Exposure to bright light and darkness to treat physiologic maladaptation to night work

Working at night results in a misalignment between the sleep-wake cycle and the output of the hypothalamic pacemaker that regulates the circadian rhythms of certain physiologic and behavioral variables. We evaluated whether such physiologic maladaptation to nighttime work could be prevented effectively by a treatment regimen of exposure to bright light during the night and darkness during the day. We assessed the functioning of the circadian pacemaker in five control and five treatment studies in order to assess the extent of adaptation in eight normal young men to a week of night work. In the control studies, on the sixth consecutive night of sedentary work in ordinary light (approximately 150 lux), the mean (+/- SEM) nadir of the endogenous temperature cycle continued to occur during the night (at 3:31 +/- 0:56 hours), indicating a lack of circadian adaptation to the nighttime work schedule. In contrast, the subjects in the treatment studies were exposed to bright light (7000 to 12,000 lux) at night and to nearly complete darkness during the day, and the temperature nadir shifted after four days of treatment to a significantly later, midafternoon hour (14:53 +/- 0:32; P less than 0.0001), indicating a successful circadian adaptation to daytime sleep and nighttime work. There were concomitant shifts in the 24-hour patterns of plasma cortisol concentration, urinary excretion rate, subjective assessment of alertness, and cognitive performance in the treatment studies. These shifts resulted in a significant improvement in both alertness and cognitive performance in the treatment group during the night-shift hours. We conclude that maladaptation of the human circadian system to night work, with its associated decline in alertness, performance, and quality of daytime sleep, can be treated effectively with scheduled exposure to bright light at night and darkness during the day.     

Enhancement of nighttime alertness and performance with bright ambient light

Objective levels of alertness and performance efficiency were measured in twenty-five healthy young adults during two simulated night shifts. Following the first night shift, during which all subjects worked under dim ambient light (10-20 lux), subjects were assigned to one of three ambient lighting conditions (10-20 lux, 100 lux or 1000 lux) for the second night of work. Subjects exposed to 1000 lux ambient light maintained significantly higher levels of alertness across the 8-hour shift than did subjects exposed to the dimmer lighting conditions. Cognitive performance was also significantly enhanced under the bright light condition, whereas simple reaction time was not. The findings indicate clearly that ambient lighting levels can have a substantial impact on nighttime alertness and performance and that bright ambient illumination may be effective in maintaining optimal levels of alertness during night shift operations.     

Complete or partial circadian re-entrainment improves performance, alertness, and mood during night-shift work

STUDY OBJECTIVES: To assess performance, alertness, and mood during the night shift and subsequent daytime sleep in relation to the degree of re-alignment (re-entrainment) of circadian rhythms with a night-work, day-sleep schedule. DESIGN: Subjects spent 5 consecutive night shifts (11:00 pm-7:00 am) in the lab and slept at home in darkened bedrooms (8:30 am-3:30 pm). Subjects were categorized by the degree of re-entrainment attained after the 5 night shifts. Completely re-entrained: temperature minimum in the second half of daytime sleep; partially re-entrained: temperature minimum in the first half of daytime sleep; not re-entrained: temperature minimum did not delay enough to reach daytime sleep. SETTING: See above. PARTICIPANTS: Young healthy adults (n = 67) who were not shift workers. INTERVENTIONS: Included bright light during the night shifts, sunglasses worn outside, a fixed dark daytime sleep episode, and melatonin. The effects of various combinations of these interventions on circadian re-entrainment were previously reported. Here we report how the degree of re-entrainment affected daytime sleep and measures collected during the night shift. MEASUREMENTS AND RESULTS: Salivary melatonin was collected every 30 minutes in dim light (<20 lux) before and after the night shifts to determine the dim light melatonin onset, and the temperature minimum was estimated by adding a constant (7 hours) to the dim light melatonin onset. Subjects kept sleep logs, which were verified by actigraphy. The Neurobehavioral Assessment Battery was completed several times during each night shift. Baseline sleep schedules and circadian phase differed among the 3 re-entrainment groups, with later times resulting in more re-entrainment. The Neurobehavioral Assessment Battery showed that performance, sleepiness, and mood were better in the groups that re-entrained compared to the group that did not re-entrain, but there were no significant differences between the partial and complete re-entrainment groups. Subjects slept almost all of the allotted 7 hours during the day, and duration did not significantly differ among the re-entrainment groups. CONCLUSIONS: In young people, complete re-entrainment to the night-shift day-sleep schedule is not necessary to produce substantial benefits in neurobehavioral measures; partial re-entrainment (delaying the temperature minimum into the beginning of daytime sleep) is sufficient. The group that did not re-entrain shows that a reasonable amount of daytime sleep is not enough to produce good neurobehavioral performance during the night shift. Therefore, some re-alignment of circadian rhythms is recommended.     

