Alcohol is one of the most commonly abused substances worldwide. In Canada, the annual volume of alcohol consumption has increased over the last decade as has the prevalence of high-risk drinking. Abuse is also very common in the United States, with a prevalence of about 14%. This excessive consumption has a very significant impact on the health-care system and society, including increases in violent crime, accident rates, pharmaceutical expenses, and hospitalizations (Laramee et al. Alcohol. Jan 2013, e-pub ahead of print).
Sleep disturbance as a risk factor for alcohol intake
Alcohol is often used by the general population as self-medication to treat sleeplessness due to its sedating effect. An international survey found that almost one quarter of the general population complained of not sleeping well with about 31% reporting insomnia; these subjects were also more likely to report alcohol use(Soldatos et al. Sleep Med. 2005;6[1]:5). Epidemiologic studies have confirmed that adults with insomnia have a much higher risk of developing alcohol abuse compared with adults without insomnia, even in absence of associated psychiatric disorders. Shift workers with sleep problems, especially those who work predominantly at night, are more likely to use alcohol as a sleep aid and to have heavy alcohol consumption compared with day-workers without sleep problems (Morikawa et al. Alcohol. Nov 2012, e-pub ahead of print).
Sleep curtailment, defined as less than 7 to 8 hours of sleep, is becoming increasingly prevalent in modern society. Adults reporting less than 6 hours per night were found to have increased alcohol intake compared with longer sleepers, more so if they also demonstrated a high degree of disinhibited eating behaviors (Chaput et al. Appetite. 2012;59[3]:650); short sleepers were also more likely to binge drink.
Effects of acute alcohol intake on sleep
As patients afflicted with insomnia will report, a lack of good quality sleep can have a major impact on quality of life, leading some to turn to alcohol as treatment. Unfortunately, despite its initial sedative effect, alcohol can lead to significant sleep disruption. The effect of alcohol use prior to bedtime was studied in healthy subjects (Feige et al. Alcohol Clin Exp Res. 2006;30[9]:1527); at the level of "social drinking," there was no significant impact on sleep architecture or subjective complaints. As the dose of alcohol increased, a hypnotic-like effect was noted, leading to shortened sleep latency, reduced number of awakenings after sleep onset, increased delta sleep, and decreased REM density; this effect was more pronounced during the first part of the night due to the fairly rapid metabolism of ethanol. During the latter half of the night, more disrupted sleep was noted along with rebound REM sleep, which may account for the increased frequency of nightmares reported by some patients as their sleep fragmentation awakens them from their dreams.
Given the described association between sleep and memory consolidation, it is not surprising that acute alcohol intake can affect memory. Heavy social drinking just before bedtime can impair recall the following morning, despite the absence of detectable alcohol in the blood at that time. Studies have also demonstrated that more modest levels of alcohol ingestion before bed impair subsequent memory for recently learned procedural and cognitive tasks in alcohol-naïve subjects, compared with the use of alcohol in the afternoon (Smith et al. Sleep. 2003; 26:185).
Some reviews have suggested an association between acute alcohol use and the incidence of parasomnias; given the known association between parasomnias and other agents that bind to the same GABAA receptors as alcohol (such as zolpidem and zaleplon), it seems reasonable to conclude that alcohol would also induce nocturnal behaviors. However, few case reports linking the two have been published. Because parasomnias are usually diagnosed clinically, it is also possible that reports of alcohol-induced sleepwalking might actually represent episodes of nocturnal wandering during intoxicated awakenings.
Acute alcohol intake can decrease the dilating force of the pharyngeal muscles, leading to upper airway narrowing and can also alter chemosensitivity to carbon dioxide and oxygen tensions. Strangely, alcohol intake has not been shown to induce snoring among nonsnorers in published studies, though acute nocturnal intake can worsen the incidence and intensity of snoring among chronic snorers. Large quantities of alcohol have also been shown to exacerbate sleep-disordered breathing, especially in men. However, even moderate amounts of alcohol intake can worsen obstructive physiologic function and oxygenation indices among patients with mild-to-moderate obstructive sleep apnea (Izumi et al. Environ Health Prev Med. 2005;10[1]:16).
Effects of chronic alcohol intake on sleep
Sleep problems are more common among long-term alcohol abusers than in the general population. Many studies have shown that alcohol intake prolongs sleep latency in patients who chronically use alcohol, compared with nonalcoholic healthy subjects. These findings may suggest that alcoholic subjects have developed a tolerance to its sedative effects. Chronic alcoholics who are actively abusing have been reported to demonstrate decreased total sleep time, increased delta sleep, and an increased REM sleep latency with decreased REM sleep. However, these effects may not persist, with at least one review suggesting that prolonged continuous drinking can lead to reduced delta sleep, possibly related to drug tolerance (Landholt et al. CNS Drugs. 2001;15[5]:413). Most chronic alcoholics have a higher rate of dissatisfaction with their sleep compared with the general population and will report symptoms of insomnia if they stop drinking.