 | |
| Clinical data | |
|---|---|
| Routes of administration | Common: Oral Uncommon: suppository, inhalation, ocular, insufflation, injection[1] |
| Drug class | Analgesic; Anaphrodisiac; Anxiolytic; Depressant; Euphoriant; General anesthetic; Sedative |
| Pharmacokinetic data | |
| Bioavailability | 80%+[2][3] |
| Protein binding | Weakly or not at all[2][3] |
| Metabolism | Liver (90%):[4][6] • Alcohol dehydrogenase • MEOS (CYP2E1) |
| Metabolites | Acetaldehyde; Acetic acid; Acetyl-CoA; Carbon dioxide; Ethyl glucuronide; Ethyl sulfate; Water |
| Onset of action | Peak concentrations:[4][2] • Range: 30–90 minutes • Mean: 45–60 minutes • Fasting: 30 minutes |
| Elimination half-life | Constant-rate elimination at typical concentrations:[5][6][4] • 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[3][2] |
| Duration of action | 6–16 hours (amount of time that levels are detectable)[7] |
| Excretion | • Major: metabolism (into carbon dioxide and water)[2] • Minor: urine, breath, sweat (5–10%)[4][2] |
The pharmacology of ethanol involves both pharmacodynamics (how it affects the body) and pharmacokinetics (how the body processes it). In the body, ethanol primarily affects the central nervous system, acting as a depressant and causing sedation, relaxation, and decreased anxiety. The complete list of mechanisms remains an area of research, but ethanol has been shown to affect ligand-gated ion channels, particularly the GABAA receptor.
After oral ingestion, ethanol is absorbed via the stomach and intestines into the bloodstream. Ethanol is highly water-soluble and diffuses passively throughout the entire body, including the brain. Soon after ingestion, it begins to be metabolized, 90% or more by the liver. One standard drink is sufficient to almost completely saturate the liver's capacity to metabolize alcohol. The main metabolite is acetaldehyde, a toxic carcinogen. Acetaldehyde is then further metabolized into ionic acetate by the enzyme aldehyde dehydrogenase (ALDH). Acetate is not carcinogenic and has low toxicity,[8] but has been implicated in causing hangovers.[9][10] Acetate is further broken down into carbon dioxide and water and eventually eliminated from the body through urine and breath. 5 to 10% of ethanol is excreted unchanged in the breath, urine, and sweat.
- ^ 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): 467–477. doi:10.1038/npp.2011.206. PMC 3242308. PMID 21956438.
- ^ a b c d e f Principles of Addiction: Comprehensive Addictive Behaviors and Disorders. Academic Press. 17 May 2013. pp. 162–. ISBN 978-0-12-398361-9.
- ^ a b c Holford NH (November 1987). "Clinical pharmacokinetics of ethanol". Clinical Pharmacokinetics. 13 (5): 273–292. doi:10.2165/00003088-198713050-00001. PMID 3319346. S2CID 19723995.
- ^ a b c d 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.
- ^ Cite error: The named reference
PMID 5457514was invoked but never defined (see the help page). - ^ a b Levine B (2003). Principles of Forensic Toxicology. Amer. Assoc. for Clinical Chemistry. pp. 161–. ISBN 978-1-890883-87-4.
- ^ Iber FL (26 November 1990). Alcohol and Drug Abuse as Encountered in Office Practice. CRC Press. pp. 74–. ISBN 978-0-8493-0166-7.
- ^ "Acetate, Ion chromatography standard solution, Safety Data Sheet". Thermo Fisher Scientific. 1 Apr 2024. p. 4.
- ^ Maxwell CR, Spangenberg RJ, Hoek JB, Silberstein SD, Oshinsky ML (December 2010). "Acetate causes alcohol hangover headache in rats". PLOS ONE. 5 (12): e15963. Bibcode:2010PLoSO...515963M. doi:10.1371/journal.pone.0015963. PMC 3013144. PMID 21209842.
- ^ 'Is coffee the real cure for a hangover?' by Bob Holmes, New Scientist, Jan. 15 2011, p. 17.
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