I am trying to puzzle my way thru the scientific issues myself. I would love for this to work, since I started TSM 6 days ago, but it would be nice to understand why.

From my reading, AL has effects on multiple neurotransmitter and reward systems. The endorphin system is but one of many. In fact, the endorphin effect can't even be that strong. Consider that giving naltrexone acutely to a drunk has little effect, while it would sent someone on heroin into severe withdrawal.

I think that the GABA/glutamate system is the primary pathway, and the endorphins feed into that. The theory behind TSM seems clear on a superficial level, but gets murky fast. That's why I would rather look at the experimental results.

In contrast to TSM, where naltrexone blocks the opioid receptors, Baclofen potentiates GABA effects. In other words, where NAL blocks the pleasure receptors, BAC takes the place of alcohol. This means BAC cannot be used in an extinction "cure" like NAL.

My understanding of this, anyways.

A lot of people on the my way out forum are having great results from Bac.I did concider it prior to starting Nal but was just too chicken on account of the SE's of those high doses,sleep paralysis in particular.

Adding to the converstion, my doctor told me to increase my dosage to 100mg yesterday. I started at 25mg for the first two weeks, went to 50mg for another 2 weeks, then 75mg for the next 12 weeks. Starting in week 17, I am at 100mg.

When I asked why, and wondered if all that served to do was increase the length of time Nal was blocking receceptors, she said she had seen a few other patients finally turn the corner at 100mg, because that dosage seemed to really reduce cravings FOR THOSE INDIVIDUALS. She said (as has been noted elsewhere in this thread) that this treatement is highly individual, as everyone responds differently.

My very non-scientific hypotheis is, even though I am a small person, perhaps I have lots and lots of receptors to block, with my family history and number of years of heavy drinking. Just a guess, no science behind that, and no way to really test beyond trying different doses!

One thing that puzzled me was an earlier comment about trading off drinking for nightmares, if the dose was too high. But since you don't take Nal when you are not drinking, why would you have nightmares from Nal when not drinking? I am fortunate, I tolerate Nal very well, no side effects beyond that spacey irritable feeling I had the first week.

regarding the science and the many rewards systems that may be in play with al dependence, i sure wish we had more information from the professionals on this. why is it when we have so much research on neurotransmitters for depressive issues, and a plethora of drugs to treat it, we couldn't have some of that research be on how those neurotransmitters relate to addiction and al? seems crazy that we are here asking these questions instead of the pro's. i am worried that i am one that uses al for serotonin boosting, as anti-anxiety/stress, ie. GABA, and as a super efficient sugar delivery system (don't know what pathway that is ). hopefully endorphins also play a significant role. sure wish i wasn't left to be guessing about it all. thanks to all of you here who have more concrete information to share, i just wish there was more of it and it was more definitive.
ok rant over
path