Variation in photoperiod response corresponds to differences in circadian light sensitivity in northern and southern Nasonia vitripennis lines.

The circadian clock times physiological and behavioural processes and resets on a daily basis to synchronize with the environment. The involvement of the circadian clock in photoperiodic time measurement synchronising annual rhythms is still under debate and different models have been proposed explaining their integration. Insects overcome unfavourable conditions in diapause, a form of dormancy. A latitudinal cline in diapause induction in the parasitoid wasp Nasonia vitripennis as well as a difference in circadian light sensitivity between north and south provide us with additional evidence that the circadian system of Nasonia is involved in photoperiodic time measurement and that latitude-specific seasonality drives adaptive evolution in photoperiodism partly through adaptation responses in the circadian system. We tested diapause induction in a range of T-cycles and photoperiods and found diapause induction in short photoperiods in all T-cycles in the northern line but in the southern line, diapause only occurred in T-cycles close to 24 h. Due to a lower light sensitivity in the southern line, a wider distribution of phase angles of entrainment can be expected at a specific T-cycle duration, while the range of entrainment will decrease. Taking these oscillator properties into account, our data can be explained by an external coincidence model involving a single oscillator with a light-sensitive phase that drives annual timing of diapause in Nasonia vitripennis.

Melanopsin- and L-cone-induced pupil constriction is inhibited by S- and M-cones in humans.

The human retina contains five photoreceptor types: rods; short (S)-, mid (M)-, and long (L)-wavelength-sensitive cones; and melanopsin-expressing ganglion cells. Recently, it has been shown that selective increments in M-cone activation are paradoxically perceived as brightness decrements, as opposed to L-cone increments. Here we show that similar effects are also observed in the pupillary light response, whereby M-cone or S-cone increments lead to pupil dilation whereas L-cone or melanopic illuminance increments resulted in pupil constriction. Additionally, intermittent photoreceptor activation increased pupil constriction over a 30-min interval. Modulation of L-cone or melanopic illuminance within the 0.25-4-Hz frequency range resulted in more sustained pupillary constriction than light of constant intensity. Opposite results were found for S-cone and M-cone modulations (2 Hz), mirroring the dichotomy observed in the transient responses. The transient and sustained pupillary light responses therefore suggest that S- and M-cones provide inhibitory input to the pupillary control system when selectively activated, whereas L-cones and melanopsin response fulfill an excitatory role. These findings provide insight into functional networks in the human retina and the effect of color-coding in nonvisual responses to light, and imply that nonvisual and visual brightness discrimination may share a common pathway that starts in the retina.

Daytime melatonin and light independently affect human alertness and body temperature.

Light significantly improves alertness during the night (Cajochen, Sleep Med Rev, 11, 2007 and 453; Ruger et al., AJP Regul Integr Comp Physiol, 290, 2005 and R1413), but results are less conclusive at daytime (Lok et al., J Biol Rhythms, 33, 2018 and 589). Melatonin and core body temperature levels at those times of day may contribute to differences in alerting effects of light. In this experiment, the combined effect of daytime exogenous melatonin administration and light intensity on alertness, body temperature, and skin temperature was studied. The goal was to assess whether (a) alerting effects of light are melatonin dependent, (b) soporific effects of melatonin are mediated via the thermoregulatory system, and (c) light can improve alertness after melatonin-induced sleepiness during daytime. 10 subjects (5 females, 5 males) received melatonin (5 mg) in dim (10 lux) and, on a separate occasion, in bright polychromatic white light (2000 lux). In addition, they received placebo both under dim and bright light conditions. Subjects participated in all four conditions in a balanced order, yielding a balanced within-subject design, lasting from noon to 04:00 pm. Alertness and performance were assessed half hourly, while body temperature and skin temperature were measured continuously. Saliva samples to detect melatonin concentrations were collected half hourly. Melatonin administration increased melatonin concentrations in all subjects. Subjective sleepiness and distal skin temperature increased after melatonin ingestion. Bright light exposure after melatonin administration did not change subjective alertness scores, but body temperature and proximal skin temperature increased, while distal skin temperature decreased. Light exposure did not significantly affect these parameters in the placebo condition. These results indicate that (a) exogenous melatonin administration during daytime increases subjective sleepiness, confirming a role for melatonin in sleepiness regulation, (b) bright light exposure after melatonin ingestion significantly affected thermoregulatory parameters without altering subjective sleepiness, therefore temperature changes seem nonessential for melatonin-induced sleepiness, (c) subjective sleepiness was increased by melatonin ingestion, but bright light administration was not able to improve melatonin-induced sleepiness feelings nor performance. Other (physiological) factors may therefore contribute to differences in alerting effects of light during daytime and nighttime.

