Short-term effects of alcohol consumption

The definition of a unit of alcohol ranges between 8 and 14 grams of pure ethanol depending on the country.{{cite web |url=http://www.drinkingandyou.com/site/pdf/Sensibledrinking.pdf |title=Sensible Drinking Guidelines |date=2018 |website=Alcohol in Moderation }} There is no agreement on definitions of a low, moderate or high dose of alcohol either. The U.S. National Institute on Alcohol Abuse and Alcoholism defines a moderate dose as alcohol intake up to two standard drinks or 28 grams for men and one standard drink or 14 grams for women.{{cite web |url=https://www.niaaa.nih.gov/alcohol-health/overview-alcohol-consumption/moderate-binge-drinking |title=Drinking Levels Defined |website=National Institute on Alcohol Abuse and Alcoholism |date=14 September 2011 }} The immediate effect of alcohol depends on the drinker's blood alcohol concentration (BAC). BAC can be different for each person depending on their age, sex, pre-existing health condition, even if they drink the same amount of alcohol.{{cite journal | vauthors = Cederbaum AI | title = Alcohol metabolism | journal = Clinics in Liver Disease | volume = 16 | issue = 4 | pages = 667–685 | date = November 2012 | pmid = 23101976 | pmc = 3484320 | doi = 10.1016/j.cld.2012.08.002 }}

Different BACs have different effects. The following lists describe the common effects of alcohol on the body depending on the BAC. However, tolerance varies considerably between individuals, as does individual response to a given dosage; the effects of alcohol differ widely between people. Hence in this context, BAC percentages are just estimates used for illustrative purposes.

File:Relative risk of an accident based on blood alcohol levels (linear scale).jpg

File:BAC and the impacts on the human mind and body.pdf

{{Main|Drunk driving#Effects on driving}}

Research shows an exponential increase of the relative risk for a crash with a linear increase of BAC.{{Cite web|url=http://www.euro.who.int/__data/assets/pdf_file/0003/87564/E82659.pdf|title=Preventing road traffic injury: A public health perspective for Europe|website=Euro.who.int|access-date=2 March 2022}} NHTSA reports that the following blood alcohol levels (BAC) in a driver will have the following predictable effects on his or her ability to drive safely: (1) A BAC of .02 will result in a "[d]ecline in visual functions (rapid tracking of a moving target), a decline in the ability to perform two tasks at the same time (divided attention)"; (2) A BAC of .05 will result in "[r]educed coordination, reduced ability to track moving objects, difficulty steering, reduced response to emergency driving situations"; (3) A BAC of .08 will result in "[c]oncentration, short-term memory loss, speed control, reduced information processing capability (e.g., signal detection, visual search), impaired perception"; (4) A BAC of .10 will result in "[r]educed ability to maintain lane position and brake appropriately"; and (5) A BAC of .15 will result in "[s]ubstantial impairment in vehicle control, attention to driving task, and in necessary visual and auditory information processing."{{cite web|last=NHTSA|date=2016-10-04|title=Drunk Driving – How Alcohol Affects Driving Ability|url=https://www.nhtsa.gov/risky-driving/drunk-driving|url-status=live|access-date=2021-03-19|website=NHTSA|language=en|archive-url=https://web.archive.org/web/20161226050807/https://www.nhtsa.gov/risky-driving/drunk-driving |archive-date=2016-12-26 }}

Ethanol inhibits the ability of glutamate to open the cation channel associated with the N-Methyl-D-aspartic acid (NMDA) subtype of glutamate receptors. Stimulated areas include the cortex, hippocampus, and nucleus accumbens, which are all responsible for both thinking and pleasure seeking. Another one of alcohol's agreeable effects is body relaxation, which is possibly caused by neurons transmitting electrical signals in an alpha waves-pattern; such waves are actually observed (with the aid of EEGs) whenever the body is relaxed.{{Citation needed|date=November 2010}}

