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Author Santhi, N.; Thorne, H.C.; van der Veen, D.R.; Johnsen, S.; Mills, S.L.; Hommes, V.; Schlangen, L.J.M.; Archer, S.N.; Dijk, D.-J.
Title The spectral composition of evening light and individual differences in the suppression of melatonin and delay of sleep in humans Type Journal Article
Year 2012 Publication (up) Journal of Pineal Research Abbreviated Journal J Pineal Res
Volume 53 Issue 1 Pages 47-59
Keywords Human Health; Adult; *Circadian Clocks; Cross-Sectional Studies; Electroencephalography; Female; Humans; Male; Melatonin/*metabolism; Photic Stimulation; *Photoperiod; Rod Opsins/*metabolism; *Sleep; *Sleep Disorders, Circadian Rhythm/etiology/metabolism/physiopathology; Time Factors
Abstract The effect of light on circadian rhythms and sleep is mediated by a multi-component photoreceptive system of rods, cones and melanopsin-expressing intrinsically photosensitive retinal ganglion cells. The intensity and spectral sensitivity characteristics of this system are to be fully determined. Whether the intensity and spectral composition of light exposure at home in the evening is such that it delays circadian rhythms and sleep also remains to be established. We monitored light exposure at home during 6-8wk and assessed light effects on sleep and circadian rhythms in the laboratory. Twenty-two women and men (23.1+/-4.7yr) participated in a six-way, cross-over design using polychromatic light conditions relevant to the light exposure at home, but with reduced, intermediate or enhanced efficacy with respect to the photopic and melanopsin systems. The evening rise of melatonin, sleepiness and EEG-assessed sleep onset varied significantly (P<0.01) across the light conditions, and these effects appeared to be largely mediated by the melanopsin, rather than the photopic system. Moreover, there were individual differences in the sensitivity to the disruptive effect of light on melatonin, which were robust against experimental manipulations (intra-class correlation=0.44). The data show that light at home in the evening affects circadian physiology and imply that the spectral composition of artificial light can be modified to minimize this disruptive effect on sleep and circadian rhythms. These findings have implications for our understanding of the contribution of artificial light exposure to sleep and circadian rhythm disorders such as delayed sleep phase disorder.
Address Surrey Sleep Research Centre, Faculty of Health and Medical Sciences, University of Surrey, Guildford, UK. n.santhi@surrey.ac.uk
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0742-3098 ISBN Medium
Area Expedition Conference
Notes PMID:22017511 Approved no
Call Number LoNNe @ kagoburian @ Serial 802
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Author Mottram, V.; Middleton, B.; Williams, P.; Arendt, J.
Title The impact of bright artificial white and 'blue-enriched' light on sleep and circadian phase during the polar winter Type Journal Article
Year 2011 Publication (up) Journal of Sleep Research Abbreviated Journal J Sleep Res
Volume 20 Issue 1 Pt 2 Pages 154-161
Keywords Adult; Circadian Rhythm/*physiology; *Cold Climate; Female; Humans; *Light; Male; Medical Records; Questionnaires; Sleep/*physiology; Time Factors; blue light
Abstract Delayed sleep phase (and sometimes free-run) is common in the Antarctic winter (no natural sunlight) and optimizing the artificial light conditions is desirable. This project evaluated sleep when using 17,000 K blue-enriched lamps compared with standard white lamps (5000 K) for personal and communal illumination. Base personnel, 10 males, five females, 32.5+/-8 years took part in the study. From 24 March to 21 September 2006 light exposure alternated between 4-5-week periods of standard white (5000 K) and blue-enriched lamps (17,000 K), with a 3-week control before and after extra light. Sleep and light exposure were assessed by actigraphy and sleep diaries. General health (RAND 36-item questionnaire) and circadian phase (urinary 6-sulphatoxymelatonin rhythm) were evaluated at the end of each light condition. Direct comparison (rmanova) of blue-enriched light with white light showed that sleep onset was earlier by 19 min (P=0.022), and sleep latency tended to be shorter by 4 min (P=0.065) with blue-enriched light. Analysing all light conditions, control, blue and white, again provided evidence for greater efficiency of blue-enriched light compared with white (P<0.05), but with the best sleep timing, duration, efficiency and quality in control natural light conditions. Circadian phase was earlier on average in midwinter blue compared with midwinter white light by 45 min (P<0.05). Light condition had no influence on general health. We conclude that the use of blue-enriched light had some beneficial effects, notably earlier sleep, compared with standard white light during the polar winter.
Address British Antarctic Survey Medical Unit, Derriford Hospital, Plymouth, UK
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0962-1105 ISBN Medium
Area Expedition Conference
Notes PMID:20723022 Approved no
Call Number IDA @ john @ Serial 348
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Author Kovac, J.; Husse, J.; Oster, H.
Title A time to fast, a time to feast: the crosstalk between metabolism and the circadian clock Type Journal Article
Year 2009 Publication (up) Molecules and Cells Abbreviated Journal Mol Cells
Volume 28 Issue 2 Pages 75-80
Keywords Human Health; Animals; Biological Clocks/*physiology; CLOCK Proteins/genetics/metabolism; Circadian Rhythm/*physiology; Energy Metabolism/*physiology; Gene Expression Regulation; Homeostasis; Humans; Period Circadian Proteins/genetics/metabolism; Time Factors
Abstract The cyclic environmental conditions brought about by the 24 h rotation of the earth have allowed the evolution of endogenous circadian clocks that control the temporal alignment of behaviour and physiology, including the uptake and processing of nutrients. Both metabolic and circadian regulatory systems are built upon a complex feedback network connecting centres of the central nervous system and different peripheral tissues. Emerging evidence suggests that circadian clock function is closely linked to metabolic homeostasis and that rhythm disruption can contribute to the development of metabolic disease. At the same time, metabolic processes feed back into the circadian clock, affecting clock gene expression and timing of behaviour. In this review, we summarize the experimental evidence for this bimodal interaction, with a focus on the molecular mechanisms mediating this exchange, and outline the implications for clock-based and metabolic diseases.