Climate change relaxes the time constraints for late-born offspring in a long-distance migrant.

Animals in seasonal environments need to fit their annual-cycle stages, such as moult and migration, in a tight schedule. Climate change affects the phenology of organisms and causes advancements in timing of these annual-cycle stages but not necessarily at the same rates. For migratory birds, this can lead to more severe or more relaxed time constraints in the time from fledging to migration, depending on the relative shifts of the different stages. We tested how a shift in hatch date, which has advanced due to climate change, impacts the organization of the birds' whole annual cycle. We experimentally advanced and delayed the hatch date of pied flycatcher chicks in the field and then measured the timing of their annual-cycle stages in a controlled laboratory environment. Hatch date affected the timing of moult and pre-migratory fattening, but not migration. Early-born birds hence had a longer time to fatten up than late-born ones; the latter reduced their interval between onset of fattening and migration to be able to migrate at the same time as the early-born birds. This difference in time constraints for early- and late-born individuals may explain why early-born offspring have a higher probability to recruit as a breeding bird. Climate change-associated advancements of avian egg-lay dates, which in turn advances hatch dates, can thus reduce the negative fitness consequences of reproducing late, thereby reducing the selection for early egg-laying migratory birds.

Railway Suicide in The Netherlands Lower Than Expected.

Background: Increasing rail transportation requires appropriate railway suicide preventive measures. Aims: The investigation of trends in railway suicide during 2008-2018, a period in which preventive measures were taken by Dutch railway infrastructure manager ProRail. Methods: Generalized linear regression models for railway suicide were developed for the period 1970-2007 with general suicide rate, railway traffic intensity, and a combination of these variables as regressors. Subsequently, the best-fitting model was used to investigate trends in railway suicide after 2007 by comparing in retrospect observed values with the expected outcomes of the regression model. Results: An adequate regression model for railway suicide was obtained using both general suicide rate and railway traffic intensity as regressors. Based on this model, while national suicide mortality and railway traffic increased, a distinct relative decline in railway suicides was found from 2012 onward. Conclusions: This decline of railway suicides in the Netherlands may indicate that preventive measures taken by ProRail were effective and prevented around 85 railway suicides annually, a reduction of 30%.

Effects of artificial dawn on sleep inertia, skin temperature, and the awakening cortisol response.

The effect of artificial dawn during the last 30 min of sleep on subsequent dissipation of sleep inertia was investigated, including possible involvement of cortisol and thermoregulatory processes. Sixteen healthy subjects who reported difficulty with waking up participated in random order in a control and an artificial dawn night. Sleep inertia severity was measured by subjective ratings of sleepiness and activation, and by performance on an addition and a reaction time task measured at 1, 15, 30, 45, 60, and 90 min after waking up at habitual wake up time at workdays. At all intervals, saliva samples were collected for cortisol analysis. Sleep electroencephalogram was recorded during the 30 min prior to waking up; core body temperature and skin temperatures were recorded continuously until 90 min after waking up. Subjective sleepiness was significantly decreased and subjective activation increased after waking up in the artificial dawn condition as compared with control, in which lights were turned on at waking up. These effects can be explained by effects of artificial dawn on skin temperature and amount of wakefulness during the 30 min prior to the alarm. Artificial dawn accelerated the decline in skin temperature and in the distal-to-proximal skin temperature gradient after getting up. No significant effects of artificial dawn on performance, core body temperature, and cortisol were found. These results suggest that the physiology underlying the positive effects of artificial dawn on the dissipation of sleep inertia involves light sleep and an accelerated skin temperature decline after awakening.

