Drug Addiction: Sleeping For Days, Why?

Sleep and substance abuse are interconnected, such that changes in one can have consequences for the other. Acute exposure to drugs of abuse can disrupt sleep by affecting sleep latency, duration, and quality. With chronic administration, sleep disruption becomes more severe, and during abstinence, insomnia with a negative effect prevails, which drives drug craving and contributes to impulsivity and relapse.

Substance abuse can lead to nighttime wakefulness, less good sleep, lower overall sleep time, and strong daytime sleepiness (hypersomnia). This can create a cycle of use for stimulants like cocaine, caffeine, and nicotine, as individuals attempt to counter the negative effects of their substance abuse.

Additionally, withdrawal from drugs can cause sleep problems or make them worse, and these issues can increase the chances of relapse.

Drug withdrawal and sleep

Drug withdrawal can have a significant impact on sleep, and this can be a challenging aspect of the recovery process for many individuals. Sleep disturbances are common during substance withdrawal and can manifest in various forms, including insomnia, broken sleep, strange dreams, and restless leg syndrome. These issues can take a toll on both mental and physical health, making the recovery journey more difficult.

The link between drug withdrawal and sleep disturbances is bidirectional. Substance use can disrupt sleep patterns, but a persistent sleep disorder can also contribute to the development or relapse of substance use problems. This connection may be due to the role of sleep in memory consolidation and extinction. Poor sleep may interfere with the learning of non-reinforced drug associations, which are crucial for recovery.

During acute exposure to drugs, sleep latency, duration, and quality are affected. With chronic drug use, sleep disruption becomes more severe, and insomnia often prevails during abstinence. This insomnia can drive drug cravings, impulsivity, and relapse. Additionally, sleep impairments associated with drug abuse can contribute to cognitive dysfunction in individuals struggling with addiction.

Opioid withdrawal, in particular, has been associated with hyperarousal and insomnia. Alpha-2-adrenergic antagonists, such as lofexidine and clonidine, are used to attenuate opioid and alcohol withdrawal symptoms, including insomnia, anxiety, and restlessness. However, their effectiveness in suppressing insomnia during protracted abstinence and its associated adverse consequences, such as irritability and cognitive impairments, remains to be fully explored.

Treating sleep disorders alongside substance use disorders is essential. Creating a consistent sleep and wake schedule, setting aside time to relax before bed, and developing strategies to manage sleep problems without resorting to drugs or alcohol are crucial steps in the recovery process. Behavioral interventions and medications are the two primary approaches to treating sleep-wake disorders co-occurring with substance use disorders. While there is no single form of psychotherapy that has proven universally successful, progressive relaxation training has shown some promise in addressing insomnia in alcoholic patients.

In summary, drug withdrawal can have a significant impact on sleep, and addressing sleep disturbances is an important component of the recovery process. Treating sleep disorders can help reduce drug cravings and improve overall mental and physical health during recovery from substance use disorders.

Alcohol and insomnia

Alcohol is a depressant and can make people feel sleepy, but it can also negatively impact sleep quality. Research shows that between 35% and 70% of individuals who use alcohol have insomnia. Insomnia is defined as either a problem falling asleep, staying asleep, or waking up early and being unable to get back to sleep. The loss of sleep is enough to cause problems in day-to-day life and is occurring at least 3 nights per week for over 3 months.

Alcohol can interfere with fundamental aspects of sleep quality, including REM sleep. REM sleep is the stage of sleep where dreaming and moving around more occur. With higher doses of alcohol, sleep is often disrupted, particularly during the second half of the night. Studies also show that alcohol may exacerbate sleep-disordered breathing, such as snoring and even obstructive sleep apnea.

Research suggests that there may be a link between higher levels of alcohol consumption and an increased risk of obstructive sleep apnea, a potentially serious sleep disorder in which breathing repeatedly stops and starts. Obstructive sleep apnea affects an estimated 15% of men and 5% of women, and current research indicates that heavy alcohol use worsens sleep apnea symptoms. A meta-analysis of 21 studies found that, relative to people who did not consume any alcohol, those who did had a 25% higher risk of having obstructive sleep apnea.

