In the last three decades the two‐process model of sleep regulation has served as a major conceptual framework in sleep research. It has been applied widely in studies on fatigue and performance and to dissect individual differences in sleep regulation. The model posits that a homeostatic process (Process S) interacts with a process controlled by the circadian pacemaker (Process C), with time‐courses derived from physiological and behavioural variables. The model simulates successfully the timing and intensity of sleep in diverse experimental protocols. Electrophysiological recordings from the suprachiasmatic nuclei ( SCN ) suggest that S and C interact continuously. Oscillators outside the SCN that are linked to energy metabolism are evident in SCN ‐lesioned arrhythmic animals subjected to restricted feeding or methamphetamine administration, as well as in human subjects during internal desynchronization. In intact animals these peripheral oscillators may dissociate from the central pacemaker rhythm. A sleep/fast and wake/feed phase segregate antagonistic anabolic and catabolic metabolic processes in peripheral tissues. A deficiency of Process S was proposed to account for both depressive sleep disturbances and the antidepressant effect of sleep deprivation. The model supported the development of novel non‐pharmacological treatment paradigms in psychiatry, based on manipulating circadian phase, sleep and light exposure. In conclusion, the model remains conceptually useful for promoting the integration of sleep and circadian rhythm research. Sleep appears to have not only a short‐term, use‐dependent function; it also serves to enforce rest and fasting, thereby supporting the optimization of metabolic processes at the appropriate phase of the 24‐h cycle.
This European guideline for the diagnosis and treatment of insomnia was developed by a task force of the European Sleep Research Society, with the aim of providing clinical recommendations for the management of adult patients with insomnia. The guideline is based on a systematic review of relevant meta‐analyses published till June 2016. The target audience for this guideline includes all clinicians involved in the management of insomnia, and the target patient population includes adults with chronic insomnia disorder. The GRADE (Grading of Recommendations Assessment, Development and Evaluation) system was used to grade the evidence and guide recommendations. The diagnostic procedure for insomnia, and its co‐morbidities, should include a clinical interview consisting of a sleep history (sleep habits, sleep environment, work schedules, circadian factors), the use of sleep questionnaires and sleep diaries, questions about somatic and mental health, a physical examination and additional measures if indicated (i.e. blood tests, electrocardiogram, electroencephalogram; strong recommendation, moderate‐ to high‐quality evidence). Polysomnography can be used to evaluate other sleep disorders if suspected (i.e. periodic limb movement disorder, sleep‐related breathing disorders), in treatment‐resistant insomnia, for professional at‐risk populations and when substantial sleep state misperception is suspected (strong recommendation, high‐quality evidence). Cognitive behavioural therapy for insomnia is recommended as the first‐line treatment for chronic insomnia in adults of any age (strong recommendation, high‐quality evidence). A pharmacological intervention can be offered if cognitive behavioural therapy for insomnia is not sufficiently effective or not available. Benzodiazepines, benzodiazepine receptor agonists and some antidepressants are effective in the short‐term treatment of insomnia (≤4 weeks; weak recommendation, moderate‐quality evidence). Antihistamines, antipsychotics, melatonin and phytotherapeutics are not recommended for insomnia treatment (strong to weak recommendations, low‐ to very‐low‐quality evidence). Light therapy and exercise need to be further evaluated to judge their usefulness in the treatment of insomnia (weak recommendation, low‐quality evidence). Complementary and alternative treatments (e.g. homeopathy, acupuncture) are not recommended for insomnia treatment (weak recommendation, very‐low‐quality evidence).
The aim of the current study was to examine sleep patterns and rates of insomnia in a population‐based study of adolescents aged 16–19 years. Gender differences in sleep patterns and insomnia, as well as a comparison of insomnia rates according to DSM ‐ IV , DSM ‐ V and quantitative criteria for insomnia ( Behav. Res. Ther ., 41 , 2003, 427), were explored. We used a large population‐based study in H ordaland county in N orway, conducted in 2012. The sample included 10 220 adolescents aged 16–18 years (54% girls). Self‐reported sleep measurements included bedtime, rise time, time in bed, sleep duration, sleep efficiency, sleep onset latency, wake after sleep onset, rate and frequency and duration of difficulties initiating and maintaining sleep and rate and frequency of tiredness and sleepiness. The adolescents reported short sleep duration on weekdays (mean 6:25 hours), resulting in a sleep deficiency of about 2 h. A majority of the adolescents (65%) reported sleep onset latency exceeding 30 min. Girls reported longer sleep onset latency and a higher rate of insomnia than boys, while boys reported later bedtimes and a larger weekday–weekend discrepancy on several sleep parameters. Insomnia prevalence rates ranged from a total prevalence of 23.8 ( DSM ‐ IV criteria), 18.5 ( DSM ‐ V criteria) and 13.6% (quantitative criteria for insomnia). We conclude that short sleep duration, long sleep onset latency and insomnia were prevalent in adolescents. This warrants attention as a public health concern in this age group.