The progression of circadian phase during light exposure in animals and humans.

Studies in humans and mice revealed that circadian phase shifting effects of light are larger at the beginning of a light exposure interval than during subsequent exposure. Little is known about the dynamics of this response reduction phenomenon. Here the authors propose a method to obtain information on the progression of phase during light exposure. Phase response curves to intervals of light exposure over a wide range in duration are available for flesh flies, mice, and humans. By comparing the phase shifts induced by pulses of various durations but starting at the same circadian phase, the progression of phase during a long interval (hours) of light exposure is reconstructed for each of these 3 species. For flies, the phase progression curves show that light pulses-if long enough- eventually make the pacemaker stabilize around InT18 (near subjective dusk), as is typical for strong resetting. The progression of phase toward the final value never shows advances larger than 7 h, while delays can be as large as 18 h. By applying the phase progression curve method presented in this study, differences between advances and delays in type-0 phase response curves can be distinguished clearly. In flesh flies (Sarcophaga) this bifurcation between delays and advance occurs when light exposure starts at InT0 (subjective midnight). The present study confirms earlier findings in mice showing that the beginning of the light pulse generates stronger phase shifts than subsequent hours of light. Response reduction is complete within 1 h of exposure. It is argued that the variation is not so much due to light adaptation processes, but rather to response saturation. In contrast to light adaptation, response saturation is fundamental to proper functioning of the circadian pacemaker during natural entrainment. For understanding entrainment of the pacemaker to natural light, phase progression curves in which naturalistic light profiles are applied could be an important tool.

Evidence for differential human slow-wave activity regulation across the brain.

The regulation of the timing of sleep is thought to be linked to the temporal dynamics of slow-wave activity [SWA, electroencephalogram (EEG) spectral power in the approximately 0.75-4.5 Hz range] in the cortical non-rapid eye movement (NREM) sleep EEG. In the two-process model of sleep regulation, SWA was used as a direct indication of sleep debt, or Process S. Originally, estimation of the latter was performed in a gross way, by measuring average SWA across NREM-REM sleep cycles, fitting an exponential curve to the values thus obtained and estimating its time constant. In later studies, SWA was assumed to be proportional to the instantaneous decay rate of Process S, rather than taken as a direct reflection of S. Following up on this, we extended the existing model of SWA dynamics in which the effects of intrusions of REM sleep and wakefulness were incorporated. For each subject, a 'gain constant' can be estimated that quantifies the efficiency of SWA in dissipating S. As the course of SWA is variable across cortical locations, local differences are likely to exist in the rate of discharge of S, eventually leading to different levels of S in different cortical regions. In this study, we estimate the extent of local differences of SWA regulation on the basis of the extended model of SWA dynamics, for 26 locations on the scalp. We observed higher efficiency of SWA in dissipation of S in frontal EEG derivations, suggesting that SWA regulation has a clear local aspect. This result further suggests that the process involved in (local) SWA regulation cannot be identical to the Process S involved (with Process C) in effectual determination of sleep timing - a single behaviour that cannot vary between locations on the scalp. We therefore propose to distinguish these two representations and characterize the former, purely SWA-related, as 'Process Z', which then is different for different locations on the scalp. To demonstrate those differences, we compare the gain constants derived for the medial EEG derivations (Fz, Cz, Pz, Oz) with each other and with the decay rate derived from SWA values per NREM-REM sleep cycle.

Emergence of circadian and photoperiodic system level properties from interactions among pacemaker cells.