Address Circadian Rhythms Group, Max Planck Institute of Biophysical Chemistry, 37077, Gottingen, Germany
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 1016-8478 ISBN Medium
Area Expedition Conference
Notes PMID:19714310 Approved no
Call Number LoNNe @ kagoburian @ Serial 772
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Author Filipski, E.; Subramanian, P.; Carriere, J.; Guettier, C.; Barbason, H.; Levi, F.
Title Circadian disruption accelerates liver carcinogenesis in mice Type Journal Article
Year 2009 Publication (up) Mutation Research Abbreviated Journal Mutat Res
Volume 680 Issue 1-2 Pages 95-105
Keywords Human Health; Animals; Alanine Transaminase/blood; Animals; Aspartate Aminotransferases/blood; Bile Duct Neoplasms/chemically induced/pathology; Bile Ducts, Intrahepatic/drug effects/pathology; Body Weight/drug effects; Carcinogens/administration & dosage/*toxicity; Carcinoma, Hepatocellular/chemically induced/pathology; Cholangiocarcinoma/chemically induced/pathology; Circadian Rhythm/*drug effects; Diethylnitrosamine/administration & dosage/*toxicity; Dose-Response Relationship, Drug; Injections, Intraperitoneal; Liver/drug effects/pathology; Liver Neoplasms/blood/*chemically induced/pathology; Male; Mice; Neoplasms, Multiple Primary/chemically induced/pathology; Sarcoma/chemically induced/pathology; Time Factors
Abstract BACKGROUND: The circadian timing system rhythmically controls behavior, physiology, cellular proliferation and xenobiotic metabolism over the 24-h period. The suprachiasmatic nuclei in the hypothalamus coordinate the molecular clocks in most mammalian cells through an array of circadian physiological rhythms including rest-activity, body temperature, feeding patterns and hormonal secretions. As a result, shift work that involves circadian disruption is probably carcinogenic in humans. In experimental models, chronic jet-lag (CJL) suppresses rest-activity and body temperature rhythms and accelerates growth of two transplantable tumors in mice. CJL also suppresses or significantly alters the expression rhythms of clock genes in liver and tumors. Circadian clock disruption from CJL downregulates p53 and upregulates c-Myc, thus favoring cellular proliferation. Here, we investigate the role of CJL as a tumor promoter in mice exposed to the hepatic carcinogen, diethylnitrosamine (DEN). METHODS: In experiment 1 (Exp 1), the dose-dependent carcinogenicity of chronic intraperitoneal (i.p.) administration of DEN was explored in mice. In Exp 2, mice received DEN at 10 mg/kg/day (cumulative dose: 243 mg/kg), then were randomized to remain in a photoperiodic regimen where 12 h of light alternates with 12 h of darkness (LD 12:12) or to be submitted to CJL (8-h advance of light onset every 2 days). Rest-activity and body temperature were monitored. Serum liver enzymes were determined repeatedly. Mice were sacrificed and examined for neoplastic lesions at 10 months. RESULTS: In Exp 1, DEN produced liver cancers in all the mice receiving 10 mg/kg/day. In Exp 2, mice on CJL had increased mean plasma levels of aspartate aminotransferase and more liver tumors as compared to LD mice at approximately 10 months (p = 0.005 and 0.028, respectively). The mean diameter of the largest liver tumor was twice as large in CJL vs LD mice (8.5 vs 4.4 mm, p = 0.027). In LD, a single histologic tumor type per liver was observed. In CJL, up to four different types were associated in the same liver (hepatocellular- or cholangio-carcinomas, sarcomas or mixed tumors). DEN itself markedly disrupted the circadian rhythms in rest-activity and body temperature in all the mice. DEN-induced disruption was prolonged for >or= 3 months by CJL exposure. CONCLUSIONS: The association of circadian disruption with chronic DEN exposure suggests that circadian clocks actively control the mechanisms of liver carcinogenesis in mice. Persistent circadian coordination may further be critical for slowing down and/or reverting cancer development after carcinogen exposure.
Address INSERM, U776 Rythmes Biologiques et Cancers, Hopital Paul Brousse, Villejuif F-94807, France
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0027-5107 ISBN Medium
Area Expedition Conference
Notes PMID:19833225 Approved no
Call Number LoNNe @ kagoburian @ Serial 747
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Author Owens, B.
Title Obesity: heavy sleepers Type Journal Article
Year 2013 Publication (up) Nature Abbreviated Journal Nature
Volume 497 Issue 7450 Pages S8-9
Keywords Human Health; Animals; Body Mass Index; CLOCK Proteins/genetics/metabolism; Circadian Rhythm/physiology; Energy Metabolism/*physiology; Ghrelin/metabolism; Humans; Insulin Resistance/physiology; Leptin/metabolism; Male; Mice; Obesity/*physiopathology; Satiety Response/physiology; Sleep/*physiology; Suprachiasmatic Nucleus/physiology; Time Factors; Weight Gain/physiology; Weight Loss/physiology
Abstract
Address
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0028-0836 ISBN Medium
Area Expedition Conference
Notes PMID:23698508 Approved no
Call Number LoNNe @ christopher.kyba @ Serial 503
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