Existing research has demonstrated associations between sleep duration and obesity, diabetes, cardiovascular disease and mortality. Sleep disorders research has shown that sleep apnoea, insomnia and other sleep disorders confer risk for cardiometabolic disease, particularly in the presence of reduced sleep duration. The aim of the present study was to examine the associations between general sleep disturbance, operationalized as ‘difficulty falling asleep, staying asleep, or sleeping too much’ as measured in a large, nationally representative sample, and self‐reported history of myocardial infarction, stroke, coronary artery disease, diabetes and obesity. Data from the Behavioral Risk Factor Surveillance System were analysed. Complete data were available for 138 201 individuals. A hierarchical logistic regression analysis examined associations before and after adjustment for demographic, socioeconomic, medical and psychological factors. After adjusting for demographic, socioeconomic and health risk factors, sleep duration was associated with obesity [odds ratio (OR) = 1.18, P < 0.0005), diabetes (OR = 1.18, P < 0.005), myocardial infarction (OR = 1.36, P < 0.0005), stroke (OR = 1.22, P < 0.05) and coronary artery disease (OR = 1.59, P < 0.0005). In fully adjusted models that included physical health, significant relationships remained for obesity (OR = 1.14, P < 0.0005), myocardial infarction (OR = 1.23, P < 0.005) and coronary artery disease (OR = 1.43, P < 0.0005). Sleep disturbance is a significant risk factor for obesity, diabetes, myocardial infarction, stroke and coronary artery disease, and effects for obesity, myocardial infarction and coronary artery disease are the most robust after adjustment. This study demonstrates that sleep disturbance is a novel risk factor that is potentially modifiable. Future research should determine whether sleep intervention could reduce the cardiometabolic consequences of sleep disturbance.
Insomnia co‐occurs with many health problems, but less is known about the prospective associations. The aim of the current study was to investigate if insomnia predicts cumulative incidence of mental and physical conditions. Prospective population‐based data from the two last N ord‐ T røndelag H ealth S tudies ( HUNT 2 in 1995–97 and HUNT 3 in 2006–08), comprising 24 715 people in the working population, were used to study insomnia as a risk factor for incidence of physical and mental conditions. Insomnia was defined according to the 4th edition of the Diagnostic and Statistical Manual of Mental Disorders ( DSM ‐ IV ). Insomnia at HUNT 2 was a significant risk factor for incidence of a range of both mental and physical conditions at HUNT 3 11 years later. Most effects were only slightly attenuated when adjusting for confounding factors, and insomnia remained a significant risk factor for the following conditions in the adjusted analyses: depression [odds ratio ( OR ): 2.38, 95% confidence interval ( CI ): 1.91–2.98], anxiety ( OR : 2.08, 95% CI : 1.63–2.64), fibromyalgia ( OR : 2.05, 95% CI : 1.51–2.79), rheumatoid arthritis ( OR : 1.87, 95% CI : 1.29–2.52), whiplash ( OR : 1.71, 95% CI : 1.21–2.41), arthrosis ( OR : 1.68, 95% CI : 1.43–1.98), osteoporosis ( OR : 1.52, 95% CI : 1.14–2.01, headache ( OR : 1.50, 95% CI : 1.16–1.95, asthma ( OR : 1.47, 95% CI : 1.16–1.86 and myocardial infarction ( OR : 1.46, 95% CI : 1.06–2.00). Insomnia was also associated significantly with incidence of angina, hypertension, obesity and stroke in the crude analyses, but not after adjusting for confounders. We conclude that insomnia predicts cumulative incidence of several physical and mental conditions. These results may have important clinical implications, and whether or not treatment of insomnia would have a preventive value for both physical and mental conditions should be studied further.
