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.

Studies have published strong evidence for certain functions of ethanol in specific systems, but other laboratories have found that these findings do not replicate with different neuronal types and heterologously expressed receptors.

[24] In the past, alcohol was believed to be a non-specific pharmacological agent affecting many neurotransmitter systems in the brain,[25] but progress has been made over the last few decades.

[20][21] Ethanol has long shown a similarity in its effects to positive allosteric modulators of the GABAA receptor like benzodiazepines, barbiturates, and various general anesthetics.

[46] In accordance, it was theorized and widely believed that the primary mechanism of action of ethanol is GABAA receptor positive allosteric modulation.

[26][21] Although ethanol exhibits positive allosteric binding properties to GABAA receptors, its effects are limited to pentamers containing the δ-subunit rather than the γ-subunit.

[46] Ro15-4513, a close analogue of the benzodiazepine antagonist flumazenil (Ro15-1788), has been found to bind to the same site as ethanol and to competitively displace it in a saturable manner.

One study showed the nature of ethanol binding to L-type calcium channels is according to first-order kinetics with a Hill coefficient around 1.

[53] The lower levels of vasopressin from the consumption of alcohol have been linked to ethanol acting as an antagonist to voltage-gated calcium channels (VGCCs).

[54] Similar results have shown to be true in single-channel recordings from isolated nerve terminal of rats that ethanol does in fact block VGCCs.

[56] Other experiments done by Malysz et al. have looked into ethanol effects on voltage-gated calcium channels on detrusor smooth muscle cells in guinea pigs.

[60] Although acetaldehyde has been associated with some of the adverse and toxic effects of ethanol, it appears to play a central role in the activation of the mesolimbic dopamine system.

[31] With acute alcohol consumption, dopamine is released in the synapses of the mesolimbic pathway, in turn heightening activation of postsynaptic D1 receptors.

[62] These modifications to CREB function in the mesolimbic pathway induce expression (i.e., increase gene expression) of ΔFosB in the NAcc,[62] where ΔFosB is the "master control protein" that, when overexpressed in the NAcc, is necessary and sufficient for the development and maintenance of an addictive state (i.e., its overexpression in the nucleus accumbens produces and then directly modulates compulsive alcohol consumption).

[48] Slightly higher levels of 5 to 10 mM, which are associated with light social drinking, produce measurable effects including changes in visual acuity, decreased anxiety, and modest behavioral disinhibition.

[67][68] In the upper range of recreational ethanol concentrations of 20 to 50 mM, depression of the central nervous system is more marked, with effects including complete drunkenness, profound sedation, amnesia, emesis, hypnosis, and eventually unconsciousness.

Hypoglycaemia occurs due to ethanol's inhibition of gluconeogenesis, especially in children, and may cause lactic acidosis, ketoacidosis, and acute kidney injury.

[72] Fermentation is a biochemical process during which yeast and certain bacteria convert sugars to ethanol, carbon dioxide, as well as other metabolic byproducts.

[80] The absorption rate of ethanol is typically modeled as a first-order kinetic process depending on the concentration gradient and specific membrane.

[81] Due to irregular gastric emptying patterns, the rate of absorption of ethanol is unpredictable, varying significantly even between drinking occasions.

[13][90] Once in systematic circulation, ethanol distributes throughout the body, diffusing passively and crossing all biological membranes including the blood-brain barrier.

has units of dose per body weight (g/kg) divided by concentration (g/L blood) - calculation gives values of 0.64 L/kg for men and 0.52 L/kg for women, lower than the original.

If the reaction stops part way through the metabolic pathways, which happens because acetic acid is excreted in the urine after drinking, then not nearly as much energy can be derived from alcohol, indeed, only 215.1 kJ/mol.

[102] Evidence suggests that humans evolved the ability to metabolize dietary ethanol between 7 and 21 million years ago, in a common ancestor shared with chimpanzees and gorillas but not orangutans.

[citation needed] An "abnormal" liver with conditions such as hepatitis, cirrhosis, gall bladder disease, and cancer is likely to result in a slower rate of metabolism.

to release superoxide radicals and induce the oxidation of polyunsaturated fatty acids to toxic aldehyde products like 4-hydroxynonenal (HNE).

[118] Explanations for the gender difference are quite varied and include liver size, secondary effects of the volume of distribution, and sex-specific hormones.

[78] Peak blood alcohol concentrations may be estimated by dividing the amount of ethanol ingested by the body weight of the individual and correcting for water dilution.

The model is most accurate when used to estimate BAC a few hours after drinking a single dose of alcohol in a fasted state, and can be within 20% CV of the true value.