Delayed melatonin circadian timing, lower melatonin output, and sleep disruptions in myopic, or short-sighted, children.

STUDY OBJECTIVES: This study investigated the differences in melatonin circadian timing and output, sleep characteristics, and cognitive function in myopic and non-myopic (or emmetropic) children, aged 8-15 years. METHODS: Twenty-six myopes (refractive error [mean ±â€…standard error mean] -2.06 ±â€…0.23 diopters) and 19 emmetropes (-0.06 ±â€…0.04 diopters), aged 11.74 ±â€…2.31 years were recruited. Circadian timing was assessed using salivary dim-light melatonin onset (DLMO), collected half-hourly for 7 hours, beginning 5 hours before and finishing 2 hours after individual average sleep onset in a sleep laboratory. Nocturnal melatonin output was assessed via aMT6s levels from urine voids collected from 05:30 pm to 8:00 am the following morning. Actigraphy-derived objective sleep timing were acquired for a week prior to the sleep laboratory visit. Cognitive assessments of sustained attention (using psychomotor vigilance task [PVT]) and working memory (using digit spans) were performed on the night of sleep laboratory. RESULTS: Myopic children (9:07 pm ±â€…14 minutes) exhibited a DLMO phase-delay of 1 hour 8 minutes compared to emmetropes (7:59 pm ±â€…13 minutes), p = 0.002. aMT6s melatonin levels were significantly lower among myopes (18.70 ±â€…2.38) than emmetropes (32.35 ±â€…6.93, p = 0.001). Myopes also exhibited significantly delayed sleep onset, delayed wake-up time, poor and reduced sleep, and more evening-type diurnal preference than emmetropes (all p < 0.05). Finally, myopes showed a slower reaction time in the PVT (p < 0.05), but not digit span tasks at night. CONCLUSIONS: These findings suggest a potential association between circadian rhythm dysfunction and myopia in children.

Circadian aspects in the aetiology and pathophysiology of insomnia.

Because the endogenous circadian pacemaker is a very strong determinant of alertness/sleep propensity across the 24 h period, its mistiming may contribute to symptoms of insomnia (e.g., difficulties initiating sleep and maintaining sleep) and to the development of insomnia disorder. Despite the separation of insomnia and circadian rhythm disorders in diagnostic nosology implying independent pathophysiology, there is considerable evidence of co-morbidity and interaction between them. Sleep onset insomnia is associated with later timed circadian rhythms and can be treated with morning bright light to shift rhythms to an earlier timing. It is also possible that the causal link may go in both directions and that having a delayed circadian rhythm can result in enough experiences of delayed sleep onset to lead to some conditioned insomnia or insomnia disorder further exacerbating a delayed circadian rhythm. Early morning awakening insomnia is associated with an advanced circadian phase (early timing) and can be treated with evening bright light resulting in a delay of rhythms and an improved ability to sleep later in the morning and to obtain more sleep. There is some evidence suggesting that sleep maintenance insomnia is associated with a blunted amplitude of circadian rhythm that may be treated with increased regularity of sleep and light exposure timing. However, this is an insomnia phenotype that requires considerably more circadian research as well as further insomnia clinical research with the other insomnia phenotypes incorporating circadian timing measures and treatments.

Electric lighting, adolescent sleep and circadian outcomes, and recommendations for improving light health.

Light is a potent circadian entraining agent. For many people, daily light exposure is fundamentally dysregulated with reduced light during the day and increased light into the late evening. This lighting schedule promotes chronic disruption to circadian physiology resulting in a myriad of impairments. Developmental changes in sleep-wake physiology suggest that such light exposure patterns may be particularly disruptive for adolescents and further compounded by lifestyle factors such as early school start times. This narrative review describes evidence that reduced light exposure during the school day delays the circadian clock, and longer exposure durations to light-emitting electronic devices in the evening suppress melatonin. While home lighting in the evening can suppress melatonin secretion and delay circadian phase, the patterning of light exposure across the day and evening can have moderating effects. Photic countermeasures may be flexibly and scalably implemented to support sleep-wake health; including manipulations of light intensity, spectra, duration and delivery modality across multiple contexts. An integrative approach addressing physiology, attitudes, and behaviors will support optimization of light-driven sleep-wake outcomes in adolescents.

