Curr Psychiatry Rep (2014) 16:487 DOI 10.1007/s11920-014-0487-3

SLEEP DISORDERS (P GEHRMAN, SECTION EDITOR)

Sleep and Substance Use Disorders: An Update Deirdre A. Conroy & J. Todd Arnedt

Published online: 19 August 2014 # Springer Science+Business Media New York 2014

Abstract Substance use disorders (SUD) are common and individuals who suffer from them are prone to relapse. One of the most common consequences of the use of and withdrawal from substances of abuse is sleep disturbance. Substances of abuse affect sleep physiology, including the neurotransmitter systems that regulate the sleep-wake system. Emerging research now highlights an interactive effect between sleep disorders and substance use. New findings in alcohol and sleep research have utilized sophisticated research designs and expanded the scope of EEG and circadian rhythm analyses. Research on marijuana and sleep has progressed with findings on the effects of marijuana withdrawal on objective and subjective measures of sleep. Treatment studies have focused primarily on sleep in alcohol use disorders. Therapies for insomnia in cannabis disorders are needed. Future research is poised to further address mechanisms of sleep disturbance in alcoholics and the effect of medical marijuana on sleep and daytime functioning.

Keywords Sleep latency (SL) . Wake after sleep onset (WASO) . Total sleep time (TST) . Sleep efficiency (SE; TST/ time between “lights out” and “lights on”) . Percentages of stages 1 (S1%), 2 (S2%), 3 (S3%), 4 (S4%), Slow wave activity (SWA) . Slow wave sleep (SWS%) . Rapid eye movement (REM%) Sleep . REM latency (REM-L; duration between “sleep onset” and “REM onset”)

This article is part of the Topical Collection on Sleep Disorders D. A. Conroy (*) : J. T. Arnedt University of Michigan Department of Psychiatry, 4250 Plymouth Road, SPC 5740, Ann Arbor, MI 48109-2700, USA e-mail: [email protected]

Introduction Substance use disorders (SUDs) are common and persistent, and individuals who suffer from them are prone to relapse. Each year, substances of abuse affect millions of adults and families, cost medical, economic, criminal, and social sectors of society more than half a trillion dollars, and contribute to more than 75,000 deaths in the U.S [1]. This common disorder can develop in any individual, but the risk of SUDs can be higher given an individual’s biological predisposition (e.g., genetic vulnerability), environment, and developmental stage (e.g., adolescence). SUDs also commonly co-occur with mental illness, which is associated with these same shared risk factors [2]. The chronic use of substances of abuse may result from a desire to alleviate negative affect, such as anxiety or depressed mood, alleviate physical pain, to improve sleep, or to enhance experience of pleasure. Once dependence has developed, withdrawal from the substance can be associated with a number of unpleasant consequences. One of the most common consequences of the use of and withdrawal from substances of abuse is sleep disturbance. Sleep disturbances have been reported to occur in up to 90 % of alcoholics [3]. The following review will focus on sleep disturbance associated with substance use disorders. Over the past several decades, sleep disturbances have been well characterized in several substances of abuse such as in alcohol [4, 5], marijuana [6], nicotine [7], caffeine [8], and cocaine [9] . For more details on these and other substances of abuse, please see Table 1. Discoveries utilizing animal research have been increasing over the past several years, particularly with respect to the interaction between alcohol and the circadian [18–21] and homeostatic [22•] systems. This review will primarily focus on these interactions in human studies. It will also focus primarily on the effects of alcohol and cannabis use disorders on sleep.

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Table 1 Effects of substances of abuse on sleep and wakefulness in humans1 Substance of abuse

Alcohol Intoxication

Sleep continuity

Sleep architecture

Other

SL

TST

SE

REM-L

REM%

SWS%



↑ to ↓

↔ to ↓



↔ to ↓













↓ ↔

↓ ↔ to ↓

↑ to ↓ ↔

↔ ↔

↓ ↔

↓ ↑ to ↓

↓ ↓

↑ ↓

↓ ↑ to ↔

↓ ↔ to ↓

↔ ↓

↔ ↓

↓ ↓

↓ ↑

↑ ↓

↓ ↑

↓ ↑

↑ ↓

↓ ↑

↑ to ↔ ↓

↓ daytime sleepiness on MSLT [15] ↑ daytime sleepiness on MSLT [16]









↔ to ↓

↑ central sleep apnea and irregular breathing patterns with chronic opiate therapy[17]

