Extremely small amounts of alcohol have been shown to interfere with glutamate action. This interference could affect multiple brain functions, including memory, and it may account for the short-lived condition referred to as “alcoholic blackout.” Because of its inhibitory effect on glutamate, chronic consumption of alcohol leads to up-regulation of glutamate receptor sites in the hippocampus, an area that is crucial to memory and often involved in epileptic seizures. During alcohol withdrawal, glutamate receptors that have adapted to the continual presence of alcohol may become overactive. Glutamate overactivity has been linked repeatedly to cell death in situations ranging from strokes to seizures. Deficiencies of thiamine and magnesium, which are common in alcoholics as a result of malnutrition, may contribute to this potentially destructive overactivity.
