SLEEP

Arvis, Laura; Doye, Emilie; Perge, Kevin; Zhang, Min; Thieux, Marine; Guyon, Aurore; Franco, Patricia; Villanueva, Carine

doi: 10.1093/sleep/zsac281pmid: 36433727

Study ObjectivesNarcolepsy with cataplexy is associated with obesity in children. We proposed to assess whether metabolic complications were linked to narcolepsy regardless of obesity. The second aim of the study was to compare endocrine comorbidities in obese children with narcolepsy and control patients.MethodsWe performed a case-control study in Pediatric Sleep Unit and Pediatric Endocrinology Unit of Woman Mother Child Hospital (Lyon, France) comparing 22 children with narcolepsy with 22 sex-, pubertal stage-, and BMI-matched non-syndromic obese patients. Clinical examination, biological measurements including an oral glucose tolerance test, and abdominal ultrasound were performed.ResultsNo difference regarding glucidic, lipid profile, hepatic, respiratory, and cardiovascular parameters were found between narcoleptic and control participants. Insulin sensitivity did not differ between the two groups. Control patients had more first-degree family history of overweight or obesity than children with narcolepsy (83% vs. 50%, p = .05). Prevalence of precocious puberty in children with narcolepsy was not higher than in control participants, but all the cases of advanced puberty involved children with narcolepsy who were diagnosed before 11 years old. All cases of central hypothyroidism belong to the narcoleptic group, who presented lower thyroid-stimulating hormone and fTA values compared to control children (respectively p = .03 and p = .001).ConclusionsNo difference regarding metabolic complications was found between children with narcolepsy and control participants. Thus, metabolic disorders may be related to weight gain rather than a narcolepsy-specific risk. The presence of hypothyroidism and advanced puberty suggests a global involvement of hypothalamic structures in children with narcolepsy.

Ong, Ju Lynn; Massar, Stijn A A; Lau, TeYang; Ng, Ben K L; Chan, Lit Fai; Koek, Daphne; Cheong, Karen; Chee, Michael W L

doi: 10.1093/sleep/zsac315pmid: 36546351

Study ObjectivesWe evaluated the efficacy of a digitally delivered, small and scalable incentive-based intervention program on sleep and wellbeing in short-sleeping, working adults.MethodsA 22-week, parallel-group, randomized-controlled trial was conducted on 21–40 y participants gifted with FitbitTM devices to measure sleep for ≥2 years, as part of a broader healthy lifestyle study. About 225 short sleepers (141 males; average time-in-bed, TIB < 7h) were randomly assigned in a 2:1 ratio to Goal-Setting or Control groups. The Goal-Setting group received health vouchers (~USD 0.24) for meeting each sleep goal (i.e. increasing weeknight TIB by 30 min/sleeping before midnight).The study spanned three phases: (1) 2-week Baseline, (2) 10-week Intervention, and (3) 10-week Follow-Up. Wellbeing questionnaires were administered on Weeks 1–2, 11–12, and 21–22.ResultsBaseline weeknight TIB (mean ± SD) was 387 ± 43 min (Goal-Setting) and 399 ± 44 min (Control), while bedtime was 00:53 ± 01:13 (Goal-Setting), and 00:38 ± 00:56 (Control). No difference in sleep outcomes was observed at study endpoints, but exploratory week-by-week analysis showed that on Weeks 3–5, TIB in the Goal-Setting group increased (9–18 min; ps < 0.05) while on Week 5, bedtimes shifted earlier (15 min; p < 0.01) compared to Baseline. Morning sleepiness was reduced in the Goal-Setting group (mean[SEM] = −3.17(1.53); p = 0.04) compared to Baseline, although between-group differences were not significant (p = 0.62). Main barriers to sleeping longer were work hours (35%), followed by leisure activities (23%) and family commitments (22%).ConclusionOur program resulted in encouraging subjective sleep improvements and short-term sleep extension, but sustained transformation of sleep will probably require structural measures to overcome significant obstacles to sleep.Trial RegistrationClinicalTrials.gov Identifier: NCT04878380 (hiSG Sleep Health Study (hiSG-SHS); https://clinicaltrials.gov/ct2/show/NCT04878380)

Wiechers, Cornelia; Uhlig, Simone; Poets, Anette; Weise, Christina; Naros, Andreas; Krimmel, Michael; Koos, Bernd; Poets, Christian F; Quante, Mirja

