Gorica Micic

Does one hour of bright or short-wavelength filtered tablet screenlight have a meaningful effect on adolescents’ pre-bedtime alertness, sleep, and daytime functioning?

Electronic media use is prevalent among adolescent populations, as is the frequency of sleeplessness. One mechanism proposed for technology affecting adolescents’ sleep is the alerting effects from bright screens. Two explanations are provided. First, screens emit significant amounts of short-wavelength light (i.e. blue), which produces acute alertness and alters sleep timing. Second, later chronotypes are hypothesised to be hypersensitive to evening light. This study analysed the pre-sleep alertness (GO/NOGO task speed, accuracy; subjective sleepiness), sleep (sleep diary, polysomnography), and morning functioning of 16 healthy adolescents (M = 17.4 ± 1.9 yrs, 56% f) who used a bright tablet screen (80 lux), dim screen (1 lux) and a filtered short-wavelength screen (f.lux; 50 lux) for 1 hr before their usual bedtime in a within-subjects protocol. Chronotype was analysed as a continuous between-subjects factor; however, no significant interactions occurred. Significant effects occurred between bright and dim screens for GO/NOGO speed and accuracy. However, the magnitude of these differences was small (e.g. GO/NOGO speed = 23 ms, accuracy = 13%), suggesting minimal clinical significance. No significant effects were found for sleep onset latency, slow-rolling eye movements, or the number of SWS and REM minutes in the first two sleep cycles. Future independent studies are needed to test short (1 hr) vs longer (>2 hrs) screen usage to provide evidence for safe-to-harmful levels of screenlight exposure before adolescents’ usual bedtime.

Delayed sleep phase disorder in an Australian school-based sample of adolescents.

STUDY OBJECTIVES To establish the extent to which the developmental changes in sleep timing experienced by Australian adolescents meet the International Classification of Sleep Disorders (ICSD-2) diagnostic criteria for delayed sleep phase disorder (DSPD), and whether adolescents with DSPD engage in poorer lifestyle choices, and are more impaired compared to good sleeping adolescents. METHODS Three-hundred seventy-four Australian adolescents (mean age 15.6 years, SD 1.0) participants completed a 7-day sleep diary, wore wrist actigraphy, and completed a battery of questionnaires to assess DSPD criteria. RESULTS The ICSD-2 criteria for DSPD were met by 1.1% (N = 4) of the adolescents sampled. The majority of adolescents (51.9%, N = 194) met one criterion, 14% (N = 52) of the adolescents met 2 criteria, while 33.2% (N = 124) did not fulfill any DSPD criteria. Despite having significantly delayed sleep timing, adolescents who met all criteria for DSPD reported similar lifestyle habits and daytime functioning. However, there were trends for greater alcohol and caffeine consumption, less sport participation, yet more time spent on extracurricular activities (i.e., learning to play a musical instruments for adolescents with DSPD. CONCLUSIONS Despite the majority of adolescents reporting DSPD symptoms, only a small minority met full diagnostic criteria. Adolescents with DSPD reported similar lifestyle habits and daytime functioning to those with some or no symptoms. Future investigations of non-school-attending DSPD adolescents are needed to confirm the trends for lifestyle behaviors found in the present study.

Nocturnal Melatonin Profiles in Patients with Delayed Sleep-Wake Phase Disorder and Control Sleepers

A significant delay in the timing of endogenous circadian rhythms has been associated with delayed sleep phase disorder (DSPD). More recently, other mechanisms have also been proposed to account for this disorder. To further explore the etiology of DSPD, the present study compared nocturnal melatonin profiles of 26 DSPD patients (18 males, 8 females; age, 21.73 ± 4.98 years) and 17 normally timed good sleepers (10 males, 7 females; age, 23.82 ± 5.23 years) in a time-free, dim-light (<10 lux) laboratory environment. A 30-h modified constant routine with alternating 20-min sleep opportunities and 40 min of enforced wakefulness was used to measure the endogenous melatonin circadian rhythm. Salivary melatonin was sampled half-hourly from 1820 h to 0020 h and then hourly from 0120 h to 1620 h. DSPD patients had significantly later timed melatonin profiles that were delayed by approximately 3 h compared to normal sleepers, and there were no notable differences in the relative duration of secretion between groups. However, melatonin secretion between dim-light melatonin onset (DLMO) and acrophase was less prominent in DSPD patients compared to good sleepers, who showed a more acute initial surge of melatonin following the DLMO. Although the regulatory role of melatonin is unknown, abnormal melatonin profiles have been linked to psychiatric and neurological disorders (e.g., major depression, obsessive compulsive disorder, Parkinson disease). These results therefore suggest that in addition to a delayed endogenous circadian rhythm, a diminished initial surge of melatonin secretion following DLMO may contribute to the etiology of DSPD.

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.

Circadian Melatonin and Temperature Taus in Delayed Sleep-wake Phase Disorder and Non-24-hour Sleep-wake Rhythm Disorder Patients: An Ultradian Constant Routine Study.

