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Short sleep duration and decreased sleep quality are emerging risk factors for obesity and its associated morbidities. Chronotype, an attribute that reflects individual preferences in the timing of sleep and other behaviors, is a continuum from morningness to eveningness. The importance of chronotype in relation to obesity is mostly unknown. Evening types tend to have unhealthy eating habits and suffer from psychological problems more frequently than Morning types, thus we hypothesized that eveningness may affect health parameters in a cohort of obese individuals reporting sleeping less than 6.5 hours per night. BASELINE DATA FROM OBESE (BMI: 38.5±6.4 kg/m(2)) and short sleeping (5.8±0.8 h/night by actigraphy) participants (n = 119) of the Sleep Extension Study were analyzed (www.ClinicalTrials.gov, identifier NCT00261898). Assessments included the Horne and Ostberg Morningness-Eveningness questionnaire, a three-day dietary intake diary, a 14-day sleep diary, 14 days of actigraphy, and measurements of sleep apnea. Twenty-four hour urinary free cortisol, 24 h urinary norepinephrine and epinephrine levels, morning plasma ACTH and serum cortisol, fasting glucose and insulin, and lipid parameters were determined. Eveningness was associated with eating later in the day on both working and non-working days. Progression towards eveningness was associated with an increase in BMI, resting heart rate, food portion size, and a decrease in the number of eating occasions and HDL-cholesterol. Evening types had overtly higher 24 h urinary epinephrine and morning plasma ACTH levels, and higher morning resting heart rate than Morning types. In addition, Evening types more often had sleep apnea, independent of BMI or neck circumference. Eveningness was associated with eating later and a tendency towards fewer and larger meals and lower HDL-cholesterol levels. In addition, Evening types had more sleep apnea and higher stress hormones. Thus, eveningness in obese, chronically sleep-deprived individuals compounds the cardiovascular risk associated with obesity.

Sleep-disordered breathing (SDB) is common in individuals with established cardiovascular disease (CVD), particularly those with heart failure (HF). There are two main types of SDB, central sleep apnoea (CSA) and obstructive sleep apnoea (OSA) which frequently overlap as mixed SDB. Investigating for SDB could be considered in patients with excessive daytime sleepiness, male sex, high body mass index, low ejection fraction, atrial fibrillation (AF), in patients with no dipping blood pressure pattern, recurrent paroxysms of nocturnal dyspnoea or when an apnoea is witnessed. Excessive daytime sleepiness is less likely to be reported by patients with HF than by the general population. In patients with CVD and OSA, continuous positive airway pressure (CPAP) ventilation for over 4 hours daily reduced the risk of major adverse cardiovascular events, but there was no reduction in mortality. In patients with AF and OSA treated with AF ablation, CPAP use was associated with a reduced risk of recurrence of AF. In patients with HF and OSA, small studies have demonstrated that CPAP improves symptoms, brain natriuretic peptide levels and ejection fraction, but data on survival are lacking. Treatment remains unclear in patients with HF and CSA. The presence of CSA may be a defensive adaptive response to HF, and effectively treating CSA as demonstrated in a randomised clinical trial of adaptive servo-ventilation caused more harm than benefit when compared to optimal medical therapy. Thus, the focus of treating CSA should remain on improving the underlying HF by optimising medical therapy and, if indicated, cardiac resynchronisation therapy.

Abstract Study Objectives Sleep-disordered breathing (SDB) is prevalent among children and is associated with adverse health outcomes. Worldwide, approximately 250 million individuals reside at altitudes higher than 2000 meters above sea level (masl). The effect of chronic high-altitude exposure on children with SDB is unknown. This study aims to determine the impact of altitude on sleep study outcomes in children with SDB dwelling at high altitude. Methods A single-center crossover study was performed to compare results of high-altitude home polysomnography (H-PSG) with lower altitude laboratory polysomnography (L-PSG) in school-age children dwelling at high altitude with symptoms consistent with SDB. The primary outcome was apnea-hypopnea index (AHI), with secondary outcomes including obstructive AHI; central AHI; and measures of oxygenation, sleep quality, and pulse rate. Results Twelve participants were enrolled, with 10 included in the final analysis. Median altitude was 1644 masl on L-PSG and 2531 masl on H-PSG. Median AHI was 2.40 on L-PSG and 10.95 on H-PSG. Both obstructive and central respiratory events accounted for the difference in AHI. Oxygenation and sleep fragmentation were worse and pulse rate higher on H-PSG compared to L-PSG. Conclusions These findings reveal a clinically substantial impact of altitude on respiratory, sleep, and cardiovascular outcomes in children with SDB who dwell at high altitude. Within this population, L-PSG underestimates obstructive sleep apnea and central sleep apnea compared to H-PSG. Given the shortage of high-altitude pediatric sleep laboratories, these results suggest a role for home sleep apnea testing for children residing at high altitude.

