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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.

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.

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.

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.

Background Several studies have shown a favorable effect of supervised exercise training on obstructive sleep apnea (OSA). This meta-analysis was conducted to analyze the data from these studies on the severity of OSA (primary outcome) in adults. Secondary outcomes of interest included body mass index (BMI), sleep efficiency, daytime sleepiness and cardiorespiratory fitness. Methods Two independent reviewers searched PubMed and Embase (from inception to March 6, 2013) to identify studies on the effects of supervised exercise training in adults with OSA. Pre- and postexercise training data on our primary and secondary outcomes were extracted. Results A total of 5 studies with 6 cohorts that enrolled a total of 129 study participants met the inclusion criteria. The pooled estimate of mean pre- to postintervention (exercise) reduction in AHI was −6.27 events/h (95 % confidence interval [CI] −8.54 to −3.99; p  < 0.001). The pooled estimates of mean changes in BMI, sleep efficiency, Epworth sleepiness scale and VO 2 peak were −1.37 (95 % CI −2.81 to 0.07; p  = 0.06), 5.75 % (95 % CI 2.47–9.03; p  = 0.001), −3.3 (95 % CI −5.57 to −1.02; p  = 0.004), and 3.93 mL/kg/min (95 % CI 2.44–5.42; p  < 0.001), respectively. Conclusions This meta-analysis shows a statistically significant effect of exercise in reducing the severity of sleep apnea in patients with OSA with minimal changes in body weight. Additionally, the significant effects of exercise on cardiorespiratory fitness, daytime sleepiness, and sleep efficiency indicate the potential value of exercise in the management of OSA.

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.

Air pollution may influence sleep through airway inflammation or autonomic nervous system pathway alterations. Epidemiological studies may provide evidence of relationships between chronic air pollution exposure and sleep apnea. To determine whether ambient-derived pollution exposure is associated with obstructive sleep apnea and objective sleep disruption. We analyzed data from a sample of participants in MESA (Multi-Ethnic Study of Atherosclerosis) who participated in both the Sleep and Air studies. Mean annual and 5-year exposure levels to nitrogen dioxide (NO ) and particulate matter ≤ 2.5 μm in aerodynamic diameter (PM ) were estimated at participants' homes using spatiotemporal models based on cohort-specific monitoring. Participants completed in-home full polysomnography and 7 days of wrist actigraphy. We used multivariate models, adjusted for demographics, comorbidities, socioeconomic factors, and site, to assess whether air pollution was associated with sleep apnea (apnea-hypopnea index ≥ 15) and actigraphy-measured sleep efficiency. The participants (n = 1,974) were an average age of 68 (±9) years, 46% male, 36% white, 24% Hispanic, 28% black, and 12% Asian; 48% had sleep apnea and 25% had a sleep efficiency of ≤88%. A 10 ppb annual increase in NO exposure was associated with 39% greater adjusted odds of sleep apnea (95% confidence interval [CI], 1.03-1.87). A 5 μg/m greater annual PM exposure was also associated with 60% greater odds of sleep apnea (95% CI, 0.98-2.62). Sleep efficiency was not associated with air pollution levels in fully adjusted models. Individuals with higher annual NO and PM exposure levels had a greater odds of sleep apnea. These data suggest that in addition to individual risk factors, environmental factors also contribute to the variation of sleep disorders across groups, possibly contributing to health disparities.

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.

Abstract Study Objectives Over 80% of people with tetraplegia have sleep-disordered breathing (SDB), but whether this is predominantly obstructive or central is unclear. This study aimed to estimate the prevalence of central sleep apnea (CSA) in tetraplegia and the contributions of central, obstructive, and hypopnea respiratory events to SDB summary indices in tetraplegia. Methods Research and clinical data from 606 individuals with tetraplegia and full overnight polysomnography were collated. The proportions of different respiratory event types were calculated; overall and for mild, moderate, and severe disease. The prevalence of Predominant CSA (Central Apnea Index [CAI] ≥ 5 and more central than obstructive apneas) and Any CSA (CAI ≥ 5) was estimated. Prevalence of sleep-related hypoventilation (SRH) was estimated in a clinical sub-cohort. Results Respiratory events were primarily hypopneas (71%), followed by obstructive (23%), central (4%), and mixed apneas (2%). As severity increased, the relative contribution of hypopneas and central apneas decreased, while that of obstructive apneas increased. The prevalence of Predominant CSA and Any CSA were 4.3% (26/606) and 8.4% (51/606) respectively. Being male, on opiates and having a high tetraplegic spinal cord injury were associated with CSA. SRH was identified in 26% (26/113) of the clinical sub-cohort. Conclusions This is the largest study to characterize SDB in tetraplegia. It provides strong evidence that obstructive sleep apnea is the predominant SDB type; 9–18 times more prevalent than CSA. The prevalence of CSA was estimated to be 4%–8%, significantly lower than previously reported. Graphical Abstract Graphical Abstract

Obstructive sleep apnea (OSA) is a common disorder that describes recurrent collapse of the upper airway during sleep. Animal models have been pivotal to the understanding of OSA pathogenesis, consequences, and treatment. In this review, we highlight the history of OSA research in animals and include the discovery of animals with spontaneous OSA, the induction of OSA in animals, and the emulation of OSA using exposures to intermittent hypoxia and sleep fragmentation.