Does Alcohol Makes You Sleepy?

Does Alcohol Makes You Sleepy
Why Alcohol Makes Me Sleepy – The Connection Between Alcohol and Sleep – Alcohol is considered a depressant and directly affects the central nervous system. Once alcohol enters the bloodstream, it circulates to the brain, where it proceeds to slow down the firing of neurons.

Why does alcohol make you sleepy?

Alcohol and Sleep | Sleep Foundation Medical Disclaimer: The content on this page should not be taken as medical advice or used as a recommendation for any specific treatment or medication. Always consult your doctor before taking a new medication or changing your current treatment.

  1. Alcohol is a central nervous system depressant that causes brain activity to slow down.
  2. 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.
  3. People with alcohol use disorders commonly experience insomnia symptoms.

Studies have shown that alcohol use can exacerbate the symptoms of sleep apnea. Drinking alcohol 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.

After a person consumes alcohol, the substance is absorbed into their bloodstream Centers for Disease Control and Prevention (CDC) As the nation’s health protection agency, CDC saves lives and protects people from health threats. 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 through the body.

The effects of alcohol largely depend on the person. Important factors include the amount of alcohol and how quickly it is consumed, as well as the person’s age and body composition. The relationship between alcohol and sleep National Institutes of Health (NIH) The NIH, a part of the U.S.

Department of Health and Human Services, is the nation’s medical research agency — making important discoveries that improve health and save lives. has been studied since the 1930s, yet many aspects of this relationship are still unknown. Research has shown that those who drink large amounts of alcohol before bed are often prone to decreased sleep onset latency, meaning they take less time to fall asleep.

As liver enzymes metabolize the alcohol during the night and blood alcohol levels decrease, these individuals are also more likely to experience sleep disruptions and decreases in sleep quality. Does Alcohol Makes You Sleepy Does Alcohol Makes You Sleepy To understand how alcohol impacts sleep, it is important to understand the different stages of the human sleep cycle. A normal sleep cycle consists of : three non-rapid eye movement (NREM) stages and one rapid eye movement (REM) stage.

  • Stage 1 (NREM) : This initial stage is the transition period between wakefulness and sleep, during which the body will begin to wind down. The sleeper’s heartbeat, breathing, and eye movements start to slow down and their muscles will relax. Brain activity also begins to decrease. This phase is also known as light sleep.
  • Stage 2 (NREM) : The sleeper’s heartbeat and breathing rates continue to slow 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.
  • Stage 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 begins about 90 minutes after the individual initially falls asleep. Eye movements will restart and the sleeper’s breathing rate and heartbeat will quicken. Dreaming primarily takes place during REM sleep. This stage is also thought to play a role in memory consolidation National Center for Biotechnology Information The National Center for Biotechnology Information advances science and health by providing access to biomedical and genomic information.,

These four NREM and REM stages repeat in cyclical fashion throughout the night. Each cycle should last roughly 90 to 120 minutes Merck Manual First published in 1899 as a small reference book for physicians and pharmacists, the Manual grew in size and scope to become one of the most widely used comprehensive medical resources for professionals and consumers.

, 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 later cycles. Drinking alcohol before bed can increase 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 imbalance decreases overall sleep quality, which can result in shorter sleep duration and more sleep disruptions., the most common sleep disorder, is marked by periods of difficulty falling or staying asleep.

Insomnia occurs despite the opportunity and desire to sleep, and leads to 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 National Center for Biotechnology Information The National Center for Biotechnology Information advances science and health by providing access to biomedical and genomic information.

  1. The following day.
  2. This can lead them into a vicious cycle National Center for Biotechnology Information The National Center for Biotechnology Information advances science and health by providing access to biomedical and genomic information.
  3. 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 National Center for Biotechnology Information The National Center for Biotechnology Information advances science and health by providing access to biomedical and genomic information., as well as middle-aged and older adults National Center for Biotechnology Information The National Center for Biotechnology Information advances science and health by providing access to biomedical and genomic information.

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.

  • The Matt Walker Podcast’s Scientific Advisor 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.
  • Occurs due to physical blockages in the back of the throat, while 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 suggest that alcohol contributes to sleep apnea because it causes the throat muscles to relax, which in turn creates more resistance during breathing.

  1. This can exacerbate OSA symptoms and lead to disruptive breathing episodes, as well as heavier snoring.
  2. Additionally, consuming just one serving of alcohol before bed can lead to symptoms of OSA and heavy snoring, even for people who have not been diagnosed with sleep apnea.
  3. The relationship between sleep apnea and alcohol has been researched fairly extensively.

The general consensus based on various studies is that consuming alcohol increases the risk of sleep apnea National Library of Medicine, Biotech Information The National Center for Biotechnology Information advances science and health by providing access to biomedical and genomic information. 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.

  • 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 typically have a more negative impact on sleep than light or moderate alcohol consumption.

  1. However, since the effects of alcohol are different from person to person, even small amounts of alcohol can reduce sleep quality for some people.
  2. One 2018 study compared sleep quality National Library of Medicine, Biotech Information The National Center for Biotechnology Information advances science and health by providing access to biomedical and genomic information.

among subjects who consumed various amounts of alcohol.

  • Low amounts of alcohol : Having fewer than two servings of alcohol per day for men or one serving per day for women decreased sleep quality by 9.3%.
  • Moderate amounts of alcohol : Having two servings of alcohol per day for men or one serving per day for women decreased sleep quality by 24%.
  • High amounts of alcohol : Having more than two servings of alcohol 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? You can manage the negative effects of alcohol on sleep by giving your body ample time to metabolize alcohol before falling asleep. To reduce the risk of sleep disruptions, you should stop drinking alcohol at least four hours National Library of Medicine, Biotech Information The National Center for Biotechnology Information advances science and health by providing access to biomedical and genomic information.