Melatonin rhythms in night shift workers.

For some time, it has remained uncertain whether the circadian rhythms of permanent night shift workers are adapted to their night-active schedule. Previous studies of this question have often been limited by "masking" (evoked) effects of sleep and activity on body temperature and cortisol, used as marker rhythms. In this study, the problem of masking was minimized by measuring the timing of melatonin production under dim light conditions. Nine permanent night shift workers were admitted to the Clinical Research Center (CRC) directly from their last work shift of the week and remained in dim light while blood samples were obtained hourly for 24 hours. Melatonin concentrations were measured in these samples using a gas-chromatographic mass-spectrometric method. Sleep diaries were completed for two weeks prior to the admission to the CRC. Overall, the onset of the melatonin rhythm was about 7.2 hours earlier (or 16.8 hours later) in the night workers compared to day-active controls. It was not possible to know whether the phase of the melatonin rhythm was the result of advances or delays. In night shift workers, sleep was initiated (on average) about three hours prior to the onset of melatonin production. In contrast, day-active subjects initiated sleep (on average) about three hours after their melatonin onset. Thus, the sleep times selected by night shift workers may not be well-synchronized to their melatonin rhythm, assumed to mark the phase of their underlying circadian pacemaker.     

Bright light exposure at night and light attenuation in the morning improve adaptation of night shift workers

With practical applicability in mind, we wanted to observe whether nocturnal alertness, performance, and daytime sleep could be improved by light exposure of tolerable intensity and duration in a real work place. We also evaluated whether attenuating morning light was important in adaptation of real night shift workers. Twelve night shift nurses participated in this study. The study consisted of three different treatment procedures: Room Light (RL), Bright Light (BL), and Bright Light with Sunglasses (BL/S). In RL, room light exposure was given during the night shift and followed by 1 hr exposure to sunlight or 10,000 lux light the next morning (from 08:30 to 09:30). In BL, a 4-hour nocturnal light exposure of 4,000-6,000 lux (from 01:00 to 05:00) was applied and followed by the same morning light exposure as in RL. In BL/S, the same nocturnal light exposure as in BL was done with light attenuation in the morning. Each treatment procedure was continued for 4 days in a repeated measures, cross-over design. Nocturnal alertness was measured by a visual analog scale. Computerized performance tests were done. Daytime sleep was recorded with actigraphy. The most significant overall improvement of sleep was noted in BL/S. BL showed less improvement than BL/S but more than RL. Comparison of nocturnal alertness among the 3 treatments produced similar results: during BL/S, the subjects were most alert, followed by BL and then by RL. Real night shift workers can improve nocturnal alertness and daytime sleep by bright light exposure in their work place. These improvements can be maximized by attenuating morning light on the way home.     

Shaping the light/dark pattern for circadian adaptation to night shift work

This is the second in a series of simulated night shift studies designed to achieve and subsequently maintain a compromise circadian phase position between complete entrainment to the daytime sleep period and no phase shift at all. We predict that this compromise will yield improved night shift alertness and daytime sleep, while still permitting adequate late night sleep and daytime wakefulness on days off. Our goal is to delay the dim light melatonin onset (DLMO) from its baseline phase of ∼ 21:00 to our target of ∼ 3:00. Healthy young subjects (n = 31) underwent three night shifts followed by two days off. Two experimental groups received intermittent bright light pulses during night shifts (total durations of 75 and 120 min per night shift), wore dark sunglasses when outside, slept in dark bedrooms at scheduled times after night shifts and on days off, and received outdoor light exposure upon awakening from sleep. A control group remained in dim room light during night shifts, wore lighter sunglasses, and had unrestricted sleep and outdoor light exposure. After the days off, the DLMO of the experimental groups was ∼ 00:00-1:00, not quite at the target of 3:00, but in a good position to reach the target after subsequent night shifts with bright light. The DLMO of the control group changed little from baseline. Experimental subjects performed better than control subjects during night shifts on a reaction time task. Subsequent studies will reveal whether the target phase is achieved and maintained through more alternations of night shifts and days off.     