Light-based methods for predicting circadian phase in delayed sleep-wake phase disorder.

Methods for predicting circadian phase have been developed for healthy individuals. It is unknown whether these methods generalize to clinical populations, such as delayed sleep-wake phase disorder (DSWPD), where circadian timing is associated with functional outcomes. This study evaluated two methods for predicting dim light melatonin onset (DLMO) in 154 DSWPD patients using ~ 7 days of sleep-wake and light data: a dynamic model and a statistical model. The dynamic model has been validated in healthy individuals under both laboratory and field conditions. The statistical model was developed for this dataset and used a multiple linear regression of light exposure during phase delay/advance portions of the phase response curve, as well as sleep timing and demographic variables. Both models performed comparably well in predicting DLMO. The dynamic model predicted DLMO with root mean square error of 68 min, with predictions accurate to within ± 1 h in 58% of participants and ± 2 h in 95%. The statistical model predicted DLMO with root mean square error of 57 min, with predictions accurate to within ± 1 h in 75% of participants and ± 2 h in 96%. We conclude that circadian phase prediction from light data is a viable technique for improving screening, diagnosis, and treatment of DSWPD.

Myopia, or near-sightedness, is associated with delayed melatonin circadian timing and lower melatonin output in young adult humans.

STUDY OBJECTIVES: Myopia, or near-sightedness, is the most common refractive vision disorder and predisposes the eye to many blinding conditions in adulthood. Recent research has suggested that myopia is associated with increased endogenous melatonin production. Here we investigated the differences in melatonin circadian timing and output in young adult myopes and non-myopes (or emmetropes) as a pathogenesis for myopia. METHODS: A total of 18 myopic (refractive error [mean ± standard deviation] -4.89 ± 2.16 dioptres) and 14 emmetropic participants (-0.09 ± 0.13 dioptres), aged 22.06 ± 2.35 years were recruited. Circadian timing was assessed using salivary dim light melatonin onset (DLMO), collected half-hourly for 7 h, beginning 5 h before and finishing 2 h after individual average sleep onset in a sleep laboratory. Total melatonin production was assessed via aMT6s levels from urine voids collected from 06:00 pm and until wake-up time the following morning. Objective measures of sleep timing were acquired a week prior to the sleep laboratory visit using an actigraphy device. RESULTS: Myopes (22:19 ± 1.8 h) exhibited a DLMO phase-delay of 1 hr 12 min compared with emmetropes (21:07 ± 1.4 h), p = 0.026, d = 0.73. Urinary aMT6s melatonin levels were significantly lower among myopes (29.17 ± 18.67) than emmetropes (42.51 ± 23.97, p = 0.04, d = 0.63). Myopes also had a significant delay in sleep onset, greater sleep onset latency, shorter sleep duration, and more evening-type diurnal preference than emmetropes (all p < 0.05). CONCLUSIONS: These findings suggest a potential association between circadian rhythms and myopia in humans.

A PERIOD3 variable number tandem repeat polymorphism modulates melatonin treatment response in delayed sleep-wake phase disorder.

We examined whether a polymorphism of the PERIOD3 gene (PER3; rs57875989) modulated the sleep-promoting effects of melatonin in Delayed Sleep-Wake Phase Disorder (DSWPD). One hundred and four individuals (53 males; 29.4 ±10.0 years) with DSWPD and a delayed dim light melatonin onset (DLMO) collected buccal swabs for genotyping (PER34/4 n = 43; PER3 5 allele [heterozygous and homozygous] n = 60). Participants were randomised to placebo or 0.5 mg melatonin taken 1 hour before desired bedtime (or ~1.45 hours before DLMO), with sleep attempted at desired bedtime (4 weeks; 5-7 nights/week). We assessed sleep (diary and actigraphy), Pittsburgh Sleep Quality Index (PSQI), Insomnia Severity Index (ISI), Patient-Reported Outcomes Measurement Information System (PROMIS: Sleep Disturbance, Sleep-Related Impairment), Sheehan Disability Scale (SDS) and Patient- and Clinician-Global Improvement (PGI-C, CGI-C). Melatonin treatment response on actigraphic sleep onset time did not differ between genotypes. For PER34/4 carriers, self-reported sleep onset time was advanced by a larger amount and sleep onset latency (SOL) was shorter in melatonin-treated patients compared to those receiving placebo (P = .008), while actigraphic sleep efficiency in the first third of the sleep episode (SE T1) did not differ. For PER3 5 carriers, actigraphic SOL and SE T1 showed a larger improvement with melatonin (P < .001). Melatonin improved ISI (P = .005), PROMIS sleep disturbance (P < .001) and sleep-related impairment (P = .017), SDS (P = .019), PGI-C (P = .028) and CGI-C (P = .016) in PER34/4 individuals only. Melatonin did not advance circadian phase. Overall, PER34/4 DSWPD patients have a greater response to melatonin treatment. PER3 genotyping may therefore improve DSWPD patient outcomes.