  1. Centers for Disease Control. (2020, January 15). Alcohol and Public Health: Frequently Asked Questions. Centers for Disease Control and Prevention., Retrieved February 6, 2023, from
  2. Roehrs, T., & Roth, T. Sleep, Sleepiness, and Alcohol Use. National Institute on Alcohol Abuse and Alcoholism., Retrieved February 6, 2023, from
  3. Rasch, B., & Born, J. (2013). About Sleep’s Role in Memory. Physiological Reviews, 93(2), 681–766.
  4. Schwab, R. (2020, June). Insomnia and Excessive Daytime Sleepiness (EDS). Merck Manual Consumer Version., Retrieved February 6, 2023, from
  5. Park, S., Oh, M., Lee, B., Kim, H., Lee, W., Lee, J., Lim, J., & Kim, J. (2015). The Effects of Alcohol on Quality of Sleep. Korean Journal of Family Medicine, 36(6), 294–299.
  6. Coltrain, I., Nicholas, C., & Baker, F. (2018). Alcohol and the Sleeping Brain. Handbook of Clinical Neurology, 125, 415–431., Retrieved from
  7. Popovici, I., & French, M. (2013). Binge Drinking and Sleep Problems among Young Adults. Drug and Alcohol Independence, 132, 207–215.
  8. Canham, S., Kaufmann, C., Mauro, P., Mojtabai, R., & Spira, A. (2015). Binge Drinking and Insomnia in Middle-aged and Older Adults: The Health and Retirement Study. International Journal of Geriatric Psychiatry, 30(3), 284–291.
  9. Simou, E., Britton, J., & Leonardi-Bee, J. (2018). Alcohol and the risk of sleep apnoea: A systematic review and meta-analysis. Sleep Medicine, 42, 38–46.
  10. Pietilä, J., Helander, E., Korhonen, I., Myllymäki, T., Kujala, U., & Lindholm, H. (2018). Acute Effect of Alcohol Intake on Cardiovascular Autonomic Regulation During the First Hours of Sleep in a Large Real-World Sample of Finnish Employees: Observational Study. JMIR Mental Health, 5(1), e23.
  11. Stein, M.D., & Friedmann, P.D. (2005). Disturbed sleep and its relationship to alcohol use. Subst Abuse, 26(1):1-13.

: Alcohol and Sleep | Sleep Foundation

Does alcohol make you sleep better?

How alcohol affects your sleep patterns – Regular drinking can affect the quality of your sleep making you feel tired and sluggish. This is because drinking disrupts your sleep cycle.1 Some people may find alcohol helps them get to sleep initially, but this is outweighed by the negative effect on sleep quality through the night.

  1. The alcohol in your system will mean you spend less time in the important Rapid Eye Movement (REM) stage of sleep, 2 with the end result that you wake up feeling less refreshed.
  2. Even just a couple of drinks will have an effect.
  3. Several sleepless nights can have an impact on your day-to-day mental function – for example, your mood, concentration and decision-making.

Of course, if you’ve had a lot to drink, you may well wake up with a hangover too. So, as well as feeling tired, you might find you have a headache, or you’re more stressed and irritable. If you get a hangover, only time will help you sober up, but you could avoid getting one in the first place by limiting how many alcoholic drinks you have, and alternating with water or soft drinks, to help avoid dehydration.

Does alcohol cause daytime sleepiness?

ALCOHOL ALERT The study of alcohol’s effects on sleep dates back to the late 1930s. Since then, an extensive literature has described alcohol’s effects on the sleep of healthy, nonalcoholic people. For example, studies found that in nonalcoholics who occasionally use alcohol, both high and low doses of alcohol initially improve sleep, although high alcohol doses can result in sleep disturbances during the second half of the nocturnal sleep period.

Furthermore, people can rapidly develop tolerance to the sedative effects of alcohol. Researchers have investigated the interactive effects of alcohol with other determinants of daytime sleepiness. Such studies indicate that alcohol interacts with sleep deprivation and sleep restriction to exacerbate daytime sleepiness and alcohol-induced performance impairments.

Alcohol’s effects on other physiological functions during sleep have yet to be documented thoroughly and unequivocally. KEY WORDS: sleep disorder; physiological AODE (effects of alcohol or other drug use, abuse, and dependence); REM (rapid eye movement) sleep; NREM (nonrapid eye movement) sleep; circadian rhythm; melatonin; prolactin; body temperature; attention; time of day; insomnia; dose-response relationship Alcohol affects sleep, daytime alertness, and certain physiological processes that occur during sleep.

  1. Its impact on human sleep has received much scientific study dating back to early experiments by Kleitman (1939), described in his book Sleep and Wakefulness,
  2. In that monograph, the author summarizes the effects that alcohol consumed 60 minutes before bedtime has on body temperature and motility during sleep in healthy nonalcoholic people.
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In the 1960s and 1970s, after scientists had identified various sleep states (e.g., rapid eye movement sleep) and had standardized electrophysiological methods to document sleep, research on alcohol’s effects on the sleep of healthy nonalcoholic and noninsomniac volunteers and on the sleep of alcoholics increased substantially.

More recently, with the emergence of the field of sleep-disorders medicine, researchers and clinicians have focused their attention on alcohol’s effect on primary sleep disorders, such as sleep apneas, which are short (i.e., 10 to 30 seconds long) episodes of breathing obstruction. This attention to sleep disorders also has sensitized investigators and clinicians to the impact that disrupted and shortened sleep has on daytime alertness.

As a result, various studies have investigated the potential interactive effects of alcohol with daytime alertness and daytime functioning in both healthy people and patients with sleep disorders. This article provides an overview of alcohol’s effects on normal sleep, sleep physiology, and daytime alertness in nonalcoholic people.

(The accompanying article by Brower, pp.110-125 in this issue, discusses alcohol’s effects on sleep in alcoholics.) The current article reviews normal sleep physiology, describes alcohol’s effects on the various sleep states and sleep stages, and explores some of the mechanisms through which alcohol may exert those effects.

It then summarizes the relationship of nocturnal sleep to daytime alertness and how alcohol affects this relationship. The article ends with a discussion of alcohol’s effects on sleep in people with primary insomnia. Normal Sleep Physiology As most people know from their own experience, sleep is not uniform through-out the night.

  1. For example, at certain times during the night, it is very difficult to wake a sleeping person, whereas at other times, the slightest sound will alert the sleeper.
  2. Extensive studies have identified two different sleep states: REM sleep and nonrapid eye movement (NREM) sleep.
  3. Furthermore, NREM sleep can be divided into four stages based on how easy it is to arouse a sleeper (i.e., how “deep” the sleep is).

These different sleep states and sleep stages are defined based on scoring criteria for three electrophysiological measurements that were first published in 1968 and have been employed ever since in sleep laboratories around the world. The three electrophysiological measurements are recorded simultaneously and comprise the following:

The electroencephalogram (EEG), which traces the electrical activity of the brain through electrodes placed on the scalp. These measurements produce characteristic brain waves called alpha, beta, delta, and theta rhythms, which differ in their frequencies. The electrooculogram (EOG), which measures eye movements through electrodes placed on the skin around the eyes and records tiny electric signals that occur when the eyes move. The electromyogram (EMG), which measures the electrical activity of muscles through electrodes placed on the skin in various body regions. This technique can measure even small muscle movement during sleep, such as twitching.

The following paragraphs describe how these measurements are used to distinguish different sleep states and sleep stages. Stages of NREM and REM Sleep When comparing the EEG readings of various sleep stages, researchers and clinicians assess the frequency of the brain waves, measured in hertz (Hz), and the size, or amplitude, of the brain waves, measured in microvolts.

