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Author (up) Arendt, J.; Middleton, B. url  doi
openurl 
  Title Human seasonal and circadian studies in Antarctica (Halley, 75 degrees S) Type Journal Article
  Year 2018 Publication General and Comparative Endocrinology Abbreviated Journal Gen Comp Endocrinol  
  Volume 258 Issue Pages 250-258  
  Keywords Human Activities; Acclimatization/*physiology; Actigraphy; Adult; Antarctic Regions; Behavior/*physiology; Circadian Rhythm/*physiology; Darkness; Female; Heart Rate/physiology; Humans; Libido; Light; Male; Melatonin/blood; Photoperiod; *Seasons; Sleep/physiology; Young Adult; *Antarctica; *Circadian; *Light; *Melatonin; *Seasonal  
  Abstract Living for extended periods in Antarctica exposes base personnel to extremes of daylength (photoperiod) and temperature. At the British Antarctic Survey base of Halley, 75 degrees S, the sun does not rise for 110 d in the winter and does not set for 100 d in summer. Photoperiod is the major time cue governing the timing of seasonal events such as reproduction in many species. The neuroendocrine signal providing photoperiodic information to body physiology is the duration of melatonin secretion which reflects the length of the night: longer in the short days of winter and shorter in summer. Light of sufficient intensity and spectral composition serves to suppress production of melatonin and to set the circadian timing and the duration of the rhythm. In humans early observations suggested that bright (>2000 lux) white light was needed to suppress melatonin completely. Shortly thereafter winter depression (Seasonal Affective Disorder or SAD) was described, and its successful treatment by an artificial summer photoperiod of bright white light, sufficient to shorten melatonin production. At Halley dim artificial light intensity during winter was measured, until 2003, at a maximum of approximately 500 lux in winter. Thus a strong seasonal and circadian time cue was absent. It seemed likely that winter depression would be common in the extended period of winter darkness and could be treated with an artificial summer photoperiod. These observations, and predictions, inspired a long series of studies regarding human seasonal and circadian status, and the effects of light treatment, in a small overwintering, isolated community, living in the same conditions for many months at Halley. We found little evidence of SAD, or change in duration of melatonin production with season. However the timing of the melatonin rhythm itself, and/or that of its metabolite 6-sulphatoxymelatonin (aMT6s), was used as a primary marker of seasonal, circadian and treatment changes. A substantial phase delay of melatonin in winter was advanced to summer phase by a two pulse 'skeleton' bright white light treatment. Subsequently a single morning pulse of bright white light was effective with regard to circadian phase and improved daytime performance. The circadian delay evidenced by melatonin was accompanied by delayed sleep (logs and actigraphy): poor sleep is a common complaint in Polar regions. Appropriate extra artificial light, both standard white, and blue enriched, present throughout the day, effectively countered delay in sleep timing and the aMT6s rhythm. The most important factor appeared to be the maximum light experienced. Another manifestation of the winter was a decline in self-rated libido (men only on base at this time). Women on the base showed lower aspects of physical and mental health compared to men. Free-running rhythms were seen in some subjects following night shift, but were rarely found at other times, probably because this base has strongly scheduled activity and leisure time. Complete circadian adaptation during a week of night shift, also seen in a similar situation on North Sea oil rigs, led to problems readapting back to day shift in winter, compared to summer. Here again timed light treatment was used to address the problem. Sleep, alertness and waking performance are critically dependent on optimum circadian phase. Circadian desynchrony is associated with increased risk of major disease in shift workers. These studies provide some groundwork for countering/avoiding circadian desynchrony in rather extreme conditions.  
