The short-term effects of alcohol (also known formally as ethanol)
consumption–due to drinking beer, wine, distilled spirits or other
alcoholic beverages–range from a decrease in anxiety and motor
skills and euphoria at lower doses to intoxication (drunkenness),
stupor, unconsciousness, anterograde amnesia (memory "blackouts"), and
central nervous system depression at higher doses. Cell membranes are
highly permeable to alcohol, so once alcohol is in the bloodstream it
can diffuse into nearly every cell in the body.
The concentration of alcohol in blood is measured via blood alcohol
content (BAC). The amount and circumstances of consumption play a
large part in determining the extent of intoxication; for example,
eating a heavy meal before alcohol consumption causes alcohol to
absorb more slowly. The amount of alcohol consumed largely
determines the extent of hangovers, although hydration also plays a
role. After excessive drinking, stupor and unconsciousness can occur.
Extreme levels of consumption can lead to alcohol poisoning and death
(a concentration in the blood stream of 0.40% will kill half of those
affected). Alcohol may also cause death indirectly, by
asphyxiation from vomit.
Alcohol can greatly exacerbate sleep problems. During abstinence,
residual disruptions in sleep regularity and sleep
patterns[clarification needed] are the greatest predictors of
1 Effects by dosage
1.1 Moderate doses
1.2 Excessive doses
2 Allergic reaction-like symptoms
3.1 Moderate alcohol consumption and sleep disruptions
3.2 Alcohol consumption and sleep improvements
3.3 Alcohol consumption and fatigue
3.4 Alcohol abstinence and sleep disruptions
4 Alcohol consumption and balance
7 See also
9 External links
Effects by dosage
Different concentrations of alcohol in the human body have different
effects on the subject.
The following lists the common effects of alcohol on the body,
depending on the blood alcohol concentration (BAC).[medical citation
needed] However, tolerance varies considerably between individuals, as
does individual response to a given dosage; the effects of alcohol
differ widely between people. Hence, BAC percentages are just
estimates used for illustrative purposes.
Euphoria (BAC = 0.03% to 0.12%)
Overall improvement in mood and possible euphoria
Shortened attention span
Impaired fine muscle coordination
Lethargy (BAC = 0.09% to 0.25%)
Impaired memory and comprehension
Ataxia; balance difficulty; unbalanced walk
Blurred vision; other senses may be impaired
Confusion (BAC = 0.18% to 0.30%)
Increased ataxia; impaired speech; staggering
Dizziness often associated with nausea ("the spins")
Stupor (BAC = 0.25% to 0.40%)
Lapses in and out of consciousness
Vomiting (death may occur due to inhalation of vomit (pulmonary
aspiration) while unconscious)
Respiratory depression (potentially life-threatening)
Decreased heart rate (usually results in coldness and/or numbness of
Coma (BAC = 0.35% to 0.80%)
Depressed reflexes (i.e., pupils do not respond appropriately to
changes in light)
Marked and life-threatening respiratory depression
Markedly decreased heart rate
Most deaths from alcohol poisoning are caused by dosage levels in this
Ethanol inhibits the ability of glutamate to open the cation channel
associated with the
N-methyl-D-aspartate (NMDA) subtype of glutamate
receptors. Stimulated areas include the cortex, hippocampus and
nucleus accumbens, which are responsible for thinking and pleasure
seeking. Another one of alcohol's agreeable effects is body
relaxation, possibly caused by neurons transmitting electrical signals
in an alpha waves-pattern; such waves are observed (with the aid of
EEGs) when the body is relaxed.
Short-term effects of alcohol include the risk of injuries, violence
and fetal damage. Alcohol has also been linked with lowered
inhibitions, though it is unclear to what degree this is chemical
versus psychological as studies with placebos can often duplicate the
social effects of alcohol at low to moderate doses. Some studies have
suggested that intoxicated people have much greater control over their
behavior than is generally recognized, though they have a reduced
ability to evaluate the consequences of their behavior. Behavioral
changes associated with drunkenness are, to some degree,
Areas of the brain responsible for planning and motor learning are
sharpened. A related effect, caused by even low levels of alcohol, is
the tendency for people to become more animated in speech and
movement. This is due to increased metabolism in areas of the brain
associated with movement, such as the nigrostriatal pathway. This
causes reward systems in the brain to become more active, which may
induce certain individuals to behave in an uncharacteristically loud
and cheerful manner.