Samples of electrophysiological measurements of various sleep stages. The four panels represent the measurements obtained during (A) wakefulness; (B) stage 2 nonrapid eye movement (NREM) sleep (i.e., light sleep); (C) stages 3 to 4 NREM sleep (deep or slow-wave sleep); and (D) rapid eye movement (REM) sleep, which is associated with dreaming. For each panel, the graphs labeled LOC and ROC represent measurements of the left and right eye movements, respectively. The graph labeled “chin” represents a measurement of small body movements, such as of the chin muscles. The graphs labeled C3-A2 and O2–A1 represent two electroencephalogram (EEG) readings measuring brain activity in certain brain regions. Finally, the electrocardiogram (EKG) measures the heart rate. Each sleep stage is characterized by a specific pattern of those readings. For example, during REM sleep the eyes move rapidly compared with stage 2 NREM sleep. At the same time, the EEG readings during REM sleep exhibit a higher frequency (i.e., number of waves per second) and a lower amplitude (i.e., height of the peaks and valleys of the waves) compared with stage 2 NREM sleep.

During active wakefulness (i.e., when the person is awake and pursuing normal activities), the EEG is characterized by high frequencies (i.e., 16 to 25 Hz) and low voltage (i.e., 10 to 30 microvolts). EOG readings during wakefulness exhibit REMs, and EMG readings generally show a high amplitude indicative of large muscle movements.

  • During relaxed wakefulness (i.e., when a person is awake but has his or her eyes closed and is relaxed), the EEG is characterized by a pattern of alpha waves with a frequency of 8 to 12 Hz and an amplitude of 20 to 40 microvolts.
  • EOG readings show slow, rolling movements at the transition to NREM sleep.

EMG readings show reduced amplitudes. During NREM sleep, the frequency of the brain waves slows further, whereas the amplitude continues to increase. Thus, when the arousal threshold is highest (i.e., sleep is “deepest”), the EEG shows slow-wave sleep with a frequency of 0.5 to 2.0 Hz and an amplitude of 75 microvolts or greater.

  • EOG tracings indicate cessation of eye movements, and EMG readings are gradually reduced, even though episodic repositioning of the body and other motor events occur.
  • Based on the simultaneous analysis of all three measurements, NREM sleep is classified into four stages that are characterized by increasing arousal thresholds.

Thus, stage 1 (i.e., drowsy sleep) has the lowest arousal threshold; stage 2 (i.e., light sleep) is intermediate; and stages 3 and 4 (i.e., deep sleep), which collectively are also called slow-wave sleep (SWS), have the highest arousal threshold. During REM sleep, cortical EEG readings revert to the low-voltage-mixed-frequency pattern seen during drowsy sleep.

The EOG displays the bursts of rapid eye movements that give this stage its name. The EMG is reduced to its lowest level for the night. In fact, most major voluntary muscle groups are paralyzed, because certain nerve cells in the spinal cord (i.e., motor neurons) are not responding to nerve signals. Arousal thresholds in REM are relatively low, similar to NREM stages 1 or 2.

Tonic and Phasic Periods of REM Sleep REM sleep can be further subdivided into tonic and phasic periods. During the tonic periods, which account for the majority of REM sleep, muscle tone is decreased and the EEG is similar to that seen during stage 1 NREM sleep.

  1. These tonic periods are interrupted by intermittent phasic REM events.
  2. For example, the eye movements characteristic of REM sleep occur in bursts during these phasic periods, which are followed by the tonic periods of EOG quiescence.
  3. Coupled with the bursts of eye movements are phasic muscle twitches, typically involving peripheral muscles, although the reduced muscle tone (i.e., atonia) characteristic of the tonic periods continues in most muscle groups.

In addition, bursts of activity occur during the phasic periods in body functions that are controlled by the autonomic nervous system 1 ( 1 The autonomic nervous system controls involuntary vital functions, such as the activities of the heart, lungs, gastrointestinal tract, and glands.) ; these bursts of activity are reflected by irregularities in cardiopulmonary function (e.g., heart rate and breathing rate).

NREM–REM Cycles An ultradian process-a biorhythm with a cycle of less than 24 hours- within sleep controls the alternation between NREM and REM sleep throughout the night. This ultradian process creates cycles of NREM sleep followed by REM sleep that last approximately 90 to 120 minutes, yielding four to five such cycles over a standard 8-hour sleep period.

In the first two of those cycles, slow-wave NREM sleep predominates, whereas the REM periods are generally quite short (i.e., 5 to 10 minutes). Conversely, in the last two or three cycles, REM sleep predominates, sometimes continuing uninterrupted for 30 to 40 minutes, and slow-wave NREM sleep is almost nonexistent.

(The significance of this ultradian cycling of NREM and REM sleep to alcohol’s effects on sleep is described in the following section of this article.) Alcohol’s Effects on Sleep Physiology To assess alcohol’s effects on sleep, investigators conducting a typical sleep study administer alcohol to their subjects approximately 30 to 60 minutes before bedtime.

As a result of this schedule, alcohol concentrations in the breath or blood usually peak at “lights-out.” Using this approach, researchers have extensively studied alcohol’s effects in healthy people at doses ranging from 0.16 to 1.0 grams of alcohol per kilogram of body weight (g/kg) (Williams and Salamy 1972).

These doses, which correspond to approximately one to six standard drinks, 2 ( 2 A standard drink is defined as one 12-ounce bottle of beer or wine cooler, one 5-ounce glass of wine, and 1.5 ounces of 80 proof distilled spirits.) yield breath alcohol concentrations (BrACs) as high as 0.105 percent.3 ( 3 Breath alcohol concentrations are another way of quantifying alcohol levels in the body and are approximately the same as blood alcohol concentrations after a given alcohol dose.) Some studies using this range of alcohol doses reported that the study participants fell asleep faster (i.e., had reduced sleep latency) than without alcohol consumption.

One study found an increased sleep time at a low alcohol dose (i.e., 0.16 g/kg) but detected no such effect at higher alcohol doses (i.e., 0.32 and 0.64 g/kg) (Stone 1980). Some investigators have separately analyzed alcohol’s effects during the first and second half of the nighttime sleep period.

These studies found that particularly at higher alcohol doses, increased wake periods or light stage 1 sleep periods occurred during the second half of the sleep period (Williams et al.1983; Roehrs et al.1991). This second-half disruption of sleep continuity is generally interpreted as a “rebound effect” once alcohol has been completely metabolized and eliminated from the body.

