Research Article: Sleep abnormalities associated with alcohol, cannabis, cocaine, and opiate use: a comprehensive review

Date Published: April 26, 2016

Publisher: BioMed Central

Author(s): Gustavo A. Angarita, Nazli Emadi, Sarah Hodges, Peter T. Morgan.


Sleep abnormalities are associated with acute and chronic use of addictive substances. Although sleep complaints associated with use and abstinence from addictive substances are widely recognized, familiarity with the underlying sleep abnormalities is often lacking, despite evidence that these sleep abnormalities may be recalcitrant and impede good outcomes. Substantial research has now characterized the abnormalities associated with acute and chronic use of alcohol, cannabis, cocaine, and opiates. This review summarizes this research and discusses the clinical implications of sleep abnormalities in the treatment of substance use disorders.

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Sleep problems are commonly associated with drug and alcohol use. Nearly 70 % of patients admitted for detoxification report sleep problems prior to admission, and 80 % of those who report sleep problems relate them to their substance use [169]. The association between substance use and sleep problems appears to be bidirectional [105, 110], with sleep problems increasing risk for developing substance use disorders [31, 89, 210], and acute and chronic substance use leading to acute and chronic problems with sleep [44, 47, 89, 97, 104, 138, 156, 168]. Evidence also indicates that long-term abstinence from chronic substance use can reverse some sleep problems [13, 37]. This paper aims to explore and clarify the strong yet not entirely understood connection between abnormalities in sleep and substance use. By improving our understanding of sleep disorders that either predispose to substance use or are the result of chronic substance use, we may be better able to prevent and treat substance use disorders.

This is a narrative, non-systematic review of clinical trials conducted in humans. For the literature search, Pubmed, Ovid Medline, and Web of Science databases were used. For each drug (e.g., alcohol, cannabis/marijuana, cocaine, and opioids/heroin) keywords included terms describing abnormal/pathological use (e.g., alcohol use disorders, alcohol abuse, alcohol dependence, and alcohol addiction, etc.) combined with terms referring to sleep or sleep abnormalities [e.g., sleep, insomnia, polysomnography, total sleep time, slow-wave sleep, rapid eye movement (REM) sleep, sleep latency, REM latency; these terms are defined in Table 1]. In addition to extracting data available in each of the retrieved articles, reference lists from each retrieved article were examined to identify articles missed by the initial search. For each drug, the available literature on subjective measurements, objective measurements, the relationship between subjective and objective measurements, clinical and laboratory correlates of sleep outcomes, and pharmacotherapies related to sleep were summarized.Table 1Sleep terminologyHomeostatic sleep driveThe drive to sleep that progressively builds with continued wakefulnessInsomniaA sleep disorder in which the quantity or quality of sleep is less than desired, usually characterized by difficulty falling or staying asleep, or waking too early, and experiencing daytime consequences of reduced sleepPolysomnography (PSG)A technique that records brain activity, eye movements, and muscle tone in order to study sleep and diagnose sleep disordersRapid eye movement (REM) sleepThe phase of sleep characterized by conjugate eye movements, paralysis of other muscles, and brain activity that is most similar to wakefulnessREM densityThe frequency of rapid eye movements occurring during REM sleep. REM density increases over the course of the sleep period and is greatest when homeostatic sleep drive (sleep pressure) is lowestREM latencyThe amount of time from the onset of sleep to the onset of REM sleepREM reboundThe characteristic increase in REM sleep after REM sleep deprivationSelf-administrationA method involving research participants administering a substance to themselves under observation in a clinical settingSleep architectureThe structure of sleep, including non-REM (stages N1, N2, and N3) and REM (stage R) sleepSleep efficiency (SE)The percent of time in bed spent sleeping, calculated as total sleep time divided by time in bedSleep fragmentationDisruption in sleep characterized by awakenings and transitions to light (stage N1) sleep from deeper sleepSleep latency (SL)The amount of time from lights out to sleep onsetSlow-wave sleep (SWS)Also known as stage N3 sleep, slow wave sleep is characterized by low frequency and high amplitude wavesTotal sleep time (TST)The amount of sleep in one complete episode of sleeping, usually reported in minutesWake after sleep onset (WASO)The amount of time awake after the onset of sleep and before final wakening

Overwhelming evidence points to chronic alterations in sleep from chronic use of addictive substances that may be distinct from some or all of the acute effects of those substances. Interestingly, the effects of chronic use on sleep are similar among both CNS stimulants and depressants. Decreased sleep time, increased sleep latency and wake time after sleep onset, and deficiency in slow-wave sleep generation appear to be common to chronic use of alcohol, cocaine, cannabis, and opiates. REM sleep is also affected by acute and chronic use, but may be more sensitive to the pattern or quantity of recent use and time from last use, as results vary more among studies. Also linking these abnormalities are connections with ongoing use and relapse. However, treatment with typical sleep promoting agents that increase sleep time or efficiency by increasing light sleep may be counterproductive. Agents that address deficiency in slow-wave sleep generation and alterations in REM sleep may prove to be more useful in addressing the connection between chronically-altered sleep physiology and ongoing use and relapse, but substantial research still needs to be done to explore this possibility.