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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.

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.

Understanding the sleep problems related to substance use disorders requires characterizing them both subjectively and objectively, while considering how sleep responds to periods of use and abstinence. This review will describe such research with regard to alcohol, cannabis, cocaine, and opioids. In addition, this review will discuss evidence that sleep abnormalities predict use and relapse, and that sleep abnormalities can be modulated to improve clinical outcome. This paper will also review potential pharmacological agents that modulate sleep. Psychotherapy options, albeit evidence-based and of clear clinical value, will not be discussed in this review as these are addressed elsewhere [15, 110].

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.

Alcohol is widely used as a sleep-promoting agent. However, as the consumption of alcohol becomes chronic, alcohol has less of an hypnotic effect [196]. Significant, self-reported sleep problems are highly prevalent among alcohol users with rates of clinical insomnia between approximately 35 and 70 % depending on the setting and stage of use, among other parameters [35, 48]. These rates are substantially higher than those observed in the general population (i.e. 15 to 30 %) [32]. Complaints typically include difficulty falling asleep, frequent awakenings, daytime sleepiness, and abnormal sleep quality [15, 34, 196], but could also include hypersomnia [196]. Notably, sleep complaints associated with alcohol use disorders are one of the most refractory problems to resolve [34, 69, 82], and insomnia is the most frequent complaint among alcoholics after they stop drinking [132].

Objective measurement of sleep in persons with alcohol use disorders confirms self-reported sleep problems in many respects, and provides additional insight into the nature of the underlying sleep abnormalities.

Although it is known that alcohol can decrease sleep latency when consumed by healthy persons [124], chronic use leads to increased sleep latency, consistent with individual self-report. Published studies show that SL is prolonged during periods of drinking [9, 33, 85, 199, 221], during acute withdrawal (e.g., weeks 1 and 2 of abstinence) [9, 33, 85, 199, 221], and during post-acute withdrawal (e.g., weeks 2 through 8) [33], (Table 2) with evidence for sleep latency prolongation in inpatient and outpatient settings (e.g., [83, 123, 183]), and when controlled for age and sex, among other variables [26]. After the second month of abstinence, sleep latency may still be increased [213], or normalized [174], with evidence for normalization also present after five [69] and 9 months of abstinence [213].

Congruent with increased sleep latency, total sleep time is reduced in persons with alcohol use disorders during periods of drinking, acute withdrawal, and post-acute withdrawal [33, 85, 86, 199, 221], with very few exceptions [9]. Numerous studies examining total sleep time from 2 to 4 weeks of abstinence document reduced sleep time compared to healthy controls [69, 83, 183] (Table 2). Reduced total sleep time has also been observed in study designs that control for age and sex, among other variables [26].

Considerable evidence points to deficits in slow wave sleep time (i.e. stage 3 and stage 4 sleep, or stage N3 sleep in the newer nomenclature) or slow-wave sleep activity (i.e. EEG spectral power in the slow wave frequency range) in persons with alcohol use disorders [33]. Most of this evidence comes from studies reporting results from the first few weeks of abstinence, including acute withdrawal [196], subacute withdrawal (i.e. days 8 and 12); [106] (Table 2), and beyond [26, 69, 83, 127].

Intriguingly, acute alcohol use has been shown to reverse the chronic slow wave sleep deficits observed in chronic alcohol users [33, 86]. Given the widespread importance of slow-wave sleep [65] in factors including sleep continuity, learning, and memory, as well as other types of cognitive performance, the deficits associated with chronic use (and their reversal with acute use of alcohol) suggests the particular importance of slow-wave sleep in alcohol use disorders. More specifically, as the brain processes that underlie the generation of these slow waves appear to be chronically altered by chronic alcohol use, and to be temporarily restored by acute use, this chronic alteration is implicated as a potential factor in relapse.

Notwithstanding the above findings, the literature on alcohol and REM sleep has some inconsistencies (Table 2). For example, a meta-analysis examined six studies that did not consider covariates and four studies that controlled for variables such as age and sex (all participants abstinent for at least 3 weeks). Even though the analyses among all subjects showed no differences in REM measured as the percentage of total sleep (REM%), the analyses did find increased REM% in persons with AUD compared to controls when controlling for some variables [26]. Other studies have found no difference in REM% between chronic alcohol users and normal controls in the second [106] and third [83] week of abstinence. Additionally, supporting the finding of no difference in REM between chronic alcohol users and controls, a study examining REM time after 4 weeks of abstinence found no difference between subjects with AUD and normal controls [183]. Another discrepancyappears in the form of a study that found REM% among participants with AUD to be reduced after 12 weeks of abstinence in comparison with REM% after 4 weeks of abstinence, arguing against a lasting REM rebound [171].

Data on REM latency in persons with alcohol use disorders is more limited but also show some discrepancies. For instance, while some studies report that REM latency is decreased during the second week of abstinence [69, 106], as well as up to two years later [69], other studies do not report differences in REM latency [26, 32] (Table 2). One potential explanation for the inconsistencies in this measure could lie in the heterogeneity of subjects with AUD with regard to co-occurring conditions like depression. Supporting this idea is the finding that AUD subjects with secondary depression exhibit shorter REM latency compared to AUD subjects who do not have secondary depression [83].

Although there is limited published data on the relationship between subjective and objective sleep measurement in persons with alcohol use disorders, one group studied 172 individuals with alcohol use disorders of whom 104 had insomnia as determined by the Sleep Disorders Questionnaire [35]. They found that participants with baseline insomnia had longer sleep latency and lower sleep efficiency at an average of approximately 1 month abstinent than those without, suggesting a correspondence between self-report and objective measurement.

In a small study, increased sleep latency associated with chronic alcohol use was linked with lower overall melatonin levels as well as with a delay in the onset and peak of melatonin [123]. A much larger study fo