scholarly journals Daytime Sleep Propensity After Moderate Circadian Phase Shifts Induced With Bright Light Exposure

SLEEP ◽  
1997 ◽  
Vol 20 (1) ◽  
pp. 11-17 ◽  
Author(s):  
Marie Dumont ◽  
Julie Carrier
1997 ◽  
Vol 272 (2) ◽  
pp. R482-R486 ◽  
Author(s):  
A. Cagnacci ◽  
R. Soldani ◽  
S. S. Yen

We investigated whether the contemporaneous administration of melatonin can modify circadian phase shifts induced by bright light stimuli. After a baseline evaluation, 10 women were exposed for three consecutive nights to a 4-h bright light stimulus (>3,000 lx) initiated at the time of the estimated core body temperature (BT(c)) nadir. Along with light, each woman orally received, randomly and in a double-blind fashion, placebo (n = 5) or melatonin (n = 5; 1 mg 30 min before and 0.75 mg 120 min after the start of light exposure). Daily rhythms were reevaluated at the end of treatment. Bright light phase advanced, by about 90-120 min, BT(c) (P < 0.01), cortisol (P < 0.05), and melatonin (P < 0.01) rhythms. Contemporaneous administration of melatonin antagonized the phase advances of the cortisol and BT(c) rhythms, as well as the melatonin peak and melatonin offset. The phase advance of the melatonin onset was instead enhanced (P < 0.05). Contemporaneous melatonin administration modifies the capability of light to induce circadian phase shifts.


2001 ◽  
Vol 49 (1) ◽  
pp. 30-40 ◽  
Author(s):  
E.B. Klerman ◽  
J.F. Duffy ◽  
D.-J. Dijk ◽  
C.A. Czeisler

2003 ◽  
Vol 5 (4) ◽  
pp. 399-413

Chronobiological disorders and syndromes include seasonal affective disorder (SAD), total blindness, advanced and delayed sleep phase syndrome, jet lag, and shift work maladaptation. These disorders are treated by adjusting circadian phase, using appropriately timed bright light exposure and melatonin administration (at doses of 0.5 mg or less). In some cases, it may be necessary to measure internal circadían phase, using the time when endogenous melatonin levels rise.


2018 ◽  
Vol 2018 ◽  
pp. 1-16 ◽  
Author(s):  
Sevag Kaladchibachi ◽  
Fabian Fernandez

Circadian timekeeping can be reset by brief flashes of light using stimulation protocols thousands of times shorter than those previously assumed to be necessary for traditional phototherapy. These observations point to a future where flexible architectures of nanosecond-, microsecond-, and millisecond-scale light pulses are compiled to reprogram the brain’s internal clock when it has been altered by psychiatric illness or advanced age. In the current review, we present a chronology of seminal experiments that established the synchronizing influence of light on the human circadian system and the efficacy of prolonged bright-light exposure for reducing symptoms associated with seasonal affective disorder. We conclude with a discussion of the different ways that precision flashes could be parlayed during sleep to effect neuroadaptive changes in brain function. This article is a contribution to a special issue onCircadian Rhythms in Regulation of Brain Processes and Role in Psychiatric Disorderscurated by editors Shimon Amir, Karen Gamble, Oliver Stork, and Harry Pantazopoulos.


1997 ◽  
Vol 12 (1) ◽  
pp. 5-15 ◽  
Author(s):  
Paula J. Mitchell ◽  
Erin K. Hoese ◽  
Liwen Liu ◽  
Louis F. Fogg ◽  
Charmane I. Eastman

2016 ◽  
Vol 310 (8) ◽  
pp. R759-R765 ◽  
Author(s):  
Helen J. Burgess ◽  
Muneer Rizvydeen ◽  
Louis F. Fogg ◽  
Ali Keshavarzian

Central circadian timing influences mental and physical health. Research in nocturnal rodents has demonstrated that when alcohol is consumed, it reaches the central hypothalamic circadian pacemaker (suprachiasmatic nuclei) and can directly alter circadian phase shifts to light. In two separate studies, we examined, for the first time, the effects of a single dose of alcohol on circadian phase advances and phase delays to light in humans. Two 23-day within-subjects placebo-controlled counterbalanced design studies were conducted. Both studies consisted of 6 days of fixed baseline sleep to stabilize circadian timing, a 2-day laboratory session, a 6-day break, and a repeat of 6 days of fixed sleep and a 2-day laboratory session. In the phase advance study ( n = 10 light drinkers, 24–45 yr), the laboratory sessions consisted of a baseline dim light phase assessment, sleep episode, alcohol (0.6 g/kg) or placebo, 2-h morning bright light pulse, and final phase assessment. In the phase-delay study ( n = 14 light drinkers, 22–44 yr), the laboratory sessions consisted of a baseline phase assessment, alcohol (0.8 g/kg) or placebo, 2-h late night bright light pulse, sleep episode, and final phase assessment. In both studies, alcohol either increased or decreased the observed phase shifts to light (interaction P ≥ 0.46), but the effect of alcohol vs. placebo on phase shifts to light was always on average smaller than 30 min. Thus, no meaningful effects of a single dose of alcohol vs. placebo on circadian phase shifts to light in humans were observed.


2000 ◽  
Vol 48 (11) ◽  
pp. 1098-1104 ◽  
Author(s):  
Niki Lindblom ◽  
Taina Hätönen ◽  
Maija-Liisa Laakso ◽  
Aino Alila-Johansson ◽  
Marja-Leena Laipio ◽  
...  

2002 ◽  
Vol 63 (4) ◽  
pp. 316-321 ◽  
Author(s):  
Sami J. Leppamaki ◽  
Timo T. Partonen ◽  
Jukka Hurme ◽  
Jari K. Haukka ◽  
Jouko K. Lonnqvist

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