Alcohol induced sleep disorder

Alcohol and Sleep | Sleep Foundation

Alcohol is a central nervous system depressant that causes brain activity to slow down. Alcohol has sedative effects that can induce feelings of relaxation and sleepiness, but the consumption of alcohol – especially in excess – has been linked to poor sleep quality and duration. People with alcohol use disorders commonly experience insomnia symptoms. Studies have shown that alcohol use can exacerbate the symptoms of sleep apnea.

Drinking in moderation is generally considered safe but every individual reacts differently to alcohol. As a result, alcohol’s impact on sleep largely depends on the individual.

How Does Alcohol Affect Sleep?

After a person consumes alcohol, the substance is absorbed into their bloodstream from the stomach and small intestine. Enzymes in the liver eventually metabolize the alcohol, but because this is a fairly slow process, excess alcohol will continue to circulate throughout the body. The effects of alcohol largely depend on the consumer. Important factors include the amount of alcohol and how quickly it is consumed, as well as the person’s age, sex, body type, and physical shape.

The relationship between alcohol and sleep has been studied since the 1930s, yet many aspects of this relationship are still unknown. Research has shown sleepers who drink large amounts of alcohol before going to bed are often prone to delayed sleep onset, meaning they need more time to fall asleep. As liver enzymes metabolize the alcohol during their night and the blood alcohol level decreases, these individuals are also more likely to experience sleep disruptions and decreases in sleep quality.

To understand how alcohol impacts sleep, it’s important to discuss different stages of the human sleep cycle. A normal sleep cycle consists of four different stages: three non-rapid eye movement (NREM) stages and one rapid eye movement (REM) stage.

  • Stage 1 (NREM): This initial stage is essentially the transition period between wakefulness and sleep, during which the body will begin to shut down. The sleeper’s heart beat, breathing, and eye movements start to slow down and their muscles will relax. Brain activity also begins to decrease, as well. This phase is also known as light sleep.
  • Stage 2 (NREM): The sleeper’s heartbeat and breathing rates continue to slow down as they progress toward deeper sleep. Their body temperature will also decrease and the eyes become still. Stage 2 is usually the longest of the four sleep cycle stages.
  • Stages 3 (NREM): Heartbeat, breathing rates, and brain activity all reach their lowest levels of the sleep cycle. Eye movements cease and the muscles are totally relaxed. This stage is known as slow-wave sleep.
  • REM: REM sleep kicks in about 90 minutes after the individual initially falls asleep. Eye movements will restart and the sleeper’s breathing rate and heartbeat will quicken. Dreaming mostly takes place during REM sleep. This stage is also thought to play a role in memory consolidation.

These four NREM and REM stages repeat in cyclical fashion throughout the night. Each cycle should last roughly 90-120 minutes, resulting in four to five cycles for every eight hours of sleep. For the first one or two cycles, NREM slow-wave sleep is dominant, whereas REM sleep typically lasts no longer than 10 minutes. For later cycles, these roles will flip and REM will become more dominant, sometimes lasting 40 minutes or longer without interruption; NREM sleep will essentially cease during these cycles.

Drinking alcohol before bed can add to the suppression of REM sleep during the first two cycles. Since alcohol is a sedative, sleep onset is often shorter for drinkers and some fall into deep sleep rather quickly. As the night progresses, this can create an imbalance between slow-wave sleep and REM sleep, resulting in less of the latter and more of the former. This decreases overall sleep quality, which can result in shorter sleep duration and more sleep disruptions.

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Alcohol and Insomnia

Insomnia, the most common sleep disorder, is defined as “a persistent difficulty with sleep initiation, duration, consolidation, or quality.” Insomnia occurs despite the opportunity and desire to sleep, and leads to excessive daytime sleepiness and other negative effects.

Since alcohol can reduce REM sleep and cause sleep disruptions, people who drink before bed often experience insomnia symptoms and feel excessively sleepy the following day. This can lead them into a vicious cycle that consists of self-medicating with alcohol in order to fall asleep, consuming caffeine and other stimulants during the day to stay awake, and then using alcohol as a sedative to offset the effects of these stimulants.

