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Arendt, J. (2012). Biological rhythms during residence in polar regions. Chronobiol Int, 29(4), 379–394.
Abstract: At Arctic and Antarctic latitudes, personnel are deprived of natural sunlight in winter and have continuous daylight in summer: light of sufficient intensity and suitable spectral composition is the main factor that maintains the 24-h period of human circadian rhythms. Thus, the status of the circadian system is of interest. Moreover, the relatively controlled artificial light conditions in winter are conducive to experimentation with different types of light treatment. The hormone melatonin and/or its metabolite 6-sulfatoxymelatonin (aMT6s) provide probably the best index of circadian (and seasonal) timing. A frequent observation has been a delay of the circadian system in winter. A skeleton photoperiod (2 x 1-h, bright white light, morning and evening) can restore summer timing. A single 1-h pulse of light in the morning may be sufficient. A few people desynchronize from the 24-h day (free-run) and show their intrinsic circadian period, usually >24 h. With regard to general health in polar regions, intermittent reports describe abnormalities in various physiological processes from the point of view of daily and seasonal rhythms, but positive health outcomes are also published. True winter depression (SAD) appears to be rare, although subsyndromal SAD is reported. Probably of most concern are the numerous reports of sleep problems. These have prompted investigations of the underlying mechanisms and treatment interventions. A delay of the circadian system with “normal” working hours implies sleep is attempted at a suboptimal phase. Decrements in sleep efficiency, latency, duration, and quality are also seen in winter. Increasing the intensity of ambient light exposure throughout the day advanced circadian phase and was associated with benefits for sleep: blue-enriched light was slightly more effective than standard white light. Effects on performance remain to be fully investigated. At 75 degrees S, base personnel adapt the circadian system to night work within a week, in contrast to temperate zones where complete adaptation rarely occurs. A similar situation occurs on high-latitude North Sea oil installations, especially when working 18:00-06:00 h. Lack of conflicting light exposure (and “social obligations”) is the probable explanation. Many have problems returning to day work, showing circadian desynchrony. Timed light treatment again has helped to restore normal phase/sleep in a small number of people. Postprandial response to meals is compromised during periods of desynchrony with evidence of insulin resistance and elevated triglycerides, risk factors for heart disease. Only small numbers of subjects have been studied intensively in polar regions; however, these observations suggest that suboptimal light conditions are deleterious to health. They apply equally to people living in temperate zones with insufficient light exposure.
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Dumont, M., & Beaulieu, C. (2007). Light exposure in the natural environment: relevance to mood and sleep disorders. Sleep Med, 8(6), 557–565.
Abstract: In addition to being necessary for vision, light also plays a primary role in circadian physiology. Humans are diurnal animals and their biological clock synchronizes their physiological functions in such a way that functions associated with activity happen in the daytime while functions associated with rest occur at night. A misalignment between the endogenous circadian clock and the desired sleep schedule is the main cause of circadian sleep disorders; it may be involved in certain mood disorders as well. Since light is the main environmental cue used by the biological clock to set its own timing in relation to the day-night cycle, inappropriate light exposure can be involved in the physiopathology of circadian disorders. Conversely, when handled properly, controlled light exposure can be used to treat some mood and sleep disorders. While the earliest studies in the field focused solely on exposure to bright light, contemporary studies aim at understanding how the entire profile of light-dark exposure can influence the circadian clock and, consequently, mood, sleep, and vigilance quality. Following a brief summary of the main concepts underlying the non-visual effects of light, this paper presents some studies using ambulatory measurements of light exposure to illustrate how these concepts apply in real-life situations and discusses the clinical relevance of light exposure in the natural environment for mood, sleep, and circadian disorders.
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Fonken, L. K., & Nelson, R. J. (2013). Dim light at night increases depressive-like responses in male C3H/HeNHsd mice. Behav Brain Res, 243, 74–78.