Chronic sleep deprivation is common among workers, and has been associated with negative work outcomes, including absenteeism and occupational accidents. The objective of the present study is to characterize reciprocal relationships between sleep and work. Specifically, we examined how sleep impacts work performance and how work affects sleep in individuals not at‐risk for a sleep disorder; assessed work performance outcomes for individuals at‐risk for sleep disorders, including insomnia, obstructive sleep apnea (OSA) and restless legs syndrome (RLS); and characterized work performance impairments in shift workers (SW) at‐risk for shift work sleep disorders relative to SW and day workers. One‐thousand Americans who work 30 h per week or more were asked questions about employment, work performance and sleep in the National Sleep Foundation’s 2008 Sleep in America telephone poll. Long work hours were associated with shorter sleep times, and shorter sleep times were associated with more work impairments. Thirty‐seven percent of respondents were classified as at‐risk for any sleep disorder. These individuals had more negative work outcomes as compared with those not at‐risk for a sleep disorder. Presenteeism was a significant problem for individuals with insomnia symptoms, OSA and RLS as compared with respondents not at‐risk. These results suggest that long work hours may contribute to chronic sleep loss, which may in turn result in work impairment. Risk for sleep disorders substantially increases the likelihood of negative work outcomes, including occupational accidents, absenteeism and presenteeism.
The aim of this study was to describe the clinical and PSG characteristics of narcolepsy with cataplexy and their genetic predisposition by using the retrospective patient database of the European Narcolepsy Network (EU-NN). We have analysed retrospective data of 1099 patients with narcolepsy diagnosed according to International Classification of Sleep Disorders-2. Demographic and clinical characteristics, polysomnography and multiple sleep latency test data, hypocretin-1 levels, and genome-wide genotypes were available. We found a significantly lower age at sleepiness onset (men versus women: 23.74 +/- 12.43 versus 21.49 +/- 11.83, P = 0.003) and longer diagnostic delay in women (men versus women: 13.82 +/- 13.79 versus 15.62 +/- 14.94, P = 0.044). The mean diagnostic delay was 14.63 +/- 14.31 years, and longer delay was associated with higher body mass index. The best predictors of short diagnostic delay were young age at diagnosis, cataplexy as the first symptom and higher frequency of cataplexy attacks. The mean multiple sleep latency negatively correlated with Epworth Sleepiness Scale (ESS) and with the number of sleep-onset rapid eye movement periods (SOREMPs), but none of the polysomnographic variables was associated with subjective or objective measures of sleepiness. Variant rs2859998 in UBXN2B gene showed a strong association (P = 1.28E-07) with the age at onset of excessive daytime sleepiness, and rs12425451 near the transcription factor TEAD4 (P = 1.97E-07) with the age at onset of cataplexy. Altogether, our results indicate that the diagnostic delay remains extremely long, age and gender substantially affect symptoms, and that a genetic predisposition affects the age at onset of symptoms.
This study compared parent‐reported sleep characteristics in 2‐ to 5‐year‐old children with autism spectrum disorders (ASD) to children with other developmental delays (DD) and typical development (TD). We included 529 children (303 ASD [167 males], 63 DD [46 males], and 163 TD [134 males]) enrolled in the CHARGE study, an ongoing population‐based case–control study. The mean age of participants was 3.6 years (standard deviation, 0.8 years). ASD diagnosis was confirmed with Autism Diagnostic Interview‐Revised (ADI‐R) and Autism Diagnostic Observation Schedules (ADOS). Cognitive and adaptive functioning was assessed using Mullen Scales of Early Learning (MSEL) and Vineland Adaptive Behavior Scales (VABS), respectively. Demographic, medical and sleep history information were ascertained from California birth records, telephone interview, medical assessments at clinic visit, and parent‐administered questionnaires. Fifty‐three percent of children with ASD had at least one frequent sleep problem, followed by 46% of children with DD, and 32% of the TD group ( P < 0.0001). Exploratory factor analyses of sleep history data yielded two factors: sleep onset problems and night waking. Children with ASD had marginally higher sleep onset factor scores and significantly higher night waking factor scores compared with the TD group. Factor scores for children with DD were intermediate between the ASD and TD groups. Cognitive or adaptive development did not predict severity of sleep problems in the ASD group.
