[Is Icelanders' sleep duration getting shorter? Review on sleep duration and sleeping habits].

Sleep health promotion is an ever-increasing subject of public discourse in Iceland. Prominent claims made include that the duration of sleep among Icelanders is shortening, and that changing sleeping habits constitute a significant public health risk. Like many aspects of healthcare, commercial interests and sales hype can skew perception. This review article will seek to shed light on the scientific background of these statements. International meta-analysis suggests there has been little change in sleep duration in adults over the past century. The duration of childrens sleep has shortened, but the consequences of this are not yet well established. Significant shortening of the sleep of adult Icelanders has not been demonstrated. No difference in sleep duration is found between Icelandic adults and adolescents and comparable groups in neighboring countries. The measurement methods that are used when comparing sleep studies are variable and can lead to different results. Associations have been established between sleep duration and adverse health outcomes, both physical and mental, but causality has not yet been established, and potential important mediators of the relationships are discussed. The circadian sleep phase of Icelanders is generally delayed relative to neighbors, likely related to Iceland's diurnal length variation at sub-Arctic latitudes and longitudinal discrepancies between natural light and local time.

[Prevalence of Poor Sleep Quality and Sleep Disturbances in Icelanders with Multiple Sclerosis].

BACKGROUND: Sleep disturbances are common, underdiagnosed and have negative consequences for people with multiple -sclerosis. OBJECTIVE: Gather information about the prevalence of poor sleep quality and sleep disturbances in Icelanders with multiple -sclerosis. METHOD: A cross-sectional self-report survey. POPULATION: Icelanders with multiple sclerosis. SAMPLE: People with multiple sclerosis, who were on the online mailing list or had access to Facebook groups of the Multiple-Sclerosis-Society in Iceland. An electronic link with background questions and 4 questionnaires was available to participants. Questionnaires: The Pittsburgh- Sleep-Quality-Index (PSQI), the Insomnia-Severity-Index, the STOP-Bang-questionnaire and 5 diagnostic criteria for restless legs syndrome. Questionnaires were used to screen for poor sleep quality, and 7 different factors that can cause disturbed sleep. Data was analyzed with SPSS version 25. RESULTS: Almost 40% of Icelanders with multiple sclerosis participated or 234 persons. Mean age was 47 years (range 20-92) and 77% were female. The prevalence of poor sleep quality (PSQI>5), was 68%. The factors that most often caused dis-turbed sleep were; bathroom breaks (39%), pain (37%), insomnia symptoms (30%) and sleep apnea symptoms (24%). Majority of participants or 79% had at least one sleep disturbance and on average they had close to two. Insomnia symptoms were strongly related to poor sleep quality. CONCLUSION: High prevalence of poor sleep quality and sleep disturbances in people with multiple sclerosis needs to be addressed. PSQI can be used to screen for poor sleep quality and to assess whether further sleep evaluation is needed. Screening, diagnosis and treatment of insomnia should be implemented.

Sleep-related sweating in obstructive sleep apnoea: association with sleep stages and blood pressure.

The aim of this study was to investigate sleep-related sweating as a symptom of obstructive sleep apnoea (OSA). Fifteen otherwise healthy male non-smoking patients with untreated moderate-to-severe OSA underwent polysomnography, including measurements of skin and core body temperature and electrodermal activity (EDA) as an objective indicator of sweating. Evening and morning blood pressure was measured as well as catecholamines in nocturnal urine. All measurements were repeated after 3 months on successful continuous positive airway pressure (CPAP) treatment. The untreated OSA subjects had a mean (+/-SD) apnoea-hypopnoea index of 45.3 +/- 3.9 and a mean EDA index during sleep of 131.9 +/- 22.4 events per hour. Patients with higher EDA indices had higher systolic blood pressure in the evening and morning (P = 0.001 and 0.006) and lower rapid eye movement (REM) sleep percentage (P = 0.003). The EDA index decreased significantly to 78.5 +/- 17.7 in the patients on CPAP treatment (P = 0.04). The decrease correlated with lower evening systolic and diastolic blood pressure (P = 0.05 and 0.006) and an increase in REM% (P = 0.02). No relationship was observed between EDA and skin or core body temperature, or to catecholamine levels in urine. OSA patients who experience sleep-related sweating may have increased blood pressure and decreased REM sleep compared with other OSA patients. CPAP treatment appears to lower blood pressure and increase REM sleep to a higher extent in these patients compared with other OSA patients.

Robust circadian rhythm in heart rate and its variability: influence of exogenous melatonin and photoperiod.

Heart rate (HR) and heart rate variability (HRV) undergo marked fluctuations over the 24-h day. Although controversial, this 24-h rhythm is thought to be driven by the sleep-wake/rest-activity cycle as well as by endogenous circadian rhythmicity. We quantified the endogenous circadian rhythm of HR and HRV and investigated whether this rhythm can be shifted by repeated melatonin administration while exposed to an altered photoperiod. Eight healthy males (age 24.4 +/- 4.4 years) participated in a double-blind cross-over design study. In both conditions, volunteers were scheduled to 16 h-8 h rest : wake and dark : light cycles for nine consecutive days preceded and followed by 29-h constant routines (CR) for assessment of endogenous circadian rhythmicity. Melatonin (1.5 mg) or placebo was administered at the beginning of the extended sleep opportunities. For all polysomnographically verified wakefulness periods of the CR, we calculated the high- (HF) and low- (LF) frequency bands of the power spectrum of the R-R interval, the standard deviation of the normal-to-normal (NN) intervals (SDNN) and the square root of the mean-squared difference of successive NN intervals (rMSSD). HR and HRV variables revealed robust endogenous circadian rhythms with fitted maxima, respectively, in the afternoon (16:36 hours) and in the early morning (between 05:00 and 06:59 hours). Melatonin treatment phase-advanced HR, HF, SDNN and rMSSD, and these shifts were significantly greater than after placebo treatment. We conclude that endogenous circadian rhythmicity influences autonomic control of HR and that the timing of these endogenous rhythms can be altered by extended sleep/rest episodes and associated changes in photoperiod as well as by melatonin treatment.