Guest Editorial

Melatonin, sleep, and circadian rhythms

Cancer cachexia is a severe metabolic syndrome marked by skeletal muscle atrophy. A successful clinical intervention for cancer cachexia is currently lacking. The study of cachexia mechanisms is largely based on preclinical animal models and the availability of high-throughput transcriptomic datasets of cachectic mouse muscles is increasing through the extensive use of next generation sequencing technologies.

Cachectic mouse muscle transcriptomic datasets of ten different studies were combined and mined by seven attribute weighting models, which analysed both categorical variables and numerical variables. The transcriptomic signature of cancer cachexia was identified by attribute weighting algorithms and was used to evaluate the performance of eleven pattern discovery models. The signature was employed to find the best combination of drugs (drug repurposing) for developing cancer cachexia treatment strategies, as well as to evaluate currently used cachexia drugs by literature mining.

Attribute weighting algorithms ranked 26 genes as the transcriptomic signature of muscle from mice with cancer cachexia. Deep Learning and Random Forest models performed better in differentiating cancer cachexia cases based on muscle transcriptomic data. Literature mining revealed that a combination of melatonin and infliximab has negative interactions with 2 key genes (Rorc and Fbxo32) upregulated in the transcriptomic signature of cancer cachexia in muscle.

The integration of machine learning, meta-analysis and literature mining was found to be an efficient approach to identifying a robust transcriptomic signature for cancer cachexia, with implications for improving clinical diagnosis and management of this condition.

Exposure to light at night (LAN) may influence sleep timing and regularity. Here, we test whether greater light exposure during sleep (LEDS) is bidirectionally associated with greater irregularity in sleep onset timing in a large cohort of older adults in cross-sectional and short-term longitudinal (days) analyses. Light exposure and activity patterns, measured via wrist-worn actigraphy (ActiWatch Spectrum), were analyzed in 1933 participants with 6+ valid days of data in the Multi-Ethnic Study of Atherosclerosis (MESA) Exam 5 Sleep Study. Summary measures of LEDS averaged across nights were evaluated in linear and logistic regression analyses to test the association with standard deviation (SD) in sleep onset timing (continuous variable) and irregular sleep onset timing (SD > 90 min, binary). Night-to-night associations between LEDS and absolute differences in nightly sleep onset timing were also evaluated with distributed lag non-linear models and mixed models. In between-individual linear and logistic models adjusted for demographic, health, and seasonal factors, every 5-lux unit increase in LEDS was associated with a 7.8-min increase in sleep onset SD (β = 0.13 h, 95%CI:0.09–0.17) and 32% greater odds (OR = 1.32, 95%CI:1.17–1.50) of irregular sleep onset. In within-individual night-to-night mixed model analyses, every 5-lux unit increase in LEDS the night prior was associated with a 2.2-min greater deviation of sleep onset the next night (β = 0.036 h, p < 0.05). Conversely, every 1-h increase in sleep deviation was associated with a 0.35-lux increase in future LEDS (β = 0.348 lux, p < 0.05). LEDS was associated with greater irregularity in sleep onset in between-individual analyses and subsequent deviation in sleep timing in within-individual analyses, supporting a role for LEDS in irregular sleep onset timing. Greater deviation in sleep onset was also associated with greater future LEDS, suggesting a bidirectional relationship. Maintaining a dark sleeping environment and preventing LEDS may promote sleep regularity and following a regular sleep schedule may limit LEDS.

To investigate the cross-sectional associations between real-world multiperiod bedroom light at night and sleep parameters among 365 Chinese young adults.

Bedroom light exposure was estimated at the individual level for two consecutive days using a portable illuminance meter. Subjective sleep parameters were measured with the Pittsburgh Sleep Quality Index, and objective sleep parameters were assessed by wrist-worn ActiGraph accelerometers for seven consecutive days.