Daily patterns of behavior and physiology in animals in temperate zones often differ substantially between summer and winter. In mammals, this may be a direct consequence of seasonal changes of activity of the suprachiasmatic nucleus (SCN). The purpose of this study was to understand such variation on the basis of the interaction between pacemaker neurons. Computer simulation demonstrates that mutual electrical activation between pacemaker cells in the SCN, in combination with cellular electrical activation by light, is sufficient to explain a variety of circadian phenomena including seasonal changes. These phenomena are: self-excitation, that is, spontaneous development of circadian rhythmicity in the absence of a light-dark cycle; persistent rhythmicity in constant darkness, and loss of circadian rhythmicity in pacemaker output in constant light; entrainment to light-dark cycles; aftereffects of zeitgeber cycles with different periods; adjustment of the circadian patterns to day length; generation of realistic phase response curves to light pulses; and relative independence from day-to-day variation in light intensity. In the model, subsets of cells turn out to be active at specific times of day. This is of functional importance for the exploitation of the SCN to tune specific behavior to specific times of day. Thus, a network of on-off oscillators provides a simple and plausible construct that behaves as a clock with readout for time of day and simultaneously as a clock for all seasons.

Lifespan is unaffected by size and direction of daily phase shifts in Nasonia, a hymenopteran insect with strong circadian light resetting.

Most organisms have an endogenous circadian clock with a period length of approximately 24 h that enables adaptation, synchronization and anticipation to environmental cycles. The circadian system (circa = about or around, diem = a day) may provide evolutionary benefits when entrained to the 24-h light-dark cycle. The more the internal circadian period (τ) deviates from the external light-dark cycle, the larger the daily phase shifts need to be to synchronize to the environment. In some species, large daily phase shifts reduce survival rate. Here we tested this 'resonance fitness hypothesis' on the diurnal wasp Nasonia vitripennis, which exhibits a large latitudinal cline in free-running period with longer circadian period lengths in the north than in the south. Longevity was measured in northern and southern wasps placed into light-dark cycles (T-cycles) with periods ranging from 20 h to 28 h. Further, locomotor activity was recorded to estimate range and phase angle of entrainment under these various T-cycles. A light pulse induced phase response curve (PRC) was measured in both lines to understand entrainment results. We expected a concave survival curve with highest longevity at T = τ and a reduction in longevity the further τ deviates from T (τ/T<>1). Our results do not support this resonance fitness hypothesis. We did not observe a reduction in longevity when τ deviates from T. Our results may be understood by the strong circadian light resetting mechanism (type 0 PRC) to single light pulses that we measured in Nasonia, resulting in: (1) the broad range of entrainment, (2) the wide natural variation in circadian free-running period, and (3) the lack of reduced survival when τ/T ratio's deviates from 1. Together this indicates that circadian adaption to latitude may lead to changes in circadian period and light response, without negative influences on survival.

Light, Alertness, and Alerting Effects of White Light: A Literature Overview.

Light is known to elicit non-image-forming responses, such as effects on alertness. This has been reported especially during light exposure at night. Nighttime results might not be translatable to the day. This article aims to provide an overview of (1) neural mechanisms regulating alertness, (2) ways of measuring and quantifying alertness, and (3) the current literature specifically regarding effects of different intensities of white light on various measures and correlates of alertness during the daytime. In general, the present literature provides inconclusive results on alerting effects of the intensity of white light during daytime, particularly for objective measures and correlates of alertness. However, the various research paradigms employed in earlier studies differed substantially, and most studies tested only a limited set of lighting conditions. Therefore, the alerting potential of exposure to more intense white light should be investigated in a systematic, dose-dependent manner with multiple correlates of alertness and within one experimental paradigm over the course of day.

White Light During Daytime Does Not Improve Alertness in Well-rested Individuals.

