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Your second paragraph is incorrect. Withdrawal is not an orderly transition to a previous physical state, it's the presence of previously unseen symptoms, typically due to biochemical adaptations to the presence of the foreign substance.

For example, if you drink a lot, some normal neural pathways are repressed by the regular presence of alcohol and your body compensates by increasing the affected neurotransmitters (GABA in this case). As a result, when you stop drinking, you have a corresponding oversupply of GABA, causing the physical symptoms of Delirium Tremens.

I was on Lexapro for 3 years. When I tapered off according to the standard protocol (already in place to avoid withdrawal issues), I experienced debilitating vertigo symptoms and had to change my process from a 2 week reduction to a 3 month process. It was intense.




>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.


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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