doi: 10.1093/sleep/zsac317pmid: 36566505

Study objectivesTo investigate neurocognitive and behavioral outcomes at primary school age in relation to obstructive sleep apnea (OSA) in children with Robin sequence (RS) treated with the Tuebingen palatal plate in infancy and to assess the impact of OSA in these patients.MethodsForty-two primary school-aged children (n = 21 with RS, n = 21 age- and sex-matched controls) underwent polysomnography, intelligence testing (“Wechsler Intelligence Scale for Children—Fifth Edition” [WISC-V]), and anthropometrics. Families completed a 7-day sleep diary and questionnaires on sleep and behavior (Children’s Sleep Habits Questionnaire [CSHQ] and the Child Behavior Checklist [CBCL]).ResultsIn children with RS (17 non-syndromic, four syndromic; median age 9.7 [8.5–10.8] years), the obstructive apnea-hypopnea index (OAHI) was significantly higher than in controls (1.3 [0.4–2.7]/h vs. 0.4 [0.1–0.6]/h). Two syndromic children with RS were already on nocturnal respiratory support for OSA prior to our study, and one non-syndromic child was diagnosed with severe OSA (OAHI 57/h) despite an unremarkable medical history and questionnaire. The overall intelligence quotient in children with RS was within the normal range and did not differ between children with RS and healthy peers (102 vs. 108, p = .05). However, children with RS had values in the at-risk clinical range for externalizing behavior.ConclusionsThese children with RS showed an increased risk of OSA and behavioral problems, suggesting regular screening for OSA throughout childhood. Neurocognitive scores in children with RS were within the normal range after adequate treatment of OSA during infancy.

Chouraki, Alexandre; Tournant, Julia; Arnal, Pierrick; Pépin, Jean-Louis; Bailly, Sébastien

doi: 10.1093/sleep/zsac319pmid: 36583300

Study ObjectivesIn-laboratory polysomnography is the current gold standard for objective sleep measurements in clinical trials, but this does not capture night-to-night variability in sleep parameters. This study analyzed variability in sleep parameters recorded over multiple nights of sleep in an ecological setting using a portable sleep monitor and then estimated the minimum sample sizes required to reliably account for inter- and intra-individual variability in sleep parameters.MethodsParticipants were males who self-reported the absence of sleep disorders, and used a sleep monitoring device (Dreem Headband, Dreem, France) over multiple nights of sleep. Night-to-night variability of sleep parameters was determined over five consecutive weeknights using coefficients of variation (CV), and the minimal number of individuals and nights needed to reliably determine each sleep parameter was assessed.ResultsNight-to-night variability for the whole group (n = 94; 470 nights) was high (CV 0.44–0.58) for N2, N3, sleep onset and persistent sleep latencies, and wake after sleep onset (WASO), medium (CV 0.22–0.28) for N1 and N3 percentage, awakenings and REM latency, and low (CV 0.04–0.19) for sleep efficiency, N2 and REM percentages, total sleep time (TST) and micro-arousal index. Minimum sample sizes for reliable assessment of TST and WASO were 2 nights with 10 participants and 4 nights with 50 participants, respectively.ConclusionsNight-to-night variability of sleep parameters is underestimated and under-recognized. These data on variability in commonly used sleep parameters will facilitate better estimation of sample sizes and number of nights required in clinical trials based on the outcomes of interest.

Bogh, Adrian F; Jensen, Simon B K; Juhl, Christian R; Janus, Charlotte; Sandsdal, Rasmus M; Lundgren, Julie R; Noer, Mikkel H; Vu, Nhu Q; Fiorenza, Matteo; Stallknecht, Bente M; Holst, Jens J; Madsbad, Sten; Torekov, Signe S

doi: 10.1093/sleep/zsac295pmid: 36472579

Study ObjectivesInsufficient sleep may attenuate weight loss, but the role of sleep in weight loss maintenance is unknown. Since weight regain after weight loss remains a major obstacle in obesity treatment, we investigated whether insufficient sleep predicts weight regain during weight loss maintenance.MethodsIn a randomized, controlled, two-by-two factorial study, 195 adults with obesity completed an 8-week low-calorie diet and were randomly assigned to 1-year weight loss maintenance with or without exercise and liraglutide 3.0 mg/day or placebo. Sleep duration and quality were measured before and after the low-calorie diet and during weight maintenance using wrist-worn accelerometers (GENEActiv) and Pittsburgh Sleep Quality Index (PSQI). To test associations between insufficient sleep and weight regain, participants were stratified at randomization into subgroups according to sleep duration (</≥6 h/night) or sleep quality (PSQI score ≤/>5).ResultsAfter a diet-induced 13.1 kg weight loss, participants with short sleep duration at randomization regained 5.3 kg body weight (p = .0008) and had less reduction in body fat percentage compared with participants with normal sleep duration (p = .007) during the 1-year weight maintenance phase. Participants with poor sleep quality before the weight loss regained 3.5 kg body weight compared with good quality sleepers (p = .010). During the weight maintenance phase, participants undergoing liraglutide treatment displayed increased sleep duration compared with placebo after 26 weeks (5 vs. −15 min/night) but not after 1 year. Participants undergoing exercise treatment preserved the sleep quality improvements attained from the initial weight loss.ConclusionsShort sleep duration or poor sleep quality was associated with weight regain after weight loss in adults with obesity.

Champetier, Pierre; André, Claire; Weber, Frederik D; Rehel, Stéphane; Ourry, Valentin; Laniepce, Alice; Lutz, Antoine; Bertran, Françoise; Cabé, Nicolas; Pitel, Anne-Lise; Poisnel, Géraldine; de la Sayette, Vincent; Vivien, Denis; Chételat, Gaël;