The term “rebound effect” means that certain physiological variables (e.g., sleep variables, such as the amount of REM sleep) change in the opposite direction to the changes induced by alcohol and even exceed normal levels once alcohol is eliminated from the body.

This effect results from the body’s adjustment to the presence of alcohol during the first half of the sleep period in an effort to maintain a normal sleep pattern. Once alcohol is eliminated from the body, however, these adjustments result in sleep disruption. This hypothesis is supported by the known rate of alcohol metabolism, which leads to a decrease in BrAC of 0.01 to 0.02 per-cent per hour.

Given that in such experiments, the typical peak BrACs measured shortly before sleep are 0.06 to 0.08 percent, alcohol metabolism at this rate would be completed within 4 to 5 hours of sleep onset; thus, the sleep disruption during the second half of the night would coincide with the clearance of alcohol from the body.

In addition to these effects on sleep initiation and sleep maintenance, researchers have found that alcohol consistently affects the proportions of the various sleep stages. Thus, most studies have reported a dose-dependent suppression of REM sleep at least during the first half of the sleep period (Williams and Salamy 1972).

As noted earlier, the amount of REM sleep time is lower during the first half of the night relative to the second half of the night; consequently, the full REM-suppressive effect of alcohol is probably underestimated in most studies. To determine alcohol’s full effect on REM sleep, investigators would need to administer an additional alcohol dose in the middle of the night, thereby causing alcohol’s peak concentrations to coincide with the majority of REM sleep time.

  1. No such studies have been conducted, however.
  2. Those studies that have demonstrated alcohol-induced REM suppression during the first half of the sleep period also have frequently found an REM rebound (i.e., longer-than-normal REM periods) during the second half of the night (Williams and Salamy 1972).

As a result, the overall amount of REM sleep in subjects receiving alcohol before sleeping did not differ from that in subjects receiving a nonalcoholic drink (i.e., a placebo). As with the increased periods of wakefulness or light sleep, the REM rebound during the second half of the night is associated with the completed alcohol metabolism and elimination from the body.

  1. The neurobiological mechanisms responsible for the rebound of either wakefulness or REM sleep are still unknown.
  2. Some studies also found an alcohol-related increase in the amount of SWS (i.e., stages 3 and 4 NREM sleep) in the first half of the sleep period (Williams and Salamy 1972).
  3. In addition to the alcohol dose consumed, the basal (i.e., normal) level of SWS in the study population appeared to be the most likely factor determining whether SWS was increased.

For example, in a study of insomniacs who had lower amounts of SWS than did healthy people when taking a placebo-a typical finding in insomniacs-SWS increased when they consumed alcohol (Roehrs et al.1999). Conversely, alcohol did not affect SWS in a group of age-matched healthy control subjects.

  • 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.

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). Several studies have assessed the effects of alcohol administration over several nights.

Such studies clearly demonstrated that tolerance to alcohol’s sedative and sleep-stage effects develops within 3 nights (Williams and Salamy 1972) and that the percentages of SWS and REM sleep return to basal levels after that time. Furthermore, in some studies, the discontinuation of nightly alcohol administration resulted in a REM sleep rebound-that is, an increase in REM sleep beyond basal levels (Williams and Salamy 1972).

However, not all studies found such a rebound effect. This variability in results may be related to several factors specific for each study, including the basal level of REM sleep in the participants, the degree of alcohol-related REM suppression, the extent of prior tolerance to REM suppression, and the dose and duration of alcohol administration.

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Alcohol’s Effects on Hormone Function The sleep-wake cycle is organized in a circadian rhythm. To track this rhythm in humans, researchers tend to use measurements of the core body temperature and of the secretion of the hormone melatonin from the pineal gland in the brain, both of which fluctuate in a typical pattern throughout the day.

Accordingly, one can also use these measurements to assess alcohol’s effects on the sleep-wake cycle. As noted earlier, Kleitman (1939) first reported that alcohol administration 60 minutes before nocturnal bedtime altered body temperature compared with placebo administration.

Thus, alcohol administration initially resulted in a reduction in core temperature, followed by a rebound increase in temperature. Such a temperature-reducing (i.e., effect of alcohol also has been observed in numerous other studies. Various hormones secreted by the pituitary gland in the brain also show circadian variations, with secretory peaks occurring during the usual sleep period.

Some of these hormones are linked to sleep-if sleep is delayed, their secretory peaks also are delayed. Conversely, the levels of other hormones peak at the same time every night, even if sleep is delayed. One of the pituitary hormones linked to sleep is growth hormone, whose secretion typically peaks with the onset of SWS (Takahashi et al.1969).

In an early study, administration of 0.8 g/kg alcohol before bedtime suppressed growth-hormone secretion, despite increasing the percentage of SWS (Prinz et al.1980). A later study using two different alcohol doses-0.5 and 1.0 g/kg-similarly found that alcohol suppressed growth-hormone secretion at a dose-related rate (Ekman et al.1996).

Thus, alcohol appears to affect growth-hormone secretion and SWS levels independently (i.e., to dissociate growth hormone from SWS). This hypothesis is further supported by the results of repeated alcohol administration in the first study (Prinz et al.1980).

  1. In that study, the alcohol-related suppression of growth-hormone secretion persisted over the 3 nights of alcohol administration, whereas tolerance developed to the alcohol-related enhancement of SWS.
  2. The clinical implications of alcohol’s inhibitory effects on growth hormone and the dissociation of growth hormone and SWS are unclear, particularly with chronic and excessive alcohol use.

Unfortunately, these provocative findings have not been pursued further. Another pituitary hormone linked to sleep is prolactin 4 ( 4 Together with other hormones, prolactin regulates growth and development of the mammary glands and tinitiation and maintenance of milk production in nursing women.) ; the hormone’s secretion peaks 4 to 5 hours after sleep onset (Van Cauter and Turek 1994).

To date, researchers have not determined conclusively whether alcohol affects prolactin release. In the study by Ekman and colleagues (1996), alcohol did not affect prolactin levels. However, possibly even at the 1.0 g/kg alcohol dose, alcohol levels may no longer have been high enough 4 to 5 hours after sleep onset to affect prolactin secretion.

Prinz and colleagues (1980) did not measure prolactin levels in their study. Alcohol’s Effects on Neurochemicals Alcohol’s effects on central nervous system (CNS) function are mediated by its effects on various brain chemicals (i.e., neurotransmitters and neuromodulators) that are responsible for the transmission of nerve signals from one nerve cell (i.e., neuron) to the next,

These neurotransmitters are released by the signal-emitting neuron and generally exert their actions by interacting with certain molecules (i.e., receptors) located on the surface of the signal-receiving neuron. Particularly at low doses, alcohol affects CNS function primarily by interfering with the normal actions of the neurotransmitters gammaaminobutyric acid (GABA) and glutamate, both of which also play critical roles in wake-sleep states (Koob 1996).

