Adolescence is a critical time period for human development. It is associated with major interrelated changes to the brain and sleep regulatory systems. These changes continue into young adulthood, and often coincide with the onset and acceleration of alcohol use. This is concerning as research suggests alcohol consumption may harm the developing brain and sleep systems. Indeed, sleep is an essential neurophysiological process that is necessary for optimal health, functioning, and development. Disturbances to sleep are associated with adverse physiological and psychological consequences. Alcohol is well-known for its sleep disturbing properties. Research has reliably shown that pre-sleep alcohol ingestion in light-drinking late adolescents leads to characteristic objective sleep disruption. These effects are bi-phasic, manifesting as sedation in the first half of the sleep period, followed by major sleep disruption in the second half. However, there is growing evidence that young people may be less sensitive to the initial sedative effects of alcohol. Critically, the effects of acute alcohol consumption on sleep have not yet been investigated in young people who habitually engage in heavy alcohol use. It is well-established that chronic heavy alcohol use leads to enduring sleep disturbances, such as degradations in slow wave sleep (SWS), that persist into periods of long-term abstinence. This has been investigated exclusively in adults with long-term alcohol use disorders. It is currently unknown whether heavy-drinking young people also suffer disturbances to normal sleep. Due to their ongoing development, it is possible that young people experience unique alcohol-related sleep disturbances. These disturbances could negatively impact physical and mental health. The current study aimed to investigate the effects of acute and habitual alcohol use on sleep quality, architecture, and electroencephalography (EEG) spectral power, in male and female late adolescents, aged 18 to 21 years. Forty-six late adolescents were recruited (mean +/- standard deviation): 9 light-drinking males (20.0 +/- 0.9 years; 13.5 +/- 10.3 standard drinks [10g of ethanol] in the previous 30 days), 13 light-drinking females (19.4 +/- 1.2 years; 12.3 +/- 8.0 standard drinks), 11 heavy-drinking males (20.1 +/- 0.7 years; 133.4 +/- 78.8 standard drinks), and 13 heavy-drinking females (19.2 +/- 0.9 years; 81.9 +/- 25.6 standard drinks). Following an initial adaptation night, participants completed in-laboratory polysomnography under two conditions: pre-bedtime alcohol (peak breath alcohol concentration [BrAC] .10%) and placebo (BrAC .00%) consumption. Experimental nights were non-consecutive and counterbalanced over participants. Participants abstained from alcohol for 48 hours prior to testing. This single-blind, mixed-model study design included two repeated- (acute alcohol vs. placebo consumption, first vs. second half of the sleep period) and two between- (male vs. female, habitual heavy vs. light drinking) measures factors. Sleep quality (sleep onset latency, arousals, wake after sleep onset, sleep efficiency) and architecture (stage N1 sleep, stage N2 sleep, SWS, rapid eye movement [REM] sleep) variables were independently scored using standard American Academy of Sleep Medicine (2007) criteria by two experienced sleep researchers. Discrepancies between scorers were resolved by an independent adjudicator. All scorers were blinded to participant group and experimental condition. Power spectral analysis was conducted for five EEG frequency bands: beta (16 – 30 hertz; Hz), sigma (12 – <16 Hz), alpha (8 – <12 Hz), theta (4 – <8 Hz), and delta (0.5 – <4 Hz) for each sleep stage. Data were analysed using mixed-model analysis of variance and post-hoc t-tests. Correlations between habitual alcohol consumption, and sleep quality and architecture variables, were also performed. Mean BrAC at lights out was .08 +/- .01 percent following pre-sleep alcohol, and .00 +/- .00 percent following placebo consumption. Following acute alcohol consumption, in the first half of the sleep period, both heavy- and light-drinking late adolescents demonstrated fewer arousals (p< .001), less stage N1 sleep (p< .001), more SWS (p= .007), longer REM sleep onset latencies (p< .001), and less REM sleep (p< .001), compared to placebo. There were no differences observed in sleep onset latency (p= .720), wake after sleep onset (p= .850), or sleep efficiency (p= .811). In the first half of the sleep period, alpha EEG spectral power was higher following alcohol consumption in stage N2 sleep (p< .001), SWS (p< .001), and REM sleep (p= .005). Although delta spectral power was higher in SWS (p= .008) and REM sleep (p< .001) in the first half of the sleep period, delta power was lower in stage N2 sleep (p= .006). In the second half of the sleep period, there were more arousals (p< .001), more wake after sleep onset (p< .001), lower sleep efficiency (p< .001), more stage N1 sleep (p< .001), and less SWS (p= .004), following acute alcohol consumption compared to placebo, in both heavy- and light-drinking late adolescents. No differences in EEG spectral power were observed in the second half of the sleep period. By design, heavy-drinking participants had consumed more alcohol in the previous 30 days, and across their lifetimes, than light drinkers (p< .001). There were no differences