Alcohol and insomnia: Possible risks and more

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sleep deprivation and alcohol

Subjects with AUD were significantly less likely to generate a K-complex in response to a tone and had significantly smaller amplitude responses. In a larger study, Colrain et al. 83 studied 42 abstinent long-term alcoholics (27 men) and 42 controls (19 men). Subjects with AUD were significantly less likely to produce K-complexes than controls. Frontal (but not posterior) amplitude of the average response was significantly smaller in AUD subjects.

sleep deprivation and alcohol

Can Alcohol Cause Insomnia?

European trials of acamprosate for the treatment of AUD found a significant benefit for the maintenance of abstinence following alcohol withdrawal in 15 of 18 randomized, double-blind, placebo-controlled trials 257. Several studies, including a secondary analysis of the U.S. acamprosate study 258, showed that acamprosate may help normalize AUD-related sleep disturbances 259,260,261. From a sleep architecture perspective, two of these studies showed that acamprosate improved sleep continuity, restored Stage 3 sleep, and increased REM sleep latency, all of which are related to relapse to AUD.

What is insomnia?

Hypocretin/orexin peptides have been implicated in sleep-wake regulation since their initial discovery 126. They have wide projections in the brain 127, interacting with autonomic, neuroendocrine, and neuroregulatory systems 128,129,130,131,132,133,134,135. Perhaps most well known is that the hypocretin system makes a key contribution to the etiology of narcolepsy. Human narcoleptic patients presented dramatic reductions (85–95%) of cerebrospinal fluid hypocretin-1 138 and the number of hypocretin neurons 139, 140, leading to the hypothesis that narcolepsy could be related to the ongoing loss of hypocretin neurons 141.

As the alcohol in your system begins to wear off, something called “homeostatic recovery” can occur.
Furthermore, the evidence that does exist indicates that alcohol’s effects occur through the nicotinic acetylcholine receptor (Collins 1996); however, acetylcholine-mediated induction of REM sleep occurs through muscarinic receptors (Bennington and Heller 1995).
Using this procedure, de Wit and colleagues (1987, 1989) found that moderate drinkers who preferred an alcohol dose of 0.5 g/kg, which corresponds to approximately three drinks, in the laboratory tests felt less alert at that time than did drinkers who did not prefer alcohol.

Alcohol and Insomnia: That Nightcap Might Keep You Up at Night

Singh et al. 72 studied AUD subjects after 2–3 weeks of treatment and a further week of washout from lorazepam.
If you still have trouble getting a good night’s rest after practicing good sleep habits, talk to your doctor.
Insomnia and sleep deprivation are closely related but aren’t the same thing.
However, these times are not always suited to the sleep patterns dictated by the economic interests and activities of modern life.
Thus, for the low-frequency EEG that is dominant in SWS, the frequency analysis is consistent with visual scoring.
Another rationale for the treatment of sleep disorders in AUD is that, retrospectively, subjects with AUD reported the presence of insomnia prior to the onset of AUD 251.

The combination of OSA and alcohol increases a person’s risk of heart attack, stroke and sudden death (64). Alcohol’s worsening of apneic events, increasing sleep disruption and daytime fatigue, can also impair driving and increase rates of motor vehicle accidents. Among OSA subjects who consumed 14 or more drinks per week, self-reports of sleep-related accidents are fivefold higher compared to those who drink lesser amounts (65). Another population that typically shows lower levels of SWS compared with healthy young adults are the elderly, but no studies have assessed alcohol’s effects on the sleep of healthy elderly people. In sleep deprivation studies, however, elderly participants show increases in SWS on the recovery night after the sleep-deprivation period; possibly alcohol could similarly promote SWS in elderly people. does alcohol help you sleep This finding does not imply, however, that alcohol should be considered a potential sleep therapy in elderly people, because tolerance to the SWS enhancement develops rapidly (Prinz et al. 1980).

European trials of acamprosate for the treatment of AUD found a significant benefit for the maintenance of abstinence following alcohol withdrawal in 15 of 18 randomized, double-blind, placebo-controlled trials 257.
In AUD patients, their ubiquitous, chronic, and long-lasting sleep issues are a cause of negative affect.
In terms of sleep problems, men were more likely to report sleeping less than 7 hours per night than women (63.7% men compared to 54.4% women).
Circadian rhythms thrown out of sync can weaken the lining of the gastrointestinal tract, making it more vulnerable to permeation—that’s the leakiness that allows bacteria, toxins, and food to leave the intestines and enter the bloodstream.

Selection of Studies

sleep deprivation and alcohol

For example, Ford and Kamerow 231 reported nearly double the prevalence of AUD in insomnia (7.0%) relative to those with no sleep complaints (3.8%). Weissman et al. 232 reported similar differences, with 3.3% of insomnia patients having AUD vs. 1.8% of normal sleepers. Notably, in a cross-sectional study of 1200 health maintenance organization members in Michigan, the prevalence of alcohol abuse or dependence was found to be 30% in those with insomnia. However, consistent with Ford and Kerow 231 and Weissman et al. 232, the gender-adjusted odds ratio for AUD was 2.0 (1.3–3.0) relative to those with no sleep disturbances 233. These include (in order of sleep-related prominence) hypocretin, norepinephrine, glucocorticoids, and neuroimmune factors.

Sleep duration, hypnotic drug use, and risk factors: cross- sectional study

Cognitive behavior therapy was shown to improve sleep but not drinking in two studies 247, 248. Two drugs that improved sleep but not alcohol drinking include quetiapine 249 and trazadone 250. Indeed, the photo- or chemostimulation of genetically tagged glutamate neurons commonly evokes cortical activation 222, 223, likely reflecting the fact that glutamate is a prominent neurotransmitter by Wake/Paradoxical Sleep-max active neurons 221. For the purposes of this review, we explore the effects of alcohol on the neurotransmitter systems that are considered key to the addiction cycle outlined above.

Insomnia disorders are more likely to have a chronic course, to require independent treatment, and may contribute more directly to relapse during alcohol recovery.
When collapsing the data across the whole night of sleep, a modest dose-related increase in SWS was observed.
REM reduction becomes less pronounced with continued alcohol use, but a REM rebound often appears with alcohol cessation.

The term Alcohol Use Disorder (AUD) is used throughout the manuscript, but this specific diagnosis is a relatively recent concept. Many of the studies that are cited herein used other diagnoses, such as “alcohol abuse” or “alcohol dependence” or even “alcoholism,” based on various research or clinical definitions that were available at the time the research was conducted. In 2012–2013, 70.9% of the original cohort who were still alive (age range 61–81 years), participated in phase 11.

sleep deprivation and alcohol

There is a higher prevalence of insomnia in people with ADHD and AUD, but consuming alcohol to manage insomnia generally worsens sleeplessness. Heavy drinking can make the sleep- and circadian rhythm-disrupting effects of alcohol worse. But even a regular, moderate routine of two to three drinks a day is enough to create sleep and performance problems for many people. The sleep of individuals with depressive and/or anxiety disorders resembles the sleep of persons with alcoholism (71). Similar REM sleep changes occur during withdrawal in alcoholics with and without secondary depression (54).