When substance abuse grips sleep.

By Regina Patrick, RPSGT

Patients with drug or alcohol addiction may not be willing to report these problems during a sleep study or may not see themselves as having an issue with dependency. Denial or failure to acknowledge drug or alcohol abuse can lead to negative health consequences and also can thwart effective treatment for a sleep disorder. However, when sleep professionals develop a keen eye for when illicit drugs are impacting a patient’s sleep, they can help accurately treat the patient’s sleep disorder.


Alcohol is the most widely abused substance in America. The National Institute on Alcohol Abuse and Alcoholism (NIAAA) estimates that 17.6 million adult Americans have an addiction to alcohol.1 Commonly used illicit drugs include marijuana, cocaine, heroin, methamphetamine, MDMA (ecstasy), and hallucinogen/dissociative drugs. Of these, marijuana is the second most widely abused drug in the United States. The National Institute on Drug Addiction (NIDA) reports that more than 94 million2 Americans 12 years or older have tried marijuana at least once; 1.5 million3 Americans are dependent on or are abusing cocaine; more than 300,000 adult Americans4 use heroin; 1.3 million5 Americans have used methamphetamine; and about 450,000 people6 currently use MDMA.

Alcohol and illicit drug use alter the activity of various neurotransmitters in the brain. Sleep, which depends on the activity of the same neurotransmitters, is affected by alcohol and illicit drug use.


Alcohol (more accurately, ethanol) increases the release of norepinephrine and dopamine and increases the production of beta-endorphin (a neuropeptide that binds with opiate receptors). This initially creates a “high” and sense of well-being. Despite these excitatory effects, alcohol is in actuality a central nervous system depressant. It decreases the excitation of cholinergic pathways and increases the neuroinhibitory actions of GABAergic pathways. This results in the hypnotic effect of alcohol.

Chronic alcohol abuse leads to reduced amounts of rapid eye movement (REM) sleep7 and slow wave sleep,8 and difficulty in initiating and maintaining sleep.7 Recovering alcoholics often struggle with insomnia. As a result, they will use alcohol to get to sleep, which in turn can lead to relapse.

Various studies have found that insomnia may be a predictor of relapse in recovering alcoholics. For example, a 2001 University of Michigan study by alcohol addiction researcher Kirk J. Brower et al7 compared the rate of relapse of alcoholic insomniac subjects with that of alcoholics without insomnia. Both groups had a baseline polysomnographic (PSG) recording and then were followed for 12 weeks. All subjects underwent a second PSG 6 weeks after the study began and a third PSG at 12 weeks. Sleep parameters such as sleep-onset latency, wake after sleep onset, and total sleep time were recorded for each group. Each subject took the self-administered 175-item Sleep Disorder Questionnaire (SDQ), which gives an idea of the subject’s perception of their sleep.

They were asked to estimate how long it took to go to sleep, how long they felt they were awake during the night, and how long they had slept. Brower and associates found that the subjects’ perception of insomnia was validated by PSG, which showed that the subjects had increased latency to sleep onset, increased amounts of wake after sleep onset, and lower sleep efficiency. Relapse during the first 6 weeks of the 12-week period had a high correlation with subjects who believed they had difficulty maintaining sleep. The researchers later did a follow-up assessment with 43% of the subjects an average of 5 months after they had completed their alcohol treatment program. They noted that relapse after treatment was greater among those subjects who had insomnia at the baseline PSG recording. Brower and associates concluded that questioning alcoholics about insomnia and other sleep problems could potentially prevent relapse and improve recovery.


The leaves of the marijuana plant contain the psychoactive chemical tetrahydrocannabinol (THC). THC binds to cannabinoid receptors in the brain. Cannabinoid receptors are concentrated in the basal ganglia (particularly the substantia nigra, pars reticulata, and globus pallidus), the hippocampus, and the cerebellum.9 Scientists10 suspect that THC increases central cholinergic activity, increases catecholaminergic activity, and acts on the GABAergic and serotoninergic pathways. Cannabinoid activity in these areas results in a sense of pleasure, euphoria, altered time perception, and drowsiness. Withdrawal from marijuana can impair sleep quality due to irritability, restlessness, insomnia, and physical symptoms such as nausea, sweating, and increased body temperature.11 Heavy marijuana users attempting to quit will resort to using the drug to ameliorate these withdrawal symptoms. This leads to a high relapse rate.

With the hope of improving marijuana abstinence, researchers Margaret Haney et al12 investigated using the drug divalproex (trade name Depakote) to lessen the insomnia and negative mood associated with withdrawal. Divalproex increases the neuroinhibitory activity of GABAergic neurons and has a mood-stabilizing effect. Subjects were all actively using marijuana addicts who smoked about six cigarettes each day for 6 to 7 days each week. They were given a modified St. Mary’s Hospital Sleep Questionnaire that asked them to answer questions such as: “I slept well last night,” “I woke up early this morning,” “I fell asleep easily last night,” “I feel clear-headed this morning,” “I woke up often last night,” and “I am satisfied with my sleep last night.” They rated their answer on a scale ranging from “not at all” to “extremely.” They were also asked to estimate how many hours they slept the previous night.

