Short-term effects of alcohol

Short-term effects of alcohol


The short-term effects of alcohol
consumption range from a decrease in anxiety and motor skills at lower doses
to unconsciousness, anterograde amnesia, 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. 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. Hydration also plays a
role, especially in determining the extent of hangovers. After excessive
drinking, unconsciousness can occur and extreme levels of consumption can lead
to alcohol poisoning and death. 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 are the greatest predictors of relapse.
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. 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.
=Moderate doses=Ethanol inhibits the ability of
glutamate to open the cation channel associated with the N-methyl-D-aspartate
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 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,
contextual. 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.
=Excessive doses=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 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, which is thought to
play a large role in memory formation, this is thought to be possible.
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. Ataxia is
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
Humans metabolize ethanol primarily through NAD+-dependent alcohol
dehydrogenase class I enzymes to acetaldehyde and then metabolize
acetaldehyde primarily by NAD2-dependent aldehyde dehydrogenase 2 to acetic acid.
Eastern Asians reportedly have a deficiency in acetaldehyde metabolism in
a surprisingly high percentage of their populations. The issue has been most
thoroughly investigated in native Japanese where persons with a
single-nucleotide polymorphism variant allele of the ALDH2 gene were found; the
variant allele, encodes lysine instead of glutamic acid 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, 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, 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, homozygous 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, 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
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 ALDH2 to metabolize the acetaldehyde. Notwithstanding such
considerations, experts suggest that the large proportion of alcoholic beverage
-induced allergic-like symptoms in populations with a low incidence the
glu487lys genotype reflect true allergic reactions to the natural and/or
contaminating allergens particularly those in wines and to a lesser extent
beers. 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 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 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 bedtime.
=Alcohol consumption and sleep improvements=
Low doses of alcohol 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
consumption. In Northern climates, increased alcohol consumption during the
winter is attributed to escalations in fatigue.
=Alcohol abstinence and sleep disruptions=
Hormonal imbalance and sleep disruption 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 time dependent.
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.” Pathophysiology
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 some people.
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 Ca2+ to 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 of their 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 co-ordination. Contrary to popular belief, research
suggests that acute exposure to alcohol is not neurotoxic in adults and actually
prevents NMDA antagonist-induced neurotoxicity.
Research 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, 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 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.
See also Alcohol and health
Long-term effects of alcohol References
External links Global Status Report on Alcohol 2004 by
the World Health Organization. Heberlein, Ulrike; Wolf, Fred W.;
Rothenfluh, Adrian; Guarnieri, Douglas J.. “Molecular Genetic Analysis of
Ethanol Intoxication in Drosophila Melanogaster”. Integrative and
Comparative Biology 44: 269–74. doi:10.109344.4.269. PMID 21676709.
Jane behaving badly

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