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Boivin, D. B., Boudreau, P., James, F. O., & Kin, N. M. K. N. Y. (2012). Photic resetting in night-shift work: impact on nurses' sleep. Chronobiol Int, 29(5), 619–628.
Abstract: The objective of this study was to quantify daytime sleep in night-shift workers with and without an intervention designed to recover the normal relationship between the endogenous circadian pacemaker and the sleep/wake cycle. Workers of the treatment group received intermittent exposure to full-spectrum bright light during night shifts and wore dark goggles during the morning commute home. All workers maintained stable 8-h daytime sleep/darkness schedules. The authors found that workers of the treatment group had daytime sleep episodes that lasted 7.1 +/- .1 h (mean +/- SEM) versus 6.6 +/- .2 h for workers in the control group (p = .04). The increase in total sleep time co-occurred with a larger proportion of the melatonin secretory episode during daytime sleep in workers of the treatment group. The results of this study showed reestablishment of a phase angle that is comparable to that observed on a day-oriented schedule favors longer daytime sleep episodes in night-shift workers. (Author correspondence: diane.boivin@douglas.mcgill.ca ).
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Boivin, D. B., Boudreau, P., & Tremblay, G. M. (2012). Phototherapy and orange-tinted goggles for night-shift adaptation of police officers on patrol. Chronobiol Int, 29(5), 629–640.
Abstract: The aim of the present combined field and laboratory study was to assess circadian entrainment in two groups of police officers working seven consecutive 8/8.5-h night shifts as part of a rotating schedule. Eight full-time police officers on patrol (mean age +/- SD: 29.8 +/- 6.5 yrs) were provided an intervention consisting of intermittent exposure to wide-spectrum bright light at night, orange-tinted goggles at sunrise, and maintenance of a regular sleep/darkness episode in the day. Orange-tinted goggles have been shown to block the melatonin-suppressing effect of light significantly more than neutral gray density goggles. Nine control group police officers (mean age +/- SD: 30.3 +/- 4.1 yrs) working the same schedule were enrolled. Police officers were studied before, after (in the laboratory), and during (ambulatory) a series of seven consecutive nights. Urine samples were collected at wake time and bedtime throughout the week of night work and during laboratory visits (1 x /3 h) preceding and following the work week to measure urinary 6-sulfatoxymelatonin (UaMT6s) excretion rate. Subjective alertness was assessed at the start, middle, and end of night shifts. A 10-min psychomotor vigilance task was performed at the start and end of each shift. Both laboratory visits consisted of two 8-h sleep episodes based on the prior schedule. Saliva samples were collected 2 x /h during waking episodes to assay their melatonin content. Subjective alertness (3 x /h) and performance (1 x /2 h) were assessed during wake periods in the laboratory. A mixed linear model was used to analyze the progression of UaMt6s excreted during daytime sleep episodes at home, as well as psychomotor performance and subjective alertness during night shifts. Two-way analysis of variance (ANOVA) (factors: laboratory visit and group) were used to compare peak salivary melatonin and UaMT6s excretion rate in the laboratory. In both groups of police officers, the excretion rate of UaMT6s at home was higher during daytime sleep episodes at the end compared to the start of the work week (p < .001). This rate increased significantly more in the intervention than control group (p = .032). A significant phase delay of salivary melatonin was observed in both groups at the end of study (p = .009), although no significant between-group difference was reached. Reaction speed dropped, and subjective alertness decreased throughout the night shift in both groups (p < .001). Reaction speed decreased throughout the work week in the control group (p </= .021), whereas no difference was observed in the intervention group. Median reaction time was increased as of the 5th and 6th nights compared to the 2nd night in controls (p </= .003), whereas it remained stable in the intervention group. These observations indicate better physiological adaptation in the intervention group compared to the controls.
Keywords: Human Health; Adaptation, Physiological/*physiology; Adult; Attention/physiology; Circadian Rhythm/physiology; Color; Darkness; *Eye Protective Devices/adverse effects; Female; Humans; Light; Male; Melatonin/analogs & derivatives/metabolism/urine; Phototherapy/*adverse effects; *Police; Psychomotor Performance/*physiology; Saliva/chemistry; Sleep/physiology; Work Schedule Tolerance/*physiology
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Boivin, D. B., Duffy, J. F., Kronauer, R. E., & Czeisler, C. A. (1996). Dose-response relationships for resetting of human circadian clock by light. Nature, 379(6565), 540–542.