Compared with the low-exposure group (average light intensity < 3lx), the high-exposure group (average light intensity ≥ 3lx) was associated with decreased 1.15% in sleep efficiency (sleep efficiency, 95% CI: −1.78, −0.52; p < .001), increased 3.94 minutes in wake after sleep onset (wake after sleep onset, 95% CI: 1.55, 6.33; p = .001), increased 1.05 unit in movement index (95% CI: 0.20, 1.89; p = .015), and increased 2.16 unit in sleep fragmentation index ( 95% CI: 0.63, 3.68; p = .006). In comparison, each interquartile increase in 2h-average and 1h-average intensity of preawake light (PAL) (PAL-2h and PAL-1h) was associated with 7.04 minutes of increases in total sleep time (95% CI: 0.87, 13.22; p = .025) and 6.69 minutes of increases in total sleep time (95% CI: 0.51, 12.87; p = .034), respectively.

Altogether, our results support the role of bedroom light exposure in sleep and imply the importance of bedroom light exposure management as a potential strategy to reduce the public health burden of sleep problems. Keeping the bedroom environment dark at night and allowing moderate morning light exposure may be important measures for improving the sleep quality of young adults.

The object of this article is to clarify sleep and body clock problems, specifically delayed sleep phase syndrome (DSPS), in patients with obsessive–compulsive disorder (OCD).

In this article, we provide information on prevalence of OCD, sleep problems and DSPS in patients with OCD; sleep factors; relationship between OCD and DSPS; sleep-related problems in children with OCD; and dreaming in OCD.

There appears to be some changed in the sleep of patients with OCD, but the architecture changes in normative studies are not consistent other than a general increase in sleep fragmentation. The changes in dreaming are not conclusive. The most notable aspect of this article is that in comparison to depression which has a lifetime prevalence of 7.9–17.0% and for which there are over 2000 publications, in OCD with a lower lifetime prevalence of 2.0–3.0%, there are only a few studies, indicating the extreme limitation of knowledge in this area, although there were exciting findings concerning the relationship between OCD and DSPS.

Exposure to artificial light-at-night (ALAN) is increasing globally, and there are concerns around how ALAN may impact sleep, psychological and physical health. However, there is a lack of evidence in the literature on how individuals perceive ALAN relative to their sleeping environment and habits, and how such perceptions correspond to objectively assessed night-time illuminance at the level of the residence. This cross-sectional study examined how such perceptions associate with sleep quality, sleep timing, psychological distress and cognitive failures. Further we examined the association between illuminance levels calculated as the biologically-relevant melatonin-suppression index (MSI) and the self-report of perception of ALAN. Five hundred and fifty two adult participants completed a survey addressing perception of ALAN in sleep environment along with the Pittsburgh Sleep Quality Index, Munich Chronotype Questionnaire, Cognitive Failure Questionnaire and the General Health Questionnaire. We report that perception of external ALAN in the sleeping environment was associated with poorer sleep quality, more cognitive failures and greater psychological distress, when controlling for age, sex, house location and MSI. No associations were found between the perception of external ALAN and MSI scores, and MSI scores were not associated with scores on any of the self-report measures. Internal lighting passing into the sleeping environment was associated with poorer sleep quality but not with psychological wellbeing. Habitual use of light-emitting devices was associated with poorer psychological wellbeing but not with sleep quality and sleep timing. Perception of environmental noise annoyance at night was associated with higher psychological distress and poorer quality sleep, and the perception of noise annoyance was associated with perception of ALAN. These results may suggest heightened attentional bias towards ALAN associated with poor sleep quality and higher levels of psychological distress, and highlight the need for more granular approaches in the study of ALAN and sleep and psychological health in terms of levels individual ALAN exposure, and an interpretation that seeks to integrate biological and psychological perspectives.

Nearly all mammals display robust daily rhythms of physiology and behavior. These approximately 24-h cycles, known as circadian rhythms, are driven by a master clock in the suprachiasmatic nucleus (SCN) of the hypothalamus and affect biological processes ranging from metabolism to immune function. Perhaps the most overt output of the circadian clock is the sleep-wake cycle, the integrity of which is critical for health and homeostasis of the organism. In this review, we summarize our current understanding of the circadian regulation of sleep. We discuss the neural circuitry and molecular mechanisms underlying daily sleep timing, and the trajectory of circadian regulation of sleep across development. We conclude by proposing future research priorities for the field that will significantly advance our mechanistic understanding of the circadian regulation of sleep.