Effects of an advanced sleep schedule and morning short wavelength light exposure on circadian phase in young adults with late sleep schedules.
ABSTRACT: We examined the effects of an advanced sleep/wake schedule and morning short wavelength (blue) light in 25 adults (mean age±SD=21.8±3 years; 13 women) with late sleep schedules and subclinical features of delayed sleep phase disorder (DSPD).After a baseline week, participants kept individualized, fixed, advanced 7.5-h sleep schedules for 6days. Participants were randomly assigned to groups to receive "blue" (470nm, ?225lux, n=12) or "dim" (<1lux, n=13) light for 1h after waking each day. Head-worn "Daysimeters" measured light exposure; actigraphs and sleep diaries confirmed schedule compliance. Salivary dim light melatonin onset (DLMO), self-reported sleep, and mood were examined with 2×2 ANOVA.After 6days, both groups showed significant circadian phase advances, but morning blue light was not associated with larger phase shifts than dim-light exposure. The average DLMO advances (mean±SD) were 1.5±1.1h in the dim light group and 1.4±0.7h in the blue light group.Adherence to a fixed advanced sleep/wake schedule resulted in significant circadian phase shifts in young adults with subclinical DSPD with or without morning blue light exposure. Light/dark exposures associated with fixed early sleep schedules are sufficient to advance circadian phase in young adults.
Project description:Human circadian rhythms are regulated by the interplay between circadian genes and environmental stimuli. The influence of altered sleep-wake schedules or light on human circadian gene expression patterns is not well characterized.Twenty-one young adults were asked to keep to their usual sleep schedules and two blood samples were drawn at the end of the first week from each subject based on estimated time of dim light melatonin onset (DLMO); the first sample was obtained one and a half hours before the estimated DLMO and the second three hours later, at one and a half hours after the estimated DLMO. During the second week, participants were randomized into two groups, one that received a one hour blue-light (?max=470 nm) exposure in the morning and one that received a comparable morning dim-light exposure. Two blood samples were obtained at the same clock times as the previous week at the end of the second week.We measured the expression of 10 circadian genes in response to sleep-wake schedule advancement and morning blue-light stimulation in the peripheral blood of 21 participants during a two-week field study. We found that nine of the 10 circadian genes showed significant expression changes from the first to the second week for participants in both the blue-light and dim-light groups, likely reflecting significant advances in circadian phase.This wholesale change in circadian gene expression may reflect considerable advances in circadian phase (i.e., advance in DLMO) from the first to the second week resulting from the advanced, daily personal light exposures.
Project description:Many adolescents fall asleep too late to get enough sleep (8-10 h) on school nights. Morning bright light advances circadian rhythms and could help adolescents fall asleep earlier. Morning bright light treatment before school, however, is difficult to fit into their morning schedule; weekends are more feasible. We examined phase advances in response to morning light treatment delivered over one weekend. Thirty-seven adolescents (16 males; 14.7-18.0 years) who reported short school-night sleep (?7 h) and late bedtimes (school-nights ?23:00; weekend/non-school nights ?24:00) slept as usual at home for ?2 weeks ("baseline") and then kept a fixed sleep schedule (baseline school-night bed and wake-up times ±30 min) for ?1 week before living in the lab for one weekend. Sleep behavior was measured with wrist actigraphy and sleep diary. On Saturday morning, we woke each participant 1 h after his/her midpoint of baseline weekend/non-school night sleep and 1 h earlier on Sunday. They remained in dim room light (?20 lux) or received 1.5 or 2.5 h of intermittent morning bright light (?6000 lux) on both mornings. The dim light melatonin onset (DLMO), a phase marker of the circadian timing system, was measured on Friday and Sunday evenings to compute the weekend circadian phase shift. The dim room light and 1.5-h bright light groups advanced the same amount (0.6 ± 0.4 and 0.6 ± 0.5 h). The 2.5-h bright light group advanced 1.0 ± 0.4 h, which was significantly more than the other groups. These data suggest that it is possible to phase advance the circadian clock of adolescents who have late bedtimes and short school-night sleep in one weekend using light that begins shortly after their sleep midpoint.
