Bimodal diurnal preference in undergraduate students is associated with negative health and sleep outcomes.

The bimodal preference is a fourth diurnal preference proposed by re-scoring the Morningness-Eveningness Questionnaire. The present work aimed to describe the prevalence of the bimodal preference in a sample of undergraduate students and to characterize the bimodal type in terms of their health and sleep-related outcomes. A web-based cross-sectional study conducted between September 2018 and March 2021 (convenience sampling method). The sample was composed of undergraduate students who completed an electronic form that included the Morningness and Eveningness Questionnaire, the Pittsburgh Sleep Quality Index, the Self-Compassion Scale, the Epworth Sleepiness Scale, the Hospital Anxiety and Depression Scale, and the World Health Organization Subjective Well-Being Index. The final sample consisted of 615 students (82% female, mean age: 23.4 ± 6.5 years), of whom 108 (18%) had positive bimodality indexes. Bimodal subjects comprised 48 students, 8% of the total sample. Bimodal subjects had poorer subjective sleep quality, more daytime sleepiness, lower subjective well-being, greater anxiety and depression symptoms, and lower self-compassion than morning and/or intermediate types; they did not differ from evening types. The description of bimodal diurnal preference in this population may be of interest for the design of academic policies more in line with the circadian reality of students.

Validation of a sleep staging classification model for healthy adults based on two combinations of a single-channel EEG headband and wrist actigraphy.

STUDY OBJECTIVES: The aim of this study was to develop a sleep staging classification model capable of accurately performing on different wearable devices. METHODS: Twenty-three healthy participants underwent a full-night type I polysomnography and used two device combinations: (A) flexible single-channel electroencephalogram (EEG) headband + actigraphy (n = 12) and (B) rigid single-channel EEG headband + actigraphy (n = 11). The signals were segmented into 30-second epochs according to polysomnographic stages (scored by a board-certified sleep technologist; model ground truth) and 18 frequency and time features were extracted. The model consisted of an ensemble of bagged decision trees. Bagging refers to bootstrap aggregation to reduce overfitting and improve generalization. To evaluate the model, a training dataset under 5-fold cross-validation and an 80-20% dataset split was used. The headbands were also evaluated without the actigraphy feature. Participants also completed a usability evaluation (comfort, pain while sleeping, and sleep disturbance). RESULTS: Combination A had an F1-score of 98.4% and the flexible headband alone of 97.7% (error rate for N1: combination A = 9.8%; flexible headband alone = 15.7%). Combination B had an F1-score of 96.9% and the rigid headband alone of 95.3% (error rate for N1: combination B = 17.0%; rigid headband alone = 27.7%); in both, N1 was more confounded with N2. CONCLUSIONS: We developed an accurate sleep classification model based on a single-channel EEG device, and actigraphy was not an important feature of the model. Both headbands were found to be useful, with the rigid one being more disruptive to sleep. Future research can improve our results by applying the developed model in a population with sleep disorders. CLINICAL TRIAL REGISTRATION: Registry: ClinicalTrials.gov; Name: Actigraphy, Wearable EEG Band and Smartphone for Sleep Staging; URL: https://clinicaltrials.gov/study/NCT04943562; Identifier: NCT04943562. CITATION: Melo MC, Vallim JRS, Garbuio S, et al. Validation of a sleep staging classification model for healthy adults based on 2 combinations of a single-channel EEG headband and wrist actigraphy. J Clin Sleep Med. 2024;20(6):983-990.

Leptin moderates the relationship between sleep quality and memory function: A population-based study.