Short-term effects of alcohol include the risk of injuries, violence, and fetal damage.{{cite journal | vauthors = Andréasson S, Allebeck P | title = [Alcohol as medication is no good. More risks than benefits according to a survey of current knowledge] | journal = Läkartidningen | volume = 102 | issue = 9 | pages = 632–637 | date = 28 February – 6 March 2005 | pmid = 15804034 }} Alcohol alters platelet response; moderate alcohol consumption can increase the amount of time bleeding by slowing down coagulation (as platelet aggregation decreases). Moreover, heavy alcohol consumption can lead to increased platelet aggregation thus increasing blood clotting and possibly leading to strokes and/or thrombosis.{{Cite journal |last=Piano |first=Mariann R |date=26 December 2024 |title=Alcohol's Effects on the Cardiovascular System |journal=Alcohol Research: Current Reviews |volume=38 |issue=2 |pages=219–241 |pmid=28988575 |pmc=5513687 }} Alcohol has also been linked with lowered inhibitions, although it is unclear as to what degree this is chemical or psychological as studies with placebos can often duplicate the social effects of alcohol at either low or 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.{{cite journal | vauthors = Grattan KE, Vogel-Sprott M | title = Maintaining intentional control of behavior under alcohol | journal = Alcoholism: Clinical and Experimental Research | volume = 25 | issue = 2 | pages = 192–197 | date = February 2001 | pmid = 11236832 | doi = 10.1111/j.1530-0277.2001.tb02198.x }} Behavioral changes associated with drunkenness are, to some degree, contextual.{{cite journal | vauthors = Grant NK, Macdonald TK | title = Can alcohol lead to inhibition or disinhibition? Applying alcohol myopia to animal experimentation | journal = Alcohol and Alcoholism | volume = 40 | issue = 5 | pages = 373–378 | year = 2005 | pmid = 15996970 | doi = 10.1093/alcalc/agh177 | doi-access = free }}{{Cite book | chapter-url = http://www.sirc.org/publik/drinking4.html | title=Social and Cultural Aspects of Drinking: A report to the European Commission | chapter = Culture Chemistry and Consequences | date = March 1998 | location = Oxford UK | publisher = Social Issues Research Centre }}

A related effect, which is caused by even low levels of alcohol, is the tendency for people to become more animated in speech and movement. This is caused by 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 favor 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, therefore creating excessive volumes of urine and the subsequent overall dehydration.{{Citation needed|date=November 2014}}

{{Refimprove section|date=March 2025}}

{{Main|Alcohol intoxication}}

Symptoms of ethanol overdose may include nausea, vomiting, CNS depression, coma, acute respiratory failure, or death. Levels of even less than 0.1% can cause intoxication, with unconsciousness often occurring at 0.3–0.4%.{{cite journal|url=http://my.lecom.edu/library/internetresources/journal%20articles/Acute%20Care%20for%20Alcohol%20Intoxication.pdf|archive-url=https://web.archive.org/web/20101214113109/http://my.lecom.edu/library/internetresources/journal%20articles/Acute%20Care%20for%20Alcohol%20Intoxication.pdf|archive-date=14 December 2010|title=Acute care for alcohol intoxication|journal=Postgraduate Medicine Online| vauthors = Yost DA |volume=112|issue=6|year=2002|access-date=29 September 2007}} Death from ethanol consumption is possible when blood alcohol levels reach 0.4%. A blood level of 0.5% or more is commonly fatal. The oral median lethal dose (LD₅₀) of ethanol in rats is 5,628 mg/kg. Directly translated to human beings, this would mean that if a person who weighs {{cvt|70|kg}} drank a {{cvt|500|mL|USoz}} glass of pure ethanol, they would theoretically have a 50% risk of dying.

Acute alcohol intoxication through excessive doses in general causes short- or long-term health effects. NMDA receptors 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 causing the memory impairment that many people experience. It has been asserted that GABA signals interfere with both the registration and the 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 be possible.

Anterograde amnesia, colloquially referred to as "blacking out", is another symptom of heavy drinking.{{cite journal | vauthors = Jackson J, Donaldson DI, Dering B | title = The morning after the night before: Alcohol-induced blackouts impair next day recall in sober young adults | journal = PLOS ONE | volume = 16 | issue = 5 | pages = e0250827 | date = 2021-05-03 | pmid = 33939715 | pmc = 8092761 | doi = 10.1371/journal.pone.0250827 | bibcode = 2021PLoSO..1650827J | veditors = Livesey EJ | doi-access = free }} This is the loss of memory during and after an episode of drinking.

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 if 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 causes 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.{{cite journal | vauthors = Mitoma H, Manto M, Shaikh AG | title = Mechanisms of Ethanol-Induced Cerebellar Ataxia: Underpinnings of Neuronal Death in the Cerebellum | journal = International Journal of Environmental Research and Public Health | volume = 18 | issue = 16 | pages = 8678 | date = August 2021 | pmid = 34444449 | pmc = 8391842 | doi = 10.3390/ijerph18168678 | doi-access = free }}

The Mellanby effect is the phenomenon that the behavioral impairment due to alcohol is less, at the same BAC, when the BAC is decreasing than when it is increasing.{{Cite journal |vauthors=Moskowitz H, Henderson R, Daily J |title=The Mellanby Effect in Moderate and Heavy Drinkers |journal=International Conference on Alcohol, Drugs and Traffic Safety |pages=184–189 |url=http://www.icadtsinternational.com/files/documents/1977_025.pdf |date=1979}} This effect was confirmed in a 2017 meta-analysis.{{cite journal | vauthors = Holland MG, Ferner RE | title = A systematic review of the evidence for acute tolerance to alcohol – the "Mellanby effect" | journal = Clinical Toxicology | volume = 55 | issue = 6 | pages = 545–556 | date = July 2017 | pmid = 28277803 | doi = 10.1080/15563650.2017.1296576 | s2cid = 1243192 | url = https://research.birmingham.ac.uk/portal/en/publications/a-systematic-review-of-the-evidence-for-acute-tolerance-to-alcohol--the-mellanby-effect(41c72d80-da73-447d-a774-d2ec4ba22b43).html }}