Combination of bright light and caffeine as a countermeasure for impaired alertness and performance during extended sleep deprivation

Effects of four conditions (Dim Light-Placebo, Dim Light-Caffeine, Bright Light-Placebo and Bright Light-Caffeine) on alertness, and performance were studied during the night-time hours across 45.5 h of sleep deprivation. Caffeine (200 mg) was administered at 20.00 and 02.00 hours and bright-light exposure (>2000 lux) was from 20.00 to 08.00 hours each night. The three treatment conditions, compared to the Dim Light-Placebo condition, enhanced night-time performance. Further, the combined treatment of caffeine and all-night bright light (Bright Light-Caffeine) enhanced performance to a larger degree than either the Dim Light-Caffeine or the Bright Light-Placebo condition. Beneficial effects of the treatments on performance were largest during the early morning hours (e.g. after 02.00 hours) when performance in the Dim Light-Placebo group was at its worst. Notably, the Bright Light-Caffeine condition was able to overcome the circadian drop in performance for most tasks measured. Both caffeine conditions improved objective alertness on the Maintenance of Wakefulness Test. Taken together, the above results suggest that the combined treatment of bright light and caffeine provides an effective intervention for enhancing alertness and performance during sleep loss.     

Responsiveness of the aging circadian clock to light

The present study assessed whether advances in sleep times and circadian phase in older adults might be due to decreased responsiveness of the aging circadian clock to light. Sixteen young (29.3 ± 5.6 years) and 14 older adults (67.1 ± 7.4 years) were exposed to 4 h of control dim (10 lux) or bright light (3500 lux) during the night. Phase shifts of the melatonin rhythm were assessed from the nights before and after the light exposure. Bright light delayed the melatonin midpoint in both young and older adults (p < 0.001). Phase delays for the older subjects were not significantly different from those of the young subjects for either the bright or dim light conditions. The magnitude of phase delays was correlated with both sleep offset and phase angle in the older, but not the younger subjects. The present results indicate that at light intensities commonly used in research as well as clinical practice older adults are able to phase delay to the same extent as younger subjects.     

The 24-h growth hormone rhythm in men: sleep and circadian influences questioned

The 24-h rhythm of growth hormone (GH) is thought to be controlled primarily by sleep processes with a weak circadian component. This concept has been recently questioned in sleep-deprived persons. To test the notion of a high sleep-dependency of GH release, we established simultaneous 24-h rhythms of GH and melatonin, a circadian marker, in night workers who form a model for challenging sleep and circadian processes. Ten day-active subjects and 11 night workers were studied during their usual sleep-wake schedule, with sleep from 23:00 to 07:00 hours and 07:00 to 15:00 hours, respectively. Experiments were conducted in sleep rooms under continuous nutrition, bed rest, and dim light. Melatonin and GH were measured every 10 min over 24 h. In day-active subjects, melatonin and GH showed the well-known 24-h profiles, with a major sleep-related GH pulse accounting for 52.8 +/- 3.5% of the 24-h GH production and the onset of the melatonin surge occurring at 21:53 hours +/- 18 min. In night workers, melatonin showed variable circadian adaptation, with the onset of secretion varying between 21:45 and 05:05 hours. The sleep-related GH pulse was lowered, but the reduction was compensated for by the emergence of large individual pulses occurring unpredictably during waking periods, so that the total amount of GH secreted during the 24 h was constant. One cannot predict the degree of GH adaptation from the highly variable melatonin shift. These results argue against the concept that sleep processes exert a predominant influence on GH release whatever the conditions. When sleep and circadian processes are misaligned, the blunting of the sleep-related GH pulse is counteracted, as in sleep-deprived persons, by a compensatory mechanism promoting GH pulses during wakefulness.     