Broad-spectrum light applied during the night has been shown to affect alertness in a dose-dependent manner. The goal of this experiment was to investigate whether a similar relationship could be established for light exposure during daytime. Fifty healthy participants were subjected to a paradigm (0730-1730 h) in which they were intermittently exposed to 1.5 h of dim light (<10 lux) and 1 h of experimental light (24-2000 lux). The same intensity of experimental light was used throughout the day, resulting in groups of 10 subjects per intensity. Alertness was assessed with subjective and multiple objective measures. A significant effect of time of day was found in all parameters of alertness ( p < 0.05). Significant dose-response relationships between light intensity and alertness during the day could be determined in a few of the parameters of alertness at some times of the day; however, none survived correction for multiple testing. We conclude that artificial light applied during daytime at intensities up to 2000 lux does not elicit significant improvements in alertness in non-sleep-deprived subjects.

Circadian control of the sleep-wake cycle.

It is beyond doubt that the timing of sleep is under control of the circadian pacemaker. Humans are a diurnal species; they sleep mostly at night, and they do so at approximately 24-h intervals. If they do not adhere to this general pattern, for instance when working night shifts or when travelling across time zones, they experience the stubborn influence of their circadian clock. In recent years much has been discovered about the organisation of the circadian clock. New photoreceptor cells in the retina have been found to influence the input to the clock, and much of the molecular machinery of the clock has been unravelled. It is now known that the circadian rhythm of sleep and wakefulness is only loosely coupled to the circadian rhythm of the pacemaker. New theories have been proposed for the functions of sleep and the sites at which those functions are executed. In spite of this rapid increase in knowledge of the circadian clock and of sleep regulatory processes, much remains to be discovered concerning the precise interaction between the biological clock and sleep timing. This is particularly unfortunate in view of the 24-h demands of our society for 7 days a week. Too little is known about the negative consequences of the societal pressures on well-being and performance.

Plasticity in the Period of the Circadian Pacemaker Induced by Phase Dispersion of Its Constituent Cellular Clocks.

The mammalian circadian pacemaker is commonly thought to be a rigid oscillator that generates output under a variety of circumstances that differ only in phase, period, and/or amplitude. Yet the pacemaker is composed of many cells that each can respond to varying circumstances in different ways. Computer simulations demonstrate that networks of such pacemaker cells behave differently under a light-dark cycle compared with constant darkness. The differences demonstrate that the circadian pacemaker is plastic: The pacemaker shapes its properties in response to the circumstances. A consequence is that properties of a pacemaker under a light-dark cycle cannot be derived from studies of the same system in constant darkness. In this paper we show that the dispersion of phase in a network of coupled oscillators can influence ensemble period: For the considered type of coupling, it is demonstrated that the more synchronous the cells are, the longer is the ensemble period. This is consistent with various data sets obtained in mammals, and even with a data set from fruit flies, in which circadian variation in behavior is regulated in a distinctly differently way from that in mammals. We conclude that environmental circumstances such as photoperiod and exposure to light pulses in otherwise darkness modify the phase distribution of the network and, thereby, the period of the ensemble. Our study supports the view that such properties as circadian period are not solely determined by clock genes but are also determined by the genes that regulate the communication in cellular networks.

Daily Light Exposure Patterns Reveal Phase and Period of the Human Circadian Clock.

Light is the most potent time cue that synchronizes (entrains) the circadian pacemaker to the 24-h solar cycle. This entrainment process is an interplay between an individual's daily light perception and intrinsic pacemaker period under free-running conditions. Establishing individual estimates of circadian phase and period can be time-consuming. We show that circadian phase can be accurately predicted (SD = 1.1 h for dim light melatonin onset, DLMO) using 9 days of ambulatory light and activity data as an input to Kronauer's limit-cycle model for the human circadian system. This approach also yields an estimated circadian period of 24.2 h (SD = 0.2 h), with longer periods resulting in later DLMOs. A larger amount of daylight exposure resulted in an earlier DLMO. Individuals with a long circadian period also showed shorter intervals between DLMO and sleep timing. When a field-based estimation of tau can be validated under laboratory studies in a wide variety of individuals, the proposed methods may prove to be essential tools for individualized chronotherapy and light treatment for shift work and jetlag applications. These methods may improve our understanding of fundamental properties of human circadian rhythms under daily living conditions.

