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>your body compensates by increasing the affected neurotransmitters (GABA

>you have a corresponding oversupply of GABA

Isn't it the other way around? I had thought that alcohol was a GABA agonist, so your body adapts to produce less of it. Then when you stop, you're _undersupplied_ which produces the DTs.

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Yeah correct, alcohol is technically a positive allosteric modulator of the GABA-A receptors, which means it potentiates the effects of GABA in those receptors. Over time, the receptors downregulate to compensate for being over-stimulated. Upon withdrawal from alcohol, the GABA-A receptors are unable to respond strongly enough to the GABA which exists, so in effect you're undersupplied and that contributes to the DTs. Alcohol is actually a very messy drug that acts on a huge range of receptors but the effect on the GABAergic system is probably the most significant.

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