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      Effects of light on human circadian rhythms, sleep and mood

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          Abstract

          Humans live in a 24-hour environment, in which light and darkness follow a diurnal pattern. Our circadian pacemaker, the suprachiasmatic nuclei (SCN) in the hypothalamus, is entrained to the 24-hour solar day via a pathway from the retina and synchronises our internal biological rhythms. Rhythmic variations in ambient illumination impact behaviours such as rest during sleep and activity during wakefulness as well as their underlying biological processes. Rather recently, the availability of artificial light has substantially changed the light environment, especially during evening and night hours. This may increase the risk of developing circadian rhythm sleep–wake disorders (CRSWD), which are often caused by a misalignment of endogenous circadian rhythms and external light–dark cycles. While the exact relationship between the availability of artificial light and CRSWD remains to be established, nocturnal light has been shown to alter circadian rhythms and sleep in humans. On the other hand, light can also be used as an effective and noninvasive therapeutic option with little to no side effects, to improve sleep,mood and general well-being. This article reviews our current state of knowledge regarding the effects of light on circadian rhythms, sleep, and mood.

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          Most cited references87

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          Melanopsin-expressing ganglion cells in primate retina signal colour and irradiance and project to the LGN.

          Human vision starts with the activation of rod photoreceptors in dim light and short (S)-, medium (M)-, and long (L)- wavelength-sensitive cone photoreceptors in daylight. Recently a parallel, non-rod, non-cone photoreceptive pathway, arising from a population of retinal ganglion cells, was discovered in nocturnal rodents. These ganglion cells express the putative photopigment melanopsin and by signalling gross changes in light intensity serve the subconscious, 'non-image-forming' functions of circadian photoentrainment and pupil constriction. Here we show an anatomically distinct population of 'giant', melanopsin-expressing ganglion cells in the primate retina that, in addition to being intrinsically photosensitive, are strongly activated by rods and cones, and display a rare, S-Off, (L + M)-On type of colour-opponent receptive field. The intrinsic, rod and (L + M) cone-derived light responses combine in these giant cells to signal irradiance over the full dynamic range of human vision. In accordance with cone-based colour opponency, the giant cells project to the lateral geniculate nucleus, the thalamic relay to primary visual cortex. Thus, in the diurnal trichromatic primate, 'non-image-forming' and conventional 'image-forming' retinal pathways are merged, and the melanopsin-based signal might contribute to conscious visual perception.
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            Effect of bright light and melatonin on cognitive and noncognitive function in elderly residents of group care facilities: a randomized controlled trial.

            Cognitive decline, mood, behavioral and sleep disturbances, and limitations of activities of daily living commonly burden elderly patients with dementia and their caregivers. Circadian rhythm disturbances have been associated with these symptoms. To determine whether the progression of cognitive and noncognitive symptoms may be ameliorated by individual or combined long-term application of the 2 major synchronizers of the circadian timing system: bright light and melatonin. A long-term, double-blind, placebo-controlled, 2 x 2 factorial randomized trial performed from 1999 to 2004 with 189 residents of 12 group care facilities in the Netherlands; mean (SD) age, 85.8 (5.5) years; 90% were female and 87% had dementia. Random assignment by facility to long-term daily treatment with whole-day bright (+/- 1000 lux) or dim (+/- 300 lux) light and by participant to evening melatonin (2.5 mg) or placebo for a mean (SD) of 15 (12) months (maximum period of 3.5 years). Standardized scales for cognitive and noncognitive symptoms, limitations of activities of daily living, and adverse effects assessed every 6 months. Light attenuated cognitive deterioration by a mean of 0.9 points (95% confidence interval [CI], 0.04-1.71) on the Mini-Mental State Examination or a relative 5%. Light also ameliorated depressive symptoms by 1.5 points (95% CI, 0.24-2.70) on the Cornell Scale for Depression in Dementia or a relative 19%, and attenuated the increase in functional limitations over time by 1.8 points per year (95% CI, 0.61-2.92) on the nurse-informant activities of daily living scale or a relative 53% difference. Melatonin shortened sleep onset latency by 8.2 minutes (95% CI, 1.08-15.38) or 19% and increased sleep duration by 27 minutes (95% CI, 9-46) or 6%. However, melatonin adversely affected scores on the Philadelphia Geriatric Centre Affect Rating Scale, both for positive affect (-0.5 points; 95% CI, -0.10 to -1.00) and negative affect (0.8 points; 95% CI, 0.20-1.44). Melatonin also increased withdrawn behavior by 1.02 points (95% CI, 0.18-1.86) on the Multi Observational Scale for Elderly Subjects scale, although this effect was not seen if given in combination with light. Combined treatment also attenuated aggressive behavior by 3.9 points (95% CI, 0.88-6.92) on the Cohen-Mansfield Agitation Index or 9%, increased sleep efficiency by 3.5% (95% CI, 0.8%-6.1%), and improved nocturnal restlessness by 1.00 minute per hour each year (95% CI, 0.26-1.78) or 9% (treatment x time effect). Light has a modest benefit in improving some cognitive and noncognitive symptoms of dementia. To counteract the adverse effect of melatonin on mood, it is recommended only in combination with light. controlled-trials.com/isrctn Identifier: ISRCTN93133646.
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              Role of melatonin in the regulation of human circadian rhythms and sleep.