Abstract: Daily patterns of light exposure have become increasingly variable since the widespread adoption of electrical lighting during the 20th century. Seasonal fluctuations in light exposure, shift-work, and transmeridian travel are all associated with alterations in mood. These studies implicate fluctuations in environmental lighting in the development of depressive disorders. Here we argue that exposure to light at night (LAN) may be causally linked to depression. Male C3H/HeNHsd mice, which produce nocturnal melatonin, were housed in either a standard light/dark (LD) cycle or exposed to nightly dim (5 lux) LAN (dLAN). After four weeks in lighting conditions mice underwent behavioral testing and hippocampal tissue was collected at the termination of the study for qPCR. Here were report that mice exposed to dLAN increase depressive-like responses in both a sucrose anhedonia and forced swim test. In contrast to findings in diurnal grass rats, dLAN mice perform comparably to mice housed under dark nights in a hippocampus-dependent learning and memory task. TNFalpha and IL1beta gene expression do not differ between groups, demonstrating that changes in these pro-inflammatory cytokines do not mediate dLAN induced depressive-like responses in mice. BDNF expression is reduced in the hippocampus of mice exposed to dLAN. These results indicate that low levels of LAN can alter mood in mice. This study along with previous work implicates LAN as a potential factor contributing to depression. Further understanding of the mechanisms through which LAN contributes to changes in mood is important for characterizing and treating depressive disorders.
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LeGates, T. A., Altimus, C. M., Wang, H., Lee, H. - K., Yang, S., Zhao, H., et al. (2012). Aberrant light directly impairs mood and learning through melanopsin-expressing neurons. Nature, 491(7425), 594–598.
Abstract: The daily solar cycle allows organisms to synchronize their circadian rhythms and sleep-wake cycles to the correct temporal niche. Changes in day-length, shift-work, and transmeridian travel lead to mood alterations and cognitive function deficits. Sleep deprivation and circadian disruption underlie mood and cognitive disorders associated with irregular light schedules. Whether irregular light schedules directly affect mood and cognitive functions in the context of normal sleep and circadian rhythms remains unclear. Here we show, using an aberrant light cycle that neither changes the amount and architecture of sleep nor causes changes in the circadian timing system, that light directly regulates mood-related behaviours and cognitive functions in mice. Animals exposed to the aberrant light cycle maintain daily corticosterone rhythms, but the overall levels of corticosterone are increased. Despite normal circadian and sleep structures, these animals show increased depression-like behaviours and impaired hippocampal long-term potentiation and learning. Administration of the antidepressant drugs fluoxetine or desipramine restores learning in mice exposed to the aberrant light cycle, suggesting that the mood deficit precedes the learning impairments. To determine the retinal circuits underlying this impairment of mood and learning, we examined the behavioural consequences of this light cycle in animals that lack intrinsically photosensitive retinal ganglion cells. In these animals, the aberrant light cycle does not impair mood and learning, despite the presence of the conventional retinal ganglion cells and the ability of these animals to detect light for image formation. These findings demonstrate the ability of light to influence cognitive and mood functions directly through intrinsically photosensitive retinal ganglion cells.
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Sharkey, K. M., Carskadon, M. A., Figueiro, M. G., Zhu, Y., & Rea, M. S. (2011). Effects of an advanced sleep schedule and morning short wavelength light exposure on circadian phase in young adults with late sleep schedules. Sleep Med, 12(7), 685–692.
Abstract: OBJECTIVE: We examined the effects of an advanced sleep/wake schedule and morning short wavelength (blue) light in 25 adults (mean age+/-SD=21.8+/-3 years; 13 women) with late sleep schedules and subclinical features of delayed sleep phase disorder (DSPD). METHODS: After a baseline week, participants kept individualized, fixed, advanced 7.5-h sleep schedules for 6days. Participants were randomly assigned to groups to receive “blue” (470nm, approximately 225lux, n=12) or “dim” (<1lux, n=13) light for 1h after waking each day. Head-worn “Daysimeters” measured light exposure; actigraphs and sleep diaries confirmed schedule compliance. Salivary dim light melatonin onset (DLMO), self-reported sleep, and mood were examined with 2x2 ANOVA. RESULTS: After 6days, both groups showed significant circadian phase advances, but morning blue light was not associated with larger phase shifts than dim-light exposure. The average DLMO advances (mean+/-SD) were 1.5+/-1.1h in the dim light group and 1.4+/-0.7h in the blue light group. CONCLUSIONS: Adherence to a fixed advanced sleep/wake schedule resulted in significant circadian phase shifts in young adults with subclinical DSPD with or without morning blue light exposure. Light/dark exposures associated with fixed early sleep schedules are sufficient to advance circadian phase in young adults.
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