Alcohol affects males and females differently because of difference in body fat percentage and water content. On average, for equal body weight, women have a higher body fat percentage than men. Since alcohol is absorbed into body water content, and men have more water in their bodies than women, for women there will be a higher blood alcohol concentration from the same amount of alcohol consumption.{{cite web |url=https://www.alcohol.org/faq/safe-level-of-drinking/ |title=What Is a Safe Level of Drinking? |date=15 March 2019 |website=alcohol.org |access-date=5 April 2019}} Women are also thought to have less alcohol dehydrogenase (ADH) enzyme which is required to break down alcohol. That is why the drinking guidelines are different for men and women.{{cite web |title=Drinking Guidelines |url=http://www.ccdus.ca/Eng/topics/alcohol/drinking-guidelines/Pages/default.aspx |website=Canadian Centre on Substance Use and Addiction |access-date=5 April 2019 |archive-date=7 May 2019 |archive-url=https://web.archive.org/web/20190507070826/http://www.ccdus.ca/Eng/topics/alcohol/drinking-guidelines/Pages/default.aspx |url-status=dead }}

Alcohol metabolism depends on the enzymes alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH).{{cite journal | vauthors = Edenberg HJ, McClintick JN | title = Alcohol Dehydrogenases, Aldehyde Dehydrogenases, and Alcohol Use Disorders: A Critical Review | journal = Alcoholism: Clinical and Experimental Research | volume = 42 | issue = 12 | pages = 2281–2297 | date = December 2018 | pmid = 30320893 | pmc = 6286250 | doi = 10.1111/acer.13904 }} Genetic variants of the genes coding for these enzymes can affect the rate of alcohol metabolism. Some ADH gene variants lead to higher metabolic activity, resulting in the accumulation of acetaldehyde, whereas, a null allele in ALDH2 causes an accumulation of acetaldehyde by preventing its catabolism to acetate.{{cite journal | vauthors = Chen HJ, Tian H, Edenberg HJ | title = Natural haplotypes in the regulatory sequences affect human alcohol dehydrogenase 1C (ADH1C) gene expression | journal = Human Mutation | volume = 25 | issue = 2 | pages = 150–155 | date = February 2005 | pmid = 15643610 | doi = 10.1002/humu.20127 | s2cid = 31530032 | doi-access = free }} The genetic variants of these enzymes can explain the differences in the alcohol metabolism in different races. The different isoforms of ADH showed protection against alcoholic disorders in Han Chinese and Japanese (due to presence of ADH1B*2 ) and in African (due to presence of ADH1B*3).{{cite journal | vauthors = Thomasson HR, Beard JD, Li TK | title = ADH2 gene polymorphisms are determinants of alcohol pharmacokinetics | journal = Alcoholism: Clinical and Experimental Research | volume = 19 | issue = 6 | pages = 1494–1499 | date = December 1995 | pmid = 8749816 | doi = 10.1111/j.1530-0277.1995.tb01013.x }} On the other hand, presence of ALDH2*2 in East Asians (a variant of the ALDH gene), can cause blood acetaldehyde levels of 30 to 75 μM or higher, which is more than 10 times the normal level. The excess amount of blood aldehyde produce facial flushing, nausea, rapid heartbeat, and other adverse effects.{{cite journal | vauthors = Enomoto N, Takase S, Yasuhara M, Takada A | title = Acetaldehyde metabolism in different aldehyde dehydrogenase-2 genotypes | journal = Alcoholism: Clinical and Experimental Research | volume = 15 | issue = 1 | pages = 141–144 | date = February 1991 | pmid = 2024727 | doi = 10.1111/j.1530-0277.1991.tb00532.x }}{{cite journal | vauthors = Peng Q, Gizer IR, Libiger O, Bizon C, Wilhelmsen KC, Schork NJ, Ehlers CL | title = Association and ancestry analysis of sequence variants in ADH and ALDH using alcohol-related phenotypes in a Native American community sample | journal = American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics | volume = 165B | issue = 8 | pages = 673–683 | date = December 2014 | pmid = 25270064 | pmc = 4364382 | doi = 10.1002/ajmg.b.32272 }} Presence of these alleles causes rapid conversion of alcohol to acetaldehyde which can be toxic in large amount. So, the East Asians and Africans feel the adverse effects of alcohol early and stop drinking. For Caucasians, ADH1B*1 allele is the most prevalent allele which causes slower conversion of alcohol to acetaldehyde and it makes them more vulnerable to alcohol use disorders.{{cite journal | vauthors = Dodge NC, Jacobson JL, Jacobson SW | title = Protective effects of the alcohol dehydrogenase-ADH1B*3 allele on attention and behavior problems in adolescents exposed to alcohol during pregnancy | journal = Neurotoxicology and Teratology | volume = 41 | pages = 43–50 | date = 2014 | pmid = 24263126 | pmc = 3943945 | doi = 10.1016/j.ntt.2013.11.003 | bibcode = 2014NTxT...41...43D }}

