156 Evening Light-Induced Circadian Phase Shift in Preschool-Aged Children

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A63-A64
Author(s):  
Lauren Hartstein ◽  
Lameese Akacem ◽  
Cecilia Diniz Behn ◽  
Shelby Stowe ◽  
Kenneth Wright ◽  
...  

Abstract Introduction In adults, exposure to light at night delays the timing of the circadian clock in a dose-dependent manner with intensity. Although children’s melatonin levels are highly suppressed by evening bright light, the sensitivity of young children’s circadian timing to evening light is unknown. This research aimed to establish an illuminance response curve for phase delay in preschool children as a result of exposure to varying light intensities in the hour before bedtime. Methods Healthy children (n=36, 3.0 – 4.9 years, 39% males), participated in a 10-day protocol. For 7 days, children followed a strict parent-selected sleep schedule. On Days 8-10, an in-home dim-light assessment was performed. On Day 8, dim light melatonin onset (DLMO) was measured through saliva samples collected in 20-30-min intervals throughout the evening until 1-h past habitual bedtime. On Day 9, children were exposed to a white light stimulus (semi-randomly assigned from 5lx to 5000lx) for 1-h before their habitual bedtime, and saliva was collected before, during, and after the exposure. On Day 10, children provided saliva samples in the evening for 2.5-h past bedtime for a final DLMO assessment. Phase angle of entrainment (habitual bedtime – DLMObaseline) and circadian phase delay (DLMOfinal – DLMObaseline) were computed. Results Final DLMO (Day 10) shifted between -8 and 123 minutes (M = 56.1 +/- 33.6 min; negative value = phase advance, positive value = phase delay) compared with DLMO at baseline (Day 8). Raw phase shift did not demonstrate a dose-dependent relationship with light intensity. Rather, we observed a robust phase delay across all intensities. Conclusion These data suggest preschoolers’ circadian clocks are immensely sensitive to a large range of light intensities, which may be mechanistically influenced by less mature ophthalmologic features (e.g. clearer lenses, larger pupils). With young children’s ever-growing use of light-emitting devices and evening exposure to artificial lighting, as well as the prevalence of behavioral sleep problems, these findings may inform recommendations for parents on the effects of evening light exposure on sleep timing in early childhood. Support (if any) This research was supported with funds from the Eunice Kennedy Shriver National Institute of Child Health & Human Development (R01-HD087707).

2000 ◽  
Vol 278 (2) ◽  
pp. R373-R382 ◽  
Author(s):  
Orfeu M. Buxton ◽  
Mireille L'Hermite-Balériaux ◽  
Fred W. Turek ◽  
Eve van Cauter

To systematically determine the effects of daytime exposure to sleep in darkness on human circadian phase, four groups of subjects participated in 4-day studies involving either no nap (control), a morning nap (0900–1500), an afternoon nap (1400–2000), or an evening nap (1900–0100) in darkness. Except during the scheduled sleep/dark periods, subjects remained awake under constant conditions, i.e., constant dim light exposure (36 lx), recumbence, and caloric intake. Blood samples were collected at 20-min intervals for 64 h to determine the onsets of nocturnal melatonin and thyrotropin secretion as markers of circadian phase before and after stimulus exposure. Sleep was polygraphically recorded. Exposure to sleep and darkness in the morning resulted in phase delays, whereas exposure in the evening resulted in phase advances relative to controls. Afternoon naps did not change circadian phase. These findings indicate that human circadian phase is dependent on the timing of darkness and/or sleep exposure and that strategies to treat circadian misalignment should consider not only the timing and intensity of light, but also the timing of darkness and/or sleep.


2018 ◽  
Vol 33 (6) ◽  
pp. 637-648 ◽  
Author(s):  
Renske Lok ◽  
Tom Woelders ◽  
Marijke C. M. Gordijn ◽  
Roelof A. Hut ◽  
Domien G. M. Beersma

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.