Longitudinal studies that have examined the association of insomnia with incident depression using objective sleep measures are very limited. The aim of this study was to examine the predictive role of the severity of insomnia for incident depression in a general population sample using psychometric and polysomnographic data. From a random, general population sample of 1741 individuals of the Penn State Adult Cohort, 1137 adults without depression were followed up with a structured telephone interview after 7.5 years. All subjects completed a full medical evaluation, 1‐night polysomnogram and Multiphasic Minnesota Personality Inventory at baseline. The incidence of depression was 15%. Poor sleep (odds ratio = 1.5, P = 0.001) and insomnia (odds ratio = 1.9, P = 0.031) were significantly associated with incident depression. The odds of incident depression were highest (odds ratio = 2.2, P = 0.019) in insomnia with objective short sleep duration and independent of Multiphasic Minnesota Personality Inventory Ego Strength scores, an index of poor coping resources. The persistence of insomnia and worsening of poor sleep into insomnia significantly increased the odds of incident depression (odds ratios ranged from 1.8 to 6.3), whereas their full remission did not (odds ratio ranged from 1.2 to 1.8). Insomnia with short sleep duration is associated with incident depression independent of poor coping resources, whereas the association of insomnia with normal sleep duration with incident depression was mediated by poor coping resources. Persistence and worsening of poor sleep or insomnia, but not their full remission, are significant predictors of incident depression. These data suggest that there is a significant relationship between the severity of insomnia and incident depression.
Light in the short wavelength range (blue light: 446–483 nm) elicits direct effects on human melatonin secretion, alertness and cognitive performance via non‐image‐forming photoreceptors. However, the impact of blue‐enriched polychromatic light on human sleep architecture and sleep electroencephalographic activity remains fairly unknown. In this study we investigated sleep structure and sleep electroencephalographic characteristics of 30 healthy young participants (16 men, 14 women; age range 20–31 years) following 2 h of evening light exposure to polychromatic light at 6500 K, 2500 K and 3000 K. Sleep structure across the first three non‐rapid eye movement non‐rapid eye movement – rapid eye movement sleep cycles did not differ significantly with respect to the light conditions. All‐night non‐rapid eye movement sleep electroencephalographic power density indicated that exposure to light at 6500 K resulted in a tendency for less frontal non‐rapid eye movement electroencephalographic power density, compared to light at 2500 K and 3000 K. The dynamics of non‐rapid eye movement electroencephalographic slow wave activity (2.0–4.0 Hz), a functional index of homeostatic sleep pressure, were such that slow wave activity was reduced significantly during the first sleep cycle after light at 6500 K compared to light at 2500 K and 3000 K, particularly in the frontal derivation. Our data suggest that exposure to blue‐enriched polychromatic light at relatively low room light levels impacts upon homeostatic sleep regulation, as indexed by reduction in frontal slow wave activity during the first non‐rapid eye movement episode.
The availability of a reliable system to record sleep stage measures easily and automatically in ambulatory settings could be of utility for research and clinical work. The aim of this study was to evaluate a novel wireless system (WS) that does not require skilled preparation for the automatic collection and scoring of human sleep. Twenty‐nine healthy adults underwent concurrent sleep measurement via the WS, polysomnography (PSG) and an actigraph (ACT) in a sleep laboratory for one assessment night preceded by an acclimation night. The PSG recordings were scored by two experienced trained technicians from separate laboratories. Each recording was scored by both technicians to Rechtschaffen and Kales (R&K) criteria. The WS and ACT were compared with each of the PSG scores and a consensus PSG score, and the PSG scores were compared with each other. Inter‐rater agreement was assessed for each pair over all pooled epochs by percentage agreement, Cohen’s kappa and intraclass correlation coefficient. The WS agreement with each of the two PSG scores for sleep stages was 75.8 and 74.7%, respectively. WS agreement with each of the two PSG scores for sleep/wakefulness was 92.6 and 91.1%, ACT agreement with PSG was 86.3 and 85.7%. The PSG scorers’ agreement with each other for sleep stages was 83.2%, and for sleep/wakefulness was 95.8%. The findings from the current study indicate that the WS may provide an easy to use and accurate complement to other established technologies for measuring sleep in healthy adults.
