Alcohol acts as a sedative that interacts with several neurotransmitter systems
important in the regulation of sleep. Acute administration of large amounts of alcohol
prior to sleep leads to decreased sleep onset latency and changes in sleep architecture
early in the night, when blood alcohol levels are high, with subsequent disrupted, poor
quality sleep later in the night. Alcohol abuse and dependence are associated with chronic
sleep disturbance, lower slow wave sleep, and more rapid eye movement sleep than normal,
that last long into periods of abstinence and may play a role in relapse. The chapter
outlines the evidence for acute and chronic alcohol effects on sleep architecture and
sleep EEG, evidence for tolerance with repeated administration, and possible underlying
neurochemical mechanisms for alcohol’s effects on sleep. Also discussed are sex
differences as well as effects of alcohol on sleep homeostasis and circadian regulation.
Evidence for the role of sleep disruption as a risk factor for developing alcohol
dependence is discussed in the context of research conducted in adolescents. The utility
of sleep evoked potentials in the assessment of the effects of alcoholism on sleep and the
brain and in abstinence-mediated recovery is also outlined. The chapter concludes with a
series of questions that need to be answered to determine the role of sleep and sleep
disturbance in the development and maintenance of problem drinking and the potential
beneficial effects of the treatment of sleep disorders for maintenance of abstinence in
alcoholism.