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.
Light is considered the most potent synchronizer of the human circadian system and exerts many other non-image forming effects, including those that affect brain function. These effects are mediated in part by intrinsically photosensitive retinal ganglion cells that express the photopigment melanopsin. The spectral sensitivity of melanopsin is greatest for blue light at approximately 480 nm. At present, there is little information on how the spectral composition of light to which people are exposed varies over the 24-h period and across seasons. Twenty two subjects, aged 22 ± 4 years (mean ± SD) participated during the winter months (Nov-Feb) and 12 subjects aged 25 ± 3 years, participated during the summer months (Apr-Aug). Subjects wore Actiwatch-RGB monitors, as well as Actiwatch-L monitors, for 7 consecutive days whilst living in England. These monitors measured activity, light-exposure in the red, green and blue spectral regions, in addition to broad-spectrum white light, with a two-minute resolution.Light exposure during the day was analyzed for the interval between 9:00 and 21:00 h.The time course of white light exposure significantly differed between seasons (p = 0.0022), with light exposure increasing in the morning hours, and declining in the afternoon hours, with a more prominent decline in the winter. Overall light exposure was significantly higher in summer compared to winter (p = 0.0002). Seasonal differences in the relative contribution of blue light exposure to overall light exposure were also observed (p = 0.0006), in particular during the evening hours. During the summer evenings (17:00-21:00 h), the relative contribution of blue light was significantly higher (p < 0.0001) (40.2 ± 1.1%) than during winter evenings (26.6 ± 0.9%). The present data 3 show that in addition to overall light exposure, the spectral composition of light exposure varies over the day and with season.
Subjects working a 12 h offshore night shift for 2 weeks normally adapt to the night shift and are out of synchrony when they return home to day life, with consequent problems of poor sleep. The aim of this study was to investigate the effectiveness of timed light treatment to hasten circadian adaptation and improve sleep after the night shift. Ten male shift workers worked 19.00–07.00 h (n= 4) or 18.00–06.00 h (n= 6) offshore shift schedules. They were assessed for the last 7 days of a 14 or 21 day offshore night shift and for the following 14 days at home. Either timed light treatment/sunglasses or no light treatment/no sunglasses were scheduled in a crossover design during days 1–5 after the nightshift, theoretically timed to advance the circadian system. Subjects completed the Horne Östberg questionnaire. They wore an Actiwatch‐L throughout the study to monitor light/activity and completed daily sleep diaries. Actigraphic sleep efficiency after the light/sunglasses treatment was significantly improved (days 1–5), that is, 86.7 ± 5.8% (mean ± SD; light treatment) compared to 79.4 ± 10.3% (no light treatment), P < 0.05. Objective sleep duration (days 6–14) was significantly improved in the light treatment leg; actigraphic sleep duration was longer after light treatment (6.75 ± 0.50 h) compared to 5.76 ± 0.73 h, P < 0.05. If appropriately timed, light and darkness has beneficial effects on sleep efficiency and sleep duration following a night shift.
Complaints concerning sleep are high among those who work night shifts; this is in part due to the disturbed relationship between circadian phase and the timing of the sleep-wake cycle. Shift schedule, light exposure, and age are all known to affect adaptation to the night shift. This study investigated circadian phase, sleep, and light exposure in subjects working 18:00-06:00 h and 19:00-07:00 h schedules during summer (May-August). Ten men, aged 46+/-10 yrs (mean+/-SD), worked the 19:00-07:00 h shift schedule for two or three weeks offshore (58 degrees N). Seven men, mean age 41+/-12 yrs, worked the 18:00-06:00 h shift schedule for two weeks offshore (61 degrees N). Circadian phase was assessed by calculating the peak (acrophase) of the 6-sulphatoxymelatonin rhythm measured by radioimmunoassay of sequential urine samples collected for 72 h at the end of the night shift. Objective sleep and light exposure were assessed by actigraphy and subjective sleep diaries. Subjects working 18:00-06:00 h had a 6-sulphatoxymelatonin acrophase of 11.7+/-0.77 h (mean+/-SEM, decimal hours), whereas it was significantly later, 14.6+/-0.55 h (p=0.01), for adapted subjects working 19:00-07:00 h. Two subjects did not adapt to the 19:00-07:00 h night shift (6-sulphatoxymelatonin acrophases being 4.3+/-0.22 and 5.3+/-0.29 h). Actigraphy analysis of sleep duration showed significant differences (p=0.03), with a mean sleep duration for those working 19:00-07:00 h of 5.71+/-0.31 h compared to those working 18:00-06:00 h whose mean sleep duration was 6.64+/-0.33 h. There was a trend to higher morning light exposure (p=0.07) in the 19:00-07:00 h group. Circadian phase was later (delayed on average by 3 h) and objective sleep was shorter with the 19:00-07:00 h than the 18:00-06:00 h shift schedule. In these offshore conditions in summer, the earlier shift start and end time appears to favor daytime sleep.
Introduction: High-strength mesalazine formulations play an important role in providing a convenient option to increase the dose in ulcerative colitis (UC) patients and therefore avoiding the switch to another therapeutic class. Higher doses of mesalazine may be required during periods of remission in order to prevent relapse. Aim: To investigate clinical outcomes of three mesalazine maintenance doses adapted for post induction response. Methods: In this post-hoc analysis, 675 UC patients entered an open label extension study for a total of 38 weeks (including 8-12 week induction period with 3.2 g/day mesalazine). After the induction period they were separated into three groups: remitters (in clinical and endoscopic remission), responders (decrease in Partial Mayo Clinic Score (PMCS) of ≥ 2 points and ≥ 30% from week 0) and non-responders (failed to achieve endoscopic and clinical response at week 8) and received 1.6 g/day, 3.2 g/day or 4.8 g/day of mesalazine (using a new 1600 mg mesalazine tablet), respectively. Results: 133/202 (65.8%), 108/274 (39.4%) and 59/199 (29.6%) patients achieved clinical and endoscopic remission at week 38 with 1.6 g/day, 3.2 g/day and 4.8 g/day, respectively. At week 38, 142/202 (70.3%), 93/274 (33.9%) and 61/199 (30.7%) patients achieved clinical remission (stool score of 0 and rectal bleeding score of 0) with 1.6 g/day, 3.2 g/day and 4.8 g/day, respectively. Conclusions: Patients partially responding or not responding to an initial induction dose of 3.2 g/day mesalazine could benefit from an extended treatment period at the same dose, or an increase to 4.8 g/day in an attempt to achieve combined clinical and endoscopic remission.
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