Effects of partial circadian adjustments on sleep and vigilance quality during simulated night work

In most situations, complete circadian adjustment is not recommended for night workers. With complete adjustment, workers experience circadian misalignment when returning on a day-active schedule, causing repeated circadian phase shifts and internal desynchrony. For this reason, partial circadian realignment was proposed as a good compromise to stabilize internal circadian rhythms in night shift workers. However, the extent of partial circadian adjustment necessary to improve sleep and vigilance quality is still a matter of debate. In this study, the effects of small but statistically significant partial circadian adjustments on sleep and vigilance quality were assessed in a laboratory simulation of night work to determine whether they were also of clinical significance. Partial adjustments obtained by phase delay or by phase advance were quantified not only by the phase shift of dim light salivary melatonin onset, but also by the overlap of the episode of melatonin production with the sleep-wake cycle adopted during simulated night work. The effects on daytime sleep and night-time vigilance quality were modest. However, they suggest that even small adjustments by phase delay may decrease the accumulation of sleep debt, whereas the advance strategy improves subjective alertness and mood during night work. Furthermore, absolute phase shifts, by advance or by delay, were associated with improved subjective alertness and mood during the night shift. These strategies need to be tested in the field, to determine whether they can be adapted to real-life situations and provide effective support to night workers.     

Bright light treatment used for adaptation to night work and re-adaptation back to day life. A field study at an oil platform in the North Sea

Night workers complain of sleepiness, reduced performance and disturbed sleep due to lack of adjustment of the circadian rhythm. In simulated night-work experiments scheduled exposure to bright light has been shown to reduce these complaints. Here we studied the effects of bright light treatment on the adaptation to 14 days of consecutive night work at an oil platform in the North Sea, and the subsequent readaptation to day life at home, using the Karolinska sleep/wake diary. Bright light treatment of 30 min per exposure was applied during the first 4 nights of the night-shift period and the first 4 days at home following the shift period. The bright light exposure was scheduled individually to phase delay the circadian rhythm. Bright light treatment modestly facilitated the subjective adaptation to night work, but the positive effect of bright light was especially pronounced during the re-adaptation back to day life following the return home. Sleepiness was reduced and the quality of day was rated better after exposure to bright light. The modest effect of bright light at the platform was, possibly, related to the finding that the workers seemed to adapt to night work within a few days even without bright light. These results suggest that short-term bright light treatment may help the adaptation to an extended night-work period, and especially the subsequent re-adaptation to day life.     

Advancing circadian rhythms before eastward flight: a strategy to prevent or reduce jet lag

STUDY OBJECTIVES: To develop a practical pre-eastward flight treatment to advance circadian rhythms as much as possible but not misalign them with sleep. DESIGN: One group had their sleep schedule advanced by 1 hour per day and another by 2 hours per day. SETTING: Baseline at home, treatment in lab. PARTICIPANTS: Young healthy adults (11 men, 15 women) between the ages of 22 and 36 years. INTERVENTIONS: Three days of a gradually advancing sleep schedule (1 or 2 hours per day) plus intermittent morning bright light (one-half hour approximately 5000 lux, one-half hour of <60 lux) for 3.5 hours. MEASUREMENTS AND RESULTS: The dim light melatonin onset was assessed before and after the 3-day treatment. Subjects completed daily sleep logs and symptom questionnaires and wore wrist activity monitors. The dim light melatonin onset advanced more in the 2-hours-per-day group than in the 1-hour-per-day group (median phase advances of 1.9 and 1.4 hours), but the difference between the means (1.8 and 1.5 hours) was not statistically significant. By the third treatment day, circadian rhythms were misaligned relative to the sleep schedule, and subjects had difficulty falling asleep in the 2-hours-per-day group, but this was not the case in the 1-hour-per-day group. Nevertheless, the 2-hours-per-day group did slightly better on the symptom questionnaires. In general, sleep disturbance and other side effects were small. CONCLUSIONS: A gradually advancing sleep schedule with intermittent morning bright light can be used to advance circadian rhythms before eastward flight and, thus, theoretically, prevent or reduce subsequent jet lag. Given the morning light treatment used here, advancing the sleep schedule 2 hours per day is not better than advancing it 1 hour per day because it was too fast for the advance in circadian rhythms. A diagram is provided to help the traveler plan a preflight schedule.     

