Most (at least 90%) of the absorbed ethanol is oxidised in the liver to acetaldehyde by the action of alcohol dehydrogenase (ADH) and the transfer of hydrogen to nicotinamide adenine dinucleotide (NAD) which forms NADH. The NADH must then be re-oxidised back to NAD before the ethanol can be oxidised. The resulting increase in NADH affects the NADH/NAD ratio, which produces changes in the ratio of all NADH/NAD-dependent metabolites leading to altered biochemical pathways and a metabolic imbalance in the liver. This imbalance is easily established when ethanol is present as it is the preferred substrate for ADH, and can displace up to 90% of all other substances normally utilised by the liver and dominate liver metabolism (Hills and Venable, 1982).

The next stage of ethanol metabolism is the conversion of acetaldehyde to acetate by aldehyde dehydrogenase. Normally acetaldehyde concentrations in the blood are moderately elevated after the ingestion of ethanol.

The average adult metabolises 7-10 g ethanol per hour (Osborn, 1998), with blood ethanol concentrations falling at a rate of 120-250 mg/l/h. The rate is largely independent of the blood ethanol concentration (Gibson et al., 1985; Baselt, 2000)

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