Alcohol (drug)

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
Pregnancy
category
  • X (Contraindicated in pregnancy)
Dependence
liability
Moderate[1]
Addiction
liability
Moderate (10–15%)[2]
Routes of
administration
Common: By mouth
Uncommon: Suppository, inhalation, ophthalmic, insufflation, injection[3]
Drug classDepressant; anxiolytic; analgesic; euphoriant; sedative; emetic; diuretic; general anesthetic
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability80%+[4][5]
Protein bindingWeakly or not at all[4][5]
MetabolismLiver (90%):[6][8]
• Alcohol dehydrogenase
MEOS (CYP2E1)
MetabolitesAcetaldehyde; acetic acid; acetyl-CoA; carbon dioxide; water; ethyl glucuronide; ethyl sulfate
Onset of actionPeak concentrations:[6][4]
• Range: 30–90 minutes
• Mean: 45–60 minutes
Fasting: 30 minutes
Elimination half-lifeConstant-rate elimination at typical concentrations:[7][8][6]
• Range: 10–34 mg/dL/hour
• Mean: 15-18 mg/dL/hr
At very high concentrations (t1/2): 4.0–4.5 hours[5][4]
Duration of action6–16 hours (amount of time that levels are detectable)[9]
Excretion• Major: metabolism (into carbon dioxide and water)[4]
• Minor: urine, breath, sweat (5–10%)[6][4]
Identifiers
IUPAC name
  • ethanol
CAS Number
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
PDB ligand
Chemical and physical data
FormulaC2H6O
Molar mass46.07 g·mol−1
3D model (JSmol)
Density0.7893 g/cm3 (at 20 °C)[10]
Melting point−114.14 ± 0.03 °C (−173.45 ± 0.05 °F) [10]
Boiling point78.24 ± 0.09 °C (172.83 ± 0.16 °F) [10]
Solubility in waterMiscible mg/mL (20 °C)
SMILES
  • CCO
InChI
  • InChI=1S/C2H6O/c1-2-3/h3H,2H2,1H3
  • Key:LFQSCWFLJHTTHZ-UHFFFAOYSA-N

Alcohol, is (an ingredient or) the active ingredient in alcoholic drinks such as beer, wine, and distilled spirits (hard liquor). Alcohol is sometimes called by its chemical name ethanol.[11]

Alcohol is a central nervous system (CNS) depressant. This means that alcohol lowers electrical activity of neurons in the brain.[12] This causes drunkenness.[13] Alcohol can also cause euphoria, decreased anxiety, sociability, sedation, and lowered cognitive, memory, motor, and sensory function.

References

  1. WHO Expert Committee on Problems Related to Alcohol Consumption: second report. Geneva, Switzerland: World Health Organization. 2007. p. 23. ISBN 978-92-4-120944-1. 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. 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.
  4. 4.0 4.1 4.2 4.3 4.4 4.5 Principles of Addiction: Comprehensive Addictive Behaviors and Disorders. Academic Press. 17 May 2013. pp. 162–. ISBN 978-0-12-398361-9.
  5. 5.0 5.1 5.2 Holford NH (November 1987). "Clinical pharmacokinetics of ethanol". Clinical Pharmacokinetics. 13 (5): 273–92. doi:10.2165/00003088-198713050-00001. PMID 3319346. S2CID 19723995.
  6. 6.0 6.1 6.2 6.3 Pohorecky LA, Brick J (1988). "Pharmacology of ethanol". Pharmacology & Therapeutics. 36 (2–3): 335–427. doi:10.1016/0163-7258(88)90109-x. PMID 3279433.
  7. Becker CE (September 1970). "The clinical pharmacology of alcohol". California Medicine. 113 (3): 37–45. PMC 1501558. PMID 5457514.
  8. 8.0 8.1 Levine B (2003). Principles of Forensic Toxicology. Amer. Assoc. for Clinical Chemistry. pp. 161–. ISBN 978-1-890883-87-4.
  9. Iber FL (26 November 1990). Alcohol and Drug Abuse as Encountered in Office Practice. CRC Press. pp. 74–. ISBN 978-0-8493-0166-7.
  10. 10.0 10.1 10.2 Haynes WM, ed. (2011). CRC Handbook of Chemistry and Physics (92nd ed.). Boca Raton, FL: CRC Press. p. 3.246. ISBN 1439855110.
  11. Collins SE, Kirouac M (2013). "Alcohol Consumption". Encyclopedia of Behavioral Medicine. pp. 61–65. doi:10.1007/978-1-4419-1005-9_626. ISBN 978-1-4419-1004-2.
  12. Costardi JV, Nampo RA, Silva GL, Ribeiro MA, Stella HJ, Stella MB, et al. (August 2015). "A review on alcohol: from the central action mechanism to chemical dependency". Revista da Associação Médica Brasileira. 61 (4): 381–387. doi:10.1590/1806-9282.61.04.381. PMID 26466222.
  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.

Further reading

  • IARC Working Group on the Evaluation of Carcinogenic Risks to Humans (1988). Alcohol Drinking. International Agency for Research on Cancer.

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