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Alcohol (drug)

Ethanol
Skeletal formula of ethanol
Ball-and-stick model of ethanol Space-filling model of ethanol
Clinical data
Pronunciation/ˈɛθənɒl/
Other namesAbsolute alcohol; Alcohol (USP); Cologne spirit; Drinking alcohol; Ethanol (JAN); Ethylic alcohol; EtOH; Ethyl alcohol; Ethyl hydrate; Ethyl hydroxide; Ethylol; Grain alcohol; Hydroxyethane; Methylcarbinol
Dependence
liability
Moderate[1]
Addiction
liability
Moderate (10–15%)[2]
Routes of
administration
Common: by mouth, topical
Uncommon: suppository, inhalation, ocular, insufflation,[3] injection[4]
Drug classAnalgesic; Depressants; Sedatives; Anxiolytics; Euphoriants; GABAA receptor positive modulators
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability80%+[5][6]
Protein bindingWeakly or not at all[5][6]
MetabolismLiver (90%):[7][9]
Alcohol dehydrogenase
MEOS (CYP2E1)
MetabolitesAcetaldehyde; Acetate; Acetyl-CoA; Carbon dioxide; Water; Ethyl glucuronide; Ethyl sulfate
Onset of actionPeak concentrations:[7][5]
• Range: 30–90 minutes
• Mean: 45–60 minutes
Fasting: 30 minutes
Elimination half-lifeConstant-rate elimination at typical concentrations:[8][9][7]
• Range: 10–34 mg/dL/hour
• Mean (men): 15 mg/dL/hour
• Mean (women): 18 mg/dL/hr
At very high concentrations (t1/2): 4.0–4.5 hours[6][5]
Duration of action6–16 hours (amount of time that levels are detectable)[10]
Excretion• Major: metabolism (into carbon dioxide and water)[5]
• Minor: urine, breath, sweat (5–10%)[7][5]
Identifiers
  • ethanol
CAS Number
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
PDB ligand
Chemical and physical data
FormulaC2H6O
Molar mass46.069 g·mol−1
3D model (JSmol)
Density0.7893 g/cm3 (at 20 °C)[11]
Melting point−114.14 ± 0.03 °C (−173.45 ± 0.05 °F) [11]
Boiling point78.24 ± 0.09 °C (172.83 ± 0.16 °F) [11]
Solubility in waterMiscible
  • CCO
  • InChI=1S/C2H6O/c1-2-3/h3H,2H2,1H3
  • Key:LFQSCWFLJHTTHZ-UHFFFAOYSA-N

Alcohol, sometimes referred to by the chemical name ethanol, is a psychoactive drug that is the active ingredient in drinks such as beer, wine, and distilled spirits (hard liquor).[12] It is one of the oldest and most common recreational substances, causing the characteristic effects of alcohol intoxication ("drunkenness").[13] Among other effects, alcohol produces happiness and euphoria, decreased anxiety, increased sociability, sedation, impairment of cognitive, memory, motor, and sensory function, and generalized depression of central nervous system function. Ethanol is only one of several types of alcohol, but it is the only type of alcohol that is found in alcoholic beverages or commonly used for recreational purposes; other alcohols such as methanol and isopropyl alcohol are significantly more toxic.[12] A mild, brief exposure to isopropanol, being only moderately more toxic than ethanol, is unlikely to cause any serious harm. Methanol, being profoundly more toxic than ethanol, is lethal in quantities as small as 10–15 milliliters (2–3 tsp).

Alcohol has a variety of short-term and long-term adverse effects. Short-term adverse effects include generalized impairment of neurocognitive function, dizziness, nausea, vomiting, and hangover-like symptoms. Alcohol can be addictive to humans, as in alcohol use disorder, and can result in dependence and withdrawal. It can have a variety of long-term adverse effects on health, for instance liver damage,[14] brain damage,[15] and its consumption is the fifth leading cause of cancer.[16][failed verification] The adverse effects of alcohol on health are most important when it is used in excessive quantities or with heavy frequency. However, some of them, such as increased risk of certain cancers, may occur even with light or moderate alcohol consumption.[17][18] In high amounts, alcohol may cause loss of consciousness or, in severe cases, death.

Alcohol works in the brain primarily by increasing the effects of a neurotransmitter called γ-aminobutyric acid, or GABA.[19] This is the major inhibitory neurotransmitter in the brain, and by facilitating its actions, alcohol suppresses the activity of the central nervous system.[19] The substance also directly affects a number of other neurotransmitter systems including those of glutamate, glycine, acetylcholine, and serotonin.[20][21] The pleasurable effects of alcohol ingestion are the result of increased levels of dopamine and endogenous opioids in the reward pathways of the brain.[22][23] Alcohol also has toxic and unpleasant actions in the body, many of which are mediated by its byproduct acetaldehyde.[24]

Alcohol has been produced and consumed by humans for its psychoactive effects for almost 10,000 years.[25] Drinking alcohol is generally socially acceptable and is legal in most countries, unlike with many other recreational substances. However, there are often restrictions on alcohol sale and use, for instance a minimum age for drinking and laws against public drinking and drinking and driving.[26] Alcohol has considerable societal and cultural significance and has important social roles in much of the world. Drinking establishments, such as bars and nightclubs, revolve primarily around the sale and consumption of alcoholic beverages, and parties, festivals, and social gatherings commonly involve alcohol consumption. Its use is also related to various societal problems, including driving accidents and fatalities, accidental injuries, sexual assaults, domestic abuse, and violent crime.[27] Alcohol remains illegal for sale and consumption in a number of countries, mainly in the Middle East.