              The circadian rhythm of pineal melatonin is the best marker of internal time under low ambient light levels. The endogenous melatonin rhythm exhibits a close association with the endogenous circadian component of the sleep propensity rhythm. This has led to the idea that melatonin is an internal sleep "facilitator" in humans, and therefore useful in the treatment of insomnia and the readjustment of circadian rhythms. There is evidence that administration of melatonin is able: (i) to induce sleep when the homeostatic drive to sleep is insufficient; (ii) to inhibit the drive for wakefulness emanating from the circadian pacemaker; and (iii) induce phase shifts in the circadian clock such that the circadian phase of increased sleep propensity occurs at a new, desired time. Therefore, exogenous melatonin can act as soporific agent, a chronohypnotic, and/or a chronobiotic. We describe the role of melatonin in the regulation of sleep, and the use of exogenous melatonin to treat sleep or circadian rhythm disorders.
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                Author and article information

                Journal
                9809663
                Somnologie (Berl)
                Somnologie (Berl)
                Somnologie : Schlafforschung und Schlafmedizin = Somnology : sleep research and sleep medicine
                1432-9123
                1439-054X
                21 August 2019
                20 August 2019
                September 2019
                18 September 2019
                : 23
                : 3
                : 147-156
                Affiliations
                [1 ]Centre for Chronobiology, Psychiatric Hospital of the University of Basel (UPK), Basel, Switzerland
                [2 ]Transfaculty Research Platform Molecular and Cognitive Neurosciences (MCN), University of Basel, Basel, Switzerland
                [3 ]Centre for Cognitive Neuroscience, University of Salzburg, Salzburg, Austria
                [4 ]Department of Experimental Psychology, University of Oxford, Oxford, UK
                Author notes
                Corresponding address: Dr. Christine BlumeCentre for Chronobiology, Psychiatric Hospital of the University of Basel (UPK) Basel, Switzerland Christine.Blume@ 123456sbg.ac.at , Dr. med. CorradoGarbazzaCentre for Chronobiology, Psychiatric Hospital of the University of Basel (UPK) Basel, Switzerland Corrado.Garbazza@ 123456upk.ch , Dr. Manuel SpitschanDepartment of Experimental Psychology, University of Oxford Oxford, UK manuel.spitschan@ 123456psy.ox.ac.uk
                Article
                EMS84169
                10.1007/s11818-019-00215-x
                6751071
                31534436
                2e1c4478-f82e-4226-a803-d85b786b899c

                This article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

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                circadian rhythms,natural light,artificial light,depression,light therapy

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