Binge-drinking – consuming an excessive amount of alcohol in a short period of time that results in a blood alcohol level of 0. 08% or higher – can be particularly detrimental to sleep quality. In recent studies, people who took part in binge-drinking on a weekly basis were significantly more likely to have trouble falling and staying asleep. These findings were true for both men and women. Similar trends were observed in adolescents and young adults, as well as middle-aged and older adults.

Researchers have noted a link between long-term alcohol abuse and chronic sleep problems. People can develop a tolerance for alcohol rather quickly, leading them to drink more before bed in order to initiate sleep. Those who have been diagnosed with alcohol use disorders frequently report insomnia symptoms.

Alcohol and Sleep Apnea

Sleep apnea is a disorder characterized by abnormal breathing and temporary loss of breath during sleep. These lapses in breathing can in turn cause sleep disruptions and decrease sleep quality. Obstructive sleep apnea (OSA) occurs due to physical blockages in the back of the throat, while central sleep apnea (CSA) occurs because the brain cannot properly signal the muscles that control breathing.

During apnea-related breathing episodes – which can occur throughout the night – the sleeper may make choking noises. People with sleep apnea are also prone to loud, disruptive snoring. Some studies have suggested that alcohol contributes to sleep apnea because it causes the throat muscles to relax, which in turn creates more resistance during breathing. This can exacerbate OSA symptoms and lead to disruptive breathing episodes, as well as heavier snoring. Additionally, consuming just one serving of alcohol before bed can lead to OSA and heavy snoring even for people who have not been diagnosed with sleep apnea.

The relationship between sleep apnea and alcohol has been researched somewhat extensively. The general consensus based on various studies is that consuming alcohol increases the risk of sleep apnea by 25%.


Alcohol and Sleep FAQ

Does Alcohol Help You Sleep?

Alcohol may aid with sleep onset due to its sedative properties, allowing you to fall asleep more quickly. However, people who drink before bed often experience disruptions later in their sleep cycle as liver enzymes metabolize alcohol. This can also lead to excessive daytime sleepiness and other issues the following day. Furthermore, drinking to fall asleep can build a tolerance, forcing you to consume more alcohol each successive night in order to experience the sedative effects.

Does Alcohol Affect Men and Women Differently?

On average, women exhibit signs of intoxication earlier and with lower doses of alcohol than men. This can mostly be attributed to two factors. First, women tend to weigh less than men and those with lower body weights often become intoxicated more quickly. Most women also have a lower amount of water in their bodies than men. Alcohol circulates through water in the body, so women are more likely to have higher blood alcohol concentrations than men after consuming the same amount of alcohol.

What Is the Difference Between Moderate Drinking and Heavy Drinking?

Definitions vary by source, but the following measurements are generally considered to constitute a single serving of alcohol:

  • 12 ounces of beer with 5% alcohol content
  • 5 ounces of wine with 12% alcohol content
  • 1 ounce of liquor or distilled spirits with 40% alcohol content

Moderate drinking is loosely defined as up to two drinks per day for men and one drink per day for women. Heavy drinking means more than 15 drinks per week for men and more than eight drinks per week for women.

Will a Small Amount of Alcohol Affect My Sleep?

Drinking to excess will probably have a more negative impact on sleep than light or moderate alcohol consumption. However, since the effects of alcohol are different from person to person, even small amounts of alcohol can reduce sleep quality for some people.

One 2018 study compared sleep quality among subjects who consumed different amounts of alcohol. The findings are as follows:

  • Low amounts of alcohol (fewer than two servings per day for men or one serving per day for women) decreased sleep quality by 9.3%.
  • Moderate amounts of alcohol (two servings per day for men or one serving per day for women) decreased sleep quality by 24%.
  • High amounts of alcohol (more than two servings per day for men or one serving per day for women) decreased sleep quality by 39. 2%.

When Should I Stop Drinking Prior To Bed To Minimize Sleep Disruption?

To reduce the risk of sleep disruptions, you should stop drinking alcohol at least four hours before bedtime.