{{Main|Alcohol tolerance}}

Alcohol tolerance is increased by regular drinking. This includes direct tolerance, speed of recovery from insobriety, and resistance to the development of alcohol use disorder.{{cite journal |date=April 1995 |title=Alcohol and Tolerance |url=http://www.niaaa.nih.gov:80/publications/aa28.htm |journal=National Institute on Alcohol Abuse and Alcoholism (NIAAA), Alcohol Alert |issue=28 |access-date=2009-08-13 |archive-url=https://web.archive.org/web/20050404172912/http://www.niaaa.nih.gov:80/publications/aa28.htm |archive-date=2005-04-04}}

{{Main|Subjective response to alcohol}}

Individuals will have unique experiences of the effects of alcohol, including measurable differences in the extent of stimulating experiences during the beginning of a drinking episode as breath alcohol content (BAC) rises and sedative effects later in a drinking episode as BAC wanes.{{Cite journal|last1=Martin|first1=Christopher S.|last2=Earleywine|first2=Mitchell|last3=Musty|first3=Richard E.|last4=Perrine|first4=M. W.|last5=Swift|first5=Robert M.|date=1 February 1993|title=Development and Validation of the Biphasic Alcohol Effects Scale|journal=Alcoholism: Clinical and Experimental Research|language=en|volume=17|issue=1|pages=140–146|doi=10.1111/j.1530-0277.1993.tb00739.x|pmid=8452195 |issn=1530-0277}} The combined influence of hedonic and aversive subjective experiences over the course of a drinking session are strong predictors of alcohol consumption and drinking consequences.{{Cite journal|last1=Roche|first1=Daniel JO|last2=Ray|first2=Lara A|date=1 May 2015|title=Subjective response as a consideration in the pharmacogenetics of alcoholism treatment|journal=Pharmacogenomics|volume=16|issue=7|pages=721–736|doi=10.2217/pgs.14.143|pmid=25950242|s2cid=7828383 |issn=1462-2416|url=http://www.escholarship.org/uc/item/4sk8b7hx}} There is also mounting evidence for consideration of SR as an endophenotype with some studies suggesting that it accounts for a significant proportion of genetic risk for the development of alcohol use disorder.{{cite journal|last2=Corbin|first2=William R.|last3=Treat|first3=Teresa A.|date=December 2015|title=Evaluating the accuracy of alcohol expectancies relative to subjective response to alcohol|journal=Addictive Behaviors|volume=51|pages=197–203|doi=10.1016/j.addbeh.2015.07.027|pmid=26291291|last1=Morean|first1=Meghan E.|pmc=4772766}}

{{main|Alcohol-induced respiratory reactions|Alcohol flush reaction}}

Humans metabolize ethanol primarily through NAD{{sup|+}}-dependent alcohol dehydrogenase (ADH) class I enzymes (i.e. ADH1A, ADH1B, and ADH1C) to acetaldehyde and then metabolize acetaldehyde primarily by NAD{{smallsup|2}}-dependent aldehyde dehydrogenase 2 (ALDH2) to acetic acid.Ann Ist Super Sanita. 2006;42(1):8–16{{cite journal | vauthors = Crabb DW, Matsumoto M, Chang D, You M | title = Overview of the role of alcohol dehydrogenase and aldehyde dehydrogenase and their variants in the genesis of alcohol-related pathology | journal = The Proceedings of the Nutrition Society | volume = 63 | issue = 1 | pages = 49–63 | date = February 2004 | pmid = 15099407 | doi = 10.1079/PNS2003327 | doi-access = free }} 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.{{cite journal | vauthors = Wolff PH | title = Ethnic differences in alcohol sensitivity | journal = Science | volume = 175 | issue = 4020 | pages = 449–450 | date = January 1972 | pmid = 5007912 | doi = 10.1126/science.175.4020.449 | s2cid = 29099223 | bibcode = 1972Sci...175..449W }}{{cite journal | vauthors = Takao A, Shimoda T, Kohno S, Asai S, Harda S | title = Correlation between alcohol-induced asthma and acetaldehyde dehydrogenase-2 genotype | journal = The Journal of Allergy and Clinical Immunology | volume = 101 | issue = 5 | pages = 576–580 | date = May 1998 | pmid = 9600491 | doi = 10.1016/s0091-6749(98)70162-9 | doi-access = free }} 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.{{cite journal | vauthors = Koppaka V, Thompson DC, Chen Y, Ellermann M, Nicolaou KC, Juvonen RO, Petersen D, Deitrich RA, Hurley TD, Vasiliou V | display-authors = 6 | title = Aldehyde dehydrogenase inhibitors: a comprehensive review of the pharmacology, mechanism of action, substrate specificity, and clinical application | journal = Pharmacological Reviews | volume = 64 | issue = 3 | pages = 520–539 | date = July 2012 | pmid = 22544865 | pmc = 3400832 | doi = 10.1124/pr.111.005538 }} 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.{{cite journal | vauthors = Adams KE, Rans TS | title = Adverse reactions to alcohol and alcoholic beverages | journal = Annals of Allergy, Asthma & Immunology | volume = 111 | issue = 6 | pages = 439–445 | date = December 2013 | pmid = 24267355 | doi = 10.1016/j.anai.2013.09.016 }} 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.{{cite journal | vauthors = Macgregor S, Lind PA, Bucholz KK, Hansell NK, Madden PA, Richter MM, Montgomery GW, Martin NG, Heath AC, Whitfield JB | display-authors = 6 | title = Associations of ADH and ALDH2 gene variation with self report alcohol reactions, consumption and dependence: an integrated analysis | journal = Human Molecular Genetics | volume = 18 | issue = 3 | pages = 580–593 | date = February 2009 | pmid = 18996923 | pmc = 2722191 | doi = 10.1093/hmg/ddn372 }}