Our objectives were to investigate the period lengths (i.e., taus) of the endogenous core body temperature rhythm and melatonin rhythm in delayed sleep-wake phase disorder patients (DSWPD) and non-24-h sleep-wake rhythm disorder patients (N24SWD) compared with normally entrained individuals. Circadian rhythms were measured during an 80-h ultradian modified constant routine consisting of 80 ultrashort 1-h “days” in which participants had 20-min sleep opportunities alternating with 40 min of enforced wakefulness. We recruited a community-based sample of 26 DSWPD patients who met diagnostic criteria (17 males, 9 females; age, 21.85 ± 4.97 years) and 18 healthy controls (10 males, 8 females; age, 23.72 ± 5.10 years). Additionally, 4 full-sighted patients (3 males, 1 female; age, 25.75 ± 4.99 years) were diagnosed with N24SWD and included as a discrete study group. Ingestible core temperature capsules were used to record minute temperatures that were averaged to obtain 80 hourly data points. Salivary melatonin concentration was assessed every half-hour to determine time of dim light melatonin onset at the beginning and end of the 80-h protocol. DSWPD patients had significantly longer melatonin rhythm taus (24 h 34 min ± 17 min) than controls (24 h 22 min ± 15 min, p = 0.03, d = 0.70). These results were further supported by longer temperature rhythm taus in DSWPD patients (24 h 34 min ± 26 min) relative to controls (24 h 13 min ± 15 min, p = 0.01, d = 0.80). N24SWD patients had even longer melatonin (25 h ± 19 min) and temperature (24 h 52 min ± 17 min) taus than both DSWPD (p = 0.007, p = 0.06) and control participants (p < 0.001, p = 0.02, respectively). Between 12% and 19% of the variance in DSWPD patients’ sleep timing could be explained by longer taus. This indicates that longer taus of circadian rhythms may contribute to the DSWPD patients’ persistent tendency to delay, their frequent failure to respond to treatment, and their relapse following treatment. Additionally, other factors can contribute to misalignments in DSWPD and N24SWD disorders.

An investigation of the longitudinal relationship between sleep and depressed mood in developing teens

Objective The prospective, bidirectional relationship between sleep disturbance and depressed mood was assessed in a school-based sample of adolescents. Method One hundred and thirty-eight Australian adolescents (mean age time 1 =15.69, standard deviation =0.92; 64% male) completed questionnaires to assess sleep parameters and depressed mood, on two occasions over 1 year. Results Cross-sectional associations were observed between depressed mood and sleep duration, as well as wakefulness in bed. Prospective analyses revealed depressed mood predicted less total sleep time on school nights and a longer latency to sleep onset on weekends 1 year later. There was no prospective support for sleep predicting later depressed mood. Conclusion Contrary to prediction, our results suggest in this case that depressed mood may act as a precursor to poor sleep rather than the converse.

Intensive Sleep Re-Training: From Bench to Bedside

Intensive sleep re-training is a promising new therapy for chronic insomnia. Therapy is completed over a 24-h period during a state of sleep deprivation. Improvements of sleep and daytime impairments are comparable to the use of stimulus control therapy but with the advantage of a rapid reversal of the insomnia. The initial studies have been laboratory based and not readily accessible to the patient population. However, new smart phone technology, using a behavioral response to external stimuli as a measure of sleep/wake state instead of EEG determination of sleep, has made this new therapy readily available. Technological improvements are still being made allowing the therapy to provide further improvements in the effectiveness of Intensive Sleep Re-training.

Can the circadian phase be estimated from self-reported sleep timing in patients with Delayed Sleep Wake Phase Disorder to guide timing of chronobiologic treatment?

ABSTRACT Introduction: The efficacy of bright light and/or melatonin treatment for Delayed Sleep Wake Phase Disorder (DSWPD) is contingent upon an accurate clinical assessment of the circadian phase. However, the process of determining this circadian phase can be costly and is not yet readily available in the clinical setting. The present study investigated whether more cost-effective and convenient estimates of the circadian phase, such as self-reported sleep timing, can be used to predict the circadian phase and guide the timing of light and/or melatonin treatment (i.e. dim-light melatonin onset, core body temperature minimum and melatonin secretion mid-point) in a sample of individuals with DSWPD. Method: Twenty-four individuals (male = 17; mean age = 21.96, SD = 5.11) with DSWPD were selected on the basis of ICSD-3 criteria from a community-based sample. The first 24-hours of a longer 80-hour constant laboratory ultradian routine were used to determine core body temperature minimum (cBTmin), dim-light melatonin onset (DLMO) and the midpoint of the melatonin secretion period (DLMmid = [DLM°ff–DLMO]/2). Prior to the laboratory session subjective sleep timing was assessed using a 7-day sleep/wake diary, the Pittsburgh Sleep Quality Index (PSQI), and the Delayed Sleep Phase Disorder Sleep Timing Questionnaire (DSPD-STQ). Results: Significant moderate to strong positive correlations were observed between self-reported sleep timing variables and DLMO, cBTmin and DLMmid. Regression equations revealed that the circadian phase (DLMO, cBTmin and DLMmid) was estimated within ±1.5 hours of the measured circadian phase most accurately by the combination of sleep timing measures (88% of the sample) followed by sleep diary reported midsleep (83% of the sample) and sleep onset time (79% of the sample). Discussion: These findings suggest that self-reported sleep timing may be useful clinically to predict a therapeutically relevant circadian phase in DSWPD.