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See More

Disturbed Sleep and Its Relationship to Alcohol Use

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Sleep disorders in alcoholism

The close relationship between sleep disorders and mental illness has long been known, which led to the identification of a separate group of secondary insomnias, including those associated with alcoholism and drug addiction [1]. In the latest, 3rd version of the International Classification of Sleep Disorders [2], all types of secondary chronic insomnia are combined into one group. Nevertheless, numerous studies of the subjective and objective characteristics of sleep in mentally ill patients have made it possible to identify the features of sleep disturbances characteristic of each of these diseases. Moreover, data were obtained that a change in some sleep indicators (representation of delta sleep, latency of REM sleep) makes it possible to predict the severity of the course and the approach of the next relapse of the disease. When examining patients with sleep disorders, 50% have associated symptoms of mental distress [3]. It has been shown that the risk of developing a depressive disorder in patients with insomnia during their lifetime is 4 times higher than in those without it [4]. Insomnia may precede the onset of a mental disorder, manifest itself simultaneously with its development, or occur in a detailed picture of the disease. The high efficiency of such insomnia treatment methods as cognitive-behavioral therapy aimed at normalizing the emotional state and behavior also testifies in favor of the presence of a close pathogenetic relationship between sleep disorders and mental disorders.

Alcoholism is one of the mental disorders associated with sleep disorders. But in this area, the effect of different doses of alcohol is reasonably differentiated. Despite the obvious toxic effect of ethanol on all organs and systems, there is also evidence of its beneficial effect when used in small doses. This has led to the fact that a number of scientists and medical organizations do not exclude moderate alcohol consumption for preventive purposes [5]. At the household level, it is widely believed that alcohol is used as an affordable sleeping pill; taking a "glass or two" accelerates the onset of sleep. At 1939 N. Kleitman first described such an effect of ethanol taken 60 minutes before sleep (quoted from [6]).

Assessment of the alcohol content in the body is carried out by measuring its concentration in the exhaled air, which depends not only on the amount of ethanol taken, but also on the type of alcoholic beverage, its absorption rate in the gastrointestinal tract, water content in the body, which varies depending on gender and age. It should be borne in mind that the highest level of ethanol in the blood is observed in the first 1-1.5 hours after ingestion. When examining the concentration of alcohol in the exhaled air, two peaks are revealed (after 15-20 minutes and 75 minutes after ingestion), the first of which is associated with the absorption of ethanol in the oral cavity, the second with absorption from the gastrointestinal tract [7]. 4-5 hours after taking alcohol at night, i.e. in the second half of the night, the effect of removing it from the body is observed.

Women reach peak blood alcohol concentration faster than men due to their lower water content in their bodies. The removal of ethanol from the blood also occurs faster in women [8].

It is worth noting the difficulties in conducting placebo-controlled studies of the effectiveness of alcohol, since it is obvious to the subjects that the presence of ethanol in the drink they offer, starting with the amount of alcohol sufficient to achieve 0.07% ethanol content in exhaled air [9]. This creates particular problems in assessing subjective effects (feeling of cheerfulness, concentration of attention), depending on the individual expectations of the subjects from the reception.

The effect of ethanol on the central nervous system (CNS) is mediated by the improvement of GABAergic and inhibition of glutamate mediation, two systems that reciprocally affect the mechanisms of sleep and wakefulness. The effect of ethanol on precisely these neurotransmitter systems was proven in laboratory studies in which alcohol intake increased or, conversely, slowed down the work of GABA or glutamate-dependent ion channels [10, 11]. The GABAergic system of the reticular formation, thalamus, hypothalamus, and basal forebrain is inhibitory, responsible for the generation of slow-wave sleep, and is the target for the action of the most common hypnotics (barbiturates, benzodiazepine and nonbenzodiazepine GABA-receptor agonists) [12]. Glutamate, in contrast, is an activating neurotransmitter present both in the reticular formation and in the brainstem and forebrain. NMDA receptors are the most numerous group of glutamate receptors, which become the target of the inhibitory action of ethanol, as well as some sedatives and anesthetics [6, 12]. In addition to GABA and glutamate systems, the mediator mediating the hypnotic effect of ethanol is adenosine, which presumably provides the homeostatic mechanism of the sleep-wake cycle (during wakefulness, adenosine accumulates in the CNS, and during sleep, its concentration gradually decreases). Ethanol accelerates synthesis, impairs adenosine reuptake, and can also directly activate adenosine receptors [13].