  Address Biochemistry and Physiology, Faculty of Health and Medical Sciences, University of Surrey, Guildford GU2 7XH, UK. Electronic address: b.middleton@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 0016-6480 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28526480 Approved no  
  Call Number IDA @ john @ Serial 2248  
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Author (up) Obayashi, K.; Saeki, K.; Iwamoto, J.; Ikada, Y.; Kurumatani, N. url  doi
openurl 
  Title Association between light exposure at night and nighttime blood pressure in the elderly independent of nocturnal urinary melatonin excretion Type Journal Article
  Year 2014 Publication Chronobiology International Abbreviated Journal Chronobiol Int  
  Volume 31 Issue 6 Pages 779-786  
  Keywords Actigraphy; circadian rhythm; elderly; light at night; melatonin; nighttime blood pressure; geriatrics  
  Abstract Circadian misalignment between internal and environmental rhythms dysregulates blood pressure (BP) variability because of disruption of the biological clock, resulting in increased nighttime BP. Although exposure to light-at-night is associated with the circadian misalignment, it remains unclear whether exposure to light-at-night in home settings is associated with nighttime BP. In this cross-sectional analysis of 528 elderly individuals (mean age: 72.8 years), we measured bedroom light intensity at 1-min intervals on two consecutive nights along with ambulatory BP, overnight urinary melatonin excretion and actigraphy. With regard to adjusted mean comparisons using analysis of covariance, the light-at-night group (average: >/=5 lux; n = 109) showed significantly higher nighttime systolic BP (SBP; adjusted mean: 120.8 vs. 116.5 mmHg, p = 0.01) and diastolic BP (70.1 vs. 67.1 mmHg, p < 0.01) compared with the Darker group (average: <5 lux; n = 419) independently of potential confounding factors including overnight urinary melatonin excretion and actigraphic sleep quality. We observed consistent associations between light-at-night and nighttime BP in different cutoff values for light-at-night intensity (i.e. 3 and 10 lux). In conclusion, exposure to light-at-night in home settings is significantly associated with increased nighttime BP in elderly individuals independently of overnight urinary melatonin excretion. A 4.3 mmHg increase in nighttime SBP is associated with a 6.1% increase in total mortality, which corresponds to approximately 10 000 annual excess deaths in Japanese elderly population.  
  Address Department of Community Health and Epidemiology, Nara Medical University School of Medicine , Nara , Japan  
  Corporate Author Thesis  
  Publisher Informa Plc Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0742-0528 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:24673296 Approved no  
  Call Number IDA @ john @ Serial 315  
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Author (up) Wams, E.J.; Woelders, T.; Marring, I.; van Rosmalen, L.; Beersma, D.G.M.; Gordijn, M.C.M.; Hut, R.A. url  doi
openurl 
  Title Linking Light Exposure and Subsequent Sleep: A Field Polysomnography Study in Humans Type Journal Article
  Year 2017 Publication Sleep Abbreviated Journal Sleep  
  Volume 40 Issue 12 Pages  
  Keywords actigraphy; chronobiology; circadian rhythms; scoring; sleep/wake mechanisms  
  Abstract Study objectives: To determine the effect of light exposure on subsequent sleep characteristics under ambulatory field conditions. Methods: Twenty healthy participants were fitted with ambulatory polysomnography (PSG) and wrist-actigraphs to assess light exposure, rest-activity, sleep quality, timing, and architecture. Laboratory salivary dim-light melatonin onset was analyzed to determine endogenous circadian phase. Results: Later circadian clock phase was associated with lower intensity (R2 = 0.34, chi2(1) = 7.19, p < .01), later light exposure (quadratic, controlling for daylength, R2 = 0.47, chi2(3) = 32.38, p < .0001), and to later sleep timing (R2 = 0.71, chi2(1) = 20.39, p < .0001). Those with later first exposure to more than 10 lux of light had more awakenings during subsequent sleep (controlled for daylength, R2 = 0.36, chi2(2) = 8.66, p < .05). Those with later light exposure subsequently had a shorter latency to first rapid eye movement (REM) sleep episode (R2 = 0.21, chi2(1) = 5.77, p < .05). Those with less light exposure subsequently had a higher percentage of REM sleep (R2 = 0.43, chi2(2) = 13.90, p < .001) in a clock phase modulated manner. Slow-wave sleep accumulation was observed to be larger after preceding exposure to high maximal intensity and early first light exposure (p < .05). Conclusions: The quality and architecture of sleep is associated with preceding light exposure. We propose that light exposure timing and intensity do not only modulate circadian-driven aspects of sleep but also homeostatic sleep pressure. These novel ambulatory PSG findings are the first to highlight the direct relationship between light and subsequent sleep, combining knowledge of homeostatic and circadian regulation of sleep by light. Upon confirmation by interventional studies, this hypothesis could change current understanding of sleep regulation and its relationship to prior light exposure. Clinical trial details: This study was not a clinical trial. The study was ethically approved and nationally registered (NL48468.042.14).  
  Address Chronobiology Unit, Groningen Institute for Evolutionary Life Sciences, University of Groningen, The Netherlands  
  Corporate Author Thesis  
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  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0161-8105 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:29040758; PMCID:PMC5806586 Approved no  
  Call Number GFZ @ kyba @ Serial 1885  
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