I don't see the ethical problem as all that dramatic, other things being equal (i.e. the side effects of the antagonists are negligible).

Negligible compared to what? Psychoactive drugs always have non-negligible side effects - at a bare minimum, they can cause their intended effect in people who don't need that effect. And a clinical trial that demonstrates that the side effects are less bad than addiction is far cry from demonstrating that it's harmless enough to be added to the general water supply on Manhatten.

I'm not advocating compulsion.

Because "take this drug or you lose your job" isn't compulsion? That is a very scary precedent to set.

But there is a public interest in preventing financial traders from hotdogging.

Of course. That is why we have financial regulators.

But enough public interest to justify violating the principle of informed consent? We don't even do that for the polio vaccine, and wiping out polio is a clear-cut case of public interest if I've ever seen one.

If you want traders to stop gambling with other people's money, you change the rules of operation of the stock exchange so they can't do it. You don't spike their lunch with psychopharmaca. We've been down that road before, and that's a really ugly neighbourhood.

- Jake

Friends come and go. Enemies accumulate.

Nalmefene has a molecular shape that allows it 'block' neuronal endorphin receptors (like a fake key stuck in a lock that can't open the door). If endorphins enter the receptors of firing neurons, they promote new dendritic growth to neighbouring neurons that were also firing at the time of reception. That's how behaviour becomes hardwired - literally.

When neuronal receptors for endorphins are blocked, the process is 'reversed'. i.e. if the stimulation of a neuron by endorphin does not happen because of the blocking, then existing dendritic connections are weakened over time. That is essentially what the nalmefene treatment entails - 'forgetting' behaviour'. Although such behaviour can be quickly 'remembered' again by unblocked stimulation.

Whereas (if I understand it correctly) stimulated dopamine receptors modulate transmission across the synaptic gap. Which is a whole different kettle of students.

I don't know if dopaminergic antagonists have yet been discovered.

You can't be me, I'm taken

In the case of alcohol, the stimulii are hard to remove because we have learned to drink so many different drinks in so many different places at different times of the day, in different company. It is a very complex behaviour.

But theoretically, if you had only ever drunk one cider a day at 6pm, alone in a red room, wearing a monkey suit, then the unavailability of those stimulii would, over time, erase the behaviour.

Being unable to remove the stimulii, the answer to alcoholism is to prevent reinforcement with, for instance, opioid blockers. For most of us, alcohol is a learned behaviour but not a disorder. It becomes a disorder when it becomes a dominant behaviour that is personally destructive. Before this point, other treatments can be beneficial (except punishment), while alternative behaviours should be encouraged before they are suppressed by the increasingly dominant behaviour of finding and drinking alcohol.

So I agree with Frank that counselling - encouraging and facilitating alternate behaviours - does work. The old behaviours, like an old romance, can sometimes be revived. But beyond a certain point, when the drinking behaviour has become dominant - to the exclusion of all else - the only intervention is the biochemical prevention of reinforcement.

You can't be me, I'm taken