GABA is the major inhibitory neurotransmitter system in the CNS-that is, its interaction with the signal-receiving neuron dampens the ability of that neuron to generate a new nerve signal. Evidence from studies using various types of experimental approaches has indicated that alcohol at low doses enhances GABA’s actions on the signal-receiving neuron, thereby reducing that neuron’s ability to generate nerve signals even further (Mihic and Harris 1996).

This observation is significant, because many hypnotic drugs (i.e., barbiturates, benzodiazepines, and the newer nonbenzodiazepine GABA agonists 5 ) ( 5 Agonists are substances that mimic the actions of another molecule. For example, GABA agonists cause the same reactions in other neurons as does GABA.) also act by facilitating GABA function.

Scientists have long considered GABA to play a major role in sleep (Jones 2000). For example, GABA-releasing neurons are present in various brain areas that are involved in the generation of SWS, such as the brainstem reticular activation system, thalamus, hypothalamus, and basal forebrain.

  • Thus, facilitation of GABA-mediated inhibition is one possible explanation for alcohol’s sedative and SWS-promoting effects.
  • Glutamate is the major excitatory neurotransmitter in the CNS-that is, the interaction of glutamate with its receptor activates the signal-receiving neuron to generate a new nerve signal.

Four types of glutamate receptors have been identified, including the NMDA receptor (Tabakoff and Hoffman 1996). Anatomically, glutamate-releasing neurons also are present in some of the brain areas that promote SWS, such as the reticular activating system of the brainstem and the forebrain (Jones 2000).

  1. NMDA agonists produce seizures; conversely, some glutamate antagonists 6 ( 6 Antagonists are substances that inhibit or interfere with the actions of another molecule.
  2. For example, glutamate antagonists inhibit glutamate’s interactions with its receptors.) are electrophysiological used as sedatives and anesthetics (Jones 2000).

Thus, glutamate is an important element in wakefulness and activation. Numerous biochemical and studies have found that alcohol inhibits NMDA-receptor function, thereby acting as a glutamate antagonist (e.g., Tabakoff and Hoffman 1996). Consequently, alcohol inhibition of NMDA function may be another mechanism through which alcohol derives its sedative effects.

  • In addition to GABA and the glutamate-NMDA system, another agent that only recently has been considered a candidate for mediating alcohol’s sleep effects is adenosine.
  • This molecule is not a neurotransmitter itself but modulates signal transmission by other neurotransmitters, including GABA and glutamate.

In general, adenosine inhibits the function of glutamate in the CNS (Dunwiddie 1996). Alcohol appears to facilitate these inhibitory modulatory effects of adenosine through several mechanisms, such as enhancing the formation of adenosine; inhibiting the return of released adenosine into the cells, thereby prolonging its actions; and enhancing adenosine-receptor function (Dunwiddie 1996).

  • Adenosine has been hypothesized to function as the sleep homeostat-the system that monitors the accumulated amount of wakefulness and sleep and signals the need for sleep (Bennington and Heller 1995).
  • Its levels in the brain rise during waking and decline during SWS.
  • Thus, alcohol also may promote SWS and rapid sleep onset by facilitating adenosine function.

The neurobiological mechanism underlying alcohol’s suppression of REM sleep is unclear. One neurotransmitter considered to play an important role in REM sleep is acetylcholine (Bennington and Heller 1995). Like other neurotransmitters, this molecule acts through several types of receptors, including nicotinic receptors and muscarinic receptors.

To date, only minimal evidence suggests a substantive alcohol effect on acetylcholine. 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).

Thus, it appears unlikely that the alcohol-related suppression of REM sleep is mediated by alcohol’s effects on the acetylcholine system. Glutamate also is involved in the induction of some REM sleep phenomena (Bennington and Heller 1995), and alcohol’s inhibition of glutamate was noted earlier in this article (Tabakoff and Hoffman 1996).

However, alcohol does not appear to exert its sedative and REM-suppressive effects through the same mechanism (e.g., glutamate inhibition), because both effects can be experimentally dissociated. For example, in a recent report, caffeine reversed alcohol’s sedative effects but not its REM suppressive effects 7 ( 7 Although unlikely at the low dose used, caffeine’s own REM-suppressive effects may have been responsible for the REM suppression observed,) (Turner et al.2000).

In sum, alcohol’s REM-suppressive effects may occur through glutamate-related mechanisms, whereas its sedative effects occur through GABA-related mechanisms. Relation of Nocturnal Sleep to Daytime Alertness As mentioned earlier, the identification and recognition of sleep disorders have sensitized clinical researchers to the importance of sleep quantity and continuity for optimal daytime alertness and performance.

In healthy people, even relatively minimal (i.e., 1 to 3 hours) reductions in nocturnal sleep time for a single night can reduce alertness and performance efficiency during the following day. Moreover, these effects can accumulate across nights (Roehrs et al.2000 a ). Similarly, a disruption of sleep continuity by auditory stimuli, without reductions in overall sleep time, results in reduced alertness and performance efficiency in healthy people (Roehrs et al.2000 a ).

This fragmentation of sleep continuity is characterized by increased amounts of stage 1 sleep and brief awakenings. Several studies have evaluated next-day performance and alertness in healthy people who consumed alcohol before bedtime. In one study, young pilots drank alcohol between 6 p.m.

And 9 p.m. in quantities sufficient to result in blood alcohol concentrations (BACs) of 0.10 and 0.12 percent right before bedtime. The following morning, more than 14 hours after consuming alcohol and with BACs at 0, the performance of pilots in a flight simulator was impaired relative to their performance after consuming a placebo (Yesavage and Leirer 1986).

To investigate whether alcohol-induced sleep disruption contributed to subsequent performance impairment, Roehrs and colleagues (1991) administered alcohol to healthy people before sleep, recorded their sleep, and assessed the participants’ alertness and performance throughout the following day.

  • The alcohol doses used resulted in a BrAC of 0.06 percent before sleep.
  • The study found that this dose was associated with an increase in the amount of stage 1 sleep in the second half of the night.
  • The next day, the investigators assessed alertness using the Multiple Sleep Latency Test (MSLT), a reliable and well-validated electrophysiological test.

Performance was evaluated with tests of auditory vigilance, in which the participants had to respond to a certain sound, or divided attention tasks, in which the participants had to perform two tasks simultaneously (Roehrs et al.2000 a ). The study found that in the alcohol-consuming participants, next-day alertness as measured by the MSLT was reduced and divided-attention performance was impaired (Roehrs et al.1991), demonstrating that alcohol can indirectly impair daytime alertness and performance through its disruptive effects on sleep.

