I found this article that explains why this is the case in no uncertain terms. We often hear in very general terms about how alcohol disrupts the GABA (inhibitory neurotransmitter)-glutamate (excitatory neurotransmitter) balance. Well, to be specific, alcohol parks itself not in a GABA receptor, but in the NMDA receptor, where glutamate should go, slowing brain activity and "taking the edge" off. As time goes on, the brain has to create more NMDA receptors so it can function normally under the sedating effects of alcohol. This is what makes AL withdrawal so dangerous. AL has rendered GABA moot, but all of a sudden, glutamate starts parking itself in all those extra NMDA receptors, basically making the brain go crazy. And there's not enough GABA to counter it.
Anyway the rest of the article deals with experiments that could lead to drugs that makes withdrawal a much safer experience. Interesting stuff:
The Rockefeller University - The alcoholic brain
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