Sleep regularity is associated with sleep-wake and circadian timing, and mediates daytime function in Delayed Sleep-Wake Phase Disorder.

BACKGROUND: In healthy populations, irregular sleep patterns are associated with delayed sleep and poor functional/mood outcomes. Currently, it is unknown whether irregular sleep contributes to poor functional/mood outcomes in individuals with Delayed Sleep-Wake Phase Disorder (DSWPD). METHODS: In 170 patients with DSWPD, we collected sleep-wake patterns, dim light melatonin onset (DLMO), and functional/mood outcomes. The Sleep Regularity Index (SRI) and other sleep timing metrics were computed. Correlations of SRI were computed with phase angle (difference between DLMO and desired bedtime), sleep timing and quality variables, daytime function, sleep-related daytime impairment, mood, and insomnia symptom severity. Path analyses assessed whether SRI or total sleep time mediated the associations between sleep onset time and phase angle with daytime functioning, sleep-related impairment, and mood outcomes. RESULTS: Higher SRI was associated with earlier sleep and longer total sleep time, but did not relate to sleep quality, daytime function, or mood outcomes. Path analysis showed that phase angle was directly associated with all outcome variables, whereas sleep onset time was not directly associated with any. SRI mediated the effects of sleep onset time and phase angle on daytime function. Total sleep time mediated the effects of sleep onset time and phase angle on sleep-related impairment. CONCLUSION: Individuals with DSWPD who have more delayed sleep and a greater phase angle also have more irregular sleep. This suggests that it is not delayed sleep timing per se that drives poor functional outcomes in DSWPD, but rather the timing of sleep relative to circadian phase and resultant irregular sleep patterns.

Increased sensitivity of the circadian system to light in delayed sleep-wake phase disorder.

KEY POINTS: This is the first study to demonstrate an altered circadian phase shifting response in a circadian rhythm sleep disorder. Patients with delayed sleep-wake phase disorder (DSWPD) demonstrate greater sensitivity of the circadian system to the phase-delaying effects of light. Increased circadian sensitivity to light is associated with later circadian timing within both control and DSWPD groups. DSWPD patients had a greater sustained pupil response after light exposure. Treatments for DSWPD should consider sensitivity of the circadian system to light as a potential underlying vulnerability, making patients susceptible to relapse. ABSTRACT: Patients with delayed sleep-wake phase disorder (DSWPD) exhibit delayed sleep-wake behaviour relative to desired bedtime, often leading to chronic sleep restriction and daytime dysfunction. The majority of DSWPD patients also display delayed circadian timing in the melatonin rhythm. Hypersensitivity of the circadian system to phase-delaying light is a plausible physiological basis for DSWPD vulnerability. We compared the phase shifting response to a 6.5 h light exposure (∼150 lux) between male patients with diagnosed DSWPD (n = 10; aged 20.8 ± 2.3 years) and male healthy controls (n = 11; aged 22.4 ± 3.3 years). Salivary dim light melatonin onset (DLMO) was measured under controlled conditions in dim light (<3 lux) before and after light exposure. Correcting for the circadian time of the light exposure, DSWPD patients exhibited 31.5% greater phase delay shifts than healthy controls. In both groups, a later initial melatonin phase was associated with a greater magnitude phase shift, indicating that increased circadian sensitivity to light may be a factor that contributes to delayed phase, even in non-clinical groups. DSWPD patients also had reduced pupil size following the light exposure, and showed a trend towards increased melatonin suppression during light exposure. These findings indicate that, for patients with DSWPD, assessment of light sensitivity may be an important factor that can inform behavioural therapy, including minimization of exposure to phase-delaying night-time light.