Alcohol dependence is also associated with insomnia, with a prevalence of between 36% and 91%. Binge drinking is also associated with disrupted sleep. Alcohol appears to inhibit neurotransmitters that activate brain cells that promote a state of wakefulness, disturbing the sleep-wake cycle and potentially predisposing a person to insomnia.

During alcohol withdrawal, insomnia and disturbed sleep are common symptoms. It is harder to fall asleep, sleep is fragmented, and the percentage and duration of REM sleep are lower. These sleep problems can continue for months or even years into recovery.

Stimulants and sleep deprivation

Stimulants are substances that increase alertness and energy, and they are commonly used to counteract the effects of sleep deprivation. However, while stimulants can provide a temporary boost in energy levels, they can also have detrimental effects on sleep and contribute to a cycle of sleep disruption and stimulant dependence.

Stimulants work by increasing the activity of certain neurotransmitters in the brain, such as dopamine, norepinephrine, and serotonin. These neurotransmitters are involved in regulating sleep and wakefulness. By altering the balance of these neurotransmitters, stimulants can disrupt the normal sleep cycle, leading to insomnia and sleep fragmentation. This disruption can be particularly severe with chronic stimulant use.

During stimulant withdrawal, individuals often experience a rebound effect, with increased sleepiness and fatigue. This can lead to a cycle of stimulant use and sleep deprivation, as individuals may turn to stimulants to counteract the negative effects of sleep deprivation. Additionally, stimulant use can alter the quality of sleep, reducing the amount of deep sleep (non-rapid eye movement sleep) and disrupting the rapid eye movement (REM) sleep stage, which is important for memory consolidation and emotional processing.

Chronic stimulant use and withdrawal can also contribute to psychiatric symptoms, including depression and anxiety, which can further impact sleep quality. Individuals with underlying sleep disorders, such as sleep apnea, may be more susceptible to the negative effects of stimulants on sleep.

Furthermore, certain stimulants, such as amphetamines and cocaine, can disrupt the circadian rhythm, leading to irregular sleep-wake patterns. This disruption can have long-lasting effects, with sleep disturbances persisting for months after stimulant withdrawal.

Overall, the interaction between stimulants and sleep is complex, and the specific effects can vary depending on the type of stimulant, the dosage, and individual factors. While stimulants may provide temporary relief from sleep deprivation, they can also exacerbate sleep issues and contribute to a cycle of stimulant dependence and sleep disruption.

Sleep-wake disorders and substance abuse

Substance abuse, defined as the maladaptive and non-medical use of psychoactive substances, is linked to disturbed sleep. Many substances of abuse have acute deleterious consequences on sleep, which may be maintained or expanded upon during chronic use and further exacerbated during withdrawal. Conversely, sleep disturbances may lead to substance abuse.

The acute effects of substance use on sleep largely depend on the substance in question. Stimulants such as cocaine and amphetamine cause light, restless, and disrupted sleep. Drugs from other classes, such as depressants (e.g. benzodiazepines, alcohol) and opiates (e.g. heroin) initially produce soporific effects, including increased daytime sleepiness and reduced sleep latency, but cause sleep disruptions later in the night due to acute withdrawal effects.

Chronic use of substances can further impact sleep quality and quantity. Unlike acute effects, the effects of chronic substance use on mood and other psychiatric symptoms are similar across different substances. Sleep-related outcomes of chronic substance use include extended sleep onset latency, reduced total sleep time, more nighttime awakenings, and decreased slow-wave sleep and rapid eye movement (REM) sleep.

Withdrawing or abstaining from substance use has its own unique impact on sleep parameters, which may be dependent on the duration of abstinence. Sleep disturbance tends to be associated with acute withdrawal from any substance, as evidenced by extended sleep onset latency, reduced total sleep time, and reduced slow-wave sleep. In addition, REM sleep often shows a rebound effect during abstinence. As the period of abstinence is extended, sleep patterns tend to return to baseline. However, some sleep characteristics, such as REM sleep disturbances, may persist well into abstinence.

