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. 2016 Apr 15;310(8):R759-65.
doi: 10.1152/ajpregu.00001.2016. Epub 2016 Mar 2.

A single dose of alcohol does not meaningfully alter circadian phase advances and phase delays to light in humans

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A single dose of alcohol does not meaningfully alter circadian phase advances and phase delays to light in humans

Helen J Burgess et al. Am J Physiol Regul Integr Comp Physiol. .

Abstract

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.

Keywords: alcohol; circadian; human; light; melatonin.

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Figures

Fig. 1.
Fig. 1.
A sample protocol for the Phase Advance study (top) and the Phase Delay study (bottom) for a subject who typically slept from 2300 to 0700. Both the Phase Advance and Phase Delay protocols consisted of 6 days of fixed sleep at home to stabilize circadian phase, a 2-day laboratory session, a 6-day study break, another 6 days of fixed sleep at home followed by another 2-day laboratory session. During the laboratory session in the Phase Advance study there was a baseline circadian phase assessment, a sleep episode, a 30-min drink window (alcohol, placebo), a 2-h bright light pulse, followed by a final circadian phase assessment. During the laboratory session in the Phase Delay study, there was a baseline circadian phase assessment, a 30-min drink window (alcohol, placebo), a 2-h bright light pulse, a sleep episode, followed by a final circadian phase assessment. The black rectangles represent scheduled sleep times. The dots represent the first and last saliva sample during the dim light circadian phase assessments. The D represents the 30-min drinking window. The L represents the 2-h bright light pulse. Square brackets indicate approximate arrival and departure times from the laboratory.
Fig. 2.
Fig. 2.
The evening rise in melatonin levels observed in two subjects in the Phase Advance study. The baseline evening rise in melatonin levels before the bright light is shown by solid circles (●), and the evening rise in melatonin levels after the bright light on the next day is shown with open circles (○). One subject (left) showed greater phase advances with alcohol than with placebo. The other subject (right) showed smaller phase advances with alcohol than with placebo.
Fig. 3.
Fig. 3.
The evening rise in melatonin levels observed in two subjects in the Phase Delay study. The baseline evening rise in melatonin levels before the bright light is shown by solid circles (●), and the evening rise in melatonin levels after the bright light on the next day is shown with open circles (○). One subject (left) showed greater phase delays with alcohol than with placebo. The other subject (right) showed smaller phase delays with alcohol than with placebo.
Fig. 4.
Fig. 4.
The phase shifts in the dim-light melatonin onset (DLMO) observed in each individual subject in the Phase Advance study (top) and phase delay study (bottom). The phase shifts for an individual subject are connected by a line. The open circles (○) represent the observed phase shift in the single subject whose baseline DLMOs varied by more than 1 h between conditions. No systematic effect of the single dose of alcohol on phase advances or phase delays to the bright light were observed (drink × time interactions in both studies P ≥ 0.46).

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