Alcohol has been known to mitigate the production of antidiuretic
hormone, which is a hormone that acts on the kidney to favour water
reabsorption in the kidneys during filtration. This occurs because
alcohol confuses osmoreceptors in the hypothalamus, which relay
osmotic pressure information to the posterior pituitary, the site of
antidiuretic hormone release. Alcohol causes the osmoreceptors to
signal that there is low osmotic pressure in the blood, which triggers
an inhibition of the antidiuretic hormone. As a consequence, one's
kidneys are no longer able to reabsorb as much water as they should be
absorbing, leading to creation of excessive volumes of urine and the
subsequent overall dehydration.
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Acute alcohol intoxication
Acute alcohol intoxication through excessive doses in general causes
short- or long-term health effects.
NMDA receptors start to become
unresponsive, slowing areas of the brain for which they are
responsible. Contributing to this effect is the activity that alcohol
induces in the gamma-aminobutyric acid (GABA) system. The GABA system
is known to inhibit activity in the brain. GABA could also be
responsible for the memory impairment that many people experience. It
has been asserted that GABA signals interfere with the registration
and consolidation stages of memory formation. As the GABA system is
found in the hippocampus (among other areas in the CNS), which is
thought to play a large role in memory formation, this is thought to
Anterograde amnesia, colloquially referred to as "blacking out", is
another symptom of heavy drinking. This is the loss of memory during
and after an episode of drinking. When alcohol is consumed at a rapid
rate, the point at which most healthy people's long-term memory
creation starts to fail usually occurs at approximately 0.20% BAC, but
can be reached as low as 0.14% BAC for inexperienced drinkers.
Another classic finding of alcohol intoxication is ataxia, in its
appendicular, gait, and truncal forms. Appendicular ataxia results in
jerky, uncoordinated movements of the limbs, as though each muscle
were working independently from the others. Truncal ataxia results in
postural instability; gait instability is manifested as a disorderly,
wide-based gait with inconsistent foot positioning.
responsible for the observation that drunk people are clumsy, sway
back and forth, and often fall down. It is presumed to be due to
alcohol's effect on the cerebellum.
Allergic reaction-like symptoms
Alcohol-induced respiratory reactions and Alcohol flush
Humans metabolize ethanol primarily through NAD+-dependent alcohol
dehydrogenase (ADH) class I enzymes (i.e. ADH1A, ADH1B, and ADH1C) to
acetaldehyde and then metabolize acetaldehyde primarily by
NAD2-dependent aldehyde dehydrogenase 2 (ALDH2) to acetic acid.
Eastern Asians reportedly have a deficiency in acetaldehyde metabolism
in a surprisingly high percentage (approaching 50%) of their
populations. The issue has been most thoroughly investigated in native
Japanese where persons with a single-nucleotide polymorphism (SNP)
variant allele of the
ALDH2 gene were found; the variant allele,
encodes lysine (lys) instead of glutamic acid (glu) at amino acid 487;
this renders the enzyme essentially inactive in metabolizing
acetaldehyde to acetic acid. The variant allele is variously
termed glu487lys, ALDH2*2, and ALDH2*504lys. In the overall Japanese
population, about 57% of individuals are homozygous for the normal
allele (sometimes termed ALDH2*1), 40% are heterozygous for glu487lys,
and 3% are homozygous for glu487lys. Since
ALDH2 assembles and
functions as a tetramer and since
ALDH2 tetramers containing one or
more glu487lys proteins are also essentially inactive (i.e. the
variant allele behaves as a dominant negative), homozygote individuals
for glu487lys have undetectable while heterozygote individuals for
glu487lys have little
ALDH2 activity. In consequence, Japanese
individuals homozygous or, to only a slightly lesser extent,
heterozygous for glu487lys metabolize ethanol to acetaldehyde normally
but metabolize acetaldehyde poorly and are susceptible to a set of
adverse responses to the ingestion of, and sometimes even the fumes
from, ethanol and ethanol-containing beverages; these responses
include the transient accumulation of acetaldehyde in blood and
tissues; facial flushing (i.e. the "oriental flushing syndrome" or
Alcohol flush reaction), urticaria, systemic dermatitis, and
alcohol-induced respiratory reactions (i.e. rhinitis and, primarily in
patients with a history of asthma, mild to moderately
bronchoconstriction exacerbations of their asthmatic disease.
These allergic reaction-like symptoms, which typically occur within
30–60 minutes of ingesting alcoholic beverages, do not appear to
reflect the operation of classical IgE- or T cell-related
allergen-induced reactions but rather are due, at least in large part,
to the action of acetaldehyde in stimulating tissues to release
histamine, the probable evoker of these symptoms.
