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Epidemiological studies show a high prevalence of "insomnia" in adolescents. However, insomnia symptoms are not specific for insomnia disorder. Puberty is associated with circadian delay, which may cause insomnia symptoms such as problems falling asleep and daytime impairments, but also difficulties rising in the morning which is not a hallmark of insomnia disorder. The aim of this study was to investigate the extent to which adolescent insomnia symptoms may be attributed to circadian delay. The sample comprised 3,867 high-school-students. Survey instruments included the Bergen Insomnia Scale (BIS), the Munich ChronoType Questionnaire (MCTQ), the reduced Morningness-Eveningness Questionnaire (r-MEQ), and items on subjective sleep problems and sleep-related behaviors. Symptoms of circadian delay (CD) were defined as i) trouble waking on school days, ii) ability to sleep long into the day, iii) waking ≥10:00 on free days and/or iv) oversleeping for school. A total of 34.5% reported insomnia according to BIS. Among these, 88.4% reported ≥1 CD-symptom and 15.5% reported all CD-symptoms. Adolescents with insomnia and ≥1 CD-symptom were often evening-types (56.9%), had long social jetlag (2:55 h) and large school-/free day discrepancy in sleep duration (6:04 vs. 8:34 h). Results suggest circadian delay as a plausible explanation for insomnia symptoms in many adolescents.

The physiological processes governing sleep regulation show maturational changes during adolescent development. To date, data are available to specify when delays in circadian timing occur; however, no longitudinal data exist to characterize the maturation of the accumulation of sleep pressure across the evening. The aim of this longitudinal study was to test whether this change in evening sleep propensity can be identified during early adolescence. Twenty pre-pubescent boys' (Mage = 10.3, SD = 0.4 years) evening sleep homeostats were assessed using a series of sleep latency tests every hour (7:30 p.m. to 3:30 a.m.) at 6-month intervals across four waves. While results revealed shorter sleep onset latencies with increasing wakefulness (p < .001), this effect was not moderated by study wave (p = .79). Evening sleep propensity thus appears to remain stable in boys during early adolescence. Future studies should expand upon these findings by using larger samples of girls as well as boys across an extended age range during the teenage years., Competing Interests: Declaration of competing interest None, (Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.)

Study Objectives: To investigate circadian typology in a large, representative sample of Norwegian adolescents, and its implications for sleep health., Methods: The sample included 3920 1 st year high school students aged 16-17 years. Respondents completed a web-based survey, including the short version of the Horne-Ostberg Morningness-Eveningness Questionnaire (rMEQ), the Munich Chronotype Questionnaire (MCTQ) and items on sleep-related behaviors (eg electronic media usage in bed, consumption of caffeinated beverages), sleep beliefs and daytime sleepiness. Data were analyzed using one-way ANOVAs and Chi-squared tests., Results: In all, 7.8% were categorized as morning, 52.3% as intermediate and 39.9% as evening types, respectively. Evening types had later sleep timing, longer sleep latency, more social jetlag and shorter school day sleep duration than morning types, with intermediate types displaying a sleep pattern between these two extremes. None of the circadian types met the minimum recommended amount of sleep on school nights (ie 8+ hours), and only morning types had a mean sleep duration of 7+ hours (7:19 h, nearly 1 h more than evening types who slept 6:20 h, p < 0.001). Evening types reported more use of electronic media in bed, more consumption of caffeinated beverages and more daytime sleepiness than the other circadian types. They were also less satisfied with their school day sleep duration and perceived it more difficult to change their sleep pattern., Conclusions: Results from this study suggest that eveningness represents a sleep health challenge for older adolescents., (Copyright © 2021 The Author(s). Published by Elsevier B.V. All rights reserved.)

Objectives: To assess differences relating to circadian preference in objectively measured sleep patterns from childhood to adolescence over a 9-year period. We hypothesized there is developmental continuity in sleep timing and duration according to circadian preference., Study Design: Young participants (N = 111, 65% girls) from a community-based birth cohort underwent sleep actigraphy at mean ages 8.1 (SD = 0.3), 12.3 (SD = 0.5), and 16.9 (SD = 0.1) years. A short version of Morningness-Eveningness Questionnaire was administered in late adolescence. At each follow-up, sleep midpoint, duration, wake after sleep onset, sleep efficiency, and weekend catch-up sleep were compared between those reporting morning, intermediate, and evening preferences in late adolescence., Results: Mixed model analyses indicated that sleep timing was significantly earlier among morning types compared with evening types at all ages (P values < .04). The mean differences in sleep midpoint between morning and evening types increased from a mean of 19 minutes (age 8), 36 minutes (age 12), to 89 minutes (age 17). The largest change occurred from age 12 to 17 years. Sleep duration, wake after sleep onset, sleep efficiency, and catch-up sleep did not differ according to circadian preference., Conclusions: This study found significant continuity in sleep timing from childhood to adolescence over 9 years, indicating that late circadian preference reported in late adolescence begins to manifest in middle childhood. Further studies are needed to establish whether sleep timing has its origins at an even earlier age., (Crown Copyright © 2017. Published by Elsevier Inc. All rights reserved.)