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.{{cite journal | vauthors = Goedde HW, Agarwal DP, Fritze G, Meier-Tackmann D, Singh S, Beckmann G, Bhatia K, Chen LZ, Fang B, Lisker R | display-authors = 6 | title = Distribution of ADH2 and ALDH2 genotypes in different populations | journal = Human Genetics | volume = 88 | issue = 3 | pages = 344–346 | date = January 1992 | pmid = 1733836 | doi = 10.1007/bf00197271 | s2cid = 20451607 }} 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.{{cite journal | vauthors = Linneberg A, Fenger RV, Husemoen LL, Vidal C, Vizcaino L, Gonzalez-Quintela A | title = Immunoglobulin E sensitization to cross-reactive carbohydrate determinants: epidemiological study of clinical relevance and role of alcohol consumption | journal = International Archives of Allergy and Immunology | volume = 153 | issue = 1 | pages = 86–94 | date = 2010 | pmid = 20357489 | doi = 10.1159/000301583 | s2cid = 37418991 }} 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.

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At low or moderate doses, alcohol acts primarily as a positive allosteric modulator of GABA_A. Alcohol also acts as a stimulant in low doses, as it triggers the release of dopamine in the striatum, with this mechanism also being responsible for the compound's interaction with the brain's reward system.{{cite book |last1=Hendler |first1=Reuben A. |last2=Ramchandani |first2=Vijay A. |last3=Gilman |first3=Jodi |last4=Hommer |first4=Daniel W. |date=2013 |title=Stimulant and sedative effects of alcohol |url=https://pubmed.ncbi.nlm.nih.gov/21560041/ | series = Current Topics in Behavioral Neurosciences|volume=13 |pages=489–509 |doi=10.1007/7854_2011_135 |issn=1866-3370 |pmid=21560041|isbn=978-3-642-28719-0 }} Alcohol binds to several different subtypes of GABA_A, 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.{{cite journal | vauthors = Huang Q, He X, Ma C, Liu R, Yu S, Dayer CA, Wenger GR, McKernan R, Cook JM | display-authors = 6 | title = Pharmacophore/receptor models for GABA(A)/BzR subtypes (alpha1beta3gamma2, alpha5beta3gamma2, and alpha6beta3gamma2) via a comprehensive ligand-mapping approach | journal = Journal of Medicinal Chemistry | volume = 43 | issue = 1 | pages = 71–95 | date = January 2000 | pmid = 10633039 | doi = 10.1021/jm990341r }}{{cite journal | vauthors = Platt DM, Duggan A, Spealman RD, Cook JM, Li X, Yin W, Rowlett JK | title = Contribution of alpha 1GABAA and alpha 5GABAA receptor subtypes to the discriminative stimulus effects of ethanol in squirrel monkeys | journal = The Journal of Pharmacology and Experimental Therapeutics | volume = 313 | issue = 2 | pages = 658–667 | date = May 2005 | pmid = 15650112 | doi = 10.1124/jpet.104.080275 | s2cid = 97681615 }}{{cite journal | vauthors = Duke AN, Platt DM, Cook JM, Huang S, Yin W, Mattingly BA, Rowlett JK | title = Enhanced sucrose pellet consumption induced by benzodiazepine-type drugs in squirrel monkeys: role of GABAA receptor subtypes | journal = Psychopharmacology | volume = 187 | issue = 3 | pages = 321–330 | date = August 2006 | pmid = 16783540 | doi = 10.1007/s00213-006-0431-2 | s2cid = 32950492 }}{{cite journal | vauthors = Wallner M, Hanchar HJ, Olsen RW | title = Low-dose alcohol actions on alpha4beta3delta GABAA receptors are reversed by the behavioral alcohol antagonist Ro15-4513 | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 103 | issue = 22 | pages = 8540–8545 | date = May 2006 | pmid = 16698930 | pmc = 1482527 | doi = 10.1073/pnas.0600194103 | doi-access = free | bibcode = 2006PNAS..103.8540W }}{{cite journal | vauthors = Mehta AK, Ticku MK | title = Ethanol potentiation of GABAergic transmission in cultured spinal cord neurons involves gamma-aminobutyric acidA-gated chloride channels | journal = The Journal of Pharmacology and Experimental Therapeutics | volume = 246 | issue = 2 | pages = 558–564 | date = August 1988 | doi = 10.1016/S0022-3565(25)22106-1 | pmid = 2457076 | url = http://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=2457076 | access-date = 1 August 2010 | archive-date = 31 May 2021 | archive-url = https://web.archive.org/web/20210531145604/https://jpet.aspetjournals.org/content/246/2/558.long | url-status = dead | url-access = subscription }}{{cite journal | vauthors = Becker HC, Anton RF | title = The benzodiazepine receptor inverse agonist RO15-4513 exacerbates, but does not precipitate, ethanol withdrawal in mice | journal = Pharmacology, Biochemistry, and Behavior | volume = 32 | issue = 1 | pages = 163–167 | date = January 1989 | pmid = 2543989 | doi = 10.1016/0091-3057(89)90227-X | s2cid = 6396416 }}{{cite journal | vauthors = Hanchar HJ, Chutsrinopkun P, Meera P, Supavilai P, Sieghart W, Wallner M, Olsen RW | title = Ethanol potently and competitively inhibits binding of the alcohol antagonist Ro15-4513 to alpha4/6beta3delta GABAA receptors | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 103 | issue = 22 | pages = 8546–8551 | date = May 2006 | pmid = 16581914 | pmc = 1482528 | doi = 10.1073/pnas.0509903103 | doi-access = free | bibcode = 2006PNAS..103.8546H }}

