SLEEP

Penzel, Thomas

doi: 10.1093/sleep/zsac190pmid: 35951083

Accepted manuscripts Accepted manuscripts are PDF versions of the author’s final manuscript, as accepted for publication by the journal but prior to copyediting or typesetting. They can be cited using the author(s), article title, journal title, year of online publication, and DOI. They will be replaced by the final typeset articles, which may therefore contain changes. The DOI will remain the same throughout. Article PDF first page preview Close This content is only available as a PDF. © Sleep Research Society 2022. Published by Oxford University Press on behalf of the Sleep Research Society. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact [email protected] © Sleep Research Society 2022. Published by Oxford University Press on behalf of the Sleep Research Society.

He, Lingfang; Ma, Tianqi; Li, Jinchen; Luo, Yi; Zhang, Guogang; Cheng, Xunjie; Bai, Yongping

doi: 10.1093/sleep/zsac141pmid: 35738866

Study ObjectivesTo investigate whether a healthy sleep pattern would reduce the risk of cardiometabolic multimorbidity (CMM) among hypertensives.MethodsThis is a prospective cohort analysis from the UK Biobank. A total of 69 524 hypertensives without a history of diabetes mellitus, coronary heart disease, or stroke at baseline were enrolled. Five dimensions of healthy sleep at baseline including early chronotype, sleep 7–8 h/d, free of insomnia, no snoring, and no frequent excessive daytime sleepiness were used to generate a healthy sleep score ranging from 0 to 5 (one point was given for each dimension of healthy sleep). A higher score indicated a healthier sleep pattern. We set five groups corresponding to the healthy sleep score of 5, 4, 3, 2, and 0–1, respectively. The primary outcome was the incidence of overall CMM among enrolled hypertensives. We assessed the adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) by Fine-Gray subdistribution hazard models.ResultsWe found the full-adjusted HR (95% CI) for overall CMM was 0.93 (0.91–0.95) for a 1-point increase in the healthy sleep score. Compared to hypertensives with a healthy sleep score of 0–1, those with a score of 5 had a 27% lower risk of overall CMM, and 37%, 23%, and 20% lower risks of diabetes mellitus, coronary heart disease, and stroke, respectively, after adjusting for sociodemographic characteristic, lifestyle, and clinical factors.ConclusionsOur results indicated that a healthy sleep pattern was associated with lower risks of CMM outcomes among hypertensives.

Mattingly, Stephen M; Martinez, Gonzalo; Young, Jessica; Cain, Meghan K; Striegel, Aaron

doi: 10.1093/sleep/zsac184pmid: 35951011

Study ObjectivesSnoozing was defined as using multiple alarms to accomplish waking, and considered as a method of sleep inertia reduction that utilizes the stress system. Surveys measured snoozing behavior including who, when, how, and why snoozing occurs. In addition, the physiological effects of snoozing on sleep were examined via wearable sleep staging and heart rate (HR) activity, both over a long time scale, and on the days that it occurs. We aimed to establish snoozing as a construct in need of additional study.MethodsA novel survey examined snoozing prevalence, how snoozing was accomplished, and explored possible contributors and motivators of snoozing behavior in 450 participants. Trait- and day-level surveys were combined with wearable data to determine if snoozers sleep differently than nonsnoozers, and how snoozers and nonsnoozers differ in other areas, such as personality.Results57% of participants snoozed. Being female, younger, having fewer steps, having lower conscientiousness, having more disturbed sleep, and being a more evening chronotype increased the likelihood of being a snoozer. Snoozers had elevated resting HR and showed lighter sleep before waking. Snoozers did not sleep less than nonsnoozers nor did they feel more sleepiness or nap more often.ConclusionsSnoozing is a common behavior associated with changes in sleep physiology before waking, both in a trait- and state-dependent manner, and is influenced by demographic and behavioral traits. Additional research is needed, especially in detailing the physiology of snoozing, its impact on health, and its interactions with observational studies of sleep.

Winter, Anne-Sophie; Haverkamp, Christian; Gratzke, Christian; Huber, Roman; Lederer, Ann-Kathrin

