Hi Melissa,

On days that I must not drink, I don't drink. Sometimes I don't drink because I don't feel like it. I'm not sure what ,kind of alcholic I am. Anyhoo, I was drinking when I wrote this post but I did think that the Campral was taken when you wanted to reduce cravings and only then.

Got our pills today though.

Aren't we overlooking the possibility that some people drink for GABA effects AND the dopamine hit? Or for some other reason altogether?

I'm not convinced that the GABA folks are the minority. From my research (I'll look up the studies I found again), they are the majority. If you don't have at least one copy of the A118G allele, then you're not getting any dopamine (endogenous, produced through the opioid system) at all and could only be addicted via GABA.

That said, my casual perusal of studies leads me to believe that if you are drinking for the GABA (or for both GABA and dopamine) that baclofen is more effective than Campral.

GABA is also available OTC (amino acid). It supposedly doesn't cross the blood-brain barrier, but some clinicians (notably Julia Ross) dispute this. I think if you're GABA deficient it would be worth a try, but it doesn't look promising. There is a form of it that definitely crosses the BBB (phenibut), but tolerance to it builds fast and withdrawal is scary. It's chemically very similar to baclofen. Since tolerance and withdrawal are common to both baclofen and phenibut and they are so similar, I wonder if there is a manageable daily dose of phenibut (which is MUCH cheaper than baclofen and available OTC) to combat alcoholism. There are lots of scary phenibut withdrawal stories, but they are from the internet, so who knows? Caution is definitely indicated. I've tried it (as a baclofen alternative). Like baclofen, for me all it did was potentiate alcohol impairment, but not the high. NOT GOOD.

Alcohol also increases available serotonin. Circulating levels are easily increased by taking 5-HTP or l-tryptophan, which are also inexpensive and available OTC. Again, from my casual perusal of the literature, it seems that you can't drink on them or they are rendered ineffective. Might be good for someone drinking for the serotonin who can also abstain. SSRI's do the same. Drinking to combat depression would be a clue that serotonin might be the problem. Another clue would be substituting sweets or binge eating for alcohol.

Alcohol also acts as an antidepressant for people who are GLA deficient (it makes the PGE1 - an endogenous anti-depressant - in the body available to the brain). GLA deficiency is treatable with evening primrose oil, which is also available inexpensively OTC.

Long (loooooong) story short: if you're drinking for the dopamine, adding Campral is not going to do anything but drain your wallet. If you're drinking for the GABA, same for naltrexone. If you're the rare snowflake who drinks for both, Campral + naltrexone may just be the thing. If you're drinking for other rewards, neither will help at all.

Thinking about why you drink and what you feel when you drink are, IMHO, helpful. Genetic testing would be more helpful, but I think subjective experience is quite telling.

Sorry for the ridiculously long post, but this is interesting stuff.

I think you are maybe conflating dopamine and opiates.

Dopamine comes into play as our general achievement/reward system. We get a shot of that whenever we accomplish anything, including the pitiful accomplishment of obtaining our drug, but it's not an inherent effect of the drug.

Everyone gets an opioid hit from alcohol. This is the "innate reward" we hear about. What's the diff in people who've got the gene? We don't know -- maybe it's more intense or maybe it's less intense (so that they need more) -- but they're not getting anything that the rest of us just plain aren't. Alcohol triggers the release of endorphins, natural opiates, which bind to the opiate receptors. That's just one of the things it does.

Everyone gets a GABA hit as well. That's another of the things it does.

We train ourselves to get the dopamine reward by seeking alcohol for other reasons. Once we've already learned to like it and enjoy it, then the dopamine reward kicks in. Dopamine's involved for everyone, but it's not the base problem for anyone because it doesn't factor in until we've already trained ourselves to seek alcohol.

More to follow . . . I want to write a thoughtful response to your main points, but I wanted to get that correction out there for the folks at home.

Magda, I'd like to work on this with you backchannel. We've done separate but overlapping research, and I think we could put it together into some really good stuff. PM me if you're interested.

PM sent.



I don't think so. Example: http://www.ncbi.nlm.nih.gov/pubmed/20479755





Some drugs (e.g. cocaine, meth) give all users a dopamine hit, but alcohol does give some users a huge hit right in the reward center of the brain. It's these drinkers that I think are the best candidates for TSM, since the µ opioid receptor (the one blocked by naltrexone) is the major determinant of the dopamine response to alcohol.



See the above response. People with the variant get dopamine delivered directly into the reward center of the brain. People without the variant get, as you correctly stated, NO dopamine. Everyone gets endorphins with opiate-like effects (which bind to the µ receptor), so naltrexone would block those, but I suspect that the endorphin release is not the problem per se in alcoholics, since, as you correctly stated, alcohol causes that release in everyone, yet most people can easily drink in moderation. In other words, I don't think it's the direct opiate effects that cause problem drinkers to lose control.

http://www.sciencedaily.com/releases/20 ... 190945.htm

[emphasis mine]
The increase in dopamine is no longer hypothetical. I'll have to find the newer studies.


True, but even there, some people (carriers of the GAD1 gene variant) are more vulnerable to the GABA effects of alcohol. They release GABA more slowly after ingesting alcohol and therefore are compelled to ingest more. Couple this with inherent low levels of GABA, and it's a pretty good recipe for alcohol dependence. It's these folks who I believe are good candidates for baclofen or Campral.

An old article that sums up the dopamine thing nicely: http://www.post-gazette.com/news/health ... 1006300241

Welcome to this community.
Good to hear from you.