Posted by Larry Hoover on April 17, 2007, at 9:25:40
In reply to How does alcohol cause depession?, posted by chiron on April 15, 2007, at 0:38:39
> I'm googling, but not getting the detailed answer I want. And I know there are a few wizs here that will know and can explan it to me.
Two possible reasons. It's very complicated; what we thought was true 15 years ago isn't true at all.
Here's a decently understandable slide show about the whole thing:
http://www.rsoa.org/lectures/2_02/2_02.pdfBasically, dopamine is enhanced in the reward pathway, but there's a complex interplay going on between excitation and inhibition of virtually every neurotransmitter/neuromodulator examined.
We used to think that alcohol was an indiscriminant releaser of neurochemicals, and that the hangover was due to general depletion. Chronic drinking led to chronic depletion, and thus mood depression. In fact, alcohol tends to be a general inhibitor, with some specific exceptions. It is the variable interaction between these multiple effects that causes the variable reaction to alcohol intake.
> So if someone has a depression problem, and drinks a 6 pack of Bud Light over the duration of a party, what would the implications be on his mood?
Acutely, they might enjoy the buzz, or they might become moodier. Immediately post-withdrawal, mood depression might be more likely than in the population at large. (There is some evidence that the intermediate in alcohol metabolism, the aldehyde, inhibits metabolism of neurotransmitters, leading to self-inhibitory products that would otherwise occur at very low concentrations.) After a few days, I wouldn't expect any lasting effects, unless the process is repeated before the brain can fully recover.
The slide show kind of gets into it, but there are two types of receptors influenced by alcohol. The first type are the ion channels. Changes in ion flow have an immediate impact on brain function. That's the whole disinhibition/intoxication thingie. However, other receptors, called metabotropic receptors, are also influenced. Loosely, metabotropic means "function changing". These are the receptors that (predominantly) influence the future responses of the neuron, i.e. up-regulation, down-regulation, de novo protein synthesis, etc. via second messengers like G-proteins. Chronic alcohol use changes the brain, and thus the acute experience of alcohol changes with time, too.
What is most amazing about this drug, alcohol, is the difference in threshold dosing for the metabotropic effects to become dominant. Some people can drink regularly, and remain happy. Others should avoid alcohol like it's poison. If you drink enough, alcohol will always be depressogenic. It's how much "enough" is, that differs markedly between individuals.
I've seen people speak in this thread about using alcohol as a self-medication. I see nothing whatsoever wrong with that (except for the risk of overdoing it), but if and only if the person also monitors state of mind. People who drink a couple of drinks a day tend to be healthier than total abstainers. People who drink significantly more than that are worse off than abstainers. Statistically.
Individual differences in response to alcohol *must* be given precedence over any other data considered.
> And would there be a mood effect from the tyramine problem if they were taking Emsam?I'm not sure what you mean. Low tyramine exposure might be stimulating, mood wise, but I wouldn't go looking for this to happen. If you meant an interaction with alcohol, I don't know of one.
> (But it did help me have fun at the party)
Nothing wrong with that, IMHO.
Lar
poster:Larry Hoover
thread:749942
URL: http://www.dr-bob.org/babble/20070413/msgs/750611.html