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 GABA_A subtypes in their brain.Shimizu, A. Matsubara, K. Uezono, T. Kimura, K. Shiono, H. "Reduced dorsal hippocampal glutamate release significantly correlates with the spatial memory deficits produced by benzodiazepines and ethanol". Neuroscience. P 701-706{{cite journal | vauthors = Petrakis IL, Limoncelli D, Gueorguieva R, Jatlow P, Boutros NN, Trevisan L, Gelernter J, Krystal JH | display-authors = 6 | title = Altered NMDA glutamate receptor antagonist response in individuals with a family vulnerability to alcoholism | journal = The American Journal of Psychiatry | volume = 161 | issue = 10 | pages = 1776–1782 | date = October 2004 | pmid = 15465973 | doi = 10.1176/appi.ajp.161.10.1776 | doi-access = free }}{{cite journal | vauthors = Nutt DJ | title = Alcohol alternatives--a goal for psychopharmacology? | journal = Journal of Psychopharmacology | volume = 20 | issue = 3 | pages = 318–320 | date = May 2006 | pmid = 16574703 | doi = 10.1177/0269881106063042 | s2cid = 44290147 }}{{cite journal | vauthors = Qiang M, Denny AD, Ticku MK | title = Chronic intermittent ethanol treatment selectively alters N-methyl-D-aspartate receptor subunit surface expression in cultured cortical neurons | journal = Molecular Pharmacology | volume = 72 | issue = 1 | pages = 95–102 | date = July 2007 | pmid = 17440117 | doi = 10.1124/mol.106.033043 | s2cid = 10640296 }}{{cite journal | vauthors = Dodd PR, Buckley ST, Eckert AL, Foley PF, Innes DJ | title = Genes and gene expression in the brains of human alcoholics | journal = Annals of the New York Academy of Sciences | volume = 1074 | issue = 1 | pages = 104–115 | date = August 2006 | pmid = 17105908 | doi = 10.1196/annals.1369.010 | s2cid = 35478580 | bibcode = 2006NYASA1074..104D }}{{cite journal | vauthors = Klein G, Gardiwal A, Schaefer A, Panning B, Breitmeier D | title = Effect of ethanol on cardiac single sodium channel gating | journal = Forensic Science International | volume = 171 | issue = 2–3 | pages = 131–135 | date = September 2007 | pmid = 17129694 | doi = 10.1016/j.forsciint.2006.10.012 }}{{cite journal | vauthors = Shiraishi M, Harris RA | title = Effects of alcohols and anesthetics on recombinant voltage-gated Na+ channels | journal = The Journal of Pharmacology and Experimental Therapeutics | volume = 309 | issue = 3 | pages = 987–994 | date = June 2004 | pmid = 14978193 | doi = 10.1124/jpet.103.064063 | s2cid = 18823121 }} Alcohol inhibits sodium-potassium pumps in the cerebellum and this is likely how it corrupts cerebellar computation and body co-ordination.{{cite journal | vauthors = Forrest MD | title = Simulation of alcohol action upon a detailed Purkinje neuron model and a simpler surrogate model that runs >400 times faster | journal = BMC Neuroscience | volume = 16 | issue = 27 | pages = 27 | date = April 2015 | pmid = 25928094 | pmc = 4417229 | doi = 10.1186/s12868-015-0162-6 | doi-access = free }}{{cite web |url= http://www.science20.com/michael_forrest/the_neuroscience_reason_we_fall_over_when_drunk-155301 |title=The neuroscience reason we fall over when drunk | vauthors = Forrest M |date=April 2015 |website=Science 2.0 |access-date=24 June 2015}}