2004 ◽  
Vol 287 (1) ◽  
pp. E174-E181 ◽  
Author(s):  
Claude Gronfier ◽  
Kenneth P. Wright ◽  
Richard E. Kronauer ◽  
Megan E. Jewett ◽  
Charles A. Czeisler

It has been shown in animal studies that exposure to brief pulses of bright light can phase shift the circadian pacemaker and that the resetting action of light is most efficient during the first minutes of light exposure. In humans, multiple consecutive days of exposure to brief bright light pulses have been shown to phase shift the circadian pacemaker. The aim of the present study was to determine whether a single sequence of brief bright light pulses administered during the early biological night would phase delay the human circadian pacemaker. Twenty-one healthy young subjects underwent a 6.5-h light exposure session in one of three randomly assigned conditions: 1) continuous bright light of ∼9,500 lux, 2) intermittent bright light (six 15-min bright light pulses of ∼9,500 lux separated by 60 min of very dim light of <1 lux), and 3) continuous very dim light of <1 lux. Twenty subjects were included in the analysis. Core body temperature (CBT) and melatonin were used as phase markers of the circadian pacemaker. Phase delays of CBT and melatonin rhythms in response to intermittent bright light pulses were comparable to those measured after continuous bright light exposure, even though the total exposure to the intermittent bright light represented only 23% of the 6.5-h continuous exposure. These results demonstrate that a single sequence of intermittent bright light pulses can phase delay the human circadian pacemaker and show that intermittent pulses have a greater resetting efficacy on a per minute basis than does continuous exposure.


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A45-A46
Author(s):  
Skyler Kanegi ◽  
Armen Akopian

Abstract Introduction The combination of artificial light and lack of exposure to natural light can delay the circadian clock, dysregulate the circadian cycle, and decrease alertness upon waking. This effect has been especially significant during the COVID-19 pandemic, where overexposure to artificial light at improper hours has contributed to increased rates of clinical insomnia. Artificial light may also contribute to concomitant neurological conditions such as primary headache, but the mechanisms by which light triggers sleep deprivation-induced headache are not well-understood. Methods To measure pain sensitivity, we habituated 13 wild-type male mice to von Frey filaments applied to the periorbital area until there was no response to 0.6g stimulus. We then applied 5 lux of continuous dim light to mice during their usual 12-hour dark cycle. The 12-hour light cycle remained unchanged with 200 lux continuous light. Three groups of mice experienced the dim light stimulus for one, three, or five consecutive days. Ambulation and rest activity were measured using SOF-812 Activity Monitor machines. After the experiment concluded, we waited 24 hours and measured mechanical threshold using von Frey filaments at 1, 3, 5, 8, and every 3 days subsequently until mice no longer responded to 0.6g stimulus. Results Artificial light triggered changes in circadian behavior including increased number of rest periods during 12-hour dark (dim light) cycle and shortened sleep duration during 12-hour light cycle. Following the artificial light stimulus, there was a significant decrease in mechanical threshold (P&lt;0.05), representing allodynia. The one-day group displayed one day of significant allodynia. The three-day group displayed three days of significant allodynia. The five-day group displayed five days of significant allodynia. Conclusion Artificial light may trigger circadian dysregulation, and the duration of artificial light exposure seemed to be directly correlated to the duration of allodynia up to one week after the stimulus was removed. We will repeat these experiments and analyze CNS and PNS tissue samples to understand the underlying physiological and biochemical bases of how artificial light triggers sleep deprivation-induced headache. This knowledge could increase our understanding of the pathophysiology and comorbidity of sleep deprivation and headache. Support (if any) Funding was received from the National Institute of Health (NS104200).


2018 ◽  
Vol 33 (6) ◽  
pp. 589-601 ◽  
Author(s):  
Renske Lok ◽  
Karin C. H. J. Smolders ◽  
Domien G. M. Beersma ◽  
Yvonne A. W. de Kort

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.


2016 ◽  
Vol 48 ◽  
pp. 442
Author(s):  
Kimberly A. Volterman ◽  
Daniel R. Moore ◽  
Peter Breithaupt ◽  
Elizabeth Offord-Cavin ◽  
Leonidas G. Karagounis ◽  
...  