While the effect of ethanol on slow-wave sleep is relatively well understood, the mechanisms of influence on REM sleep (REM), which is regulated by other mediator systems, remain unclear. Some researchers [6] believe that in this case the effect of alcohol is mediated by acetylcholine and glutamate, but clarity on this issue has not been achieved.

Episodic low to moderate alcohol consumption (up to 0.75 g/kg) can cause a short activating effect (due to the rapid release of dopamine and endorphins) followed by a sedative effect corresponding to the descending portion of the ethanol metabolism curve. The use of any doses of ethanol is manifested by a decrease in the time to fall asleep, as well as an increase in the representation of deep stages of sleep and a dose-dependent decrease in the proportion of REM sleep in the first half of the night [14-18]. It is worth emphasizing, however, that different sensitivity to alcohol causes a wide variation in the clinical severity of the effects of alcohol when consumed in different doses. Often, small doses of ethanol do not cause significant sedation, although sleep studies will still detect changes in sleep patterns. In this regard, there is still no general opinion about the dosage sufficient for the development of sleep and changes in its structure.

As alcohol is eliminated from the body, the so-called release of REM sleep occurs with an increase in its representation. This leads to a feeling of more superficial sleep due to frequent awakenings in FBS [19]. Thus, the overall representation of REM sleep throughout the night after episodic alcohol consumption does not differ significantly from normal indicators, but the described changes in sleep structure are more pronounced in women compared to men (due to the above metabolic features) and do not depend on the presence or absence of cases of alcohol abuse in a family history [14].

Repeated alcohol intake for three consecutive days develops tolerance to the sedative effect and effect on the sleep structure - indicators of deep slow wave sleep and REM sleep return to baseline. Some researchers [6] have observed a return of FBS after the cessation of a short period of alcohol intake: in this case, the proportion of REM sleep exceeded the baseline.

The effect of ethanol on sleep in alcoholic patients has been well studied. During periods of binges, they fall asleep very quickly, however, the duration of sleep is relatively short, and the phase of slow-wave sleep (SMS) prevails in its structure. In studies of the behavior of such patients [17], when they were provided with free access to alcohol, it was found that periods of sleep and alcohol consumption alternate at short intervals during the day. If you need to sleep for 8 hours or more, the second half of sleep becomes intermittent due to frequent awakenings in FBS [19]. Alcohol withdrawal leads to a sharp decrease in the representation of stages 3-4 of sleep, slow-wave sleep is represented mainly by stages 1-2, while the share of REM sleep increases due to an increase in the number and shortening of sleep cycles, but without an increase in duration FBS in each cycle [20]. Such changes in sleep patterns can persist even up to 2 years after cessation of alcohol intake.

The risk of developing insomnia in alcoholic disease is higher in women, patients with a family history of alcohol abuse, in patients who began to abuse alcohol at a later age (over 27 years), with a long history of abuse (more than 7 years), with concomitant mental pathology ( endogenous depression, anxiety disorders) [21, 22]. The described features, according to the authors of the relevant works, are evidence of the development of physical dependence on alcohol, since similar changes can be observed with dependence on other drugs (barbiturates, opiates, psychostimulants). Alcohol intake during the period of acute withdrawal eliminates these changes, but they increase again after the cessation of ethanol intake into the body.

In persons suffering from alcohol dependence, during the period of withdrawal, insomnia disorders are observed in 91% of cases, while the criteria for acute insomnia syndrome are met in 61% of cases [23, 24]. Insomnia is one of the 8 symptoms of alcohol withdrawal according to DSM-V (2 of 8 signs are required for the diagnosis of alcohol withdrawal) [25]. There is an assumption that hallucinations that appear after alcohol withdrawal are an invasion of "rebound" REM sleep in the waking state [26]. However, it is questioned due to the fact that not all patients with hallucinations have the phenomenon of such a "rebound". In the period of remission of alcoholic disease, sleep characteristics such as an increase in FBS pressure (decrease in latency, high proportion, density of rapid eye movements), a decrease in the representation of stages 3–4 of non-REM sleep can be predictors of a relapse of the disease in the next 5–6 months [27] . The presence and severity of sleep disorders during the period of acute withdrawal also has a significant positive relationship with the risk of relapse [21].