The main consequence of insufficient sleep is sleepiness. While measures of sleep latency, continuous encephalographical/electro‐oculographical ( EEG / EOG ) recording and performance tests are useful indicators of sleepiness in the laboratory and clinic, they are not easily implemented in large, real‐life field studies. Subjective ratings of sleepiness, which are easily applied and unobtrusive, are an alternative, but whether they measure sleepiness sensitively, reliably and validly remains uncertain. This review brings together research relevant to these issues. It is focused on the Karolinska Sleepiness Scale ( KSS ), which is a nine‐point Likert‐type scale. The diurnal pattern of sleepiness is U‐shaped, with high KSS values in the morning and late evening, and with great stability across years. KSS values increase sensitively during acute total and repeated partial sleep deprivation and night work, including night driving. The effect sizes range between 1.5 and 3. The relation to driving performance or EEG / EOG indicators of sleepiness is highly significant, strongly curvilinear and consistent across individuals. High (>6) KSS values are associated particularly with impaired driving performance and sleep intrusions in the EEG . KSS values are also increased in many clinical conditions such as sleep apnea, depression and burnout. The context has a strong influence on KSS ratings. Thus, physical activity, social interaction and light exposure will reduce KSS values by 1–2 units. In contrast, time‐on‐task in a monotonous context will increase KSS values by 1–2 units. In summary, subjective ratings of sleepiness as described here is as sensitive and valid an indicator of sleepiness as objective measures, and particularly suitable for field studies.
Rapid eye movement (REM) sleep behaviour disorder (RBD) has been suggested to predict the development of neurodegenerative disorders. Patients with RBD are acting out dream behaviour associated with loss of normal muscle atonia of REM sleep. The aim of the present study was to confirm that exogenous melatonin improves RBD. Eight consecutively recruited males (mean age 54 years) with a polysomnographically (PSG) confirmed diagnosis of RBD were included in a two‐part, randomized, double‐blind, placebo‐controlled cross‐over study. Patients received placebo and 3 mg of melatonin daily in a cross‐over design, administered between 22:00 h and 23:00 h over a period of 4 weeks. PSG recordings were performed in all patients at baseline, at the end of Part I of the trial and at the end of Part II of the trial. Compared to baseline, melatonin significantly reduced the number of 30‐s REM sleep epochs without muscle atonia (39% versus 27%; P = 0.012), and led to a significant improvement in clinical global impression (CGI: 6.1 versus 4.6; P = 0.024). Interestingly, the number of REM sleep epochs without muscle atonia remained lower in patients who took placebo during Part II after having received melatonin in Part I (–16% compared to baseline; P = 0.043). In contrast, patients who took placebo during Part I showed improvements in REM sleep muscle atonia only during Part II (i.e. during melatonin treatment). The data suggest that melatonin might be a second useful agent besides clonazepam in the treatment of RBD.
The aim of this study was to investigate long‐term trends in insomnia symptoms, tiredness and school performance among Finnish adolescents. A time–series from 1984 to 2011 was analysed from two large‐scale survey studies, the Finnish School Health Promotion Study and the Health Behavior in School‐Aged Children study. A total of 1 136 583 adolescents aged 11–18 years answered a standardized questionnaire assessing frequency of insomnia symptoms, tiredness and school performance. A clear approximately twofold increasing trend in insomnia symptoms and tiredness was found from the mid‐1990s to the end of the 2000s. The increase was evident in all participating age groups and in both genders. After 2008, the increase seems to have stopped. Insomnia symptoms and tiredness were associated with lower school performance and they were more prevalent among girls (11.9 and 18.4%) compared to boys (6.9 and 9.0%, respectively). Unexpectedly, we also observed an increasingly widening gap in school performance between normally vigilant and chronically tired pupils. The underlying causes of these phenomena are unknown, but may concern changes in the broader society. The observed recent increasing trend in adolescents’ sleep problems is worrisome: poor sleep quality has also been suggested to associate with clinical or subclinical mood or anxiety disorders and behavioural problems and predispose to sleep and psychiatric disorders later in life. Our results justify further studies and call for serious attention to be paid to adolescent's sleep in the Finnish educational system and society at large.