  1. ^ WHO Expert Committee on Problems Related to Alcohol Consumption : second report (PDF). Geneva, Switzerland: World Health Organization. 2007. p. 23. ISBN 9789241209441. Retrieved 3 March 2015. ...alcohol dependence (is) a substantial risk of regular heavy drinking...
  2. ^ Vengeliene V, Bilbao A, Molander A, Spanagel R (May 2008). "Neuropharmacology of alcohol addiction". British Journal of Pharmacology. 154 (2): 299–315. doi:10.1038/bjp.2008.30. PMC 2442440. PMID 18311194. (Compulsive alcohol use) occurs only in a limited proportion of about 10–15% of alcohol users....
  3. ^ Stogner JM, Eassey JM, Baldwin JM, Miller BL (September 2014). "Innovative alcohol use: assessing the prevalence of alcohol without liquid and other non-oral routes of alcohol administration". Drug and Alcohol Dependence. 142: 74–8. doi:10.1016/j.drugalcdep.2014.05.026. PMID 25012895.
  4. ^ Gilman JM, Ramchandani VA, Crouss T, Hommer DW (January 2012). "Subjective and neural responses to intravenous alcohol in young adults with light and heavy drinking patterns". Neuropsychopharmacology. 37 (2): 467–77. doi:10.1038/npp.2011.206. PMC 3242308. PMID 21956438.
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  8. ^ Becker CE (September 1970). "The clinical pharmacology of alcohol". California Medicine. 113 (3): 37–45. PMC 1501558. PMID 5457514.
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  10. ^ Iber FL (26 November 1990). Alcohol and Drug Abuse as Encountered in Office Practice. CRC Press. pp. 74–. ISBN 978-0-8493-0166-7.
  11. ^ a b c Haynes, William M., ed. (2011). CRC Handbook of Chemistry and Physics (92nd ed.). Boca Raton, FL: CRC Press. p. 3.246. ISBN 1439855110.
  12. ^ a b Collins SE, Kirouac M (2013). "Alcohol Consumption". Encyclopedia of Behavioral Medicine: 61–65. doi:10.1007/978-1-4419-1005-9_626. ISBN 978-1-4419-1004-2.
  13. ^ "10th Special Report to the U.S. Congress on Alcohol and Health: Highlights from Current Research" (PDF). National Institute of Health. National Institute on Alcohol Abuse and Alcoholism. June 2000. p. 134. Retrieved 21 October 2014. The brain is a major target for the actions of alcohol, and heavy alcohol consumption has long been associated with brain damage. Studies clearly indicate that alcohol is neurotoxic, with direct effects on nerve cells. Chronic alcohol abusers are at additional risk for brain injury from related causes, such as poor nutrition, liver disease, and head trauma.
  14. ^ Bruha R, Dvorak K, Petrtyl J (March 2012). "Alcoholic liver disease". World Journal of Hepatology. 4 (3): 81–90. doi:10.4254/wjh.v4.i3.81. PMC 3321494. PMID 22489260.
  15. ^ Brust JC (April 2010). "Ethanol and cognition: indirect effects, neurotoxicity and neuroprotection: a review". International Journal of Environmental Research and Public Health. 7 (4): 1540–57. doi:10.3390/ijerph7041540. PMC 2872345. PMID 20617045.
  16. ^ de Menezes RF, Bergmann A, Thuler LC (2013). "Alcohol consumption and risk of cancer: a systematic literature review". Asian Pacific Journal of Cancer Prevention. 14 (9): 4965–72. doi:10.7314/apjcp.2013.14.9.4965. PMID 24175760.
  17. ^ Bagnardi V, Rota M, Botteri E, Tramacere I, Islami F, Fedirko V, Scotti L, Jenab M, Turati F, Pasquali E, Pelucchi C, Bellocco R, Negri E, Corrao G, Rehm J, Boffetta P, La Vecchia C (February 2013). "Light alcohol drinking and cancer: a meta-analysis". Annals of Oncology. 24 (2): 301–8. doi:10.1093/annonc/mds337. PMID 22910838.
  18. ^ Yasinski, Emma, Even If You Don’t Drink Daily, Alcohol Can Mess With Your Brain, Discover (magazine), January 12, 2021
  19. ^ a b Lobo IA, Harris RA (July 2008). "GABA(A) receptors and alcohol". Pharmacology Biochemistry and Behavior. 90 (1): 90–4. doi:10.1016/j.pbb.2008.03.006. PMC 2574824. PMID 18423561.
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  22. ^ Charlet K, Beck A, Heinz A (2013). "The dopamine system in mediating alcohol effects in humans". Current Topics in Behavioral Neurosciences. 13: 461–88. doi:10.1007/7854_2011_130. ISBN 978-3-642-28719-0. PMID 21533679.
  23. ^ Méndez M, Morales-Mulia M (June 2008). "Role of mu and delta opioid receptors in alcohol drinking behaviour". Current Drug Abuse Reviews. 1 (2): 239–52. doi:10.2174/1874473710801020239. PMID 19630722.
  24. ^ Burcham PC (19 November 2013). An Introduction to Toxicology. Springer Science & Business Media. pp. 42–. ISBN 978-1-4471-5553-9.
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  26. ^ Alcohol : No Ordinary Commodity : Research and Public Policy. Babor, Thomas. (2nd ed.). Oxford: Oxford University Press. 2010. ISBN 978-0-19-955114-9. OCLC 656362316.CS1 maint: others (link)
  27. ^ Cite error: The named reference ButcherHooley2013 was invoked but never defined (see the help page).