Sleep is crucial for memory, as it promotes its encoding, consolidation, storage, and retrieval. Sleep periods following learning enhance memory consolidation. Leptin, a hormone that regulates appetite and energy balance, also influences memory and neuroplasticity. It plays a neurotrophic role in the hippocampus, enhancing synaptic function and promoting memory processes. Given these associations between sleep, memory, and leptin, this study aimed to evaluate the interplay between sleep quality, memory complaints and leptin levels. Using data from the São Paulo Epidemiologic Sleep Study (EPISONO) 2007 edition, we analyzed data from 881 participants who underwent evaluations for subjective sleep quality (Pittsburgh Sleep Quality Index), memory function (Prospective and Retrospective Memory Questionnaire), body mass index and plasmatic leptin levels. After confirming that subjects with poor sleep quality had more memory complaints in our cohort, we observed that leptin levels were increased in individuals with more memory complaints, but there was no association between leptin levels and sleep quality. Mediation analysis reinforced the direct effect of sleep quality on memory function, but leptin had no indirect effect as mediator over the sleep-memory association. Moderation analysis revealed that leptin acted as a moderator in the relationship between sleep quality and memory, with increased leptin levels enhancing the effect of sleep quality over memory function. These findings underscore the intricate interplay between sleep, memory, and metabolic factors like leptin, shedding light on potential mechanisms through which sleep influences memory and cognitive functions. Further research is needed to elucidate the exact mechanisms underlying these relationships and their implications for overall health and well-being.

The effects of social jetlag and sleep variability on sleepiness in a population-based study: The mediating role of sleep debt.

Sleepiness is a multicausal condition, and previous research has highlighted associations between this symptom and the circadian timing system, specifically concerning social jetlag and sleep variability. Recent inquiries have shown that the effects of social jetlag on sleepiness can be confounded with the consequences of sleep debt. In light of the current evidence, we aimed to assess the effects of social jetlag and sleep variability on sleepiness and the potential mediating role of sleep debt. We used data from the EPISONO study, a cross-sectional population-based study with a sample size of 1042 participants, representative of the city of Sao Paulo, Brazil. Participants completed the UNIFESP Sleep Questionnaire (self-reported bedtime and get-up time) and the Epworth Sleepiness Scale (subjective daytime sleepiness). Subsequently, sleep-corrected mid-sleep time (chronotype), total sleep time, social jetlag (absolute difference between the mid-sleep time on workdays and mid-sleep time on free days), sleep variability (standard deviation of mid-sleep time), and sleep debt (difference between total sleep time on workdays and free days) were calculated. Generalised linear models were used to test whether social jetlag and sleep variability affected sleepiness. Mediation models were used to determine if any observed significant effects were mediated by sleep debt. The prevalence of social jetlag was 23% for >1 h and 12% for >2 h. The mean sleep variability was 41 ± 30 min. Social jetlag had a significant effect on the Epworth Sleepiness Scale scores. This association was no longer statistically significant after controlling for age, sex, body mass index, work schedule, and chronotype. A significant indirect effect of social jetlag on sleep debt and subsequently on the Epworth Sleepiness Scale scores was found. No effect of sleep variability on sleepiness could be identified. In conclusion, the association between social jetlag and sleepiness was mediated by sleep debt but was not independent of demographic, work, and chronotype variables. This study provides new evidence on the importance of circadian misalignment and sleep debt for sleep health on a population level.

Sleep deprivation decreases the reproductive capacity by affecting the arrival of morulas in the uterus.

A previous animal study by our group found that sleep deprivation during preimplantation was associated with decreased pregnancy maintenance. Given its impact on human society, we aimed in the current study to assess whether sleep deprivation affects blastocyst gene expression and/or the implantation process. For this, pregnant mice (gestational day 0 [GD 0]) were assigned into paradoxical sleep deprivation (SD, 72 hr; multiple platform method) and, a control (CT) group. Animals were euthanized on GD 3.5 and blood, uterus (embryos) and fallopian tube were collected. Then, 89% of CT presented blastocysts in the uterus versus 25% from SD group. Compared to CT, SD presented lighter relative uterus weight, increased plasma concentrations of corticosterone and testosterone, decreased concentrations of progesterone and luteinizing hormone, but no statistical differences in plasma concentrations of 17ß-estradiol and follicle stimulating hormone. There were no differences in uterus and blastocyst gene expression related to embryo implantation and development, and no alteration in blastocysts global DNA methylation. Considering this, the decreased pregnancy maintenance after sleep deprivation seems not to be associated with implantation losses or developmental problems related to the blastocysts. It is likely that complications in morula development and/or its movement through the fallopian tubes affect the pregnancy rate, since only 25% of SD females presented a blastocyst on the GD 3.5. In fact, three out of four females without blastocysts in the uterus presented morula in the fallopian tubes due to a phase delay. Additionally, we suggest that the observed hormonal changes may play a role in this outcome.