The main purpose of the present analysis is to assess the influence of introducing early nasal continuous positive airway pressure ( nCPAP ) treatment on cardiovascular recurrences and mortality in patients with a first‐ever ischaemic stroke and moderate–severe obstructive sleep apnea (OSA) with an apnea–hypopnea index (AHI) ≥20 events h −1 during a 5‐year follow‐up. Patients received conventional treatment for stroke and were assigned randomly to the nCPAP group ( n = 71) or the control group ( n = 69). Cardiovascular events and mortality were registered for all patients. Survival and cardiovascular event‐free survival analysis were performed after 5‐year follow‐up using the Kaplan–Meier test. Patients in the nCPAP group had significantly higher cardiovascular survival than the control group (100 versus 89.9%, log‐rank test 5.887; P = 0.015) However, and also despite a positive tendency, there were no significant differences in the cardiovascular event‐free survival at 68 months between the n CPAP and control groups (89.5 versus 75.4%, log‐rank test 3.565; P = 0.059). Early n CPAP therapy has a positive effect on long‐term survival in ischaemic stroke patients and moderate–severe OSA.
Although melatonin and cognitive–behavioural therapy have shown efficacy in treating sleep disorders in children with autism spectrum disorders, little is known about their relative or combined efficacy. One hundred and sixty children with autism spectrum disorders, aged 4–10 years, suffering from sleep onset insomnia and impaired sleep maintenance, were assigned randomly to either (1) combination of controlled‐release melatonin and cognitive–behavioural therapy; (2) controlled‐release melatonin; (3) four sessions of cognitive–behavioural therapy; or (4) placebo drug treatment condition for 12 weeks in a 1 : 1 : 1 : 1 ratio. Children were studied at baseline and after 12 weeks of treatment. Treatment response was assessed with 1‐week actigraphic monitoring, sleep diary and sleep questionnaire. Main outcome measures, derived actigraphically, were sleep latency, total sleep time, wake after sleep onset and number of awakenings. The active treatment groups all resulted in improvements across all outcome measures, with moderate‐to‐large effect sizes from baseline to a 12‐week assessment. Melatonin treatment was mainly effective in reducing insomnia symptoms, while cognitive–behavioural therapy had a light positive impact mainly on sleep latency, suggesting that some behavioural aspects might play a role in determining initial insomnia. The combination treatment group showed a trend to outperform other active treatment groups, with fewer dropouts and a greater proportion of treatment responders achieving clinically significant changes (63.38% normative sleep efficiency criterion of >85% and 84.62%, sleep onset latency <30 min). This study demonstrates that adding behavioural intervention to melatonin treatment seems to result in a better treatment response, at least in the short term.
Early childhood is a period of dramatic change in sleep and emotion processing, as well as a time when disturbance in both domains are first detected. Although sleep is recognized as central in emotion processing and psychopathology, the great majority of experimental data have been collected in adults. We examined the effects of acute sleep restriction (nap deprivation) on toddlers’ emotion expression. Ten healthy children (seven females; 30–36 months old) followed a strict sleep schedule (≥12.5 h time in bed per 24‐h) for 5 days, before each of two randomly assigned afternoon emotion assessments following Nap and No‐Nap conditions (resulting in an 11‐day protocol). Children viewed emotion‐eliciting pictures (five positive, three neutral, three negative) and completed puzzles (one solvable, one unsolvable). Children’s faces were video‐recorded, and emotion displays were coded. When sleep restricted, children displayed less confusion in response to neutral pictures, more negativity to neutral and negative pictures, and less positivity to positive pictures. Sleep restriction also resulted in a 34% reduction in positive emotion responses (solvable puzzle), as well as a 31% increase in negative emotion responses and a 39% decrease in confused responses (unsolvable puzzle). These findings suggest sleep is a key factor in how young children respond to their world. When sleep restricted, toddlers are neither able to take full advantage of positive experiences nor are they as adaptive in challenging contexts. If insufficient sleep consistently ‘taxes’ young children’s emotion responses, they may not manage emotion regulation challenges effectively, potentially placing them at risk for future emotional/behavioral problems.