Project description:INTRODUCTION:Many sleep and circadian studies require participants to adhere to structured sleep-wake schedules designed to stabilize sleep outcomes and circadian phase prior to in-laboratory testing. The effectiveness of this approach has not been rigorously evaluated, however. We therefore investigated the differences between participants' unstructured and structured sleep over a three-week interval. METHODS:Twenty-three healthy young adults completed three weeks of sleep monitoring, including one week of unstructured sleep and two weeks of structured sleep with consistent bed and wake times. Circadian phase was assessed via salivary dim light melatonin onset (DLMO) during both the unstructured and structured sleep episodes. RESULTS:Compared to their unstructured sleep schedule, participants' bed- and wake times were significantly earlier in their structured sleep, by 34 ± 44 mins (M ± SD) and 44 ± 41 mins, respectively. During structured sleep, circadian phase was earlier in 65% of participants (40 ± 32 mins) and was later in 35% (41 ± 25 mins) compared to unstructured sleep but did not change at the group level. While structured sleep reduced night-to-night variability in sleep timing and sleep duration, and improved the alignment (phase angle) between sleep onset and circadian phase in the most poorly aligned individuals (DLMO < 1h or > 3h before sleep onset time; 25% of our sample), sleep duration and quality were unchanged. CONCLUSION:Our results show adherence to a structured sleep schedule results in more regular sleep timing, and improved alignment between sleep and circadian timing for those individuals who previously had poorer alignment. Our findings support the use of structured sleep schedules prior to in-laboratory sleep and circadian studies to stabilize sleep and circadian timing in healthy volunteers.
Project description:Dim light melatonin onset (DLMO) is the most reliable measure of human central circadian timing. Its modulation by light exposure and chronotype has been scarcely approached. We evaluated the impact of light changes on the interaction between melatonin, sleep, and chronotype in university students (n = 12) between the Antarctic summer (10 days) and the autumn equinox in Montevideo, Uruguay (10 days). Circadian preferences were tested by validated questionnaires. A Morningness-Eveningness Questionnaire average value (47 ± 8.01) was used to separate late and early participants. Daylight exposure (measured by actimetry) was significantly higher in Antarctica versus Montevideo in both sensitive time windows (the morning phase-advancing and the evening phase-delaying). Melatonin was measured in hourly saliva samples (18-24 h) collected in dim light conditions (<30 lx) during the last night of each study period. Early and late participants were exposed to similar amounts of light in both sites and time windows, but only early participants were significantly more exposed during the late evening in Antarctica. Late participants advanced their DLMO with no changes in sleep onset time in Antarctica, while early participants delayed their DLMO and sleep onset time. This different susceptibility to respond to light may be explained by a subtle difference in evening light exposure between chronotypes.
Project description:To examine, in a field study circadian phase changes associated with two different light-dark exposures patterns, one that was congruent with a phase advanced sleep schedule and one that was incongruent with an advanced schedule.Twenty-one adults (mean age±standard deviation=22.5±3.9 years; 11 women) participated in the 12day study. After a five-day baseline period, participants were all given individualized, fixed, 90-minute advanced sleep schedules for one week. Participants were randomly assigned to one of two groups, an advance group with a light-dark exposure prescription designed to advance circadian phase or a delay group with light-dark exposure prescription designed to delay circadian phase. The advance group received two morning hours of short-wavelength (blue) light (?max ? 476±1 nm, full-width-half-maximum ?20 nm) exposure and three evening hours of light restriction (orange-filtered light, ?<525 nm=0). The delay group received blue light for three hours in the evening and light restriction for two hours in the morning. Participants led their normal lives while wearing a calibrated wrist-worn light exposure and activity monitor.After seven days on the 90-minute advanced sleep schedule, circadian phase advanced 132±19 minutes for the advance group and delayed 59±7.5 minutes for the delay group.Controlling the light-dark exposure pattern shifts circadian phase in the expected direction irrespective of the fixed advanced sleep schedule.
