Review discusses alcohol's acute and chronic effects on sleep in individuals with sleep disorders, suggesting substantial disruption.
Alcohol use is often used as a sedative and administered as a self-treatment for sleep disorders. Acute moderate use may reduce sleep onset latency, but accumulating evidence suggests that alcohol does indeed cause significant disruption of normal sleep architecture. This review discusses the acute and chronic effects of alcohol on sleep physiology and sleep quality. Acutely, alcohol shortens sleep onset latency and promotes first-half-of-the-night slow-wave sleep while suppressing REM sleep and increasing sleep fragmentation throughout the second half of the night as blood alcohol levels decrease. Chronic and heavy intake accentuates insomnia, frequent awakenings, decreased sleep efficiency, and long-term circadian disruption. These effects are mediated by alcohol-induced changes in major neurotransmitter systems, including GABA, glutamate, serotonin, norepinephrine, and acetylcholine, which play a crucial role in regulating sleep-wake functions. High rates of insomnia among individuals with alcohol use disorders reflect the complex interrelationship between alcohol and sleep disturbance. Overall, alcohol should not be considered a therapeutic sleep aid but rather a substantial disruptor of restorative sleep.
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Beng et al. (2026) studied this question.
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