Efficacy of melatonin with behavioural sleep-wake scheduling for delayed sleep-wake phase disorder: A double-blind, randomised clinical trial.

BACKGROUND: Delayed Sleep-Wake Phase Disorder (DSWPD) is characterised by sleep initiation insomnia when attempting sleep at conventional times and difficulty waking at the required time for daytime commitments. Although there are published therapeutic guidelines for the administration of melatonin for DSWPD, to our knowledge, randomised controlled trials are lacking. This trial tested the efficacy of 0.5 mg melatonin, combined with behavioural sleep-wake scheduling, for improving sleep initiation in clinically diagnosed DSWPD patients with a delayed endogenous melatonin rhythm relative to patient-desired (or -required) bedtime (DBT). METHODS: This randomised, placebo-controlled, double-blind clinical trial was conducted in an Australian outpatient DSWPD population. Following 1-wk baseline, clinically diagnosed DSWPD patients with delayed melatonin rhythm relative to DBT (salivary dim light melatonin onset [DLMO] after or within 30 min before DBT) were randomised to 4-wk treatment with 0.5 mg fast-release melatonin or placebo 1 h before DBT for at least 5 consecutive nights per week. All patients received behavioural sleep-wake scheduling, consisting of bedtime scheduled at DBT. The primary outcome was actigraphic sleep onset time. Secondary outcomes were sleep efficiency in the first third of time in bed (SE T1) on treatment nights, subjective sleep-related daytime impairment (Patient Reported Outcomes Measurement Information System [PROMIS]), PROMIS sleep disturbance, measures of daytime sleepiness, clinician-rated change in illness severity, and DLMO time. FINDINGS: Between September 13, 2012 and September 1, 2014, 307 participants were registered; 116 were randomised to treatment (intention-to-treat n = 116; n = 62 males; mean age, 29.0 y). Relative to baseline and compared to placebo, sleep onset occurred 34 min earlier (95% confidence interval [CI] -60 to -8) in the melatonin group. SE T1 increased; PROMIS sleep-related impairment, PROMIS sleep disturbance, insomnia severity, and functional disability decreased; and a greater proportion of patients showed more than minimal clinician-rated improvement following melatonin treatment (52.8%) compared to placebo (24.0%) (P < 0.05). The groups did not differ in the number of nights treatment was taken per protocol. Post-treatment DLMO assessed in a subset of patients (n = 43) was not significantly different between groups. Adverse events included light-headedness, daytime sleepiness, and decreased libido, although rates were similar between treatment groups. The clinical benefits or safety of melatonin with long-term treatment were not assessed, and it remains unknown whether the same treatment regime would benefit patients experiencing DSWPD sleep symptomology without a delay in the endogenous melatonin rhythm. CONCLUSIONS: In this study, melatonin treatment 1 h prior to DBT combined with behavioural sleep-wake scheduling was efficacious for improving objective and subjective measures of sleep disturbances and sleep-related impairments in DSWPD patients with delayed circadian phase relative to DBT. Improvements were achieved largely through the sleep-promoting effects of melatonin, combined with behavioural sleep-wake scheduling. TRIAL REGISTRATION: This trial was registered with the Australian New Zealand Clinical Trials Registry, ACTRN12612000425897.

Prevalence of Circadian Misalignment and Its Association With Depressive Symptoms in Delayed Sleep Phase Disorder.

Study Objective: To examine the prevalence of circadian misalignment in clinically diagnosed delayed sleep phase disorder (DSPD) and to compare mood and daytime functioning in those with and without a circadian basis for the disorder. Methods: One hundred and eighty-two DSPD patients aged 16-64 years, engaged in regular employment or school, underwent sleep-wake monitoring in the home, followed by a sleep laboratory visit for assessment of salivary dim light melatonin onset (DLMO). Based on the DLMO assessments, patients were classified into two groups: circadian DSPD, defined as DLMO occurring at or after desired bedtime (DBT), or non-circadian DSPD, defined as DLMO occurring before DBT. Results: One hundred and three patients (57%) were classified as circadian DSPD and 79 (43%) as non-circadian DSPD. DLMO occurred 1.66 hours later in circadian DSPD compared to non-circadian DSPD (p < .001). Moderate-severe depressive symptoms (Beck Depression Inventory-II) were more prevalent in circadian DSPD (14.0%) than in non-circadian DSPD (3.8%; p < .05). Relative to non-circadian DSPD patients, circadian DSPD patients had 4.31 times increased odds of at least mild depressive symptoms (95% CI 1.75 to 10.64; p < .01). No group differences were found for daytime sleepiness or function, but DSPD symptoms were rated by clinicians to be more severe in those with circadian DSPD. Conclusions: Almost half of patients clinically diagnosed with DSPD did not show misalignment between the circadian pacemaker and the DBT, suggesting that the reported difficulties initiating sleep at the DBT are unlikely to be explained by the (mis)timing of the circadian rhythm of sleep propensity. Circadian misalignment in DSPD is associated with increased depressive symptoms and DSPD symptom severity.