The negative association of insomnia and internet addiction with mental health is widely documented in the literature, yet little is known about their inter‐relationships. The primary aim of this study was to examine the inter‐relationships between insomnia, internet addiction and depression. A total of 719 Chinese adolescents in Hong Kong participated in this school‐based cross‐sectional study. Participants completed the Chinese version of the Pittsburgh Sleep Quality Index (PSQI), the Chinese Internet Addiction Scale (CIAS), the 12‐item version of General Health Questionnaire (GHQ‐12) and questions assessing internet use pattern and sociodemographic characteristics. The classification of internet addiction and insomnia was based on the CIAS cutoff global score >63 and PSQI cutoff global score >5, respectively. Multiple regression analyses tested the effects of insomnia and internet addiction on depression. Among students with internet addiction (17.2%), 51.7% were also identified as insomniacs. Internet addicts scored significantly poorer on all PSQI components, except sleep duration, than their non‐addicted counterparts. After adjustment for gender and internet use time, both internet addiction (β = 0.05; Sobel test Z = 6.50, P < 0.001) and insomnia (β = 0.59; Sobel test Z = 4.49, P < 0.001) demonstrated a significant association with depression. Overall, there is high comorbidity between internet addiction and insomnia. Both insomnia and internet addiction emerged as significant explanatory factors, but they exerted differential effects on depression. Future research should be directed at determining the causal relationship between internet addiction and insomnia, and its underlying mechanism with depression.
The pervasiveness of media use in our society has raised concerns about its potential impact on important lifestyle behaviours, including sleep. Although a number of studies have modelled poor sleep as a negative outcome of media use, a critical assessment of the literature indicates two important gaps: (i) studies have almost exclusively relied on concurrent data, and thus have not been able to assess the direction of effects; and (ii) studies have largely been conducted with children and adolescents. The purpose of the present 3‐year longitudinal study, therefore, was to examine whether both sleep duration and sleep problems would be predictors or outcomes of two forms of media use (i.e. television and online social networking) among a sample of emerging adults. Participants were 942 (71.5% female) university students (M = 19.01 years, SD = 0.90) at Time 1. Survey measures, which were assessed for three consecutive years starting in the first year of university, included demographics, sleep duration, sleep problems, television and online social networking use. Results of a cross‐lagged model indicated that the association between sleep problems and media use was statistically significant: sleep problems predicted longer time spent watching television and on social networking websites, but not vice versa . Contrary to our hypotheses, sleep duration was not associated with media use. Our findings indicate no negative effects of media use on sleep among emerging adults, but instead suggest that emerging adults appear to seek out media as a means of coping with their sleep problems.
The European Sleep Research Society aimed to estimate the prevalence, determinants and consequences of falling asleep at the wheel. In total, 12 434 questionnaires were obtained from 19 countries using an anonymous online questionnaire that collected demographic and sleep‐related data, driving behaviour, history of drowsy driving and accidents. Associations were quantified using multivariate logistic regression. The average prevalence of falling asleep at the wheel in the previous 2 years was 17%. Among respondents who fell asleep, the median prevalence of sleep‐related accidents was 7.0% (13.2% involved hospital care and 3.6% caused fatalities). The most frequently perceived reasons for falling asleep at the wheel were poor sleep in the previous night (42.5%) and poor sleeping habits in general (34.1%). Falling asleep was more frequent in the Netherlands [odds ratio = 3.55 (95% confidence interval: 1.97; 6.39)] and Austria [2.34 (1.75; 3.13)], followed by Belgium [1.52 (1.28; 1.81)], Portugal [1.34 (1.13, 1.58)], Poland [1.22 (1.06; 1.40)] and France [1.20 (1.05; 1.38)]. Lower odds were found in Croatia [0.36 (0.21; 0.61)], Slovenia [0.62 (0.43; 0.89)] and Italy [0.65 (0.53; 0.79)]. Individual determinants of falling asleep were younger age; male gender [1.79 (1.61; 2.00)]; driving ≥20 000 km year [2.02 (1.74; 2.35)]; higher daytime sleepiness [7.49 (6.26; 8.95)] and high risk of obstructive sleep apnea syndrome [3.48 (2.78; 4.36) in men]. This Pan European survey demonstrates that drowsy driving is a major safety hazard throughout Europe. It emphasizes the importance of joint research and policy efforts to reduce the burden of sleepiness at the wheel for European drivers.