and D , and Table 1 ) . The increase in appetite tended to be greatest for calorie-dense foods with high carbohydrate content ( sweets , salty foods , and starchy foods : increase , 33 % to 45 % ; P= 0.06 ) ( Table 1 ) . The increase in appetite for fruits and vegetables was less consistent and of lesser magnitude ( increase , 17 % to 21 % ) ( Table 1 ) . Appetite for protein-rich nutrients ( meat , poultry , fish , eggs , and dairy foods ) was not significantly affected by sleep duration ( Table 1 ) . When we considered the changes in ghrelin and leptin in an integrated fashion by calculating the ghrelin-to-leptin ratio , the increase in hunger was proportional to the increase in ghrelin-to-leptin ratio ( r= 0.87 ) ( Figure 2 ) . Almost 70 % of the variance in increased hunger could be accounted for by the increase in the ghrelin-to-leptin ratio . Figure 1 . Effect of sleep duration on daytime leptin levels , ghrelin levels , hunger , and appetite . A. B. C D C D Table . Average Ratings of Appetite after 2 Days of Sleep Restriction or Sleep Extension Figure 2 . Association between the change in hunger ratings and the change in ghrelin-to-leptin ratio during the 12:00 noon to 9:00 p.m. time period when sleep is restricted as compared with extended . P Discussion We observed that sleep duration may affect the circulating levels of neuroendocrine factors that regulate hunger and appetite . Two days with 4 hours of time in bed each night were associated with an 18 % decrease in the levels of the anorexigenic hormone leptin . By comparison , 3 days of underfeeding by approximately 900 calories per day in healthy lean volunteers has been reported to result in a decrease of leptin levels averaging 22 % ( 4 ) . Sleep curtailment was also associated with an almost 28 % increase in daytime levels of the orexigenic factor ghrelin . The reciprocal changes in leptin and ghrelin that we observed in response to sleep restriction were associated with a 24 % increase in hunger and a 23 % increase in appetite . Appetite for calorie-dense nutrients with high carbohydrate content , including sweets , salty snacks , and starchy foods , increased by 33 % to 45 % . In contrast ,
AIM Because type 2 diabetes ( T2D ) is related to obesity , it is often associated with obstructive sleep apnoea syndrome ( OSAS ) , although OSAS is also frequently diagnosed in patients with type 1 diabetes ( T1D ) and may promote gestational diabetes .
Thus , this systematic review of the scientific evidence aim ed to evaluate the epidemiological association between OSAS and all forms of diabetes , the current underst and ing of the pathophysiological mechanisms behind these associations , the expected benefits and limitations of OSAS treatment in patients with diabetes and , finally , to propose which patients require screening for OSAS .