Sleep is a fundamental, necessary and complex behavior in humans. There are two distinct states of sleep, rapid eye movement (REM) and non-rapid eye movement (NREM) sleep, that involve different patterns of neurological activation and neurotransmitter release, and presumably different functions.
Alcohol effects many of the neurotransmitters involved in wake-sleep regulation, thus affecting sleep in a number of ways.
As evidenced by other drugs, alcohol demonstrates tolerance with repeated administration and dependence, and this tolerance is accompanied by adaptation of neurotransmitter systems [1].
Upon withdrawal, those dependent on alcohol typically have neurological manifestations that are in part, due to the consequent neurochemical imbalance.
Over time, recovery can take place to restore a normal balance of inhibitory and excitatory systems, however, it is possible that some changes induced by alcohol may be resistant to restoration.
In addition to the direct pharmacological effect of alcohol on sleep-regulation, the long-term consequences of alcohol abuse and dependence on brain macrostructure and microstructure, may lead to changes in sleep regulation or changes in electroencephalographic (EEG) manifestations of sleep.
In this article, we’ll investigate the evidence-based research for the acute effects of alcohol on sleep, the effects of short-term repeated administration of alcohol on sleep, and the observations of the long-term consequences of alcohol dependence on sleep.
While the overarching purpose of sleep remains unknown, evidence suggests that it serves several functions, including conservation of brain energy, facilitation of certain forms of learning and memory, and support of cognitive capacity including pruning and maintenance of synaptic connectivity [2].
Insufficient sleep or insomnia (difficulty initiating or maintaining sleep or non-restorative sleep) are associated with negative consequences to immune function, impaired cardiovascular and cerebrovascular health, cognitive impairment, and a change in emotional reactivity.
Insomnia is a risk factor for the development of psychiatric disorders, including depression, anxiety, and alcohol abuse [3].
Insomnia may also interfere with the recovery process and contribute to relapse among patients in recovery from alcohol dependence [4]. Therefore, it has, been suggested that treating insomnia may assist recovery in alcoholics and prevent or reduce the likelihood of relapse.
Insufficient sleep or insomnia often occurs alongside depression and/or anxiety, which can have debilitating effects on your physical performance and body composition goals.
The catabolic hormone cortisol is released when there is a lack of sleep or a lot of stress occurring simultaneously with insomnia. This can wreak havoc on your fat loss and muscle building goals.
Blood alcohol levels may continue to rise for some time during sleep, but this is dependent on the timing of sleep onset relative to consumption. Inevitably, blood levels will start to fall as a function of metabolism, the time course of which is unaltered by sleep itself.
Sleep, therefore, could be expected to be affected differently during the initial period of high alcohol levels from the subsequent elimination phase that occurs later on.
Initially, alcohol acts as a sedative.
Commonly reported experiences include shortened sleep onset latency [5] and increased slow wave sleep in the first half of the night [6].
Sleep onset latency is the length of time that it takes to accomplish the transition from full wakefulness to sleep, normally to the lightest of the non-REM sleep stages. Slow-wave sleep, often referred to as deep sleep, consists of stage three of non-rapid eye movement sleep. It usually lasts between 70 and 90 minutes and takes place during the first hours of the night.
REM sleep is suppressed, with a longer latency to REM sleep and decreased REM sleep in the first half of the night [7].
During the second half of the night, sleep is disrupted, with increased wakefulness and/or stage 1 sleep. This debilitating pattern of initial sleep augmentation followed by a period of poor-quality sleep can lead to a downward spiral.
The insomnia that ensues is self-treated with alcohol to produce a rapid sleep onset, with the subsequent poor sleep later in the night ultimately leading to daytime sleepiness that is self-treated with caffeine, which exacerbates insomnia, requiring more alcohol to fall asleep, etc.
This becomes a vicious cycle that leads to many problems.
It is estimated that alcohol is used by more than one in ten individuals as a hypnotic agent to self-medicate sleep problems [4].
Studies consistently show a high comorbidity of insomnia and alcoholism [4]. Clinical data demonstrates that between 36 – 91% of patients report insomnia either while drinking or within several weeks of stopping [8].
Many alcoholics develop poor sleep habits and irregular sleep-wake schedules when drinking, which may persist after quitting. Napping and maintaining an irregular sleep-wake schedule are associated with greater wakefulness and poorer sleep quality at night [9].
Laboratory studies also indicate a decrease in slow wave sleep as a highly consistent finding in alcoholics relative to controls [10].
In addition, there is also evidence of increased REM sleep pressure which is reasonable to expect in actively drinking or recently detoxified alcoholics, given that REM sleep is suppressed with high doses of alcohol [11].
This form of REM rebound cannot explain the increased REM in those who have been abstinent for a long time, relative to controls. It is possible that increased REM sleep may represent a predisposition to altered sleep rather than a consequence of alcohol abuse, although REM is not elevated in adolescents with a positive family history of alcoholism [12].
Another possibility is that alcohol abuse leads to long-lasting neurochemical changes in the brain stem.
Alcohol profoundly impacts sleep and its effects are dependent on acute versus chronic use. Many people utilize alcohol for its initially sedating effects, which disappear after a few hours, and cause fragmented and disturbed sleep in the second half of the night.
Serious sleep problems occur from chronic alcohol use.
Alcohol drinking binges cause ongoing sleep and circadian rhythm disruption. Even when one is abstinent from alcohol for a period of time, sleep issues persist, with insomnia and vivid dreams being common complaints.
These factors can potentially lead to relapse.
It is critically important from a clinical perspective to ascertain whether preventing sleep disorders may help prevent the development of alcohol use disorders in high-risk individuals.
Also, it’s crucial to determine which treatments are most effective in alcoholics, both in terms of improving sleep quality and supporting continued abstinence.
Current trends indicate that poly-substance dependence is common, so it will be increasingly relevant to investigate the interactive effects of substances of abuse on sleep behavior and regulation.
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References
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