A new Radiolab podcast talks about addiction, particularly focusing on the use of somewhat-newer drugs like baclofen, acamprosate, naltrexone, buprenorphine, others. It’s interesting to hear the words they use. One guy, after taking baclofen, says “I would try to use cocaine, I couldn’t feel the effects of it“. Then he says “when I was taking it, I didn’t have no cravings“. Anna Rose Childress, an addiction researcher working with this guy, says “He could get the high again, and the craving went through the ceiling”. Does this anecdotal evidence (and there are other examples in the podcast) equate euphoria with craving? Mark Willenbring says that when you use a drug like naltrexone “It’s a buzzkill…you don’t get the happy warm feeling”. It seems intuitive that this could alter addiction, but as Dews said in 1977:
“… it was supposed that the prediction of addiction liability was essentially equivalent to prediction of euphorigenic power. As with most self-evident ideas, the mere matter of there being essentially no evidence in favor of it, and much against it, had little effect on its acceptance.”
Thanks to Terry Robinson for that quote. But was Dews right? Terry says yes, and in several papers (here’s one) he says that the brain changes, or sensitizes, during drug exposure. Then he says that “the brain systems that are sensitized do not mediate the pleasurable or euphoric effects of drugs (drug “liking”), but instead they mediate a subcomponent of reward we have termed incentive salience (drug “wanting”).” So, while studies show that drugs like naltrexone reduce drug-induced euphoria, craving, and drug intake (particularly alcohol drinking), that doesn’t mean that all these things are related. It’s more likely that these drugs are non-specific, in that they affect pleasure and “craving” systems through separable biological substrates. Insert lots of neurobiological studies here. It’s a little confusing because we certainly link the opioid system to pleasure, so of course we want to equate pleasure with drug reinforcement. But opioid receptors are present on pleasure and incentive salience systems in the brain. So an opioid drug like heroin causes pleasure and leads to craving. Conversely, naltrexone reduces pleasure and craving, even though pleasure and craving are separable in the brain. Note that the story probably will be pretty different depending on the drug class.
At any rate, we’re going to hear more examples of this, equating euphoria with drug craving, because it’s so easy to think about addiction this way. In terms of treatment, however, we may want to avoid a non-specific drug that affects euphoria, because there may be mood-related consequences. Unfortunately, finding drugs that specifically reduce craving seems to be tricky.
Meyer Lab 