Project description:Photic and non-photic stimuli have been shown to shift the phase of the human circadian clock. We examined how photic and non-photic time cues may be combined by the human circadian system by assessing the phase advancing effects of one evening dose of exogenous melatonin, alone and in combination with one session of morning bright light exposure.Randomized placebo-controlled double-blind circadian protocol. The effects of four conditions, dim light (?1.9 lux, ?0.6 Watts/m(2))-placebo, dim light-melatonin (5 mg), bright light (?3000 lux, ?7 Watts/m(2))-placebo, and bright light-melatonin on circadian phase was assessed by the change in the salivary dim light melatonin onset (DLMO) prior to and following treatment under constant routine conditions. Melatonin or placebo was administered 5.75 h prior to habitual bedtime and 3 h of bright light exposure started 1 h prior to habitual wake time.Sleep and chronobiology laboratory environment free of time cues.Thirty-six healthy participants (18 females) aged 22 ± 4 y (mean ± SD).Morning bright light combined with early evening exogenous melatonin induced a greater phase advance of the DLMO than either treatment alone. Bright light alone and melatonin alone induced similar phase advances.Information from light and melatonin appear to be combined by the human circadian clock. The ability to combine circadian time cues has important implications for understanding fundamental physiological principles of the human circadian timing system. Knowledge of such principles is important for designing effective countermeasures for phase-shifting the human circadian clock to adapt to jet lag, shift work, and for designing effective treatments for circadian sleep-wakefulness disorders.
Project description:A neural network model was previously developed to predict melatonin rhythms accurately from blue light and skin temperature recordings in individuals on a fixed sleep schedule. This study aimed to test the generalizability of the model to other sleep schedules, including rotating shift work. Ambulatory wrist blue light irradiance and skin temperature data were collected in 16 healthy individuals on fixed and habitual sleep schedules, and 28 rotating shift workers. Artificial neural network models were trained to predict the circadian rhythm of (i) salivary melatonin on a fixed sleep schedule; (ii) urinary aMT6s on both fixed and habitual sleep schedules, including shift workers on a diurnal schedule; and (iii) urinary aMT6s in rotating shift workers on a night shift schedule. To determine predicted circadian phase, center of gravity of the fitted bimodal skewed baseline cosine curve was used for melatonin, and acrophase of the cosine curve for aMT6s. On a fixed sleep schedule, the model predicted melatonin phase to within ± 1 hour in 67% and ± 1.5 hours in 100% of participants, with mean absolute error of 41 ± 32 minutes. On diurnal schedules, including shift workers, the model predicted aMT6s acrophase to within ± 1 hour in 66% and ± 2 hours in 87% of participants, with mean absolute error of 63 ± 67 minutes. On night shift schedules, the model predicted aMT6s acrophase to within ± 1 hour in 42% and ± 2 hours in 53% of participants, with mean absolute error of 143 ± 155 minutes. Prediction accuracy was similar when using either 1 (wrist) or 11 skin temperature sensor inputs. These findings demonstrate that the model can predict circadian timing to within ± 2 hours for the vast majority of individuals on diurnal schedules, using blue light and a single temperature sensor. However, this approach did not generalize to night shift conditions.