Contrary to popular belief, research suggests that acute exposure to alcohol is not neurotoxic in adults and actually prevents NMDA antagonist-induced neurotoxicity.{{cite journal | vauthors = Farber NB, Heinkel C, Dribben WH, Nemmers B, Jiang X | title = In the adult CNS, ethanol prevents rather than produces NMDA antagonist-induced neurotoxicity | journal = Brain Research | volume = 1028 | issue = 1 | pages = 66–74 | date = November 2004 | pmid = 15518643 | doi = 10.1016/j.brainres.2004.08.065 | s2cid = 9346522 }}

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Alcohol causes generalized CNS depression, is a positive allosteric GABA_A modulator and is associated and related with cognitive, memory, motor, and sensory impairment. It slows and impairs cognition and reaction time and the cognitive skills, impairs judgement, interferes with motor function resulting in motor incoordination, loss of balance, confusion, sedation, numbness and slurred speech, impairs memory formation, and causes sensory impairment. At high concentrations, it can induce amnesia, analgesia, spins, stupor, and unconsciousness as result of high levels of ethanol in blood.

At very high concentrations, alcohol can cause anterograde amnesia, markedly decreased heart rate, pulmonary aspiration, positional alcohol nystagmus, respiratory depression, shock, coma and death can result due to profound suppression of CNS function alcohol overdose and can finish in consequent dysautonomia.

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Alcohol can cause nausea and vomiting in sufficiently high amounts (varying by person). Alcohol stimulates gastric juice production, even when food is not present, and as a result, its consumption stimulates acidic secretions normally intended to digest protein molecules. Consequently, the excess acidity may harm the inner lining of the stomach. The stomach lining is normally protected by a mucosal layer that prevents the stomach from, essentially, digesting itself. However, in patients who have a peptic ulcer disease (PUD), this mucosal layer is broken down. PUD is commonly associated with the bacteria Helicobacter pylori, which secretes a toxin that weakens the mucosal wall, allowing acid and protein enzymes to penetrate the weakened barrier. Because alcohol stimulates the stomach to secrete acid, a person with PUD should avoid drinking alcohol on an empty stomach. Drinking alcohol causes more acid release, which further damages the already-weakened stomach wall.[http://www.medscape.com/viewarticle/734791_2 Overview of Peptic Ulcer Disease: Etiology and Pathophysiology]. Medscape.com. Retrieved 27 April 2013. Complications of this disease could include a burning pain in the abdomen, bloating and in severe cases, the presence of dark black stools indicate internal bleeding.[http://www.webmd.com/digestive-disorders/digestive-diseases-peptic-ulcer-disease Peptic Ulcer Disease (Stomach Ulcers) Cause, Symptoms, Treatments]. Webmd.com. Retrieved 27 April 2013. A person who drinks alcohol regularly is strongly advised to reduce their intake to prevent PUD aggravation.

Ingestion of alcohol can initiate systemic pro-inflammatory changes through two intestinal routes: (1) altering intestinal microbiota composition (dysbiosis), which increases lipopolysaccharide (LPS) release, and (2) degrading intestinal mucosal barrier integrity – thus allowing LPS to enter the circulatory system. The major portion of the blood supply to the liver is provided by the portal vein. Therefore, while the liver is continuously fed nutrients from the intestine, it is also exposed to any bacteria and/or bacterial derivatives that breach the intestinal mucosal barrier. Consequently, LPS levels increase in the portal vein, liver and systemic circulation after alcohol intake. Immune cells in the liver respond to LPS with the production of reactive oxygen species, leukotrienes, chemokines and cytokines. These factors promote tissue inflammation and contribute to organ pathology.{{cite journal | vauthors = Patel S, Behara R, Swanson GR, Forsyth CB, Voigt RM, Keshavarzian A | title = Alcohol and the Intestine | journal = Biomolecules | volume = 5 | issue = 4 | pages = 2573–88 | date = October 2015 | pmid = 26501334 | pmc = 4693248 | doi = 10.3390/biom5042573 | doi-access = free }}