Sleep apnoea, one of the most common chronic diseases, is a risk factor for ischaemic stroke, stroke recurrence, and poor functional recovery after stroke. More than half of stroke survivors present with sleep apnoea during the acute phase after stroke, with obstructive sleep apnoea being the most common subtype. Following a stroke, sleep apnoea frequency and severity might decrease over time, but moderate to severe sleep apnoea is nevertheless present in up to a third of patients in the chronic phase after an ischaemic stroke. Over the past few decades evidence suggests that treatment for sleep apnoea is feasible during the acute phase of stroke and might favourably affect recovery and long-term outcomes. Nevertheless, sleep apnoea still remains underdiagnosed and untreated in many cases, due to challenges in the detection and prediction of post-stroke sleep apnoea, uncertainty as to the optimal timing for its diagnosis, and a scarcity of clear treatment guidelines (ie, uncertainty on when to treat and the optimal treatment strategy). Moreover, the pathophysiology of sleep apnoea associated with stroke, the proportion of stroke survivors with obstructive and central sleep apnoea, and the temporal evolution of sleep apnoea subtypes following stroke remain to be clarified. To address these shortcomings, the management of sleep apnoea associated with stroke should be integrated into a multidisciplinary diagnostic, treatment, and follow-up strategy.

Sleep-wake disorders are highly prevalent disorders, which can lead to negative effects on cognitive, emotional and interpersonal functioning, and can cause maladaptive metabolic changes. Recent studies support the notion that metabolic processes correlate with sleep. The study of metabolite biomarkers (metabolomics) in a large-scale manner offers unique opportunities to provide insights into the pathology of diseases by revealing alterations in metabolic pathways. This review aims to summarize the status of metabolomic analyses-based knowledge on sleep disorders and to present knowledge in understanding the metabolic role of sleep in psychiatric disorders. Overall, findings suggest that sleep-wake disorders lead to pronounced alterations in specific metabolic pathways, which might contribute to the association of sleep disorders with other psychiatric disorders and medical conditions. These alterations are mainly related to changes in the metabolism of branched-chain amino acids, as well as glucose and lipid metabolism. In insomnia, alterations in branched-chain amino acid and glucose metabolism were shown among studies. In obstructive sleep apnea, biomarkers related to lipid metabolism seem to be of special importance. Future studies are needed to examine severity, subtypes and treatment of sleep-wake disorders in the context of metabolite levels.

Weight loss medications are emerging candidates for pharmacotherapy of sleep-disordered breathing (SDB). A melanocortin 4 receptor (MC4R) agonist, setmelanotide (Set), is used to treat obesity caused by abnormal melanocortin and leptin signaling. We hypothesized that Set can treat SDB in mice with diet-induced obesity. We performed a proof-of-concept randomized crossover trial of a single dose of Set versus vehicle and a 2-week daily Set versus vehicle trial, examined colocalization of Mc4r mRNAs with the markers of CO2-sensing neurons Phox2b and neuromedin B in the brainstem, and expressed Cre-dependent designer receptors exclusively activated by designer drugs (DREADDs) or caspase in obese Mc4r-Cre mice. Set increased minute ventilation across sleep/wake states, enhanced the hypercapnic ventilatory response (HCVR), and abolished apneas during sleep. Phox2b+ neurons in the nucleus of the solitary tract (NTS) and the parafacial region expressed Mc4r. Chemogenetic stimulation of the MC4R+ neurons in the parafacial region, but not in the NTS, augmented HCVR without any changes in metabolism. Caspase elimination of the parafacial MC4R+ neurons abolished effects of Set on HCVR. Parafacial MC4R+ neurons projected to the respiratory premotor neurons retrogradely labeled from C3-C4. In conclusion, MC4R agonists enhance the HCVR and treat SDB by acting on the parafacial MC4R+ neurons.

RationaleHighly prevalent and severe sleep-disordered breathing caused by acute cervical spinal cord injury (quadriplegia) is associated with neurocognitive dysfunction and sleepiness and is likely to impair rehabilitation.ObjectiveTo determine whether 3 months of autotitrating CPAP would improve neurocognitive function, sleepiness, quality of life, anxiety and depression more than usual care in acute quadriplegia.Methods and measurementsMultinational, randomised controlled trial (11 centres) from July 2009 to October 2015. The primary outcome was neurocognitive (attention and information processing as measure with the Paced Auditory Serial Addition Task). Daytime sleepiness (Karolinska Sleepiness Scale) was a priori identified as the most important secondary outcome.Main results1810 incident cases were screened. 332 underwent full, portable polysomnography, 273 of whom had an apnoea hypopnoea index greater than 10. 160 tolerated at least 4 hours of CPAP during a 3-day run-in and were randomised. 149 participants (134 men, age 46±34 years, 81±57 days postinjury) completed the trial. CPAP use averaged 2.9±2.3 hours per night with 21% fully ‘adherent’ (at least 4 hours use on 5 days per week). Intention-to-treat analyses revealed no significant differences between groups in the Paced Auditory Serial Addition Task (mean improvement of 2.28, 95% CI −7.09 to 11.6; p=0.63). Controlling for premorbid intelligence, age and obstructive sleep apnoea severity (group effect −1.15, 95% CI −10 to 7.7) did not alter this finding. Sleepiness was significantly improved by CPAP on intention-to-treat analysis (mean difference −1.26, 95% CI −2.2 to –0.32; p=0.01).ConclusionCPAP did not improve Paced Auditory Serial Addition Task scores but significantly reduced sleepiness after acute quadriplegia.Trial registration numberACTRN12605000799651.

