Circadian light.

Lighting Research Center, Rensselaer Polytechnic Institute, 21 Union Street, Troy, NY 12180, USA. .
Journal of Circadian Rhythms 02/2010; 8(1):2. DOI: 10.1186/1740-3391-8-2
Source: DOAJ

ABSTRACT The present paper reflects a work in progress toward a definition of circadian light, one that should be informed by the thoughtful, century-old evolution of our present definition of light as a stimulus for the human visual system. This work in progress is based upon the functional relationship between optical radiation and its effects on nocturnal melatonin suppression, in large part because the basic data are available in the literature. Discussed here are the fundamental differences between responses by the visual and circadian systems to optical radiation. Brief reviews of photometry, colorimetry, and brightness perception are presented as a foundation for the discussion of circadian light. Finally, circadian light (CLA) and circadian stimulus (CS) calculation procedures based on a published mathematical model of human circadian phototransduction are presented with an example.

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    ABSTRACT: BACKGROUND: Human circadian rhythms are regulated by the interplay between circadian genes and environmental stimuli. The influence of altered sleep-wake schedules or light on human circadian gene expression patterns is not well characterized. METHODS: Twenty-one young adults were asked to keep to their usual sleep schedules and two blood samples were drawn at the end of the first week from each subject based on estimated time of dim light melatonin onset (DLMO); the first sample was obtained one and a half hours before the estimated DLMO and the second three hours later, at one and a half hours after the estimated DLMO. During the second week, participants were randomized into two groups, one that received a one hour blue-light (λmax=470nm) exposure in the morning and one that received a comparable morning dim-light exposure. Two blood samples were obtained at the same clock times as the previous week at the end of the second week. RESULTS: We measured the expression of 10 circadian genes in response to sleep-wake schedule advancement and morning blue-light stimulation in the peripheral blood of 21 participants during a two-week field study. We found that nine of the 10 circadian genes showed significant expression changes from the first to the second week for participants in both the blue-light and dim-light groups, likely reflecting significant advances in circadian phase. CONCLUSIONS: This wholesale change in circadian gene expression may reflect considerable advances in circadian phase (i.e., advance in DLMO) from the first to the second week resulting from the advanced, daily personal light exposures.
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    ABSTRACT: OBJECTIVE: To examine, in a field study circadian phase changes associated with two different light-dark exposures patterns, one that was congruent with a phase advanced sleep schedule and one that was incongruent with an advanced schedule. METHODS: Twenty-one adults (mean age±standard deviation=22.5±3.9years; 11 women) participated in the 12day study. After a five-day baseline period, participants were all given individualized, fixed, 90-minute advanced sleep schedules for one week. Participants were randomly assigned to one of two groups, an advance group with a light-dark exposure prescription designed to advance circadian phase or a delay group with light-dark exposure prescription designed to delay circadian phase. The advance group received two morning hours of short-wavelength (blue) light (λmax≈476±1nm, full-width-half-maximum≈20nm) exposure and three evening hours of light restriction (orange-filtered light, λ<525nm=0). The delay group received blue light for three hours in the evening and light restriction for two hours in the morning. Participants led their normal lives while wearing a calibrated wrist-worn light exposure and activity monitor. RESULTS: After seven days on the 90-minute advanced sleep schedule, circadian phase advanced 132±19 minutes for the advance group and delayed 59±7.5 minutes for the delay group. CONCLUSIONS: Controlling the light-dark exposure pattern shifts circadian phase in the expected direction irrespective of the fixed advanced sleep schedule.
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    ABSTRACT: 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). 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, ∼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 2×2 ANOVA. 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. 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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