The measurable disruption of normal sleep architecture and quality caused by the consumption of ethanol, a psychoactive substance. Clinically, this impact is characterized by changes in sleep latency, a reduction in REM sleep proportion, and increased sleep fragmentation, which compromises the restorative processes.
Origin
This concept originates from chronobiology and sleep medicine, addressing the pharmacological effects of alcohol on the central nervous system’s sleep-wake regulatory centers. The physiological consequences are directly observed in polysomnography studies following ethanol ingestion.
Mechanism
Alcohol initially acts as a sedative, decreasing sleep latency by enhancing GABAergic activity in the brain, which is an inhibitory neurotransmitter. As the alcohol is metabolized by the liver, the resultant rebound effect leads to sympathetic nervous system activation, resulting in fragmented sleep, suppression of the crucial REM phase, and an overall decrease in the sleep cycle utility necessary for hormonal regulation and cognitive consolidation.
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