Adolescents are vulnerable to inadequate sleep due to a unique constellation of risk factors. In particular, the puberty-related phase delay in the timing of the circadian system postpones the onset of sleep. Resultantly, disordered sleep is common among teenagers and young adults, with the most common sleep problem being delayed sleep wake-phase disorder (DSWPD). Although current treatments for DSWPD show promise, novel ways to improve our youth's sleep are needed. The purpose of this review is to critically evaluate the evidence for the role of exercise as a method to shift and/or regulate circadian timing, and thus improve sleep, in adolescents and young adults. A growing body of evidence suggests that nocturnal exercise can delay circadian timing. However, exercise administered at different times of the 24-h day may result in phase advances, particularly when the timing of exercise is gradually advanced in small daily increments. The implications of these results for young people's sleep health are discussed and suggestions are provided for ways that exercise could be used clinically, to improve the treatment of DSWPD., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

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., (© 2016 The Author(s).)

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 (cBT min ), dim-light melatonin onset (DLMO) and the midpoint of the melatonin secretion period (DLM mid = [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, cBT min and DLM mid . Regression equations revealed that the circadian phase (DLMO, cBT min and DLM mid ) 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.

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., (© 2015 The Author(s).)

Objective: Daylight is an important zeitgeber for entraining the circadian rhythm to a 24 h clock cycle, especially within the Polar circle, which has long Polar nights several months each year. Phase delays in sleep timing may occur, but the mean shift is normally small. However, the individual variation in phase shifts is large, implicating moderating factors. Here we examined the role of several self-regulatory variables (mood and fatigue, behavioral habits, and psychological self-regulation) as moderators of seasonality in sleep timing and chronotype., Methods: A sample of 162 young adults (76% females; mean age: females 23.4 years, males 24.3 years) participated in a prospective study across three seasons (September, December, March) in Tromsø/Norway at 69°39′N Sleep diary and sleep/health-related questionnaire data were collected at each time-point., Results: Sleep timing and chronotype were delayed during the dark period (December) compared with brighter photoperiods (September and March). Comparable effects were observed for insomnia, fatigue, mood (depression and anxiety), subjective health complaints, physical activity, and school-related stress. Most importantly, depression and fatigue moderated the degree of seasonal shifting in sleep timing, whereas the other self-regulation indicators did not (ie eating habits, physical activity, and psychological self-regulation)., Conclusion: Seasonality in sleep timing and chronotype was confirmed, and it seems that depressive symptoms during the dark period exacerbate phase-shifting problems for people living in sub-Arctic regions.

The currently assumed aetiology for delayed sleep phase disorder (DSPD) is a delay of the circadian system. Clinicians have sought to use bright light therapy, exogenous melatonin or chronotherapy to correct the disorder. However, these treatments have achieved unreliable outcomes for DSPD patients and, as such, one suggestion has been that the disorder may be caused by a longer than normal circadian rhythm period length (i.e. tau). The present study investigated this premise using a 78-h ultradian, ultra-short sleep-wake cycle. This constant bedrest routine was used to simulate a series of 1-h long 'days' by alternating 20-min sleep opportunities and 40 min of enforced wakefulness. Thirteen participants were recruited for the study including, six people diagnosed with DSPD according to the International Classification of Sleep Disorders-2 [mean age = 22.0, standard deviation (SD) = 3.3] and seven good sleepers (mean age = 23.1, SD = 3.9) with normal sleep timing. The DSPD participants' core temperature rhythm tau (mean = 24 h 54 min, SD = 23 min) was significantly longer (t = -2.33, P = 0.04, Cohen's d = 1.91) than the good sleepers' (mean 24 h 29 min, SD = 16 min). The temperature rhythm of the DSPD participants delayed more rapidly (i.e. >25 min day(-1) ) than the good sleepers'. These findings provide an explanation for the difficulty that DSPD patients have in phase advancing to a more conventional sleep time and their frequent relapse following treatment. The outcomes of this study support a vigorous and continued application of chronobiological and behavioural therapies to entrain DSPD patients to their desired earlier sleep times., (© 2013 European Sleep Research Society.)

Skin temperature circadian rhythms have been explored relatively recently. It has been suggested that distal and proximal skin temperature changes play a role in the regulation of the core temperature circadian rhythm and sleepiness. The authors investigated the circadian finger and core temperature rhythms in conjunction with the circadian rhythms of subjective and objective sleepiness. Fourteen healthy, young, good sleepers participated in a modified constant-routine procedure in which palmar finger temperature, rectal temperature, subjective sleepiness, and objective sleep latency were measured half-hourly across a 48-h period of enforced wakeful bed rest. Individual curves were adjusted to the group mean temperature minimum time of 0500 h and averaged to create the 4 mean curves. The 5 possible cross-correlation curves between these 4 measures were calculated for half-hourly phase lags from 12 h before to 12 h after the group mean core temperature minimum time. Maximum cross-correlations for each curve suggested that finger temperature preceded core temperature by 3 h (r = -0.22), and subjective sleepiness followed core temperature by 0.5 h (r = -0.33) and objective sleepiness by 2 h (r = 0.29). Although these data are correlational, they are consistent with the notion that finger temperature changes drive core temperature changes, which determine changes of subjective and objective sleepiness.