Withdrawal ↑ Caffeine Intoxication ↑ Withdrawal ↑ to ↔ Nicotine Intoxication ↑ Withdrawal ↑ to ↓ Marijuana Intoxication ↑ to ↓ Withdrawal ↑ Cocaine and other stimulants Intoxication ↑ Withdrawal ↓ Heroin and other opiates Intoxication ↑ to ↔ Withdrawal GHB2

0

0



0





Intoxication Withdrawal Rohypnol3 Intoxication Withdrawal

↔ to ↓ 0

↔ 0

↔ 0

↓ 0

↔ to ↓ 0

↑ 0

↓ 0

↑ 0

↑ 0

↑ 0

↓ 0

↔ 0

0 0

0 0

0 0

0 0

0 0

0 0

↔ ↑

↓ ↓

↔ to ↓ ↓

↔ ↓

↓ ↑

↔ ↔

Ketamine Intoxication Withdrawal MDMA Intoxication Withdrawal

↑ SDB risk with increasing consumption for men; biphasic effect on daytime sleepiness (MSLT)[10] ↑ SDB and PLMs among alcoholics[11, 12] ↓ daytime sleepiness on MSLT [13]

↑ daytime sleepiness on MSLT[14]

SL=sleep latency; TST=total sleep time; SE=sleep efficiency; REM-L=REM latency; REM%=% rapid eye movement sleep; SWS%=% slow wave sleep ↑=increased compared to baseline; ↓=decreased compared to baseline; ↔=no change compared to baseline; 0=insufficient information 1

Results reported are based on preponderance of data from laboratory studies in humans. Findings across individual studies frequently varied. Note that intoxication results for alcohol, nicotine, and club drugs refer to healthy controls 2

FDA approved for treatment of cataplexy and excessive daytime sleepiness associated with narcolepsy

3

Not approved for medical use in U.S.

The specific focus on alcohol and marijuana for this update is due to the expanding literature in the past few years on the interface among sleep, circadian rhythms, and these substances in particular. Novel findings in the field of alcohol and sleep research have utilized more sophisticated research designs and expanded the scope of EEG and circadian rhythm analyses. The field of marijuana and sleep has also progressed with respect to the effects of marijuana withdrawal on

objective and subjective measures of sleep. This emphasis may reflect the increased availability of marijuana as a result of changes in laws related to marijuana use. There are now many states that have decriminalized marijuana or passed medical marijuana laws, and some states have included insomnia as one of the symptoms for which medical marijuana may be prescribed. However, research has still been limited by variable methodologies to study marijuana dose, dosage

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timing (e.g., immediately prior to sleep onset or throughout the day), preparations of marijuana (e.g., THC vs. marijuana extract), and amount of prior drug experience among participants. This goal of this review is to bring the reader up-to-date on new findings published over the past 1-3 years.

Etiology The intermittent use of many substances of abuse can cause neurobiological or behavioral sensitization, amplifying the rewarding effects of the drug. With repeated administration, down regulation of these systems may lead to a decrease in the impact of the substance on the reward circuits of the brain, leading the abuser to substance dependence [2]. Substances of abuse can alter the homeostatic balance of neurotransmitters systems, such as acetylcholine, GABA, dopamine, glutamate, norepinephrine, and the orexin the systems [23–26]. These neurochemical changes may lead to tolerance (the need to escalate the dose of the drug to achieve the same effect) and withdrawal (consequences of not using the drug), which can further contribute to the development of dependence [2, 27]. Many of the same neurotransmitter systems affected by substances of abuse are intimately involved in the regulation of sleep-wake systems [28]. As a result, sleep disturbances and circadian dysregulation may result at various stages of substance use or withdrawal.

Early Detection and Prevention of Substance use Disorders Substances of abuse can impair sleep at any age, but this can be particularly prevalent during adolescence, a time when both sleep problems and drug seeking behaviors increase [29]. In one study, adolescents who used any illicit drug (most often marijuana) were 2.6 times more likely to report a sleep problem compared to those who remained substance-free [30]. In a nationally representative sample, adolescents with insomnia were 1.75 times as likely to report marijuana use compared to adolescents without insomnia [31]. Sleep disturbances have also been associated with substances of abuse in young adults [32–34]. The presence of a mood disorder may increase the likelihood of developing a substance use disorder with associated sleep disturbance. In a longitudinal study of 364 alcohol-dependent adults, depression and drinking quantity separately predicted insomnia severity even when controlling for age, time, and gender [35]. In summary, the abuse of substances can be influenced by a number of factors, including stage of development and/or psychological factors. Early substance abuse may contribute to sleep problems, which may play a role in the choice to escalate dose of the use of the drug, leading to the development of a substance use disorder.

