Alcohol metabolism
Zero-order ethanol elimination and how to calculate a falling blood alcohol level, the alcohol and aldehyde dehydrogenase pathway with its NADH and acetaldehyde consequences, CYP2E1 induction, the biochemistry behind alcoholic ketoacidosis and hypoglycaemia, ALDH2 and ADH1B variants, and the osmolar gap.
Tier 1Medical sciences concept
Written with AI assistance and fact-checked against the sources below. For exam study, not clinical decisions. How notes are made
At a glance
- Ethanol is eliminated by zero-order kinetics at usual drinking levels: a fixed amount per hour, not a fixed fraction. There is no useful half-life.
- The main route is alcohol dehydrogenase then ALDH2, both generating NADH. Nearly every metabolic complication of drinking follows from that shifted redox ratio or from acetaldehyde.
- CYP2E1 handles a minority of ethanol at low levels but is induced by chronic use, which explains lower paracetamol thresholds and faster clearance of some drugs.
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Sources
- Goodman & Gilman's The Pharmacological Basis of Therapeutics (14th ed.)McGraw Hill (Brunton and Knollmann, 2023), 2023
- Rang & Dale's Pharmacology (10th ed.)Elsevier (Ritter et al., 2023), 2023
- Australian Medicines HandbookAU/NZAustralian Medicines Handbook Pty Ltd, 2026
- Alcohol and aldehyde dehydrogenase polymorphisms and alcoholismAlcohol Research (Edenberg, 2007;30:5-13), 2007
- Fomepizole for the treatment of methanol poisoningNew England Journal of Medicine (Brent et al., 2001;344:424-9), 2001
- Last updated
- 14 November 2026
What changed
- 14 November 2026 Personal emails, About story and Australian-style copy