1993 ◽  
Vol 8 (3) ◽  
pp. 233-245 ◽  
Author(s):  
Wade S. Warren ◽  
Donald B. Hodges ◽  
Vincent M. Cassone

1997 ◽  
Vol 272 (2) ◽  
pp. R482-R486 ◽  
Author(s):  
A. Cagnacci ◽  
R. Soldani ◽  
S. S. Yen

We investigated whether the contemporaneous administration of melatonin can modify circadian phase shifts induced by bright light stimuli. After a baseline evaluation, 10 women were exposed for three consecutive nights to a 4-h bright light stimulus (>3,000 lx) initiated at the time of the estimated core body temperature (BT(c)) nadir. Along with light, each woman orally received, randomly and in a double-blind fashion, placebo (n = 5) or melatonin (n = 5; 1 mg 30 min before and 0.75 mg 120 min after the start of light exposure). Daily rhythms were reevaluated at the end of treatment. Bright light phase advanced, by about 90-120 min, BT(c) (P < 0.01), cortisol (P < 0.05), and melatonin (P < 0.01) rhythms. Contemporaneous administration of melatonin antagonized the phase advances of the cortisol and BT(c) rhythms, as well as the melatonin peak and melatonin offset. The phase advance of the melatonin onset was instead enhanced (P < 0.05). Contemporaneous melatonin administration modifies the capability of light to induce circadian phase shifts.


1997 ◽  
Vol 273 (5) ◽  
pp. R1800-R1809 ◽  
Author(s):  
Megan E. Jewett ◽  
David W. Rimmer ◽  
Jeanne F. Duffy ◽  
Elizabeth B. Klerman ◽  
Richard E. Kronauer ◽  
...  

Fifty-six resetting trials were conducted across the subjective day in 43 young men using a three-cycle bright-light (∼10,000 lx) stimulus against a background of very dim light (10–15 lx). The phase-response curve (PRC) to these trials was assessed for the presence of a “dead zone” of photic insensitivity and was compared with another three-cycle PRC that had used a background of ∼150 lx. To assess possible transients after the light stimulus, the trials were divided into 43 steady-state trials, which occurred after several baseline days, and 13 consecutive trials, which occurred immediately after a previous resetting trial. We found that 1) bright light induces phase shifts throughout subjective day with no apparent dead zone; 2) there is no evidence of transients in constant routine assessments of the fitted temperature minimum 1–2 days after completion of the resetting stimulus; and 3) the timing of background room light modulates the resetting response to bright light. These data indicate that the human circadian pacemaker is sensitive to light at virtually all circadian phases, implying that the entire 24-h pattern of light exposure contributes to entrainment.


2019 ◽  
Author(s):  
Daniel S. Joyce ◽  
Manuel Spitschan ◽  
Jamie M. Zeitzer

AbstractThe human circadian system is exquisitely sensitive to light, through a pathway connecting the melanopsin-expressing intrinsically photosensitive retinal ganglion cells (ipRGCs) to the hypothalamic suprachiasmatic nuclei (SCN). ipRGCs are characterised by a delayed off-time following cessation of light exposure; we exploited this unusual physiologic property and examined how a sequence of flashes of bright light differing in intensity or duration presented in the biological night could delay the human circadian clock in vivo in healthy young participants (n=54). To understand the mechanism underlying circadian photoreception, we probed temporal integration by manipulating flash intensity and duration independently. In a 34-hour in-laboratory between-subjects design, we examined variable-intensity (3, 30, 95, 300, 950, 3000, or 9500 photopic lux; n=28 participants) flashes at fixed duration (2 ms), and variable-duration (10 μs, 100 μs, 1 ms, 10 ms, 100 ms, 1 sec, 10 sec) flashes at fixed intensity (2000 photopic lux; n=31 participants). We measured the phase shift of dim-light melatonin onset on the subsequent evening, and acute melatonin suppression and alertness during the flash sequence. In the variable-intensity study, we find a clear sigmoidal dose-response relationship for flash intensity and the induced circadian phase shift. In the variable-duration study, we find no parametric relationship between flash duration and induced circadian phase shift, indicating a relative insensitivity of the circadian system to flashes varying in duration. As the intermittent periods of darkness in our stimulation paradigm supports the recovery of extrinsic rod-cone signalling into the ipRGCs, our results strongly suggest rod-cone contributions into circadian photoreception.


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