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A Bidirectional Relationship A developing field of research, beginning nearly a decade ago [36], has begun to show that sleep disturbances experienced early in life may precede and/or predispose an individual to developing a substance use disorder. Subsequent studies have supported this finding, highlighting the relationship between sleep problems (in the absence of substance abuse) during adolescence and future involvement with substance of abuse [31, 37, 38]. Pasch et al. (2012) conducted a longitudinal study using a cross-lagged structural equation model to determine the bi-directional relationships between sleep and substance use in teens. Sleep patterns (i.e., the times teens went to sleep and woke up and the consistency of those patterns across weekdays and weekends) and duration of sleep in approximately 700 teenagers at baseline predicted the onset of cigarette, alcohol, and marijuana use after 2 years. This finding persisted even after controlling for covariates such as pubertal development, body mass index, and depressive symptoms. The reverse direction also remained; cigarette and alcohol use also predicted reduced sleep on the weekend two years later [39]. Hasler et al. (2014) also examined the longitudinal relationship between sleep and alcohol use. Data on insomnia symptoms, hypersomnia, and variability in weekday to weekend sleep duration was obtained by 696 teens with (n=347) and without (n=349) alcohol use disorder (AUD) at baseline and then at 1, 3, and 5 year follow up visits. The teens without AUD at baseline (controlling for sex, age, depression, and current alcohol symptoms) that had greater sleep complaints had more alcohol symptoms one year later. Teens with variable sleep times at baseline had more alcohol symptoms 3 and 5 years later [40]. These studies support a bidirectional component of the relationship between sleep patterns and substance use. Theoretical models to explain this relationship have highlighted influences of both the biological rhythm changes in sleep regulation as well as the effects of sleep deprivation as key changes affecting emotional regulation, self-control, and risk taking behaviors during adolescence [41–43]. Functional magnetic resonance imaging of the adolescent brain has now partially supported this as one study showed that shifts from weekend to weekday sleep schedule affected the reward sensitivity in the medial prefrontal cortex (mPFC) and striatum, key areas of the brain involved in reward functioning [44]. The studies described above have even helped to support a change in the current nomenclature for the diagnosis of insomnia. For example, “insomnia due to a drug or substance” was considered a form of secondary insomnia (i.e., caused by the substance use disorder). Now, it is considered a subtype of a chronic insomnia disorder. The term “insomnia due to a substance” is no longer used in Diagnostic and Statistical Manual-DSM-V[45] or International Classification of Sleep Disorders, third edition (ICSD-3) [46]. These changes

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acknowledge the interactive effects between sleep disorders and substance use as well as other psychiatric and medical disorders (see further details in Table 1). In summary, while these epidemiological studies are informative and suggest bidrectionality, they do not inform us regarding the relationship of amount of the substance used to affect sleep, or as to common versus reciprocal etiology. Nevertheless, current research suggests that early identification and treatment of persistent sleep difficulties should be considered.

Effects of Substances on Sleep Alcohol use Disorder An estimated 17 million Americans have an alcohol use disorder (AUD), i.e., including both alcoholism and harmful drinking that does not reach the level of dependence [47] and only 15 % ever seek treatment [48]. In a healthy control sample, high alcohol consumption (BrAC of 0.11±0.01 g%) at bedtime has been shown to result in sleep disruption, which is more significant in women than in men [49]. In individuals with alcohol dependence, studies show alcohol produces prolonged latency to sleep, decreased REM% and decreased total sleep time. Earlier studies have shown alcohol produces increases in slow wave sleep in the first half of the night [4] in alcoholics whereas other more recent protocols have not [50, 51]. Recent findings suggest that an individual’s time of day preference, or chronotype, may predispose an individual to substance use. For example, the tendency to go to bed late, or being an “evening chronotype,” has been found to be moderated by alcohol drinking and smoking [52]. One of the proposed mechanisms of sleep and circadian alterations in alcoholics is a reduction in melatonin, a circadian output hormone. Moderate amounts of alcohol have been shown to reduce nocturnal melatonin levels in healthy adults [53]. In substance abusing teens, the time interval between dim light melatonin onset and wake time was significantly and positively related to the Substance Problem Index (SPI), a scale of the severity of substance use [54]. In adult male abstinent alcohol dependent subjects, a lower level of melatonin during the early part of the night and a delay in the nocturnal rise of melatonin [55] was found. This finding was supported in two additional samples that included abstinent female alcohol dependent individuals [56, 57]. These stud ies may sugg est a ro le for chronotherapeutic options (use of therapies that target the circadian timing system, such as light or exogenous melatonin) in alcohol dependent individuals. Assessment of biomarkers of circadian phase, such as melatonin, as well as assessment of sleep/wake patterns via actigraphy or other mobile technology may become part of the comprehensive sleep and circadian assessment.