{{main|Alcohol use and sleep}}

Low doses of alcohol (one {{convert|360|mL|0|abbr=on}} 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.{{cite journal | vauthors = Stone BM | title = Sleep and low doses of alcohol | journal = Electroencephalography and Clinical Neurophysiology | volume = 48 | issue = 6 | pages = 706–709 | date = June 1980 | pmid = 6155259 | doi = 10.1016/0013-4694(80)90427-7 }} 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.{{cite journal | vauthors = Schuckit MA | title = Low level of response to alcohol as a predictor of future alcoholism | journal = The American Journal of Psychiatry | volume = 151 | issue = 2 | pages = 184–189 | date = February 1994 | pmid = 8296886 | doi = 10.1176/ajp.151.2.184 }} In insomniacs, moderate doses of alcohol improve sleep maintenance.{{cite journal | vauthors = Roehrs T, Papineau K, Rosenthal L, Roth T | title = Ethanol as a hypnotic in insomniacs: self administration and effects on sleep and mood | journal = Neuropsychopharmacology | volume = 20 | issue = 3 | pages = 279–286 | date = March 1999 | pmid = 10063488 | doi = 10.1016/S0893-133X(98)00068-2 | doi-access = free }}

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 three days of alcohol consumption before bedtime.

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".{{cite web | url = http://scienceline.org/2011/02/why-does-my-head-spin-when-i%E2%80%99m-drunk/ | title = Why does my head spin when I'm drunk? | vauthors= Nuwer R | author-link = Rachel Nuwer | date = 8 February 2011 | work = Scienceline }}

Alcohol taken with a meal increases and prolongs postprandial triglyceridemia. This is true despite the observation that the relationship between alcohol consumption and triglyceridemia is "J-shaped," meaning that fasting triglycerides concentration is lower in people who drink 10–20 g/alcohol a day compared to people who either abstain from alcohol or who drink more per day.{{cite journal | vauthors = Kovář J, Zemánková K | title = Moderate alcohol consumption and triglyceridemia | journal = Physiological Research | volume = 64 | issue = Suppl 3 | pages = S371–S375 | date = 2015 | pmid = 26680670 | doi = 10.33549/physiolres.933178 | doi-access = free }}

A systematic review reported that alcohol has bi-phasic effect on blood pressure. Both systolic and diastolic blood pressure fell when they were measured couple of hours after alcohol consumption. However, the longer term measurement (20 hours average) showed a modest but statistically significant increase in blood pressure: a 2.7 mmHg rise in systolic blood pressure and 1.4 mmHg rise in diastolic blood pressure.{{cite journal | vauthors = McFadden CB, Brensinger CM, Berlin JA, Townsend RR | title = Systematic review of the effect of daily alcohol intake on blood pressure | journal = American Journal of Hypertension | volume = 18 | issue = 2 Pt 1 | pages = 276–286 | date = February 2005 | pmid = 15752957 | doi = 10.1016/j.amjhyper.2004.07.020 | doi-access = free }} A Cochrane systematic review based on only randomized controlled trials which investigates the acute effect of alcohol consumption in healthy and hypertensive adults is in progress.{{cite journal | vauthors = Mills KT, Bundy JD, Kelly TN, Reed JE, Kearney PM, Reynolds K, Chen J, He J | display-authors = 6 | title = Global Disparities of Hypertension Prevalence and Control: A Systematic Analysis of Population-Based Studies From 90 Countries | journal = Circulation | volume = 134 | issue = 6 | pages = 441–450 | date = August 2016 | pmc = 6483609 | doi = 10.1002/14651858.CD012787 | pmid = 27502908 }}

A 2015 literature review found that alcohol administration confers acute pain-inhibitory effects. It also found the relationship between alcohol consumption and pain is curvilinear; moderate alcohol use was associated with positive pain-related outcomes and heavy alcohol use was associated with negative pain-related outcomes.

{{cite journal | vauthors = Zale EL, Maisto SA, Ditre JW | title = Interrelations between pain and alcohol: An integrative review | journal = Clinical Psychology Review | volume = 37 | issue = | pages = 57–71 | date = April 2015 | pmid = 25766100 | pmc = 4385458 | doi = 10.1016/j.cpr.2015.02.005 }}

• Alcohol and health
• Long-term effects of alcohol consumption

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• {{cite report | url = https://www.who.int/publications/i/item/9789241565639 | title = Global Status Report on Alcohol | date = 2018 | location = Geneva | publisher = World Health Organization }}
• {{cite journal | vauthors = Heberlein U, Wolf FW, Rothenfluh A, Guarnieri DJ | title = Molecular Genetic Analysis of Ethanol Intoxication in Drosophila melanogaster | journal = Integrative and Comparative Biology | volume = 44 | issue = 4 | pages = 269–274 | date = August 2004 | pmid = 21676709 | doi = 10.1093/icb/44.4.269 | citeseerx = 10.1.1.536.262 }}

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{{alcohealth}}

{{DEFAULTSORT:Short-Term Effects of Alcohol}}

Category:Drinking culture

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