Project description:For over 30 years, delayed sleep phase disorder (DSPD) has been defined as a debilitating sleep condition. Recently, there is more awareness of DSPD in young people, yet considerable information is needed to understand its cause and treatment. This review describes the latest research findings describing the clinical features, cause, and treatment of DSPD.The prevalence of DSPD in adolescents and young adults ranges from 1 to 16%. The impact on the individuals is significant, particularly in the domains of school/work performance and mental health. We describe various contributing factors including reduced homeostatic sleep pressure, a lengthened and delayed circadian rhythm, insensitivity to clock-resetting morning light, and heightened cognitive activity. Evening melatonin administration as a sole treatment appears promising, as is a combination of cognitive-behavior therapy and morning bright light.Recent findings suggest clinicians to be aware of the clinical features (i.e., significant daytime sleepiness, anxiety and depression symptoms, potential for school dropout) of DSPD, as several biological features underpinning this disorder are unseen in clinical settings. We advise clinicians to become familiar with exogenous evening melatonin administration, and cognitive and behavioral techniques to simultaneously treat the delayed circadian rhythm and associated sleep-onset insomnia.
Project description:The timing of the internal circadian clock shows large inter-individual variability across the lifespan. Although the sleep-wakefulness pattern of most toddlers includes an afternoon nap, the association between napping and circadian phase in early childhood remains unexplored. This study examined differences in circadian phase and sleep between napping and non-napping toddlers. Data were collected on 20 toddlers (34.2±2.0 months; 12 females; 15 nappers). Children followed their habitual napping and non-napping sleep schedules (monitored with actigraphy) for 5 days before an in-home salivary dim light melatonin onset (DLMO) assessment. On average, napping children fell asleep during their nap opportunities on 3.6±1.2 of the 5 days before the DLMO assessment. For these napping children, melatonin onset time was 38 min later (p = 0.044; d = 0.93), actigraphically-estimated bedtime was 43 min later (p = 0.014; d = 1.24), sleep onset time was 59 min later (p = 0.006; d = 1.46), and sleep onset latency was 16 min longer (p = 0.030; d = 1.03) than those not napping. Midsleep and wake time did not differ by napping status. No difference was observed in the bedtime, sleep onset, or midsleep phase relationships with DLMO; however, the wake time phase difference was 47 min smaller for napping toddlers (p = 0.029; d = 1.23). On average, nappers had 69 min shorter nighttime sleep durations (p = 0.006; d = 1.47) and spent 49 min less time in bed (p = 0.019; d = 1.16) than non-nappers. Number of days napping was correlated with melatonin onset time (r = 0.49; p = 0.014). Our findings indicate that napping influences individual variability in melatonin onset time in early childhood. The delayed bedtimes of napping toddlers likely permits light exposure later in the evening, thereby delaying the timing of the clock and sleep. Whether the early developmental trajectory of circadian phase involves an advance associated with the decline in napping is a question necessitating longitudinal data as children transition from a biphasic to monophasic sleep-wakefulness pattern.
Project description:This study investigated the utility of the pupillary light reflex as a method of differentiating DSPD patients with delayed melatonin timing relative to desired/required sleep time (circadian type) and those with non-delayed melatonin timing (non-circadian type). All participants were young adults, with a total of 14 circadian DSPD patients (M = 28.14, SD = 5.26), 12 non-circadian DSPD patients (M = 29.42, SD = 11.51) and 51 healthy controls (M = 21.47 SD = 3.16) completing the protocol. All participants were free of central nervous system acting medications and abstained from caffeine and alcohol on the day of the assessment. Two pupillary light reflex measurements were completed by each participant, one with a 1s dim (~10 lux) light exposure, and one with a 1s bright (~1500 lux) light exposure. Circadian DSPD patients showed a significantly faster pupillary light reflex than both non-circadian DSPD patients and healthy controls. Non-circadian patients and healthy controls did not differ significantly. Receiver operating characteristic curves were generated to determine the utility of mean and maximum constriction velocity in differentiating the two DSPD phenotypes, and these demonstrated high levels of sensitivity (69.23--100%) and specificity (66.67-91.67%) at their optimal cut offs. The strongest predictor of DSPD phenotype was the mean constriction velocity to bright light (AUC = 0.87). These results support the potential for the pupillary light reflex to clinically differentiate between DSPD patients with normal vs. delayed circadian timing relative to desired bedtime, without the need for costly and time-consuming circadian assessments.