Personality differences in patients with delayed sleep-wake phase disorder and non-24-h sleep-wake rhythm disorder relative to healthy sleepers.

OBJECTIVE/BACKGROUND: Delayed sleep-wake phase disorder (DSWPD) is associated with a delayed timing of circadian rhythms, and this delay is suggested to be the basis of the disorder. However, this has been questioned due to frequent relapses following treatment based on this aetiology. Recent studies have emerged suggesting personality factors may contribute to sleep patterns in DSWPD. The aim of this study was to further investigate circadian and personality factors in DSWPD patients as well as patients with non-24-h sleep-wake rhythm disorder (N24SWD) relative to control sleepers. PATIENTS/METHODS: This sample consisted of 16 DSWPD (age = 21.1 ± 2.8, 10 m, 7 f), and three N24SWD patients (age = 24.0 ± 4.4, 2 m, 1 f). Controls were seven males and seven females (age = 23.4 ± 5.9). Before starting an 80-h modified constant routine, eligible participants' sleep patterns were monitored for a week and they completed a personality questionnaire (NEO PI-R). An ultradian routine with alternating 20-min sleep opportunities and 40 min of enforced wakefulness was used to measure the timing of endogenous circadian temperature and melatonin rhythms. RESULTS: As compared with controls, DSWPD patients reported higher neuroticism, significantly lower extraversion, conscientiousness and agreeableness. Similarly, N24SWD patients' patterns of personality traits were similar to that of DSWPD. Conscientiousness, in particular, was associated with phase timings of circadian rhythms as well as sleep measures and lifestyle factors within the DSWPD group. CONCLUSIONS: These findings suggest that circadian rhythm sleep-wake disorders (CRSWDs) may not only stem from circadian abnormalities but personality factors may also drive lifestyle choices, including sleep timing.

Developing a successful treatment for co-morbid insomnia and sleep apnoea.

Insomnia and sleep apnoea are the two most common sleep disorders, found in 6% and 23-50% of the general population respectively. These disorders also frequently co-occur, with 39-58% of sleep apnoea patients reporting symptoms indicative of co-morbid insomnia. When these disorders co-occur, clinicians are faced with difficult treatment decisions, patients experience the additive detrimental impacts of both disorders, and the effectiveness of discrete treatments for each disorder may be impaired. A common finding is that co-morbid insomnia and sleep apnoea (COMISA) is more difficult to treat than either disorder presenting alone. Co-morbid insomnia reduces the initial acceptance of, and later adherence to, continuous positive airway pressure (CPAP) therapy for obstructive sleep apnoea. This has resulted in recent recommendations that treatment approaches should initially target COMISA patients' insomnia to remove this barrier to CPAP treatment, and improve patient outcomes. However, no randomised controlled trial outcomes investigating this treatment approach currently exist. The current article aims to review and integrate recent research examining the prevalence, characteristics, and theoretical mechanistic relationships between co-occurring insomnia and OSA, and discuss previous treatment attempts.

The etiology of delayed sleep phase disorder.