The study was a double-blind crossover study. Subjects, while continuing to smoke marijuana, were initially given either a placebo drug or divalproex for 14 days as an outpatient. The subjects then went into an inpatient setting where they were given divalproex for 15 days and marijuana use could be controlled for three conditions: baseline (days 1 to 4), active marijuana (days 5 to 8), or placebo marijuana (days 9 to 14). (The subjects moved out on day 15.) After completing this, the subjects were crossed over to take either divalproex or the placebo drug for 14 days as an outpatient. They then underwent another 15-day inpatient treatment.

Haney and associates found that when divalproex was taken during the inpatient placebo marijuana days 9 to 14 (ie, withdrawal condition), subjects reported a worsened mood and subjectively believed they had increased problems with sleepiness, difficulty maintaining sleep, and awakening earlier than desired. Objectively, PSG showed that divalproex had actually improved the subjects’ total sleep time. Despite this objective improvement, divalproex did not prove useful in enhancing recovery. Haney and associates believe that marijuana addiction recovery involves improving both the objective measures of sleep and the subjective perception of sleep quality.


Cocaine is a powdered substance derived from leaves of the cocoa plant. It blocks the reuptake of dopamine and exerts this effect on dopaminergic neurons in the ventral tegmental area (VTA) and the nucleus accumbens—the “reward” pathways in the brain. The excess dopaminergic stimulation in these areas results in a burst of euphoria and energy. Chronic cocaine use can lead to problems with insomnia and restlessness.

Recovering cocaine addicts note improved sleep after a period of abstinence, but a group of Yale University School of Medicine researchers headed by Peter T. Morgan13 recently found that recovering cocaine addicts may actually suffer from hidden insomnia. In a 23-day study, PSG recording of 12 abstinent cocaine addicts revealed that total sleep time and sleep latency were at their worst by days 10 to 14. Continued abstinence to day 23 of the study did not improve sleep, yet the subjects believed their sleep had improved. Morgan and associates concluded that abstinent cocaine addicts, while subjectively feeling better, are unaware of having hidden insomnia. Other researchers14 have similarly found that sleep quality worsens with continued abstinence and caution that this may increase the risk of relapse in the cocaine addict.


Heroin is a synthetic substance similar in chemical structure to morphine. It crosses the blood-brain barrier and is converted into morphine in the brain. Heroin binds to opiate receptors located in areas involved in emotion (eg, amygdala) and the reward system (eg, ventral tegmentum). This leads to the euphoria experienced by users. Chronic heroin use results in increased wakefulness, frequent arousals during sleep, decreased total sleep time,15 and decreased amounts of slow wave sleep and REM sleep with REM sleep being more disrupted than slow wave sleep.16 Insomnia resulting from opiate abuse can lead to depression, which in turn can result in drug relapse.17


Methamphetamine is a stimulant structurally similar to dopamine. It exerts its effect on the ventral tegmental area (located at the upper portion of the brainstem), the hippocampus, frontal cortex, substantia nigra, and striatum. It causes neurons to release dopamine into the synaptic cleft while blocking the reuptake of dopamine from the synaptic cleft. The excessive stimulation of dopaminergic neurons through repeated use of methamphetamine ultimately destroys the neurons.

MDMA is an acronym for 3,4-methylenedioxymethamphetamine. It is a synthetic stimulant similar to methamphetamine. It causes neurons to release serotonin, dopamine, and norepinephrine. Compared to methamphetamine, it causes a greater release of serotonin than dopamine. Therefore, repeated use of MDMA damages serotoninergic neurons.

Chronic use of methamphetamine or MDMA can result in insomnia. Chronic MDMA use results in decreased total sleep time and decreased stage 2 sleep.18 Withdrawal from amphetamine drugs can cause hypersomnia, irritability, and restlessness. These symptoms may lead a person to relapse.

A drug-dependent person may come to a sleep center with complaints of sleep problems such as insomnia or excessive sleepiness, but may not admit to or be aware of the role that alcohol or drug addiction may be playing in their problems and therefore may not mention the drug use. Ironically, a preexisting sleep problem can be a risk factor for addiction since a person may self-medicate in an effort to sleep or remain awake. These factors make improving sleep difficult in someone with suspected drug addiction. However, careful questioning about drug use and sleep symptoms may reveal hidden drug usage and improve treatment efforts for a sleep disorder and drug-addiction recovery.

Regina Patrick, RPSGT, is a contributing writer for Sleep Review.


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