Circadian rhythms of melatonin, cortisol, and clock gene expression during simulated night shift work

STUDY OBJECTIVES: The synchronization of peripheral circadian oscillators in humans living on atypical sleep/wake schedules is largely unknown. In this night shift work simulation, we evaluate clock gene expression in peripheral blood mononuclear cells (PBMCs) relative to reliable markers of the central circadian pacemaker. DESIGN: Participants were placed on a 10-hr delayed sleep/wake schedule simulating nighttime work followed by a daytime sleep episode. SETTING: Baseline, intermediate and final circadian evaluations were performed in the temporal isolation laboratory. PARTICIPANTS: Five healthy candidates, 18-30 years. INTERVENTIONS: Polychromatic white light of (mean +/-SEM) 6,036 +/-326 lux (approximately 17,685 +/-955 W/m2) during night shifts; dim light exposure after each night shift; an 8-hr sleep/darkness episode beginning 2 hrs after the end of each night shift. MEASUREMENTS: Melatonin and cortisol in plasma; clock genes HPER1, HPER2 and HBMAL1 RNA in PBMCs. RESULTS: Following 9 days on the night schedule, hormonal rhythms were adapted to the shifted schedule. HPER1 and HPER2 expression in PBMCs displayed significant circadian rhythmicity, which was in a conventional relationship with the shifted sleep/wake schedule. Changes in the pattern of clock gene expression were apparent as of 3 days on the shifted sleep/wake schedule. CONCLUSIONS: This preliminary study is the first documentation of the effects of a shifted sleep/wake schedule on the circadian expression of both peripheral circadian oscillators in PBMCs and centrally-driven hormonal rhythms. In light of evidence associating clock gene expression with tissue function, the study of peripheral circadian oscillators has important implications for understanding medical disorders affecting night shift workers.     

Effects of nocturnal bright light on saliva melatonin, core body temperature and sleep propensity rhythms in human subjects

Nine healthy male volunteers (mean age of 24) participated in two experimental sessions of random crossover design: a bright light (5000 lux for 5 h from 00:00 to 05:00 h) session and a dim light (10 lux for 5 h from 00:00 to 05:00 h) session. Subsequently participants entered an ultra-short sleep-wake schedule for 26 h, in which a sleep-wake cycle consisting of 10-min sleep EEG recording on a bed and 20-min resting awake on a semi-upright chair were repeated. Saliva melatonin level and core body temperature was measured throughout the experiment. Bright light significantly delayed rhythms of melatonin secretion (01:58 h), core body temperature (01:12 h) and sleep propensity (02:00 h), compared as dim light session. Significant positive correlation was found between bright light-induced phase change in core body temperature and that in sleep propensity rhythm. Light-induced melatonin suppression significantly positively correlated with the phase change in core body temperature and that in sleep propensity rhythm. Assuming that light-induced melatonin suppression represents an acute impact of light on the circadian pacemaker, our results suggest that such an impact may be directly reflected in phase changes of sleep propensity and core body temperature rhythms rather than in melatonin rhythm.     

Practice parameters for the clinical evaluation and treatment of circadian rhythm sleep disorders. An American Academy of Sleep Medicine report

The expanding science of circadian rhythm biology and a growing literature in human clinical research on circadian rhythm sleep disorders (CRSDs) prompted the American Academy of Sleep Medicine (AASM) to convene a task force of experts to write a review of this important topic. Due to the extensive nature of the disorders covered, the review was written in two sections. The first review paper, in addition to providing a general introduction to circadian biology, addresses "exogenous" circadian rhythm sleep disorders, including shift work disorder (SWD) and jet lag disorder (JLD). The second review paper addresses the "endogenous" circadian rhythm sleep disorders, including advanced sleep phase disorder (ASPD), delayed sleep phase disorder (DSPD), irregular sleep-wake rhythm (ISWR), and the non-24-hour sleep-wake syndrome (nonentrained type) or free-running disorder (FRD). These practice parameters were developed by the Standards of Practice Committee and reviewed and approved by the Board of Directors of the AASM to present recommendations for the assessment and treatment of CRSDs based on the two accompanying comprehensive reviews. The main diagnostic tools considered include sleep logs, actigraphy, the Morningness-Eveningness Questionnaire (MEQ), circadian phase markers, and polysomnography. Use of a sleep log or diary is indicated in the assessment of patients with a suspected circadian rhythm sleep disorder (Guideline). Actigraphy is indicated to assist in evaluation of patients suspected of circadian rhythm disorders (strength of recommendation varies from "Option" to "Guideline," depending on the suspected CRSD). Polysomnography is not routinely indicated for the diagnosis of CRSDs, but may be indicated to rule out another primary sleep disorder (Standard). There is insufficient evidence to justify the use of MEQ for the routine clinical evaluation of CRSDs (Option). Circadian phase markers are useful to determine circadian phase and confirm the diagnosis of FRD in sighted and unsighted patients but there is insufficient evidence to recommend their routine use in the diagnosis of SWD, JLD, ASPD, DSPD, or ISWR (Option). Additionally, actigraphy is useful as an outcome measure in evaluating the response to treatment for CRSDs (Guideline). A range of therapeutic interventions were considered including planned sleep schedules, timed light exposure, timed melatonin doses, hypnotics, stimulants, and alerting agents. Planned or prescribed sleep schedules are indicated in SWD (Standard) and in JLD, DSPD, ASPD, ISWR (excluding elderly-demented/nursing home residents), and FRD (Option). Specifically dosed and timed light exposure is indicated for each of the circadian disorders with variable success (Option). Timed melatonin administration is indicated for JLD (Standard); SWD, DSPD, and FRD in unsighted persons (Guideline); and for ASPD, FRD in sighted individuals, and for ISWR in children with moderate to severe psychomotor retardation (Option). Hypnotic medications may be indicated to promote or improve daytime sleep among night shift workers (Guideline) and to treat jet lag-induced insomnia (Option). Stimulants may be indicated to improve alertness in JLD and SWD (Option) but may have risks that must be weighed prior to use. Modafinil may be indicated to improve alertness during the night shift for patients with SWD (Guideline).     