According to classification manuals for sleep disorders, nine disorders are directly related to biological clock timing misalignments. Of all, delayed sleep phase disorder (DSPD) is the most commonly diagnosed, predominantly affecting adolescents, young adults, and insomnia patients. It is a persistent inability to fall asleep at earlier, more desirable and socially conventional times, coupled with extreme difficulty awakening in the morning. Considerable evidence shows a delay in the circadian clock to be associated with DSPD. Therefore, treatments have mainly focused on advancing the biological clock and sleep timing through pharmacotherapy, phototherapy and behavioral therapies. The clinical evidence indicates that these treatments are efficacious, at least in the short term. However, follow up studies show frequent patient relapse, leading researchers to speculate that alternative etiologies may be contributing to sleep and circadian clock delays in DSPD. The aim of the present paper is to review and collate current literature related to DSPD etiology in order to outline gaps in current knowledge and suggest future research.

The relationship between a night's sleep and subsequent daytime functioning in older poor and good sleepers.

Those suffering insomnia symptoms generally report daytime impairments. However, research has not assessed whether this relationship holds on a nightly basis, despite the strongly held belief that a night of poor sleep impairs mood and functioning the following day. The objective of this study was to test this relationship in a group of older poor sleepers with insomnia symptoms compared with good sleepers. This study utilized a within-subjects design to investigate day-to-day subjective daytime functioning and its relation to the previous night's sleep. Seventeen older individuals (mean age: 67.5 years) were identified with a retrospective questionnaire and 2 weeks of sleep-wake diary to have poor sleep consistent with insomnia. Seventeen good sleepers (mean age: 67.8 years) were selected using the same measures. Participants reported their beliefs about sleep and daytime functioning on the Dysfunctional Beliefs and Attitudes about Sleep Scale (DBAS-16). One week later they commenced a 14-day period of sleep-wake diaries and concurrent responses to a modified Daytime Insomnia Symptom Scale (DISS). Results showed significant night-to-day covariation between sleep efficiency and daytime functioning for individuals with poor sleep (r = 0.34), but not for good sleepers (r = 0.08). Those poor sleepers who held this covariation belief most strongly were those who subsequently showed this night-to-day relationship the most strongly (r = 0.56). This was not true for good sleepers. For those suffering insomnia, these findings demonstrate their belief that a poor sleep is followed by an impaired daytime, consistent with their experience.

Beliefs about the 'shape' and continuity of healthy sleep as a function of age.

OBJECTIVE: Treating insomnia includes challenging unrealistic beliefs that may contribute to anxieties and wakefulness. This study explored beliefs about the shape and continuity of healthy adult sleep at different adult ages. METHODS: Younger (n=113, M=21.4 (2.4)) and older adults (n=110, M=72.3 (7.7)) depicted their concept of the normal sleep of both a healthy 18 and 65 year olds. Plots were drawn to show sleep depth and awakenings across the night. RESULTS: Seventy percent conceptualized healthy sleep as an unbroken U shape and 18 year olds were depicted with deeper sleep than 65 year olds. About 95% of younger adults and three quarters of older adults showed both healthy 18 and 65 year olds sleep without awakenings. CONCLUSION: Unrealistic sleep beliefs are widespread, with healthy sleep usually being mistakenly conceptualized as unbroken, even in older adults. Education that awakenings are part of normal sleep may have preventative health implications and reduce sleep anxieties.

The impact of sleep on adolescent depressed mood, alertness and academic performance.

The present study developed and tested a theoretical model examining the inter-relationships among sleep duration, sleep quality, and circadian chronotype and their effect on alertness, depression, and academic performance. Participants were 385 adolescents aged 13-18 years (M = 15.6, SD = 1.0; 60% male) were recruited from eight socioeconomically diverse high schools in South Australia. Participants completed a battery of questionnaires during class time and recorded their sleep patterns in a sleep diary for 8 days. A good fit was found between the model and the data (χ(2)/df = 1.78, CFI = .99, RMSEA = .04). Circadian chronotype showed the largest association with on adolescent functioning, with more evening-typed students reporting worse sleep quality (ß = .50, p < .001) and diminished alertness (ß = .59, p < .001). Sleep quality was significantly associated with poor outcomes: adolescents with poorer sleep quality reported less sleep on school nights (ß = -.28, p < .001), diminished daytime alertness (ß = .33, p < .001), and more depressed mood (ß = .47, p < .001). Adolescents with poor sleep quality and/or more evening chronotype were also more likely to report worse grades, through the association with depression. Sleep duration showed no direct effect on adolescent functioning. These results identified the importance of two lesser-studied aspects of sleep: circadian chronotype and sleep quality. Easy-to-implement strategies to optimize sleep quality and maintain an adaptive circadian body clock may help to increase daytime alertness, elevate mood, and improve academic performance.

