Pattern of desynchronized sleep during deprivation and recovery induced in the rat by changes in ambient temperature

The pattern of desynchronized sleep (DS) occurrence in the rat was studied during exposure to an ambient temperature (Ta) of 0 degrees C for 48 h and during a 12 h recovery period at laboratory Ta (23 degrees C) following the first and second 24 h of cold exposure. The exposure to low Ta induces a DS deprivation which is followed, during recovery, by a clear DS rebound. Both the decrease and the following increase in the amount of DS are due to changes in the frequency rather than in the duration of DS episodes. The frequency distribution of the intervals between the end of one DS episode and the beginning of the next (DS interval) has shown that two populations of DS intervals exist, i.e. short DS intervals (3 min). On the basis of this, two types of DS episodes have been identified: the 'single DS episode', which is both preceded and followed by a long DS interval, and the 'sequential DS episode', which is a DS episode occurring within a cluster or a sequence of DS episodes and is characteristically separated by short DS intervals. The occurrence of such sequential DS episodes in a 'DS cluster', allows a high amount of DS to occur without increasing the duration of the DS episode. DS clusters are repressed during cold exposure, when the DS drive is counteracted by the need to thermoregulate, and enhanced during recovery, when the DS drive is unrestrained. In contrast, the occurrence of single DS episodes is much less affected by such different experimental conditions.     

Changes in sleep duration and recreational screen time among Canadians, 1998–2010

It is commonly claimed that sleep duration has declined in recent years – over a period coinciding with a marked increase in personal electronics and communications use. The aim of this study was to assess change in sleep duration among Canadians from 1998 to 2010, and examine any associations with non‐work‐related screen time. The analysis uses population‐representative data from Statistics Canada's General Social Survey cycles of 1998 and 2010; the respective samples numbered 10 749 and 15 390 individuals. Response rates were 80% in 1998 and 55% in 2010. Respondents were aged 15 years and older, residing in private households in the 10 Canadian provinces. The General Social Survey is administered by computer‐assisted telephone interviewing. Data on sleep duration (excluding naps outside essential sleep time) and recreational screen time were obtained using a 24‐h time‐use diary. Survey weights were applied to adjust for non‐response and non‐landline households. Frequencies (respondent characteristics) and averages (time‐use variables) were estimated by age group and sex. Sleep duration was examined by weighted quartile of screen time. Confidence intervals (95%) were calculated around estimates. Average sleep duration increased from 8.1 h in 1998 to 8.3 h in 2010. Average screen time increased from 140 min in 1998 to 154 min in 2010. Sleep duration and screen time were positively related in both years. The percentage of people averaging less than 6 h sleep decreased from 9.6% in 1998 to 8.6% in 2010. Between 1998 and 2010, increases in screen time did not occur at the expense of sleep duration.     

Relationships of sleep duration with sociodemographic and health‐related factors,psychiatric disorders and sleep disturbances in a community sample of Korean adults

The aim of this study is to examine relationships of sleep duration with sociodemographic and health‐related factors, psychiatric disorders and sleep disturbances in a nationwide sample in Korea. A total of 6510 subjects aged 18–64 years participated in this study. Logistic regression was used to calculate the odd ratios and 95% confidence intervals of the covariates, psychiatric disorders and sleep disturbances across the following sleep duration categories: 5 h or less, 6, 7, 8 and 9 h or more per day. Low levels of education, unemployment and physical illness were associated with sleeping for 5 h or less and 9 h or more. Being older and widowed/divorced/separated, high levels of physical activity, pain/discomfort, obesity and high scores on the General Health Questionnaires were associated with sleeping for 5 h or less. Female, being younger and underweight were associated with sleeping for 9 h or more. Alcohol dependence, anxiety disorder and social phobia were associated significantly with sleeping for 5 h or less and 9 h or more. Other psychiatric disorders were more common in subjects who slept for 5 h or less (e.g. alcohol use disorder, mood disorder, major depressive disorder, dysthymic disorder, obsessive‐compulsive disorder and specific phobia) or 9 h or more (e.g. post‐traumatic stress disorder). In addition, subjects who slept for 5 h or less reported more sleep disturbances than did subjects who slept for 7 h. Short or long sleep is associated with psychiatric disorders and/or sleep disturbance, therefore attention to the mental health of short or long sleepers is needed.     

Association between sleep duration and all‐cause mortality in old age: 9‐year follow‐up of the Bambuí Cohort Study,Brazil

This study investigates the association of sleep duration with risk of all‐cause mortality among elderly Brazilians using data from a 9‐year population‐based cohort study and applying a multivariable longitudinal categorical and continuous analysis using Cox’s proportional hazards models. This analysis used data from the Bambui Health and Ageing Study (BHAS), conducted in Bambuí city (approximately 15 000 inhabitants) in southeastern Brazil. The study population comprised 1512 (86.8%) of all eligible 1742 elderly residents. In multivariable analysis, using sleep duration as categorical variable and controlling for multiple measures of sociodemographic and health status, those who slept 9 h or more per night were found to be at higher risk of mortality than those who slept 7 h [hazard ratio (HR): 1.53; 95% confidence interval (CI): 1.12–2.09]. Excluding those whose deaths occurred within 2 years after entry, this association remained significant (HR: 1.56; 95% CI: 1.12–2.18). In analyses using sleep duration as a continuous variable, a linear correlation was found between sleep duration and mortality in all adjusted models in the whole sample (HR: 1.08; 95% CI: 1.02–1.15) and following exclusion of those whose deaths occurred within 2 years after entry (HR: 1.13; 95% CI: 1.06–1.21). Both linear and quadratic terms were significant, reflecting a predicted relationship, with mortality predominantly increasing in association with long sleep duration but with the addition of a slight decrease in association with shorter sleep duration. In conclusion, long rather than short sleep duration was associated principally with all‐cause mortality in this sample. It is therefore reasonable to suggest that clinicians should be aware of the potential adverse prognosis associated with prolonged sleep.     