The locus coeruleus (LC)-norepinephrine (NE) system, a diffuse forebrain-projecting system involved in arousal, is a primary target of drugs of abuse, including nicotine, stimulants, opioids, and cannabinoids. LC-NE neuronal activity is positively correlated with the state of arousal, and LC neurons are most active during waking and are off during REM sleep. Selective LC activation is sufficient to elicit cortical arousal, and selective LC inhibition prevents cortical activation by stressors.

The raphe nuclei (including the dorsal raphe nucleus) serotonin (5-HT) neurons also modulate sleep and wakefulness through widespread forebrain projections. Raphe nucleus lesions trigger insomnia, and during the awake state, the cumulative 5-HT released from the raphe into the basal forebrain is believed to serve as a sleep-promoting factor. However, 5-HT neurons are active during waking, decrease their activity during slow-wave sleep, and cease firing during REM sleep, as is the case for LC-NE neurons.

The histamine (HA) neurons of the tuberomammillary nucleus form another diffusely projecting arousal system that is active during waking only, and these neurons are activated by opioids, which can further contribute to sleep disruption associated with chronic opioid use. HA promotes arousal through activation of cortical and basal forebrain neurons, effects that are primarily mediated by H1 receptors.

The endogenous cannabinoid system (ECS) that signals through cannabinoid CB1 and CB2 receptors, which are targets of marijuana, is also involved in the regulation of the sleep-wake cycle. Acutely, cannabis is sleep-promoting and decreases sleep latency, increases sleep time, increases slow-wave sleep, and decreases REMs. With chronic use, tolerance occurs to the sleep-enhancing effects of cannabis, and abstinence is characterized by unusual dreams and poor sleep quality that is predictive of relapse.

The orexin system, which derives from the posterior lateral hypothalamus, is essential for sustaining the waking state, as its disruption in patients with narcolepsy leads to periodic and abrupt interruptions of the conscious state. Orexin neurons are activated by reward and project to the DA neurons in the VTA that innervate the nucleus accumbens and mediate reward, which they also influence via their direct projections to it. Chronic opioid exposure upregulates orexin in humans and rodents, and orexin antagonists may provide a two-fold benefit by preventing two distinct but interrelated effects of orexin, potentiation of reward and arousal effects, which could help attenuate drug reward and improve sleep disturbances.

Treatment for sleep-wake disorders and substance abuse

Sleep-wake disorders and substance abuse are interconnected, with one often leading to the other. Treatment for these co-occurring disorders involves addressing both issues simultaneously.

Behavioural Interventions

Behavioural interventions for sleep-wake disorders and substance abuse include creating a home environment that is conducive to healthy sleep patterns. This may involve:

• Creating a consistent sleeping and waking schedule.
• Setting aside time to relax and unwind before bed.
• Coming up with a plan to deal with inevitable sleep problems without having to use drugs or alcohol.

Medications

Medications can also be used to treat sleep-wake disorders and substance abuse. However, it is important to be cautious when prescribing medications to this patient population, as some drugs can be addictive. Some medications that have been used to treat these co-occurring disorders include:

• Benzodiazepines: These drugs have been used to treat insomnia and other sleeping issues, but they have the potential for misuse and dependence.
• Z-drugs (e.g. zaleplon, zolpidem, eszopiclone): This class of medications is also used to treat insomnia, but they may have a similar misuse potential to benzodiazepines.
• Gabapentin: This drug has been found to improve sleep in alcoholic patients, but more research is needed to confirm its efficacy.
• Antidepressants (e.g. mirtazapine, nefazodone): These drugs can improve sleep architecture and shorten the time needed to fall asleep in patients with depression.

Long-Term Treatment

Long-term treatment for sleep-wake disorders and substance abuse may involve short-term counselling and long-term therapy, including group and family meetings, peer-led support groups, and years of careful and healthy living.

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