doi: 10.1093/sleep/zsac122pmid: 35640263

Study ObjectivesPostoperative sleep disturbances appear to be a common complication after surgery being treated with sleep-promoting medication such as valerian, but robust data and evidence of medicinal approaches are lacking.MethodsWe performed a retrospective cohort analysis of all 21 168 urological, gynecological, and general surgical patients of the University Medical Center Freiburg, Germany, who underwent surgery between 2015 and 2020. Target parameters were the usage of sleep-promoting medication to estimate the occurrence of postoperative sleep disturbances as well as the kind of sleep medication with a special focus on herbal medication such as valerian.ResultsDrug-treated sleep disturbances occurred in 15% (n = 3083) of the patients. Valerian was the second most applied drug (n = 814, 26.4%) after classic benzodiazepines (n = 1 138, 36.9%). The majority of patients got valerian as monotherapy. Age, length of stay, and comorbidities were associated with demand for sleep medication in general (p < .001). Valerian monotherapy was more common in women (OR 1.53, 95% CI: 1.33–1.77, p < .001), elderly patients (OR 1.50, 95% CI: 1.29–1.75, p < .001), and patients with prolonged hospital stay (OR 2.23, 95% CI: 1.91–2.61, p < .001).ConclusionsValerian plays an important role in the treatment of postoperative sleep disturbances clinically, and it appears to be a promising therapeutic approach especially in women, older and sicker patients, and those with prolonged hospital stay. Further research has to clarify the efficacy of valerian postoperatively.Clinical trial registrationDRKS00027903, https://www.drks.de/drks_web/navigate.do?navigationId=trial.HTML&TRIAL_ID=DRKS00027903

Li, Wen-Yang; Jin, Hongyu; Zou, Ying; Huang, Hong; Wei, Zhijing; Kang, Jian; Xue, Yixue; Wang, Wei

doi: 10.1093/sleep/zsac170pmid: 35867628

Study ObjectivesThe mechanical efficiency of upper airway (UA) muscles are pivotal in maintaining UA stability. We aimed to investigate if different tongue training approaches could differently induce signs of neuroplastic in the corticomotor pathways and upper airway stability changes.Methods36 Sprague–Dawley rats were trained daily for eight weeks to lick an isotonic force-sensing disc at targeting forces using 30%–50% of maximal achieved lick force (MALF) for tongue task training (TTT) or targeting force set above 50%, 60%, and 70% of MALF progressively for tongue strength training (TST). Corticomotor excitability was dynamically assessed by GG response to transcortical magnetic stimulation (TMS) at different sessions. GG EMG activity, GG ultrastructure and myosin heavy chain (MHC), UA dynamics were assessed after eight weeks.ResultsAfter 4 weeks, GG TMS latencies decreased in both tongue training groups when compared with the control group (p < .05) and this excitability was more stable in TTT group. After 8 weeks, both GG TMS response and EMG activity revealed increased excitability in TTT and TST groups. The apoptotic pathological morphology changes of GG ultrastructure were observed in TST group, but not TTT. Percentage of GG MHC type I fibers in TST group was higher than the control and TTT groups (p < .05). The UA Pcrit decreased significantly in TTT group (p < .05) and tend to decrease in TST group (p = .09).ConclusionTTT could improve the UA stability and induce the neuroplastic changes more efficiently without training-induced muscle injury, while TST revealed a fatigue-resistance change in GG.

Kendle, Anthony M; Salemi, Jason L; Jackson, Chandra L; Buysse, Daniel J; Louis, Judette M

doi: 10.1093/sleep/zsac175pmid: 35901516

Study ObjectivesUsing a large, nationally representative database, we aimed to estimate the prevalence and trends of insomnia among pregnant women over a 12-year period. In addition, we aimed to examine the interplay among insomnia, maternal comorbidities, and severe maternal morbidity (SMM).MethodsWe conducted a serial cross-sectional analysis of pregnancy-related hospitalizations in the United States from the 2006 to 2017 National Inpatient Sample (NIS). ICD-9 and ICD-10 codes were used to capture diagnoses of insomnia and obstetric comorbidities during delivery and non-delivery hospitalizations. The primary outcome was the diagnosis of SMM at delivery. We used logistic regression to assess the association between insomnia and SMM. Joinpoint regression was used to estimate trends in insomnia and SMM.ResultsOf nearly 47 million delivery hospitalizations, 24 625 women had a diagnosis of insomnia, or 5.2 per 10 000 deliveries. The annual incidence increased from 1.8 to 8.6 per 10 000 over the study period. The crude rate of insomnia was 6.3 times higher for non-delivery hospitalizations. Patients with insomnia had more comorbidities, particularly neuromuscular disease, mental health disorders, asthma, and substance use disorder. Prevalence of non-blood transfusion SMM was 3.6 times higher for patients with insomnia (2.4% vs. 0.7%). SMM increased annually by 11% (95% CI = 3.0% to 19.7%) in patients with insomnia. After adjusting for comorbidities, there remained a 24% increased likelihood of SMM for patients with insomnia.ConclusionsCoded diagnosis of insomnia during pregnancy has increased over time, and this burden disparately affects women of low socioeconomic status. Diagnosis of insomnia is an independent predictor of SMM.

