Glutamate is the major excitatory neurotransmitter in the brain and plays an essential role in regulating wakefulness and REM sleep (Jones, 2019). Indeed, glutamatergic system dysregulation in AUD is a likely substrate for several sleep disturbances (Koob and Colrain, 2019). Thus, when baseline levels of SWS% were less than 20 percent, heavy drinking produced either no change or a decrease in SWS%.

These limitations reflect the fact that the studies generally were designed to focus on sleep outcomes rather than alcohol outcomes. Moreover, these studies varied in whether the patients were seeking or engaged in AUD treatment, and whether they were required to be abstinent at study start. Several studies during the past 25 years have demonstrated a relationship between alcohol induced insomnia baseline sleep problems when patients enter alcoholism treatment and subsequent relapse to drinking. Sleep predictors of relapse include insomnia, especially difficulty falling asleep, and various polysomnographic abnormalities, such as increased sleep latency, REM%, and REM density as well as decreased SWS, REM sleep latency, sleep efficiency, and total sleep time.

How Alcohol Affects Sleep

Thus, persistent REM sleep abnormalities were most evident in depressed alcoholics (Gillin et al. 1990a; Moeller et al. 1993) and alcoholics who subsequently relapsed (Gillin et al. 1994; Brower et al. 1998). The acute withdrawal phase after cessation of alcohol consumption lasts approximately 1 to 2 weeks. Some withdrawal-like symptoms, such as insomnia, craving, and mood instability, however, persist even beyond that period, a phenomenon variously called “subacute withdrawal,” “protracted abstinence,” or “protracted withdrawal” (Gross and Hastey 1976; Satel et al. 1993).

2020 research suggests that alcohol impacts the part of sleep known as rapid eye movement (REM). Drinking heavily over time can also disrupt the chemical messengers in the brain, which can affect sleep. Application of the inclusion and exclusion criteria resulted in 26 RCT on the efficacy and/or safety of disulfiram, acamprosate, naltrexone, and nalmefene. All the relevant characteristics and outcomes of the studies are summarized in Table 3. The key is to drink in moderation and give yourself time before going to bed so the alcohol can clear your system.

The serotonin theory of depression: a systematic umbrella review of the evidence

Heavy consumption of alcohol over an extended period of time leads to increased tolerance and this tolerance is accompanied by adaptation of the neurotransmitter systems5. Furthermore, long-term consequences of alcohol may lead to changes in sleep regulation. The influence of alcohol on sleep therefore needs to be evaluated by exploring both the short term effects on sleep (cross sectional data) and the long-term consequences (longitudinal data of repeated measures).

alcohol induced insomnia

Those who have been diagnosed with alcohol use disorders frequently report insomnia symptoms. Finally, similar trends for increased insomnia were observed with nalmefene, although much less evidence was available, and the statistical significance was null or not reported. These results are not surprising, given that both naltrexone and nalmefene act on opioid receptors, although with different mechanisms. More studies are required to establish the exact mechanisms of the opioid-induced effects on sleep–wake cycle. In turn, alcohol intake, through its neurotoxic effects, may induce sleep disorders.

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