These reductions in alertness and performance were relatively minor in terms of percentage of the baseline values; in the performance of difficult tasks (e.g., driving a car or flying an airplane), however, even such minor impairments might have significant consequences. Direct Alcohol Effects on Daytime Alertness Although alcohol generally is classified as a depressant drug, in fact it has both sedative and stimulatory effects.

These differential (i.e., biphasic) effects are dependent on the alcohol dose consumed and on the phase of the BAC (Pohorecky 1977). Thus, stimulatory effects are evident primarily at low-to moderate alcohol doses and when BACs ascend to a peak. Conversely, alcohol’s sedative effects occur at higher alcohol doses and when BACs decline.

  • Nighttime sleep studies that demonstrated alcohol’s sedative effects (i.e., reduced sleep latencies) in healthy people typically used alcohol doses that resulted in BrACs above 0.05 percent (Williams and Salamy 1972).
  • Furthermore, the alcohol generally was administered 30 to 60 minutes before sleep, thus allowing for alcohol concentrations to peak before bedtime.

In other studies that also were conducted during the descending BAC phase, alcohol reduced sleep latency, as measured by a standard MSLT, and impaired both attention and reaction-time performance in a dose-dependent manner. These impairing effects persisted for at least 2 hours after the alcohol had been completely metabolized as evidenced by BrACs of 0 (Roehrs and Roth 1998).

  1. Only one daytime study using a modified MSLT assessed alcohol’s sleep effects during both the ascending and descending phase of the BrACs.
  2. That study found increased sleep latencies at peak BrACs relative to placebo, consistent with alcohol’s stimulatory effects under these conditions (Papineau et al.1988).

During the subsequent descending phase of the BrACs, however, sleep latencies were reduced relative to placebo, confirming alcohol’s biphasic effects. A series of studies explored the modulation of alcohol’s daytime sedative and performance-disrupting effects by a person’s basal level of sleepiness (Roehrs and Roth 1998).

In these studies, the investigators first either shortened or extended the participants’ scheduled nocturnal sleep time and then administered alcohol doses of 0.4 to 0.8 g/kg the following day. Subsequently, the researchers assessed the participants’ levels of sleepiness or alertness as well as psychomotor performance for approximately 8 hours.

The results indicated that the level of sleepiness or alertness at the time of alcohol administration altered alcohol’s subsequent sedating and performance-disrupting effects. Thus, increased sleepiness compounded alcohol’s effects, whereas increased alertness diminished alcohol’s effects.

Furthermore, the investigators observed those effects whether they compared sleepy versus alert healthy people, whether they studied the same person before and after both sleep restriction and sleep extension, or whether they studied the same person at various times of the day when the levels of sleepiness are known to differ according to the typical circadian rhythm.

Relationships Between Nocturnal Sleep, Daytime Alertness, and Alcohol-Consumption History Until now, this article has explored alcohol’s effects on nocturnal sleep and daytime alertness. The relationship between sleepiness-alertness and alcohol consumption, however, may be bidirectional.

  1. Thus, some survey and laboratory data suggest that variations in the duration of nocturnal sleep and level of day-time sleepiness may play an important role in modulating alcohol consumption.
  2. For example, a British survey found a negative correlation between sleep times and alcohol consumption in men- that is, shorter periods of sleep were associated with heavier drinking (Palmer et al.1980).

Similarly, in a U.S. study of young adults, participants who reported needing only 6 hours of sleep or less had an earlier age of drinking onset and drank more per month than did participants who needed more sleep (Schuckit and Bernstein 1981), leading the investigators to hypothesize that short sleep is associated with heavier alcohol intake.

Laboratory studies of alcohol and mood have identified some interesting relations between daytime sleepiness-alertness and drinking. In such studies, the participants’ preference for alcohol is studied by offering them several beverage choices presented in color-coded cups in which the participants do not know which of the cups contain an alcoholic beverage.

After the participants have tasted each beverage, they can choose which beverage they prefer. 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.

Furthermore, participants who preferred alcohol in those studies generally experienced alcohol as increasing their elation and vigor, whereas participants who did not prefer alcohol generally experienced alcohol as increasing their sleepiness. In an alcohol challenge study, in which healthy young men received a certain alcohol dose, the men’s drinking histories predicted their subjective responses to alcohol (Schuckit and Klein 1991).

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Those participants with histories of greater alcohol consumption showed less self-rated sleepiness after the alcohol challenge than did participants with histories of lower alcohol consumption. Researchers do not know whether these individual differences in response to alcohol reflect different physiological states (i.e., whether people are actually more or less sleepy) or differences in the perception of a common physiological state (i.e., whether all people experience the same physiological state but differ in whether they perceive that state as “being sleepy”).

  • In the latter case, the different perceptions of alcohol’s effects may result from differential expectations regarding alcohol’s effects.
  • Alcohol’s Effects on the Sleep of Insomniacs Approximately 10 to 15 percent of the U.S.
  • General population experiences difficulties falling asleep or maintaining sleep, or suffer from nonrestorative sleep (i.e., sleep that does not result in a feeling of being rested) (Roehrs et al.2000 b ).

Moreover, 30 percent of people with persistent insomnia in the general population have reported using alcohol to help them sleep in the past year, and 67 percent of those people have reported that alcohol was effective in inducing sleep (Ancoli-Israel and Roth 2000).

  • For several reasons, studies conducted in healthy people sleeping at their usual bedtimes, such as the studies reviewed in this article, do not adequately represent the hypnotic potential of alcohol in people with insomnia.
  • First, in healthy people, sleep latency and sleep efficiency are already optimal, and further improvement is difficult to demonstrate.

Consequently, as previously noted, alcohol’s effects on measures of sleep induction and maintenance in healthy people are minimal and inconsistent. Second, the doses used in sleep studies are generally much larger (i.e., resulting in BrACs greater than 0.05 percent, which corresponds to more than three drinks) than the doses that insomniacs typically report using (i.e., one to two drinks).

  1. Third, the same alcohol dose may have different effects in healthy people and insomniacs.
  2. A recent study compared the effects of an alcohol dose of 0.5 g/kg on the sleep of insomniacs and age-matched healthy people (Roehrs et al.1999).
  3. In the insomniacs, but not in the healthy control subjects, this alcohol dose improved sleep compared with a placebo.

Further-more, the sleep disruption during the second half of the night that occurs in healthy people after higher alcohol doses was not observed in the insomniacs. Specifically, alcohol consumption in the insomniacs increased their SWS to the levels of the age-matched control subjects.