A three pulse phase response curve to three milligrams of melatonin in humans

Exogenous melatonin is increasingly used for its phase shifting and soporific effects. We generated a three pulse phase response curve (PRC) to exogenous melatonin (3 mg) by administering it to free-running subjects. Young healthy subjects (n = 27) participated in two 5 day laboratory sessions, each preceded by at least a week of habitual, but fixed sleep. Each 5 day laboratory session started and ended with a phase assessment to measure the circadian rhythm of endogenous melatonin in dim light using 30 min saliva samples. In between were three days in an ultradian dim light (< 150 lux)-dark cycle (LD 2.5 : 1.5) during which each subject took one pill per day at the same clock time (3 mg melatonin or placebo, double blind, counterbalanced). Each individual's phase shift to exogenous melatonin was corrected by subtracting their phase shift to placebo (a free-run). The resulting PRC has a phase advance portion peaking about 5 h before the dim light melatonin onset, in the afternoon. The phase delay portion peaks about 11 h after the dim light melatonin onset, shortly after the usual time of morning awakening. A dead zone of minimal phase shifts occurred around the first half of habitual sleep. The fitted maximum advance and delay shifts were 1.8 h and 1.3 h, respectively. This new PRC will aid in determining the optimal time to administer exogenous melatonin to achieve desired phase shifts and demonstrates that using exogenous melatonin as a sleep aid at night has minimal phase shifting effects.     

Use of bright light to treat maladaptation to night shift work and circadian rhythm sleep disorders

SUMMARY  Night work is associated with increased sleepiness and disturbed sleep. Maladaptation of the circadian system, which is phase-adjusted to day time work and thus promotes sleepiness during its nadir at night and wakefulness (or disturbed sleep) during the day, contributes substantially to this problem. A major cause of suboptimal circadian phase adjustment among night workers is the exposure to morning light, which prevents the delay needed for optimal adjustment to night work. Several laboratory studies indicate that careful application of bright light may cause the circadian system to shift to any desired phase. Furthermore, studies of simulated night work demonstrate that night exposure to bright light can virtually eliminate circadian maladjustment among night workers. While the results are promising, there is still, however, an urgent need for longitudinal studies of bright light application in. real-life settings.     