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Cannabis use Disorder Marijuana, also known as cannabis, is one of the most commonly used drugs in the United States. It is most prevalent in the United States (US) among 18-25 year olds with approximately 32 % of non-college, 35 % of college-attending reporting past year use, and roughly 40-75 % of adults aged 18 to 45 years reporting experience with it during their lifetime. As many as one third of 12th graders report having used marijuana at least once during the past year, with one in 20 teens reporting daily use [58–61]. More individuals in recent years are reporting self-treating with marijuana for a number of medical and psychiatric symptoms, most commonly pain, anxiety, insomnia related to PTSD [62, 63] and sleep[64]. The subjective impressions of the effect of marijuana on sleep are that it facilitates sleep onset. One of the initial studies conducted on this topic in 1973 showed that higher doses of THC (20 mg) significantly reduced self-reported latency to fall asleep and had no effect on sleep continuity in sample of males with insomnia [65]. A 2004 double-blind, placebo-controlled study compared administration of placebo, 15 mg Delta-9tetrahydrocannabinol (THC), 5 mg THC combined with 5 mg cannabidiol (CBD), and 15 mg THC combined with 15 mg CBD at bedtime in chronic marijuana users. With the higher dose combination, subjects reported increased sleepiness and changes in mood the next day. The authors suggested that 15 mg THC is sedative, while 15 mg CBD may be alerting as it increased WASO and counteracted the residual sedative activity of 15 mg THC [66]. This study highlights the complexity that the dose and combined effects of the cannabis components may introduce in its effects on sleep. Despite the subjective impressions of faster sleep onset, most polysomnographic (PSG) studies show no change in sleep latency (SL) or wakefulness during the night following acute marijuana administration or with continued use [67], except at higher doses when both can be acutely prolonged [68]. Acute reductions in stage 3 percent (S3%) and increases in stage 4 percent (S4%) with an overall slight increase in SWS have been observed [66, 67, 69] but reductions in SWS may result with continued use [69]. Reductions in REM sleep time, REM density (number of eye movements during REM sleep), and occasionally latency to REM sleep (REM-L ) have also been documented [67]. In summary, subjective impressions suggest an improvement of sleep onset and continuity, but polysomnographic studies reveal either no change or longer SL and wake after sleep onset (WASO) at higher doses. This may reflect a form of sleep state misperception with marijuana, similar to alcohol dependent individuals with insomnia [70].

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Withdrawal

Marijuana

Alcohol

Many studies that have evaluated sleep indices in marijuana users have done so in heavy marijuana users who have sought substance abuse treatment [6, 82, 83•, 84•]. Discontinuation of marijuana following chronic use reliably produces a withdrawal syndrome of equivalent severity and duration to that following tobacco cessation [85]. A review of the literature prior to 2004 revealed that up to 76 % of heavy marijuana users who stop abruptly report disturbed sleep [86]. On the first night without marijuana, young adult heavy marijuana users (marijuana use ≥5 times per week over the past 3 months) show decreased total sleep time and less slow wave sleep compared to controls [6]. In a community sample of non-treatment seeking marijuana users, difficulty sleeping was reported by 32 % of the sample; the sleep problem developed relatively quickly, 2.74 (+/-3.77) days after last marijuana use. Most (69 %) of the participants in that sample then used marijuana, alcohol, or took a “tranquilizer” to aid in sleep [87]. Objective sleep measured by PSG appears to show the continued worsening of sleep over time. After two weeks of marijuana abstinence, total sleep time (TST), rapid eye movement (REM) sleep, WASO, and sleep efficiency (SE%) worsen [88]. This sleep disturbance has been shown to persist for more than 45 days into a marijuana abstinence period [85]. A subset of withdrawal symptoms are reversed with oral THC administration, but sleep disturbances remained across a 10 day period. [89]. Identifying sleep disturbance in marijuana withdrawal is important as it may interfere with maintaining abstinence during a quit attempt. Studies conducted in younger samples show that one in five young adults who use marijuana (and no other illicit drugs) report insomnia (e.g., have trouble going to sleep or staying asleep most or all of the time); significantly higher than persons not using marijuana [30, 31]. In a sample of 100 military veterans attempting to quit marijuana, those who reported poor sleep quality (via the Pittsburgh Sleep Quality Index) did not reduce marijuana use as much as veterans who perceived their sleep quality as good at baseline [82]. In addition, poor sleep quality was found to moderate the relationship between depression symptoms and “problematic” marijuana use [83•] and was a risk factor for a lapse following a quit attempt [84•]. In the sleep laboratory setting, sleep disturbances worsened among daily marijuana smokers abstaining for three days, and returned to baseline when marijuana use was reinitiated [90]. In summary, both subjective and objective sleep disturbances have been observed acutely and persistently following discontinuation of heavy marijuana use. In summary, given the studies reviewed above showing that sleep disturbance during abstinence from marijuana can precipitate relapse to cannabis use, sleep focused treatment interventions are needed. Current studies supported by the