Studies conducted in the UK and the USA [28, 29] have shown that people who start drinking alcohol at an earlier age and consume it in greater quantities, the daily duration of sleep is significantly less.

Studies of the effects of daytime alcohol consumption, in which subjects had free access to alcoholic beverages before bedtime, gave conflicting results in the form of both subjectively lower levels of alertness and energy, and increased performance [30]. When evaluating them, as mentioned above, one should take into account the difficulties of their interpretation without taking into account individual expectations from drinking alcohol.

With insomnia syndrome, which occurs in the general population in 6% (and some symptoms disturb 48% of people from time to time), 30% of patients resort to alcohol as a sleeping pill, 67% of whom note a positive effect [31]. Moreover, the positive effect of ethanol on the rate of falling asleep and the depth of sleep in those suffering from insomnia is manifested in doses that are lower than those required to achieve the same effect in healthy people [32]. At the same time, tolerance quickly develops to the sedative effect of alcohol both at the receptor and psychological levels - this leads to the fact that patients with insomnia increase the amount of alcohol taken before bedtime. As a result, "therapeutic" alcohol use can quietly transform into alcohol addiction. In studies with free access to alcoholic beverages, patients with insomnia were more likely to choose alcohol before bed than healthy subjects. This is also consistent with epidemiological data showing that people with sleep problems are twice as likely to suffer from alcoholism than those who did not have sleep problems: 7 and 3.8%, respectively [4, 33].

In the event that alcohol abuse has developed against the background of existing insomnia, insomnia complaints intensify in the withdrawal period, which creates conditions for a relapse. Thus, a kind of "vicious circle" arises, for the destruction of which it is necessary to make great efforts both on the part of the patient and the doctor, since the selection of drug therapy in such patients is complicated by a higher risk of developing drug dependence. Thus, benzodiazepine receptor agonists, which have a high risk of developing addiction and addiction, affecting the structure of sleep and causing "rebound" insomnia upon withdrawal, are not recommended for the relief of insomnia in the withdrawal period, with the exception of cases of delirium tremens [21]. An additional risk of taking benzodiazepines is associated with the possibility of their overdose when used with alcohol.

In the period of abstinence from taking alcohol, antidepressants and anticonvulsants are preferred as sleeping pills, taking into account the increased risk of developing an epileptic seizure as a result of reactivation of suppressed excitatory systems. Studies of the effect of carbamazepine and gabapentin on the symptoms of insomnia in the withdrawal period have shown that their effectiveness exceeds that of benzodiazepines [34, 35]. The more favorable spectrum of side effects of gabapentin should also be noted, the metabolism of which does not depend on liver enzymes and which has a lower potential for dependence and abuse.

If long-term treatment of insomnia and depression, especially noted before the onset of alcohol abuse, is required, antidepressants of the sedative spectrum become the drugs of choice. The inevitable damaging effect of alcohol on the liver necessitates the choice of a drug with a minimal effect on it. High subjective and objective efficacy in relation to the symptoms of insomnia, including alcohol withdrawal, a low risk of developing dependence and abuse of trazodone (in Russia it is represented by the drug trittico) has been proven in a number of foreign and domestic studies [21, 36, 37]. The extrahepatic metabolism of this drug allows it to be prescribed to patients with liver disease.

Trazodone is a triazolopyridine derivative and, as an antidepressant, belongs to a unique class of serotonin receptor antagonists/serotonin reuptake inhibitors. Its multifaceted therapeutic effect is primarily explained by its effect on serotonin transmission. Trazodone is a 5HT1A receptor agonist, 5HT2A-, 5HT2B-, 5HT2C receptor antagonist, and serotonin reuptake inhibitor. In addition, it has a blocking effect on α1- and α2-adrenergic receptors and h2-histamine receptors. The drug is approved in many countries as a treatment for major depressive disorder in adults. Trazodone has been shown to be effective in clinical trials comparable to tricyclic antidepressants, selective serotonin reuptake inhibitors (SSRIs) and serotonin/norepinephrine reuptake inhibitors. It is important to note that the use of this drug does not cause serious side effects characteristic of SSRIs, such as insomnia, increased anxiety, and sexual dysfunction [38].