Daytime exposure to bright light, as compared to dim light, decreases sleepiness and improves psychomotor vigilance performance

STUDY OBJECTIVES: This study examined the effects of bright light exposure, as compared to dim light, on daytime subjective sleepiness, incidences of slow eye movements (SEMs), and psychomotor vigilance task (PVT) performance following 2 nights of sleep restriction. DESIGN: The study had a mixed factorial design with 2 independent variables: light condition (bright light, 1,000 lux; dim light, < 5 lux) and time of day. The dependent variables were subjective sleepiness, PVT performance, incidences of SEMs, and salivary melatonin levels. SETTING: Sleep research laboratory at Monash University. PARTICIPANTS: Sixteen healthy adults (10 women and 6 men) aged 18 to 35 years (mean age 25 years, 3 months). INTERVENTIONS: Following 2 nights of sleep restriction (5 hours each night), participants were exposed to modified constant routine conditions. Eight participants were exposed to bright light from noon until 5:00 pm. Outside the bright light exposure period (9:00 am to noon, 5:00 pm to 9:00 pm) light levels were maintained at less than 5 lux. A second group of 8 participants served as controls for the bright light exposure and were exposed to dim light throughout the entire protocol. MEASUREMENTS AND RESULTS: Bright light exposure reduced subjective sleepiness, decreased SEMs, and improved PVT performance compared to dim light. Bright lights had no effect on salivary melatonin. A significant positive correlation between PVT reaction times and subjective sleepiness was observed for both groups. Changes in SEMs did not correlate significantly with either subjective sleepiness or PVT performance. CONCLUSIONS: Daytime bright light exposure can reduce the impact of sleep loss on sleepiness levels and performance, as compared to dim light. These effects appear to be mediated by mechanisms that are separate from melatonin suppression. The results may assist in the development of treatments for daytime sleepiness.     

Nighttime dim light exposure alters the responses of the circadian system

The daily light dark cycle is the most salient entraining factor for the circadian system. However, in modern society, darkness at night is vanishing as light pollution steadily increases. The impact of brighter nights on wild life ecology and human physiology is just now being recognized. In the present study, we tested the possible detrimental effects of dim light exposure on the regulation of circadian rhythms, using CD1 mice housed in light/dim light (LdimL, 300 lux:20 lux) or light/dark (LD, 300 lux:1 lux) conditions. We first examined the expression of clock genes in the suprachiasmatic nucleus (SCN), the locus of the principal brain clock, in the animals of the LD and LdimL groups. Under the entrained condition, there was no difference in PER1 peak expression between the two groups, but at the trough of the PER 1 rhythm, there was an increase in PER1 in the LdimL group, indicating a decrease in the amplitude of the PER1 rhythm. After a brief light exposure (30 min, 300 lux) at night, the light-induced expression of mPer1 and mPer2 genes was attenuated in the SCN of LdimL group. Next, we examined the behavioral rhythms by monitoring wheel-running activity to determine whether the altered responses in the SCN of LdimL group have behavioral consequence. Compared to the LD controls, the LdimL group showed increased daytime activity. After being released into constant darkness, the LdimL group displayed shorter free-running periods. Furthermore, following the light exposure, the phase shifting responses were smaller in the LdimL group. The results indicate that nighttime dim light exposure can cause functional changes of the circadian system, and suggest that altered circadian function could be one of the mechanisms underlying the adverse effects of light pollution on wild life ecology and human physiology.     

Short nights reduce light-induced circadian phase delays in humans

STUDY OBJECTIVE: Short sleep episodes are common in modern society. We recently demonstrated that short nights reduce phase advances to light. Here we show that short nights also reduce phase delays to light. DESIGN: Two weeks of 6-hour sleep episodes in the dark (short nights) and 2 weeks of long 9-hour sleep episodes (long nights) in counterbalanced order, separated by 7 days. Following each series of nights, there was a dim-light phase assessment to assess baseline phase. Three days later, subjects were exposed to a phase-delaying light stimulus for 2 days, followed by a final phase assessment. SETTING: Subjects slept at home in dark bedrooms but came to the laboratory for the phase assessments and light stimulus. PARTICIPANTS: Seven young healthy subjects. INTERVENTIONS: The 3.5-hour light stimulus was four 30-minute pulses of bright light (-5000 lux) separated by 30-minute intervals of room light. The stimulus began 2.5 hours after each subject's dim-light melatonin onset, followed by a 6- or 9-hour sleep episode. On the second night, the bright light and sleep episode began 1 hour later. MEASUREMENTS AND RESULTS: The dim-light melatonin onset and dimlight melatonin offset phase delayed 1.4 and 0.7 hours less in the short nights, respectively (both p < or = .015). CONCLUSIONS: These results indicate for the first time that short nights can reduce circadian phase delays, that long nights can increase phase delays to light, or both. People who curtail their sleep may inadvertently reduce their circadian responsiveness to evening light.