Alcohol tolerance may result from ethanol-induced up-regulation in response to the continued consumption of alcohol. Alcohol dependence may result from overactivity of the same pathway after the ethanol effect starts vanishing and before the system has time to return to a normal state. GABA is believed to play an important role in tolerance.
It can cause metabolic consequences because of the ethanol oxidation in the liver, liver injury that is caused by the toxicity of the metabolic byproducts of alcohol as well as inflammation caused by these products. Chronic alcohol consumption can also cause dysregulation of fatty acid oxidation and synthesis, and activation of the innate immune system.
Wernicke-Korsakoff-syndrome is caused by a thiamine deficiency and is characterized by the paralysis of external eye muscles, ataxia, and a confused state that can lead to a coma and/or death. This is rarely seen in the absence of alcoholism. It is treated with parenteral thiamine.
Fetal alcohol syndrome is caused by chronic maternal alcohol abuse during pregnancy. It is associated with teratogenic effects which include mental retardation and congenital malformations. Alcohol rapidly crosses the placenta and causes the fetal blood to reach the same concentration as that of the mother. This triggers apoptotic neurodegeneration which causes neuronal and glial migration in the developing nervous system.
In acute alcohol consumptions, the most important enzymes are mostly alcohol dehydrogenase and MEOS that mostly work when concentrations are too high. In chronic alcohol consumption, the MEOS are the predominant active enzymes and their activity is induced by chronic alcohol consumption and which increases alcohol metabolism.