The percentages of glu487lys heterozygous plus homozygous genotypes
are about 35% in native
Caboclo of Brazil, 30% in Chinese, 28% in
Koreans, 11% in Thai people, 7% in Malaysians, 3% in natives of India,
3% in Hungarians, and 1% in Filipinos; percentages are essentially 0
in individuals of Native African descent, Caucasians of Western
European descent, Turks, Australian Aborigines, Australians of Western
European descent, Swedish Lapps, and Alaskan Eskimos. The
prevalence of ethanol-induced allergic symptoms in 0 or low levels of
glu487lys genotypes commonly ranges above 5%. These "ethanol reactors"
may have other gene-based abnormalities that cause the accumulation of
acetaldehyde following the ingestion of ethanol or ethanol-containing
beverages. For example, the surveyed incidence of self-reported
ethanol-induced flushing reactions in Scandinavians living in
Copenhagen as well as Australians of European descent is about 16% in
individuals homozygous for the "normal"
ADH1B gene but runs to ~23% in
individuals with the ADH1-Arg48His SNP variant; in vitro, this variant
metabolizes ethanol rapidly and in humans, it is proposed, may form
acetaldehyde at levels that exceed the capacity of
metabolize. Notwithstanding such considerations, experts
suggest that the large proportion of alcoholic beverage-induced
allergic-like symptoms in populations with a low incidence of the
glu487lys genotype reflect true allergic reactions to the natural
and/or contaminating allergens particularly those in wines and to a
lesser extent beers.
Main article: Alcohol use and sleep
Moderate alcohol consumption and sleep disruptions
Moderate alcohol consumption 30–60 minutes before sleep, although
decreasing, disrupts sleep architecture. Rebound effects occur once
the alcohol has been largely metabolized, causing late night
disruptions in sleep maintenance. Under conditions of moderate alcohol
consumption where blood alcohol levels average 0.06–0.08 percent and
decrease 0.01–0.02 percent per hour, an alcohol clearance rate of
4–5 hours would coincide with disruptions in sleep maintenance in
the second half of an 8-hour sleep episode. In terms of sleep
architecture, moderate doses of alcohol facilitate "rebounds" in rapid
eye movement (REM) following suppression in REM and stage 1 sleep in
the first half of an 8-hour sleep episode, REM and stage 1 sleep
increase well beyond baseline in the second half. Moderate doses of
alcohol also very quickly increase slow wave sleep (SWS) in the first
half of an 8-hour sleep episode. Enhancements in REM sleep and SWS
following moderate alcohol consumption are mediated by reductions in
glutamatergic activity by adenosine in the central nervous system. In
addition, tolerance to changes in sleep maintenance and sleep
architecture develops within 3 days of alcohol consumption before
Alcohol consumption and sleep improvements
Low doses of alcohol (one 360 ml (13 imp fl oz;
12 US fl oz) beer) appear to increase total sleep time
and reduce awakening during the night. The sleep-promoting benefits of
alcohol dissipate at moderate and higher doses of alcohol.
Previous experience with alcohol also influences the extent to which
alcohol positively or negatively affects sleep. Under free-choice
conditions, in which subjects chose between drinking alcohol or water,
inexperienced drinkers were sedated while experienced drinkers were
stimulated following alcohol consumption. In insomniacs, moderate
doses of alcohol improve sleep maintenance.
Alcohol consumption and fatigue
Conditions of fatigue correlate positively with increased alcohol
Alcohol abstinence and sleep disruptions
Hormonal imbalance and sleep disruptions following withdrawal from
chronic alcohol consumption are strong predictors of relapse. During
abstinence, recovering alcoholics have attenuated melatonin secretion
at onset of a sleep episode, resulting in prolonged sleep onset
latencies. Psychiatry and core body temperatures during the sleep
period contribute to poor sleep maintenance. The effect of alcohol
consumption on the circadian control of human core body temperature is
Alcohol consumption and balance
Alcohol can affect balance by altering the viscosity of the endolymph
within the otolithic membrane, the fluid inside the semicircular
canals inside the ear. The endolymph surrounds the ampullary cupula
which contains hair cells within the semicircular canals. When the
head is tilted, the endolymph flows and moves the cupula. The hair
cells then bend and send signals to the brain indicating the direction
in which the head is tilted. By changing the viscosity of the
endolymph to become less dense when alcohol enters the system, the
hair cells can move more easily within the ear, which sends the signal
to the brain and results in exaggerated and overcompensated movements
of body. This can also result in vertigo, or "the spins."