The results of successful use of trazodone for bulimia, benzodiazepine and alcohol dependence, fibromyalgia, degenerative diseases of the central nervous system, schizophrenia, chronic pain syndromes, diabetic polyneuropathy, sexual dysfunction have been published [39].

Russian multicenter study of the effectiveness of the use of trittiko for the correction of sleep disorders in depressive disorders, was conducted in 2011-2012. [36]. It included 30 patients diagnosed with a depressive episode or recurrent depression. Trittico was used at an average dose of 150 mg for 42 days, along with a decrease in the severity of anxiety and depression, there was an improvement in sleep parameters both according to questionnaires and according to the results of an objective study (polysomnography). The authors of the study concluded that the drug is effective and safe in the treatment of patients with non-psychotic depressive disorders with sleep disorders.

Concerning other groups of drugs commonly used to treat insomnia (antipsychotics, melatonin, ethanolamines), convincing evidence of their effectiveness and safety in relation to patients suffering from alcohol dependence is not yet available.

A number of studies [40, 41] have found a positive effect of the method of cognitive behavioral therapy on the quality of sleep and the severity of daytime symptoms compared with placebo. Comparative studies of the effectiveness of this kind of non-specific therapy and drug treatment in alcohol withdrawal have not been conducted. But its further study is undoubtedly promising, taking into account the toxic effect of ethanol on all organs and systems of the patient, which causes contraindications for drug therapy.

Mention should be made of the effect of alcohol consumption on sleep disorders other than those described. So, we are talking about breathing disorders during sleep, which among all sleep disorders are in second place in terms of prevalence after insomnia: 3-8% in men, 2% in women [42]. Alcohol can contribute to the manifestation of sleep apnea with an existing predisposition [43]. This is due to the ability of ethanol to inhibit the respiratory center of the medulla oblongata, reduce reflex awakening in response to respiratory arrest, and directly reduce the tone of the soft tissues of the upper respiratory tract. The considered effects of ethanol are reflected in studies [44], where alcohol consumption before bedtime led to an increase in the apnea-hypopnea index from 22 to 28 episodes per hour and a decrease in mean blood saturation from 78 to 62%, requiring the selection of a higher pressure of overmask ventilation with constant positive pressure (CPAP therapy) to eliminate breathing disorders during sleep [43]. Probably, there is also an inverse relationship, since among those suffering from alcoholism, breathing disorders during sleep are more common than among healthy people of the same age [45].

In addition to the above, it can also be added that alcohol reduces the manifestations of restless legs syndrome and periodic limb movements during sleep, but this effect disappears as tolerance develops rapidly. In addition, periodic limb movements themselves can lead to awakenings and exacerbate the fragmentation of sleep caused by alcohol elimination. By increasing the representation of deep sleep, alcohol contributes to the increase in sleepwalking and other parasomnias that occur in non-REM sleep.

Due to the development of a sedative effect, alcohol worsens the daytime manifestations of narcolepsy, which itself is characterized by bouts of imperative daytime sleepiness. Patients who have narcolepsy onset in childhood and adolescence avoid alcohol, while those with onset in adulthood are sometimes habitually prevented from giving up.

So, since alcohol has a generalized toxic effect, this cannot but affect the sleep and wake systems that are sensitive to exogenous and endogenous influences. Despite the seeming improvement in sleep with insomnia, the use of alcohol as a sleeping pill tends to increase uncontrollably and lead to difficult-to-treat sleep structure disorders and the development of addiction. It is important to remember that insomnia is often combined with other sleep disorders, which, under its mask, can cause daytime sleepiness (breathing disorders during sleep, restless legs syndrome), frequent awakenings (periodic limb movement syndrome during sleep). Drinking alcohol in these cases can not only aggravate the course of the disease, but also lead to catastrophic consequences (stopping breathing due to depression of the respiratory center during sleep apnea). Thus, alcohol, even in small doses, cannot be recommended to patients with complaints of sleep disorders. A history of abuse of alcohol or drugs that affect sleep should lead the physician to think about the risk of relapse.

Alcohol and sleep disorders | Efremov

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