Linking Light Exposure and Subsequent Sleep: A Field Polysomnography Study in Humans.

Study objectives: To determine the effect of light exposure on subsequent sleep characteristics under ambulatory field conditions. Methods: Twenty healthy participants were fitted with ambulatory polysomnography (PSG) and wrist-actigraphs to assess light exposure, rest-activity, sleep quality, timing, and architecture. Laboratory salivary dim-light melatonin onset was analyzed to determine endogenous circadian phase. Results: Later circadian clock phase was associated with lower intensity (R2 = 0.34, χ2(1) = 7.19, p < .01), later light exposure (quadratic, controlling for daylength, R2 = 0.47, χ2(3) = 32.38, p < .0001), and to later sleep timing (R2 = 0.71, χ2(1) = 20.39, p < .0001). Those with later first exposure to more than 10 lux of light had more awakenings during subsequent sleep (controlled for daylength, R2 = 0.36, χ2(2) = 8.66, p < .05). Those with later light exposure subsequently had a shorter latency to first rapid eye movement (REM) sleep episode (R2 = 0.21, χ2(1) = 5.77, p < .05). Those with less light exposure subsequently had a higher percentage of REM sleep (R2 = 0.43, χ2(2) = 13.90, p < .001) in a clock phase modulated manner. Slow-wave sleep accumulation was observed to be larger after preceding exposure to high maximal intensity and early first light exposure (p < .05). Conclusions: The quality and architecture of sleep is associated with preceding light exposure. We propose that light exposure timing and intensity do not only modulate circadian-driven aspects of sleep but also homeostatic sleep pressure. These novel ambulatory PSG findings are the first to highlight the direct relationship between light and subsequent sleep, combining knowledge of homeostatic and circadian regulation of sleep by light. Upon confirmation by interventional studies, this hypothesis could change current understanding of sleep regulation and its relationship to prior light exposure. Clinical trial details: This study was not a clinical trial. The study was ethically approved and nationally registered (NL48468.042.14).

Why and how do we model circadian rhythms?

In our attempts to understand the circadian system, we unavoidably rely on abstractions. Instead of describing the behavior of the circadian system in all its complexity, we try to derive basic features from which we form a global concept on how the system works. Such a basic concept is a model of reality. The author discusses why it is advantageous or even necessary to transform conceptual models into mathematical formulations. As examples to demonstrate those advantages, the author reviews 4 types of mathematical models: negative feedback models thought to operate within pacemaker cells, models on coupling between pacemaker cells to generate pacemaker output, oscillator models describing the behavior of the composite circadian pacemaker, and models describing how the circadian pacemaker influences behavior.

Nasal versus temporal illumination of the human retina: effects on core body temperature, melatonin, and circadian phase.

The mammalian retina contains both visual and circadian photoreceptors. In humans, nocturnal stimulation of the latter receptors leads to melatonin suppression, which might cause reduced nighttime sleepiness. Melatonin suppression is maximal when the nasal part of the retina is illuminated. Whether circadian phase shifting in humans is due to the same photoreceptors is not known. The authors explore whether phase shifts and melatonin suppression depend on the same retinal area. Twelve healthy subjects participated in a within-subjects design and received all of 3 light conditions--1) 10 lux of dim light on the whole retina, 2) 100 lux of ocular light on the nasal part of the retina, and 3) 100 lux of ocular light on the temporal part of the retina--on separate nights in random order. In all 3 conditions, pupils were dilated before and during light exposure. The protocol consisted of an adaptation night followed by a 23-h period of sustained wakefulness, during which a 4-h light pulse was presented at a time when maximal phase delays were expected. Nasal illumination resulted in an immediate suppression of melatonin but had no effect on subjective sleepiness or core body temperature (CBT). Nasal illumination delayed the subsequent melatonin rhythm by 78 min, which is significantly (p= 0.016) more than the delay drift in the dim-light condition (38 min), but had no detectable phase-shifting effect on the CBT rhythm. Temporal illumination suppressed melatonin less than the nasal illumination and had no effect on subjective sleepiness and CBT. Temporal illumination delayed neither the melatonin rhythm nor the CBT rhythm. The data show that the suppression of melatonin does not necessarily result in a reduction of subjective sleepiness and an elevation ofCBT. In addition, 100 lux of bright white light is strong enough to affect the photoreceptors responsible for the suppression of melatonin but not strong enough to have a significant effect on sleepiness and CBT. This may be due to the larger variability of the latter variables.