in objective sleep quality between heavy- and light-drinking late adolescents. However, a correlational analysis showed that, in the placebo condition, higher alcohol consumption in the previous 30 days was associated with higher wake after sleep onset (Spearman's Rho= .312, p= .035), and lower sleep efficiency (Spearman's Rho= -.327, p= .027). Heavy drinkers had less all-night visually scored SWS (p= .026), and more stage N2 sleep (p= .008), than same-aged light drinkers, in the placebo condition. Furthermore, higher previous 30-day alcohol consumption was related to lower SWS (Spearman's Rho= -.261, p= .040) and higher stage N2 sleep (Spearman's Rho= .250, p= .027) percentage, in the placebo condition. Irrespective of experimental condition, heavy drinkers had shorter REM sleep onset latencies, compared to same-aged light drinkers (p= .038). Although there were no differences in all-night REM sleep percentage, heavy drinkers had less REM sleep in the second half of the sleep period compared to light drinkers, irrespective of condition (p= .016). There were no differences in delta spectral power between heavy- and light-drinking late adolescents in any sleep stage. However, heavy-drinking late adolescents had higher sigma spectral power in SWS (p= .029), and stage N2 sleep (p= .021), than same-aged light drinkers, regardless of experimental condition. There was an interaction between sex, acute alcohol use, and habitual alcohol use, for all-night SWS percentage (p= .003). This interaction suggested that heavy-drinking males had higher all-night SWS percentage following alcohol consumption compared to placebo, however, heavy-drinking females had lower all-night SWS. In light-drinking males and females, there were no differences in all-night SWS percentage following alcohol or placebo consumption. The current study demonstrated that both heavy- and light-drinking late adolescents experience substantial sleep disruption following a high dose of alcohol prior to sleep. In contrast to the adult literature, the current investigation reported no differences in sleep onset latency, wake after sleep onset, or sleep efficiency, in the first half of the sleep period. This supports growing evidence that young people may experience less initial physiological sedation following alcohol consumption. However, a direct adult comparison is needed to verify this. This unique physiological response could potentially contribute to higher levels of alcohol use in young people, as it permits them to consume higher doses of alcohol before experiencing sedation. The current study replicated previous findings of higher alpha and delta spectral power following pre-sleep alcohol in young people. This may represent alpha-delta sleep – a potential electrophysiological indicator of sleep disruption. It is possible that these objective sleep disturbances may compromise the restorative properties of sleep and contribute to the alcohol hangover. The current study reported more wake after sleep onset, and less sleep efficiency, following acute alcohol consumption, which may contribute to sleep restriction in young people. Critically, this investigation provided novel evidence that pre-sleep alcohol consumption disrupts sleep in heavy-drinking late adolescents. This indicates that this population may be repeatedly experiencing sleep disruption during the final stages of neural development. Furthermore, these effects may be amplified in heavy-drinking young women, however further research is needed to replicate these novel findings. Finally, the present study uniquely demonstrated that heavy habitual alcohol use in young people is associated with disturbances to normal sleep, irrespective of pre-sleep alcohol consumption. Despite their relatively short drinking histories, the pattern of deficits was similar to those reported in adults with long-term alcohol use disorders, including lower all-night SWS percentage. Furthermore, some sleep abnormalities may be unique to this developing age group, such as elevated sigma spectral power during SWS and stage N2 sleep. Evidence suggests SWS plays a functional role in neurophysiological growth and repair, and learning and memory. Enduring degradations in SWS may be particularly detrimental in young people, as neural development is still ongoing, and academic pressure is high, during this time period. Although longitudinal research is required, the sleep deficits observed in the current investigation may represent alcohol-related changes to the brain and sleep systems, and/or a predisposition to heavy alcohol use. In summary, the current study provided key objective evidence that both acute and habitual alcohol use in late adolescence disrupts sleep. This could have deleterious effects on the health, functioning, and development of young people. It is imperative that action is taken to prevent or reduce alcohol-related sleep disturbances during the final stages of human development. Interventions should aim to delay and reduce alcohol consumption, enhance cognitive function, and improve sleep quality to protect the health and wellbeing of young people.

DR

Julia Chan

Lecturer, Psychology

Melbourne School of Psychological Sciences

DR

Julia Chan

Contact Julia Chan

Division

Faculty of Medicine, Dentistry and Health Sciences

DR

Julia Chan

Print

Julia Chan's Short Profile

Enquiries

Contact