Disability-adjusted life year
Disability-adjusted life year for alcohol use disorders
per 100,000 inhabitants in 2004.
less than 50
more than 1050
At low or moderate doses, alcohol acts primarily as a positive
allosteric modulator of GABAA. Alcohol binds to several different
subtypes of GABAA, but not to others. The main subtypes responsible
for the subjective effects of alcohol are the α1β3γ2, α5β3γ2,
α4β3δ and α6β3δ subtypes, although other subtypes such as
α2β3γ2 and α3β3γ2 are also affected. Activation of these
receptors causes most of the effects of alcohol such as relaxation and
relief from anxiety, sedation, ataxia and increase in appetite and
lowering of inhibitions that can cause a tendency toward violence in
Alcohol has a powerful effect on glutamate as well. Alcohol decreases
glutamate's ability to bind with
NMDA and acts as an antagonist of the
NMDA receptor, which plays a critical role in LTP by allowing
enter the cell. These inhibitory effects are thought to be responsible
for the "memory blanks" that can occur at levels as low as 0.03% blood
level. In addition, reduced glutamate release in the dorsal
hippocampus has been linked to spatial memory loss. Chronic alcohol
users experience an upregulation of
NMDA receptors because the brain
is attempting to reestablish homeostasis. When a chronic alcohol user
stops drinking for more than 10 hours, apoptosis can occur due to
excitotoxicity. The seizures experienced during alcohol abstinence are
thought to be a result of this
NMDA upregulation. Alteration of NMDA
receptor numbers in chronic alcoholics is likely to be responsible for
some of the symptoms seen in delirium tremens during severe alcohol
withdrawal, such as delirium and hallucinations. Other targets such as
sodium channels can also be affected by high doses of alcohol, and
alteration in the numbers of these channels in chronic alcoholics is
likely to be responsible for as well as other effects such as cardiac
arrhythmia. Other targets that are affected by alcohol include
cannabinoid, opioid and dopamine receptors, although it is unclear
whether alcohol affects these directly or if they are affected by
downstream consequences of the GABA/
NMDA effects. People with a family
history of alcoholism may exhibit genetic differences in the response
NMDA glutamate receptors as well as the ratios of GABAA
subtypes in their brain.
Alcohol inhibits sodium-potassium pumps in the cerebellum and this is
likely how it corrupts cerebellar computation and body
Contrary to popular belief, research suggests that acute exposure to
alcohol is not neurotoxic in adults and actually prevents NMDA
Animal models using mammals and invertebrates have been informative in
studying the effects of ethanol on not only pharmacokinetics of
alcohol but also pharmacodynamics, in particular in the nervous
system. Ethanol-induced intoxication is not uncommon in the animal
kingdom, as noted here:
"Many of us have noticed that bees or yellow jackets cannot fly well
after having drunk the juice of overripe fruits or berries; bears have
been seen to stagger and fall down after eating fermented honey; and
birds often crash or fly haphazardly while intoxicated on ethanol that
occurs naturally as free-floating microorganisms convert vegetable
carbohydrates to alcohol."
More recently, studies using animal models have begun to elucidate the
effects of ethanol on the nervous system. Traditionally, many studies
have been performed in mammals, such as mice, rats, and non-human
primates. However, non-mammalian animal models have also been
employed; in particular, the Ulrike Heberlein group at UC San
Francisco has used Drosophila melanogaster, the fruit fly, taking
advantage of its facile genetics to dissect the neural circuits and
molecular pathways, upon which ethanol acts. The series of studies
carried in the Heberlein lab has identified insulin and its related
signaling pathways as well as biogenic amines in the invertebrate
nervous system as being important in alcohol tolerance.
The value of antabuse (disulfiram) as a treatment for alcoholism has
been tested using another invertebrate animal model, the honey
bees. It is important to note that some of the analogous
biochemical pathways and neural systems have been known to be
important in alcohol's effects on humans, while the possibility that
others may also be important remains unknown. Research of alcohol's
effects on the nervous system remains a hot topic of research, as
scientists inch toward understanding the problem of alcohol addiction.
In addition to the studies carried out in invertebrates, researchers
have also used vertebrate animal models to study various effects of
ethanol on behaviors.
Alcohol and health
Long-term effects of alcohol
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Alcohol and health
Note: see Template:Psychoactive substance use for diagnoses
Alcohol-induced mood disorders
Ban on caffeinated alcoholic beverages
Alcohol server training
Recommended maximum intake of alcoholic beverages
Anti-addictive psychedelics: Ibogaine, Salvia divinorum
Disulfiram-like drugs: disulfiram, calcium carbimide, cyanamide
Religion and alcohol
Christian views on alcohol
alcohol in the Bible
Islam and alcohol
on college campuses
Alcohol-free beverage definition controversy
Blackout (alcohol-related amnesia)
College student alcoholism
Drinking games / pregaming
Driving under the influence
Adult Children of Alcoholics
High-functioning alcoholic (HFA)
Sin tax / Pigovian tax
Short-term effects of alcohol consumption
Long-term effects of alcohol