The Acute Effects of Alcohol on Sleep Architecture in Late Adolescence

Abstract

Background Alcohol consumption is prevalent in late adolescence, however little is known about its effect on sleep in this group. In mature adults, alcohol decreases sleep onset latency (SOL) and sleep efficiency (SE) and increases wake after sleep onset (WASO). It also increases slow wave sleep (SWS) and decreases REM sleep in the first half of the night, with the inverse occurring in the second half. Alcohol’s effect on sleep during late adolescence is of interest given that this age group shows both dramatic increases in alcohol consumption, and significant developmental changes in the central nervous system. This study examined the effect of alcohol on sleep architecture in women and men aged 18–21 years and whether previously reported sleep architecture effects may have been as an artificial result of changes to sleep cycle length. Methods 24 (12 female) healthy 18–21 year old light social drinkers (19.1±1.0yrs) underwent two conditions: pre-sleep alcohol (Target BAC 0.10%) and placebo administered under controlled conditions, followed by standard polysomnography. Results In the alcohol condition, mean breath alcohol concentration (BAC) at lights out was 0.084 ±0.016%. Time in bed, total sleep time and sleep onset latency (all p>.05) did not differ between conditions. However, there was less REM (p=.011) and more stage 2 sleep (p=.035) in the alcohol condition. Further, alcohol increased SWS (p=.02) and decreased REM sleep (p<.001) in the first half of the night and disrupted sleep in the second half, with increased WASO (interaction: p=.034), and decreased SE (p=.04) and SWS (p=.01) and no REM sleep rebound in the second half of the night (p=.262). Additionally, alcohol had no effect on sleep cycle length (p=.598). Conclusions The results were broadly consistent with the adult literature with the novel extension that half night sleep architecture effects could not be attributed to changes in sleep cycle length. However, alcohol did not reduce SOL, or result in a REM rebound following reduced REM in the first half of the night. The results suggest that the effects of alcohol on sleep are modified by sleep’s prevailing developmental stage.

Alcohol and the sleeping brain

“…Women also reported higher ratings of sleepiness after consuming alcohol than did men. No sex differences in the effects of alcohol on sleep were seen in the group of older adolescents studied by Chan et al (Chan et al 2013). In a study of 42 recovering alcoholics (15 women) and 42 controls (23 women), we found that women had a better sleep efficiency and more delta activity during NREM sleep than men, regardless of diagnosis (Colrain, Turlington, and Baker 2009a).…”

“…Alcohol initially acts as a sedative. Commonly reported phenomena include shortened sleep onset latency (MacLean and Cairns 1982; Roehrs et al 1999; Williams, MacLean, and Cairns 1983; Stone 1980; Scrima et al 1982) and increased SWS in the first half of the night (Williams, MacLean, and Cairns 1983; Van Reen, Jenni, and Carskadon 2006; Sagawa et al 2011; Rundell et al 1972; Chan et al 2013; MacLean and Cairns 1982; Prinz et al. 1980; Feige et al 2006; Arnedt, Rohsenow, et al 2011).…”

“…1980; Feige et al 2006; Arnedt, Rohsenow, et al 2011). REM sleep is suppressed, with a longer latency to REM sleep and decreased REM sleep in the first half of the night (Williams, MacLean, and Cairns 1983; Van Reen, Jenni, and Carskadon 2006; Sagawa et al 2011; Rundell et al 1972; Chan et al 2013) or across the whole night (Van Reen, Jenni, and Carskadon 2006; Williams, MacLean, and Cairns 1983; Roehrs et al 1999; Rundell et al 1972; Roehrs, Yoon, and Roth 1991; Arnedt, Rohsenow, et al 2011). In the second half of the night, sleep is disrupted, with increased wakefulness and/or stage 1 sleep.…”

The effect of sleep restriction on laser evoked potentials, thermal sensory and pain thresholds and suprathreshold pain in healthy subjects

“…SWS-rebound during the second night could possibly be able to mask the effects on pain of SWS-deprivation (Onen et al, 2001). However, real SWS-rebound, including any cognitive effect thereof, was probably minimal, as N3 was about 88 min in the four hours sleep group and 101 min in the nine hours sleep group, and about 80% of N3 is expected to occur within the first half of sleep in young adults (Chan et al, 2013).…”

Sleep Disturbances in Alcoholic Disease. Diagnpstics and Therapy

“…Алкоголь, принятый непосредственно перед сном, действует как транквилизатор: характерна меньшая продолжительность периода засыпания и уси-ление медленно-волновой активности в первой полови-не ночного сна [30]. Фаза быстрого REM сна подавлена и укорочена [6]. Во второй половине ночного сна сон прерывается, представленность REM-сна увеличивается.…”