Sleep architecture of the sleep EEG during protracted abstinence from alcohol shows sleep fragmentation, increased arousal during sleep, profound decrease in SWS, and increases in REM sleep [71, 72], with a gradual recovery occurring at least for some subjects [72]. Recent studies show alterations in the sleep homeostatic mechanisms in alcoholics. When compared to healthy controls, spectral analyses of the sleep EEG show that alcohol dependent men [71, 73] and women [71] have less slow wave activity (SWA) power. When undergoing a sleep “challenge”, i.e., staying awake 3 hours later than typical bedtime, alcoholics show a blunted response in SWA power in the EEG compared to depressed men [73] and healthy controls [74]. Other physiological differences have been detected in the sleep of recently recovering alcoholics. For example, reduced heart rate variability (a sign of poor autonomic nervous system functioning), was found in the first part of the night, compared to age and sex matched healthy controls [75]. Sleep evoked potentials are also impaired in recently recovering alcohol dependent subjects, but appear to show recovery over time. The evoked amplitude of the K-complex (an EEG delta wave that occurs in stage 2 sleep) in response to auditory signals was examined in 42 (27 men) alcoholics and healthy controls during sleep. The study specifically analyzed K-complexes in alcoholics because K-complexes are delta frequency waveforms, produced by the same generator mechanisms as those responsible for SWS delta EEG activity [76]. They have also been used as a measure of the ageing process. There were fewer K-complexes and the amplitudes of P2, N550, and P900 compared to healthy controls suggesting a negative impact of alcohol abuse on the process that generates K complexes [77•]. In a follow-up study, 15 alcohol dependent subjects (12 men) underwent standard sleep evoked potential protocols on two occasions separated by one year. When this sample was examined again one year later, the N550 and P900 amplitudes were significantly higher [78•]. This study is in line with several other studies that have shown structural and functional brain recovery with prolonged abstinence [79–81]. However, whether these results suggest that this is a recovery of sleep after one year is still not certain. These studies do suggest that alterations in sleep physiology occur during early abstinence and that the sleep EEG may be a window into the process by which the brain changes during recovery from alcohol dependence. Consideration of these signature brain patterns in combination with subjective sleep reports may have implications for treatment.

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National Institute of Drug Abuse are underway to examine pharmacotherapy and psychosocial therapies for insomnia in cannabis disorders (http://report.nih.gov/index.aspx, 2014).

Treatment Pharmacotherapy Most of the treatment studies conducted thus far have focused on sleep disturbances in the presence of an alcohol use disorder. Many prescribing physicians may be reluctant to prescribe traditional hypnotics that target the benzodiazepine receptors in the SUD patient because of their abuse potential, withdrawal effects, and potential for overdose if mixed with alcohol. For these reasons, clinical guidelines specific to SUDs patients have been recommended for addressing insomnia complaints in early recovery [91]. Gabapentin, at doses of 300 to 1800 mg at bedtime, has been found to be useful in treating insomnia in abstinent alcoholdependent outpatients and appears to be safe (for review see Howland 2014) [92]. It is often used as a treatment for insomnia in the SUD patient because it is not metabolized by the liver, does not lower the seizure threshold, and does not require blood monitoring for toxicity. However, a small pilot study found that the administration of gabapentin during early abstinence did not improve sleep compared to placebo, though it did delay the onset to heavy drinking [93]. Another study showed superior sleep outcomes of trazodone versus placebo over 12 weeks of treatment in alcohol-dependent patients, but heavy drinking was higher in the trazodone-treated group [94]. A combination of gabapentin with naltrexone for 16 weeks prolonged the time to first heavy drinking period in comparison with those who took naltrexone alone [95]. Sleep disturbance was associated with more drinking in the naltrexone only group. Quetiapine may be of potential benefit for sleep disturbance associated with alcohol dependence in abstinent patients [96]. In one study, quetiapine XR at bedtime (with doses titrated from 50 mg up to 400 mg across one week) (n=10) or placebo (n=10) was administered to recovering alcohol dependent patients with sleep complaints for 8 weeks. PSG assessed objective sleep and standard sleep questionnaires assessed subjective sleep. There was a reduction in PSG identified WASO and improvement in subjective ratings of insomnia among those who took the quetiapine XR, but this improvement was not sustained across the 9 week assessment period [97]. Side effects, such as dry mouth and somnolence, were noted in both the treatment and placebo condition, but were more common in the treatment condition. However, the risk of tardive dyskinesia and metabolic abnormalities associated with the use of atypical antipsychotics suggests that they should be used cautiously, if at all, for insomnia.