Otto, Michael W; Lubin, Rebecca E; Rosenfield, David; Taylor, Daniel J; Birk, Jeffrey L; Espie, Colin A; Shechter, Ari; Edmondson, Donald; Shepherd, Justin M; Zvolensky, Michael J

doi: 10.1093/sleep/zsac117pmid: 35639820

Valente, Heloisa B; Morelhão, Priscila K; Andersen, Monica L; Tufik, Sergio; Vanderlei, Luiz Carlos M

doi: 10.1093/sleep/zsac211pmid: 36111802

Dear Editor, Over the past few decades, there has been a progressive increase in the prevalence of sleep disorders, including in respect of daytime sleepiness, difficulty initiating or maintaining sleep, snoring, and sleep deprivation [1]. Some sleep disturbances have been shown to be independent risk factors for cardiovascular diseases [2], one of the main causes of mortality and disability in the world. A recent review [3] reported that a habitual sleep time of 6 hours or less has been related to increased sympathetic activity, oxidative stress, and a proinflammatory state. These factors are all risk factors for the development of cardiovascular and metabolic syndromes [3]. A reduction in sleep hours has been associated with an increase in the occurrence of major adverse events. In a prospective study by Daghlas et al., a duration of less than 6 hours of sleep was related to a higher risk for myocardial infarction [4]. Aggarwal et al. found that sleeping less than 6 hours per night increased the prevalence of stroke and myocardial infarction [5]. Given the high prevalence of habitual sleep curtailment and its relationship with the occurrence of major adverse events, identifying strategies that can increase and improve sleep time may be important in a clinical context and in respect of public health. In this scenario, sleep extension therapy may be an option to be considered in the treatment of sleep-deprived patients. Sleep extension is structured and monitored behavioral intervention that is based on lengthening the duration of nighttime sleep to produce a higher level of recuperation than that habitually obtained [6]. A growing number of studies have demonstrated favorable results with the use of sleep extension therapy. In a prospective, longitudinal, comparative parallel study, sleep extension combined with dietary restriction promoted weight loss, a significant reduction in waist circumference and a decrease in interleukin-6 and insulin levels in adolescents with obesity [7]. In a study by Leproult et al., inverse relationships were observed between 6 weeks of sleep extension and insulin and glucose levels, as well as markers of insulin sensitivity, in adults with habitual sleep restriction [8]. In another study, a reduction in mean systolic blood pressure in hypertensive individuals after a sleep extension intervention was also identified [9]. Although the underlying mechanisms have not yet been fully elucidated, it is supposed that sleep extension enhances slow-wave sleep and restores the alignment between endogenous circadian rhythm and exogenous stimuli, which neutralizes the effects caused by short sleep [9]. It is important to highlight that factors, such as obesity and inflammation, that are predictors of major adverse events [4] are controlled after an intervention based on sleep extension [7]. Furthermore, a previous study revealed that a sleep duration of 6–9 hours mitigated myocardial infarction risk, despite the genetic predisposition of individuals, and other sleep dimensions, such as quality [4]. This evidence is opportune, since sleep extension therapy has been shown to be an affordable intervention in most of the studies performed. It should be noted that research has also found that a sleep time equal to or greater than 9 hours was associated with the occurrence of major adverse events [10]. Thus, any recommendation to use sleep extension must be done with caution and only for sleep-deprived individuals, and it is not an appropriate treatment for patients with sleep disorders, such as narcolepsy and idiopathic hypersomnia. Given the evidence discussed above, we would like to draw the attention of researchers to the need to perform quality randomized controlled clinical trials to investigate whether sleep extension might be used as a potential behavioral intervention to reduce the risk of the occurrence of major adverse events in individuals with insufficient sleep. Data from these studies could be important for the development of new therapeutic strategies for sleep-deprived patients that can reduce the risk of major adverse events. Funding Our studies are supported by grants from the Associação Fundo de Incentivo à Pesquisa (AFIP). M.L.A. and S.T. are Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) fellowship recipients. Disclosure Statement None declared. References 1. Drager LF , et al. 1º Posicionamento brasileiro sobre o impacto dos distúrbios de sono nas doenças cardiovasculares da Sociedade Brasileira de Cardiologia . Arq Bras Cardiol. 2018 ; 111 ( 2 ): 290 – 340 . doi:10.5935/abc.20180154 Google Scholar PubMed OpenURL Placeholder Text WorldCat 2. Drager LF , et al. Sleep apnea and cardiovascular disease: lessons from recent trials and need for team science . Circulation 2017 ; 136 ( 19 ): 1840 – 1850 . doi:10.1161/CIRCULATIONAHA.117.029400 Google Scholar Crossref Search ADS PubMed WorldCat 3. Tobaldini E , et al. Short sleep duration and cardiometabolic risk: from pathophysiology to clinical evidence . Nat Rev Cardiol. 2019 ; 16 ( 4 ): 213 – 224 . doi:10.1038/s41569-018-0109-6 Google Scholar Crossref Search ADS PubMed WorldCat 4. Daghlas I , et al. Sleep duration and myocardial infarction . J Am Coll Cardiol. 2019 ; 74 ( 10 ): 1304 – 1314 . doi:10.1016/j.jacc.2019.07.022 Google Scholar Crossref Search ADS PubMed WorldCat 5. Aggarwal S , et al. Associations between sleep duration and prevalence of cardiovascular events . Clin Cardiol. 2013 ; 36 ( 11 ): 671 – 676 . doi:10.1002/clc.22160 Google Scholar Crossref Search ADS PubMed WorldCat 6. Mantua J , et al. Sleep extension reduces fatigue in healthy, normally-sleeping young adults . Sleep Sci. 2019 ; 12 ( 1 ): 21 – 27 . doi:10.5935/1984-0063.20190056 Google Scholar Crossref Search ADS PubMed WorldCat 7. Moreno-Frías C , et al. Sleep extension increases the effect of caloric restriction over body weight and improves the chronic low-grade inflammation in adolescents with obesity . J Adolesc Health. 2020 ; 66 ( 5 ): 575 – 581 . doi:10.1016/j.jadohealth.2019.11.301 Google Scholar Crossref Search ADS PubMed WorldCat 8. Leproult R , et al. Beneficial impact of sleep extension on fasting insulin sensitivity in adults with habitual sleep restriction . Sleep. 2015 ; 38 ( 5 ): 707 – 715 . doi:10.5665/sleep.4660 Google Scholar Crossref Search ADS PubMed WorldCat 9. Zhu B , et al. Feasibility of sleep extension and its effect on cardiometabolic parameters in free-living settings: a systematic review and meta-analysis of experimental studies . Eur J Cardiovasc Nurs. 2022 ; 21 ( 1 ): 9 – 25 . doi:10.1093/eurjcn/zvab055 Google Scholar Crossref Search ADS PubMed WorldCat 10. Wang Y , et al. Association of longitudinal patterns of habitual sleep duration with risk of cardiovascular events and all-cause mortality . JAMA Netw Open. 2020 ; 3 ( 5 ): e205246 . doi:10.1001/jamanetworkopen.2020.5246 Google Scholar Crossref Search ADS PubMed WorldCat © The Author(s) 2022. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For permissions, please e-mail: [email protected] This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/pages/standard-publication-reuse-rights) © The Author(s) 2022. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For permissions, please e-mail: [email protected]