  1. During a later phase of the same study (Roehrs et al.1999), the participants also had an opportunity to choose between beverages presented in color-coded cups that contained various alcohol concentrations or a placebo.
  2. The participants had previously experienced all of those beverages (i.e., they had taken them one at a time before bedtime on different nights) and were asked to choose the beverage that would best help them sleep.

With this approach, the insomniacs generally chose an alcohol-containing beverage, whereas the healthy people chose the placebo-containing beverage. Furthermore, the average nightly alcohol dose self-administered by the insomniacs was 0.45 g/kg (up to 0.6 g/kg was possible), which is similar to the dose previously shown to improve the sleep of the insomniacs and similar to the dose that insomniacs report using at home.

The epidemiological data and laboratory study findings indicating the preference for alcohol at bedtime by insomniacs, compared with generate several questions. For example, does this preference reflect the use of alcohol as self-medication for a sleep problem, as a way to improve mood, or as a sleep medication that subsequently becomes a “mood-altering” drug? And if alcohol use initially is, or ultimately becomes, “mood-altering” behavior, what are the “mood-altering” effects for the insomniac that reinforce alcohol consumption? Furthermore, do insomniacs develop tolerance to alcohol’s sedative effects as do other people? Do insomniacs increase their alcohol dose in successive nights? Does hypnotic use at night generalize to daytime use? And ultimately, what are the risks associated with the use of alcohol as a hypnotic? All these issues have yet to be addressed.

But these data again suggest that the alcohol-sleep relation is interactive- that is, disturbed nocturnal sleep increases the likelihood of alcohol use, and alcohol has the potential to influence sleep. Summary Alcohol has extensive effects on sleep and daytime sleepiness.

  1. In healthy people, acute high alcohol doses disturb sleep, whereas in insomniacs, lower doses may be beneficial.
  2. Data from healthy people suggest, however, that tolerance to alcohol’s sedative effects probably develops rapidly.
  3. This tolerance development may lead to excessive hypnotic use and, possibly, excessive daytime use for insomniacs.

The effects of alcohol appear to be bidirectional in that nocturnal sleep quantity and continuity and subsequent levels of daytime sleepiness also influence alcohol’s sedative and performance-impairing effects. Sleep quality and daytime sleepiness may also relate to rates of alcohol drinking and become a gateway to excessive alcohol use.

To investigate these issues and identify the mechanisms underlying the relationship between alcohol and sleep remain important tasks, as does documenting alcohol’s effects on other physiological functions during sleep. References ANCOLI-ISRAEL, S., AND ROTH, T. Characteristics of insomnia in the United States: Results of the 1991 National Sleep Foundation Survey.I.

Sleep 22:S347-S353, 2000. BENNINGTON, J.H., AND HELLER, H.C. Restoration of brain energy metabolism as the function of sleep. Progress in Neurobiology 45:347-365, 1995. COLLINS, A.C. The nicotinic cholinergic receptor as a potential site of ethanol action.

In: Dietrich, R.A., and Erwin, V.G., eds. Pharmacological Effects of Ethanol on the Nervous System, New York: CRC Press, 1996. pp.95-116. DE WIT, H.; UHLENHUTH, E.H.; PIEZ, J.; AND JOHANSON, C.E. Individual differences in behavioral and subjective responses to alcohol. Alcoholism: Clinical and Experimental Research 11:52-59, 1987.

DE WIT, H.; PIERRI, J.; AND JOHANSON, C.E. Assessing individual differences in ETOH preference using a cumulative dosing procedure. Psychopharmacology 98:113-119, 1989. DUNWIDDIE, T.V. Acute and chronic effects of ethanol on the brain: Interactions of ethanol with adenosine, adenosine transporters and adenosine receptors.

In: Dietrich, R.A., and Erwin, V.G., eds. Pharmacological Effects of Ethanol on the Nervous System, New York: CRC Press, 1996. pp.147-162. EKMAN, A.C.; VAKKURI, O.; EKMAN, M.; ET AL. Ethanol decreases nocturnal plasma levels of thyrotropin and growth hormone but not those of thyroid hormones or prolactin in man.

Journal of Clinical Endocrinology and Metabolism 81:2627- 2632, 1996. JONES, B.E. Basic mechanisms of sleep-wake states. In: Kryger, M.H.; Roth, T.; and Dement, W.C., eds. Principles and Practice of Sleep Medicine,3d ed. Philadelphia: W.B Saunders, 2000.

Pp.134-154. KLEITMAN, N. Sleep and Wakefulness, Chicago: University of Chicago Press, 1939. KOOB, G.F. The neuropharmacology of ethanol’s behavioral action: New data, new paradigms, new hope. In: Dietrich, R.A., and Erwin, V.G., eds. Pharmacological Effects of Ethanol on the Nervous System, New York: CRC Press, 1996.

pp.1-12. MIHIC, S.J., AND HARRIS, R.A. Alcohol action at the GABA receptor/chloride channel complex. In: Dietrich, R.A., and Erwin, V.G., eds. Pharmacological Effects of Ethanol on the Nervous System, New York: CRC Press, 1996. pp.51-72. PALMER, C.D.; HARRISON, G.A.; AND HIORNS, R.W.

Association between smoking and drinking and sleep duration. Annals of Human Biology 7:103-107, 1980. PAPINEAU, K.; ROEHRS, T.; PETRUCELLI, N.; ROSENTHAL, L.; AND ROTH, T. Electrophysiological assessment (Multiple Sleep Latency Test) of the biphasic effects of ethanol in humans. Alcoholism: Clinical and Experimental Research 22:231-235, 1988.

POHORECKY, L.A. Biphasic action of ethanol. Biobehavior Reviews 1:231-240, 1977. PRINZ, P.; ROEHRS, T.; VITALIANO, P.; LINNOILA, M.; AND WEITZMAN, E. Effect of alcohol on sleep and nighttime plasma growth hormone and cortisol concentrations. Journal of Clinical Endocrinology and Metabolism 51:759-764, 1980.

ROEHRS, T., AND ROTH, T. State-altering actions of ethanol, caffeine, and nicotine. In: Lydic, R., and Baghdoyan, H.A., eds. Handbook of Behavioral State Control-Cellular and Molecular Mechanisms, New York: CRC Press, 1998. pp.421-432. ROEHRS, T.; YOON, J.; AND ROTH T. Nocturnal and next-day effects of ethanol and basal level of sleepiness.

Human Psychopharmacology 6:307-311, 1991. ROEHRS, T.; PAPINEAU, K.; ROSENTHAL, L.; AND ROTH, T. Ethanol as a hypnotic in insomniacs: Self administration and effects of sleep and mood. Neuropsychopharmacology 20:279-286, 1999. ROEHRS, T.; CARSKADON, M.A.; DEMENT, W.C.; AND ROTH, T.