Twenty‐four‐hour motor activity and body temperature patterns suggest altered central circadian timekeeping in Smith–Magenis syndrome,a neurodevelopmental disorder

Smith–Magenis syndrome (SMS) is a contiguous gene syndrome linked to interstitial microdeletion, or mutation of RAI1, within chromosome 17p11.2. Key behavioral features of SMS include intellectual disability, sleep‐disturbances, maladaptive, aggressive and self‐injurious behaviors, hyperactivity, and sudden changes in mood. A distinguishing feature of this syndrome is an inverted pattern of melatonin characterized by elevated daytime and low nighttime melatonin levels. As the central circadian clock controls the 24‐hr rhythm of melatonin, we hypothesized that the clock itself may contribute to the disrupted pattern of melatonin and sleep. In this report, 24‐hr patterns of body temperature, a surrogate marker of clock‐timing, and continuous wrist activity were collected to examine the links between body temperature, sleep behavior, and the circadian clock. In addition, age‐dependent changes in sleep behavior were explored. Actigraphy‐estimated sleep time for SMS was 1 hr less than expected across all ages studied. The timing of the 24‐hr body temperature (Tb‐24) rhythm was phase advanced, but not inverted. Compared to sibling (SIB) controls, the SMS group had less total night sleep, lower sleep efficiency, earlier sleep onset, earlier final awake times, increased waking after sleep onset (WASO), and increased daytime nap duration. The timing of wake onset varied with age, providing evidence of ongoing developmental sleep changes from childhood through adolescence. Clarification of the circadian and developmental factors that contribute to the disrupted and variable sleep patterns in this syndrome will be helpful in identifying more effective individualized treatments.     

Body temperature,activity and melatonin profiles in adults with attention‐deficit/hyperactivity disorder and delayed sleep: a case–control study

Irregular sleep–wake patterns and delayed sleep times are common in adults with attention‐deficit/hyperactivity disorder, but mechanisms underlying these problems are unknown. The present case–control study examined whether circadian abnormalities underlie these sleep problems in a naturalistic home setting. We included 12 medication‐naïve patients with attention‐deficit/hyperactivity disorder and delayed sleep phase syndrome, and 12 matched healthy controls. We examined associations between sleep/wake rhythm in attention‐deficit/hyperactivity disorder and circadian parameters (i.e. salivary melatonin concentrations, core and skin temperatures, and activity patterns) of the patients and controls during five consecutive days and nights. Daily bedtimes were more variable within patients compared with controls (F = 8.19, P < 0.001), but melatonin profiles were equally stable within individuals. Dim‐light melatonin onset was about 1.5 h later in the patient group (U = 771, Z = ?4.63, P < 0.001). Patients slept about 1 h less on nights before work days compared with controls (F = 11.21, P = 0.002). The interval between dim‐light melatonin onset and sleep onset was on average 1 h longer in patients compared with controls (U = 1117, Z = ?2.62, P = 0.009). This interval was even longer in patients with extremely late chronotype. Melatonin, activity and body temperatures were delayed to comparable degrees in patients. Overall temperatures were lower in patients than controls. Sleep‐onset difficulties correlated with greater distal–proximal temperature gradient (DPG; i.e. colder hands, r² = ?0.32, P = 0.028) in patients. Observed day‐to‐day bedtime variability of individuals with attention‐deficit/hyperactivity disorder and delayed sleep phase syndrome were not reflected in their melatonin profiles. Irregular sleep–wake patterns and delayed sleep in individuals with attention‐deficit/hyperactivity disorder and delayed sleep phase syndrome are associated with delays and dysregulations of the core and skin temperatures.     

Effects of obesity on the association between long‐term sleep apnea treatment and changes in interleukin‐6 levels: the Icelandic Sleep Apnea Cohort

The aim of this study was to evaluate changes in interleukin (IL)‐6 and soluble IL‐6 receptor levels in obstructive sleep apnea patients and assess the role of positive airway pressure treatment and obesity on these changes. A total of 309 newly diagnosed subjects with sleep apnea from the Icelandic Sleep Apnea Cohort were referred for treatment and reassessed at a 2‐year follow‐up. Full treatment was defined objectively as use ≥4 h day^?1 and ≥20 days month^?1. At the 2‐year follow‐up, there were 177 full users, 44 partial users and 88 non‐users. The mean change in biomarker levels from baseline to the 2‐year follow‐up was assessed in a primary model that included adjustment for baseline biomarker levels, baseline body mass index and change in body mass index, as well as after adjustment for numerous relevant covariates. No significant overall difference in IL‐6 level change was found among full, partial and non‐users. However, in severely obese patients (body mass index ≥35), a significant increase in IL‐6 levels during the 2‐year period was found in partial and non‐users, compared to no change in full users. Results were attenuated in a smaller propensity score matched subsample, although similar trends were observed. No differences were found in soluble IL‐6 receptor levels between full users and non‐users, after adjustment for confounders. In conclusion, among untreated obese sleep apnea patients, IL‐6 levels increase substantially during 2 years, while adherence to positive airway pressure treatment may prevent further increases in this inflammatory biomarker.