Spruyt, Karen; Ferri, Raffaele

doi: 10.1093/sleep/zsac169pmid: 35830507

Accepted manuscripts Accepted manuscripts are PDF versions of the author’s final manuscript, as accepted for publication by the journal but prior to copyediting or typesetting. They can be cited using the author(s), article title, journal title, year of online publication, and DOI. They will be replaced by the final typeset articles, which may therefore contain changes. The DOI will remain the same throughout. Article PDF first page preview Close This content is only available as a PDF. © The Author(s) 2022. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For permissions, please e-mail: [email protected] This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model) © The Author(s) 2022. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For permissions, please e-mail: [email protected]

Honda, Makoto; Shigematsu, Yosuke; Shimada, Mihoko; Honda, Yoshiko; Tokunaga, Katsushi; Miyagawa, Taku

doi: 10.1093/sleep/zsac160pmid: 35810398

Study ObjectivesNarcolepsy type 1 (NT1) is associated with metabolic abnormalities but their etiology remains largely unknown. The gene for carnitine palmitoyltransferase 1B (CPT1B) and abnormally low serum acylcarnitine levels have been linked to NT1. To elucidate the details of altered fatty acid metabolism, we determined levels of individual acylcarnitines and evaluated CPT1 activity in patients with NT1 and other hypersomnia.MethodsBlood samples from 57 NT1, 51 other hypersomnia patients, and 61 healthy controls were analyzed. The levels of 25 major individual acylcarnitines were determined and the C0/(t[C16] + t[C18]) ratio was used as a CPT1 activity marker. We further performed transcriptome analysis using independent blood samples from 42 NT1 and 42 healthy controls to study the relevance of fatty acid metabolism. NT1-specific changes in CPT1 activity and in expression of related genes were investigated.ResultsCPT1 activity was lower in patients with NT1 (p = 0.00064) and other hypersomnia (p = 0.0014) than in controls. Regression analysis revealed that CPT1 activity was an independent risk factor for NT1 (OR: 1.68; p = 0.0031) and for other hypersomnia (OR: 1.64; p = 0.0042). There was a significant interaction between obesity (BMI <25, ≥25) and the SNP rs5770917 status such that nonobese NT1 patients without risk allele had better CPT1 activity (p = 0.0089). The expression levels of carnitine-acylcarnitine translocase (CACT) and CPT2 in carnitine shuttle were lower in NT1 (p = 0.000051 and p = 0.00014, respectively).ConclusionsThese results provide evidences that abnormal fatty acid metabolism is involved in the pathophysiology of NT1 and other hypersomnia.