  1. Daytime sleepiness and alertness.
  2. In: Kryger, M.H.; Roth, T.; and Dement, W.C., eds.
  3. Principles and Practice of Sleep Medicine,3d ed.
  4. Philadelphia: W.B.
  5. Saunders, 2000 a, pp.43-52.
  7. Transient and short-term insomnias.
  8. In: Kryger, M.H.; Roth, T.; and Dement, W.C., eds.
  9. Principles and Practice of Sleep Medicine,3d ed.

Philadelphia: W.B. Saunders, 2000 b, pp.624-632. SCHUCKIT, M.A., AND BERNSTEIN, L.I. Sleep time and drinking history: A hypothesis. American Journal of Psychiatry 138:528-530, 1981. SCHUCKIT, M.A., AND KLEIN, J.L. Correlations between drinking intensity and reaction of ethanol and diazepam in healthy young men.

  1. Neuropsychopharmacology 4(3):157-163, 1991.
  2. STONE, B.M.
  3. Sleep and low doses of alcohol.
  4. Electroencephalography and Clinical Neurophysiology 48:706-709, 1980.
  6. Ethanol and glutamate receptors.
  7. In: Dietrich, R.A., and Erwin, V.G., eds.
  8. Pharmacological Effects of Ethanol on the Nervous System,

New York: CRC Press, 1996. pp.73-93. TAKAHASHI, Y.; KIPNIS, D.M.; AND DAUGHADAY, W.H. Growth hormone secretion during sleep. Journal of Clinical Investigation 47:2079-2090, 1969. TURNER, L.; ROEHRS, T.; ROSENTHAL, L.; AND ROTH, T. Ethanol and caffeine effects on the sleep of insomniacs.

  • Sleep 23:S48, 2000.
  • Endocrine and other biological rhythms.
  • In: Degroot, L.J., ed.
  • Endocrinology,
  • Philadelphia: W.B.
  • Saunders, 1994.
  • Pp.487-548.
  • Dose-response effects of ethanol of the sleep of young women.
  • Journal of Studies on Alcohol 44(3): 515-523, 1983.

WILLIAMS, H., AND SALAMY, A. Alcohol and sleep. In: Kissin, B., and Begleiter, H., eds. The Biology of Alcoholism, New York: Plenum Press, 1972. pp.435-483. YESAVAGE, J.A., AND LEIRER, V.O. Hangover effects on aircraft pilots 14 hours after alcohol ingestion: A preliminary report.

At What Blood Alcohol Level Is a Person Too Impaired To Drive Safely? New findings relevant to this and other questions can be found in Alcohol Alert, the quarterly bulletin published by the National Institute on Alcohol Abuse and Alcoholism. Alcohol Alert provides timely information on alcohol research and treatment. Each issue addresses a specific topic in alcohol research and summarizes critical findings in a brief, four-page, easy-to-read format. Alcohol and Transportation Safety (No.52)-discusses the effects that even low blood alcohol concentration has on driving skills, and reviews strategies designed to reduce alcohol-related crashes and repeat drinking-and-driving offenses.
For a free subscription to Alcohol Alert, write to: National Institute on Alcohol Abuse and Alcoholism, Attn.: Alcohol Alert, Publications Distribution Center, P.O. Box 10686, Rockville, MD 20849–0686. Fax: (202) 842–0418. Alcohol Alert is also available on NIAAA’s Web site (


How does alcohol make you feel?

– Alcohol can hit you pretty fast. It typically reaches your brain within 5 minutes, and you can begin feeling the effects within 10 minutes, When the concentration of alcohol begins to increase in your bloodstream, you’ll start to feel good, You might feel happy, more social and confident, and less inhibited.

  • This is because alcohol stimulates the release of dopamine and serotonin, which are rightfully referred to as your “feel good” hormones.
  • As you get drunker, you’ll start to experience more physical symptoms.
  • This happens because alcohol depresses your central nervous system and interferes with your brain’s communication pathways, which affects how your brain processes information.

This causes symptoms like:

slurred speechloss of coordinationblurred visiondizziness

Your brain produces antidiuretic hormone (ADH), which tells your kidneys how much water to conserve. Alcohol limits ADH production, which brings us to our next body part.

How many beers a day is healthy?

Drinking in Moderation: According to the “Dietary Guidelines for Americans 2020-2025,” U.S. Department of Health and Human Services and U.S. Department of Agriculture, adults of legal drinking age can choose not to drink or to drink in moderation by limiting intake to 2 drinks or less in a day for men and 1 drink or less in a day for women, when alcohol is consumed.

NIAAA defines binge drinking as a pattern of drinking alcohol that brings blood alcohol concentration (BAC) to 0.08 percent – or 0.08 grams of alcohol per deciliter – or higher. For a typical adult, this pattern corresponds to consuming 5 or more drinks (male), or 4 or more drinks (female), in about 2 hours.

The Substance Abuse and Mental Health Services Administration (SAMHSA), which conducts the annual National Survey on Drug Use and Health (NSDUH), defines binge drinking as 5 or more alcoholic drinks for males or 4 or more alcoholic drinks for females on the same occasion (i.e., at the same time or within a couple of hours of each other) on at least 1 day in the past month.

Heavy Alcohol Use:

NIAAA defines heavy drinking as follows:

For men, consuming more than 4 drinks on any day or more than 14 drinks per week For women, consuming more than 3 drinks on any day or more than 7 drinks per week

SAMHSA defines heavy alcohol use as binge drinking on 5 or more days in the past month.

Patterns of Drinking Associated with Alcohol Use Disorder : Binge drinking and heavy alcohol use can increase an individual’s risk of alcohol use disorder. Certain people should avoid alcohol completely, including those who:

Plan to drive or operate machinery, or participate in activities that require skill, coordination, and alertness Take certain over-the-counter or prescription medications Have certain medical conditions Are recovering from alcohol use disorder or are unable to control the amount that they drink Are younger than age 21 Are pregnant or may become pregnant

How do you stop sleepiness after drinking alcohol?

– If a person plans to consume alcohol but wants to avoid disrupted sleep, they can take measures to help plan an adequate sleep. These include:

Allowing time between drinking and bedtime to metabolize alcohol: A person may want to cut off drinking a few hours before bed to prevent sleepiness or restlessness from alcohol. Reducing waking to urinate: A person can do this by going to the bathroom before bed. Avoiding drinks containing caffeine: These beverages can cause further disruptions to sleep. Maintaining a regular sleep schedule: This may help a person avoid sleepiness and sleep disruption. Being physically active regularly during the day: This may also help improve sleep hygiene.

Read more about improving sleep hygiene.