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The melatonin receptor agonist ramelteon is also an option for treating insomnia in recovering alcoholics, although controlled trials are lacking. One study to date has tested ramelteon in recovering alcoholics. Four weeks of 8 mg nightly in five recovering alcoholic patients resulted in a reduction of scores on an insomnia questionnaire, a reduction in latency to sleep, and one additional hour of total sleep time [98]. Agomelatine, an antidepressant approved by the European Agency that is a melatonergic agonist (MT1 and MT2 receptors) and a 5-HT2C antagonist indicated in the treatment of major depressive episodes, has been shown to improve sleep in a small study of nine alcohol dependent patients with sleep problems. Participants who took between 25 mg to 50 mg of agomelatine nightly had improved subjective sleep quality after 6 weeks. Mean Pittsburgh Sleep Quality Index scores dropped from 13.1 (+/1.7) to 7.8 (+/-1.7) post treatment [99]. Hepatoxicity, a common concern with agomelatine, was not evident in these doses. Cognitive Behavioral Therapy for Insomnia Cognitive-behavioral therapy for insomnia (CBT-I) is a multicomponent therapy that includes behavioral and cognitive strategies to consolidate nighttime sleep, and improve sleep quality and daytime functioning. It has been utilized as a nonpharmacological treatment approach for insomnia in alcohol dependent individuals in three studies. First, Currie and colleagues [100] randomized 60 alcoholic outpatients (mean age 43.3±10.9 years, 42 men) to individual CBT-I therapy (five sessions over seven weeks), self-help manual with five telephone support calls, or wait-list control. Post-treatment followups assessing sleep and drinking were conducted 3 and 6 months post-treatment. Participants in both active treatment groups had greater post-treatment improvements than controls on diary measures of sleep quality, SL, SE, and number of awakenings. The treatment gains were maintained at 3- and 6month follow-up. However, treatment appeared to have little positive impact on alcohol relapse. Second, in an 8-week uncontrolled trial of CBT-I in seven recovering alcoholic patients, Arnedt et al. 2007 found improvements in sleep quality and daytime functioning with no relapse to drinking [101]. Finally, a randomized controlled trial that delivered either CBT-I (n=9) or behavioral placebo treatment (n=8) to abstinent AD patients showed that sleep diary rated SE%, WASO, and daytime fatigue ratings improved more in the CBTI compared to the BPT group. No group differences were found in the number of participants who relapsed to drinking [102].

Conclusion The current conceptualization of sleep and substance use disorders has evolved over the past several years. One cannot

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assume that sleep disturbances are directly due to a substance use disorder as epidemiological studies suggest that sleep disturbances may predate the onset of the substance disorder. Nevertheless, once the substance use disorder develops, sleep disturbances are often associated with both the acute and prolonged withdrawal from the substance. In the case of alcohol and marijuana, this sleep disturbance may persist even after weeks or years of withdrawal. Future research studies are poised to further address the mechanisms of sleep disturbance in alcoholics and the effect of medical marijuana on sleep and daytime functioning.

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Compliance with Ethics Guidelines 18. Conflict of Interest Deirdre A. Conroy and J. Todd Arnedt declare that they have no conflict of interest. Human and Animal Rights and Informed Consent This article does not contain any studies with human or animal subjects performed by any of the authors.

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References

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Papers of particular interest, published recently, have been highlighted as: • Of importance

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Sleep and substance use disorders: an update.

Substance use disorders (SUD) are common and individuals who suffer from them are prone to relapse. One of the most common consequences of the use of ...
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