Abstract: Since the first report in unicells, studies across diverse species have demonstrated that light is a powerful synchronizer which resets, in an intensity-dependent manner, endogenous circadian pacemakers. Although it is recognized that bright light (approximately 7,000 to 13,000 lux) is an effective circadian synchronizer in humans, it is widely believed that the human circadian pacemaker is insensitive to ordinary indoor illumination (approximately 50-300 lux). It has been proposed that the relationship between the resetting effect of light and its intensity follows a compressive nonlinear function, such that exposure to lower illuminances still exerts a robust effect. We therefore undertook a series of experiments which support this hypothesis and report here that light of even relatively low intensity (approximately 180 lux) significantly phase-shifts the human circadian pacemaker. Our results clearly demonstrate that humans are much more sensitive to light than initially suspected and support the conclusion that they are not qualitatively different from other mammals in their mechanism of circadian entrainment.
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Bonmati-Carrion, M., Arguelles-Prieto, R., Martinez-Madrid, M., Reiter, R., Hardeland, R., Rol, M., et al. (2014). Protecting the Melatonin Rhythm through Circadian Healthy Light Exposure. IJMS, 15(12), 23448–23500.
Abstract: Currently, in developed countries, nights are excessively illuminated (light at night), whereas daytime is mainly spent indoors, and thus people are exposed to much lower light intensities than under natural conditions. In spite of the positive impact of artificial light, we pay a price for the easy access to light during the night: disorganization of our circadian system or chronodisruption (CD), including perturbations in melatonin rhythm. Epidemiological studies show that CD is associated with an increased incidence of diabetes, obesity, heart disease, cognitive and affective impairment, premature aging and some types of cancer. Knowledge of retinal photoreceptors and the discovery of melanopsin in some ganglion cells demonstrate that light intensity, timing and spectrum must be considered to keep the biological clock properly entrained. Importantly, not all wavelengths of light are equally chronodisrupting. Blue light, which is particularly beneficial during the daytime, seems to be more disruptive at night, and induces the strongest melatonin inhibition. Nocturnal blue light exposure is currently increasing, due to the proliferation of energy-efficient lighting (LEDs) and electronic devices. Thus, the development of lighting systems that preserve the melatonin rhythm could reduce the health risks induced by chronodisruption. This review addresses the state of the art regarding the crosstalk between light and the circadian system.
Keywords: human health; chronodisruption; circadian; light at night (LAN); melanopsin; melatonin
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Borniger, J. C., Maurya, S. K., Periasamy, M., & Nelson, R. J. (2014). Acute dim light at night increases body mass, alters metabolism, and shifts core body temperature circadian rhythms. Chronobiol Int, 31(8), 917–925.
Abstract: The circadian system is primarily entrained by the ambient light environment and is fundamentally linked to metabolism. Mounting evidence suggests a causal relationship among aberrant light exposure, shift work, and metabolic disease. Previous research has demonstrated deleterious metabolic phenotypes elicited by chronic (>4 weeks) exposure to dim light at night (DLAN) ( approximately 5 lux). However, the metabolic effects of short-term (<2 weeks) exposure to DLAN are unspecified. We hypothesized that metabolic alterations would arise in response to just 2 weeks of DLAN. Specifically, we predicted that mice exposed to dim light would gain more body mass, alter whole body metabolism, and display altered body temperature (Tb) and activity rhythms compared to mice maintained in dark nights. Our data largely support these predictions; DLAN mice gained significantly more mass, reduced whole body energy expenditure, increased carbohydrate over fat oxidation, and altered temperature circadian rhythms. Importantly, these alterations occurred despite similar activity locomotor levels (and rhythms) and total food intake between groups. Peripheral clocks are potently entrained by body temperature rhythms, and the deregulation of body temperature we observed may contribute to metabolic problems due to “internal desynchrony” between the central circadian oscillator and temperature sensitive peripheral clocks. We conclude that even relatively short-term exposure to low levels of nighttime light can influence metabolism to increase mass gain.
Keywords: Animals; Body temperature; calorimetry; circadian; light at night; metabolism
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