Short Blue Light Pulses (30 Min) in the Morning Support a Sleep-Advancing Protocol in a Home Setting.

Many people in our modern civilized society sleep later on free days compared to work days. This discrepancy in sleep timing will lead to so-called 'social jetlag' on work days with negative consequences for performance and health. Light therapy in the morning is often proposed as the most effective method to advance the circadian rhythm and sleep phase. However, most studies focus on direct effects on the circadian system and not on posttreatment effects on sleep phase and sleep integrity. In this placebo-controlled home study we investigated if blue light, rather than amber light therapy, can phase shift the sleep phase along with the circadian rhythm with preservation of sleep integrity and performance. We selected 42 participants who suffered from 'social jetlag' on workdays. Participants were randomly assigned to either high-intensity blue light exposure or amber light exposure (placebo) with similar photopic illuminance. The protocol consisted of 14 baseline days without sleep restrictions, 9 treatment days with either 30-min blue light pulses or 30-min amber light pulses in the morning along with a sleep advancing scheme and 7 posttreatment days without sleep restrictions. Melatonin samples were taken at days 1, 7, 14 (baseline), day 23 (effect treatment), and day 30 (posttreatment). Light exposure was recorded continuously. Sleep was monitored through actigraphy. Performance was measured with a reaction time task. As expected, the phase advance of the melatonin rhythm from day 14 to day 23 was significantly larger in the blue light exposure group, compared to the amber light group (84 min ± 51 (SD) and 48 min ± 47 (SD) respectively; t36 = 2.23, p < 0.05). Wake-up time during the posttreatment days was slightly earlier compared to baseline in the blue light group compared to slightly later in the amber light group (-21 min ± 33 (SD) and +12 min ± 33 (SD) respectively; F1,35 = 9.20, p < 0.01). The number of sleep bouts was significantly higher in the amber light group compared to the blue light group during sleep in the treatment period (F1,32 = 4.40, p < 0.05). Performance was significantly worse compared to baseline at all times during (F1,13 = 10.1, p < 0.01) and after amber light treatment (F1,13 = 17.1, p < 0.01), while only in the morning during posttreatment in the blue light condition (F1,10 = 9.8, p < 0.05). The data support the conclusion that blue light was able to compensate for the sleep integrity reduction and to a large extent for the performance decrement that was observed in the amber light condition, both probably as a consequence of the advancing sleep schedule. This study shows that blue light therapy in the morning, applied in a home setting, supports a sleep advancing protocol by phase advancing the circadian rhythm as well as sleep timing.

Comparison of the Munich Chronotype Questionnaire with the Horne-Ostberg's Morningness-Eveningness Score.

We report on results from an Internet survey of sleeping habits in a Dutch population using the Munich Chronotype Questionnaire (MCTQ), supplemented with the Horne-Ostberg Morningness-Eveningness Questionnaire (MEQ). The MCTQ was completed by 5,055 responders, of which 2,481 also completed the MEQ. MEQ score correlated well with the MCTQ assessment of time of mid-sleep on free days (MSF; r = - 0.73) and on workdays (MSW; r = - 0.61). MEQ was more strongly correlated with MSF (50% of sleep time) than with sleep onset (0%), rise time (100%), or with any other percentile (10 to 40, 60% to 90%) of sleep on free days. The study shows that chronotype (based on MSF as measured by the MCTQ) strongly correlates with morningness-eveningness (as measured by the MEQ). However, the MCTQ collects additional detailed information on sleep-wake behavior under natural conditions.