This systematic review and meta-analysis examines the associations of allergic rhinitis with sleep duration and sleep impairment. Observational studies published before August 2019 were obtained through English language literature searches in the PubMed, Embase, and CINAHL databases. Mean differences and odds ratios with 95% confidence intervals were extracted and used for meta-analysis. Heterogeneity was confirmed by the I2-heterogeneity test. Subgroup analysis was conducted to evaluate the influence of study design. The Grading of Recommendations Assessment, Development, and Evaluation approach was used to determine the level of evidence. In total, 2544 records were identified through database searches; 914 duplicate records were excluded, 1452 records were removed after screening of titles and abstracts, 151 records were excluded after full-text screening, and 27 articles were included in the final meta-analyses. A total of 240,706,026 patients (19,444,043 with allergic rhinitis) were considered. No significant difference in sleep duration between the allergic rhinitis and the control groups was found. Patients with allergic rhinitis presented with significantly higher sleep quality scores, sleep disturbances scores, and sleep latency scores; more frequent use of sleep medications; and lower sleep efficiency as measured by the Pittsburgh Sleep Quality Index and polysomnography. Meta-analyses for adjusted odds ratios showed that allergic rhinitis was also associated with higher risks of nocturnal dysfunctions, including insomnia, nocturnal enuresis, restless sleep, sleep-disordered breathing, obstructive sleep apnea, and snoring. Meta-analysis for adjusted odds ratio also showed that allergic rhinitis was associated with daytime dysfunction, including difficulty waking up, daytime sleepiness, morning headache, and the use of sleep medications. The overall quality of evidence ranged from low to very low, indicating that caution is required when interpreting these results. This study demonstrates that there is a significant association of AR with sleep characteristics.

Few patients with amyotrophic lateral sclerosis currently receive non-invasive ventilation (NIV), reflecting clinical uncertainty about the role of this intervention. We aimed to assess the effect of NIV on quality of life and survival in amyotrophic lateral sclerosis in a randomised controlled trial. 92 of 102 eligible patients participated. They were assessed every 2 months and randomly assigned to NIV (n=22) or standard care (n=19) when they developed either orthopnoea with maximum inspiratory pressure less than 60% of that predicted or symptomatic hypercapnia. Primary validated quality-of-life outcome measures were the short form 36 mental component summary (MCS) and the sleep apnoea quality-of-life index symptoms domain (sym). Both time maintained above 75% of baseline (T iMCS and T isym) and mean improvement (μMCS and μsym) were measured. NIV improved T iMCS, T isym, μMCS, μsym, and survival in all patients and in the subgroup with better bulbar function (n=20). This subgroup showed improvement in several measures of quality of life and a median survival benefit of 205 days (p=0·006) with maintained quality of life for most of this period. NIV improved some quality-of-life indices in those with poor bulbar function, including μsym (p=0·018), but conferred no survival benefit. In patients with amyotrophic lateral sclerosis without severe bulbar dysfunction, NIV improves survival with maintenance of, and improvement in, quality of life. The survival benefit from NIV in this group is much greater than that from currently available neuroprotective therapy. In patients with severe bulbar impairment, NIV improves sleep-related symptoms, but is unlikely to confer a large survival advantage.

Abstract Study Objectives Opioid medications are commonly used and are known to impact both breathing and sleep and are linked with adverse health outcomes including death. Clinical data indicate that chronic opioid use causes central sleep apnea, and might also worsen obstructive sleep apnea. The mechanisms by which opioids influence sleep-disordered breathing (SDB) pathogenesis are not established. Methods Patients who underwent clinically indicated polysomnography confirming SDB (AHI ≥ 5/hour) were included. Each patient using opioids was matched by sex, age, and body mass index (BMI) to three control individuals not using opioids. Physiology known to influence SDB pathogenesis was determined from validated polysomnography-based signal analysis. PSG and physiology parameters of interest were compared between opioid and control individuals, adjusted for covariates. Mediation analysis was used to evaluate the link between opioids, physiology, and polysomnographic metrics. Results One hundred and seventy-eight individuals using opioids were matched to 534 controls (median [IQR] age 59 [50,65] years, BMI 33 [29,41] kg/m2, 57% female, and daily morphine equivalent 30 [20,80] mg). Compared with controls, opioids were associated with increased central apneas (2.8 vs. 1.7 events/hr; p = .001) and worsened hypoxemia (5 vs. 3% sleep with SpO2 < 88%; p = .013), with similar overall apnea–hypopnea index. The use of opioids was associated with higher loop gain, a lower respiratory rate (RR), and higher RR variability. Higher loop gain and increased RR variability mediated the effect of opioids on central apnea, but did not mediate the effect on hypoxemia. Conclusions Opioids have multi-level effects impacting SDB. Targeting these factors may help mitigate the deleterious respiratory consequences of chronic opioid use.