Public health implications of sleep loss: the community burden.

Poor sleep imparts a significant personal and societal burden. Therefore, it is important to have accurate estimates of its causes, prevalence and costs to inform health policy. A recent evaluation of the sleep habits of Australians demonstrates that frequent (daily or near daily) sleep difficulties (initiating and maintaining sleep, and experiencing inadequate sleep), daytime fatigue, sleepiness and irritability are highly prevalent (20%-35%). These difficulties are generally more prevalent among females, with the exception of snoring and related difficulties. While about half of these problems are likely to be attributable to specific sleep disorders, the balance appears attributable to poor sleep habits or choices to limit sleep opportunity. Study of the economic impact of sleep disorders demonstrates financial costs to Australia of $5.1 billion per year. This comprises $270 million for health care costs for the conditions themselves, $540 million for care of associated medical conditions attributable to sleep disorders, and about $4.3 billion largely attributable to associated productivity losses and non-medical costs resulting from sleep loss-related accidents. Loss of life quality added a substantial further non-financial cost. While large, these costs were for sleep disorders alone. Additional costs relating to inadequate sleep from poor sleep habits in people without sleep disorders were not considered. Based on the high prevalence of such problems and the known impacts of sleep loss in all its forms on health, productivity and safety, it is likely that these poor sleep habits would add substantially to the costs from sleep disorders alone.

Estimating adolescent sleep patterns: parent reports versus adolescent self-report surveys, sleep diaries, and actigraphy.

BACKGROUND: In research and clinical contexts, parent reports are often used to gain information about the sleep patterns of their adolescents; however, the degree of concordance between parent reports and adolescent-derived measures is unclear. The present study compares parent estimates of adolescent sleep patterns with adolescent self-reports from surveys and sleep diaries, together with actigraphy. METHODS: A total of 308 adolescents (59% male) aged 13-17 years completed a school sleep habits survey during class time at school, followed by a 7-day sleep diary and wrist actigraphy. Parents completed the Sleep, Medical, Education and Family History Survey. RESULTS: Parents reported an idealized version of their adolescent's sleep, estimating significantly earlier bedtimes on both school nights and weekends, significantly later wake times on weekends, and significantly more sleep than either the adolescent self-reported survey, sleep diary, or actigraphic estimates. CONCLUSION: Parent reports indicate that the adolescent averages a near-optimal amount of sleep on school nights and a more than optimal amount of sleep on weekends. However, adolescent-derived averages indicate patterns of greater sleep restriction. These results illustrate the importance of using adolescent-derived estimates of sleep patterns in this age group and the importance of sleep education for both adolescents and their parents.

A cross-cultural comparison of sleep duration between US And Australian adolescents: the effect of school start time, parent-set bedtimes, and extracurricular load.

STUDY OBJECTIVE: To test whether sleep duration on school nights differs between adolescents in Australia and the United States and, if so, whether this difference is explained by cultural differences in school start time, parental involvement in setting bedtimes, and extracurricular commitments. PARTICIPANTS: Three hundred eighty-five adolescents aged 13 to 18 years (M = 15.57, SD = 0.95; 60% male) from Australia and 302 adolescents aged 13 to 19 years (M = 16.03, SD = 1.19; 35% male) from the United States. METHODS: Adolescents completed the School Sleep Habits Survey during class time, followed by an 8-day sleep diary. RESULTS: After controlling for age and gender, Australian adolescents obtained an average of 47 minutes more sleep per school night than those in the United States. Australian adolescents were more likely to have a parent-set bedtime (17.5% vs. 6.8%), have a later school start time (8:32 a.m. vs. 7:45 a.m.), and spend less time per day on extracurricular commitments (1 h 37 min vs. 2 h 41 min) than their U.S. peers. The mediating factors of parent-set bedtimes, later school start times, and less time spent on extracurricular activities were significantly associated with more total sleep. CONCLUSIONS: In addition to biological factors, extrinsic cultural factors significantly affect adolescent sleep. The present study highlights the importance of a cross-cultural, ecological approach and the impact of early school start times, lack of parental limit setting around bedtimes, and extracurricular load in limiting adolescent sleep.