Do endorphins (or their depletion) cause addiction?
Is there any scientific evidence that opiates actually supplant endorphin production, making withdrawal from opiates a severe “physical” hurdle? People on methadone claim that without the drug, their “endorphin-challenged” brain cannot function. This seems to support a true biological “need.” What do you think?
This is an excellent question, because it gets to the heart of the matter. The answer is, “No.” People love to claim that addiction to opiates is a result of the impact of opiate use on endorphins, claiming that use of heroin and other narcotics depletes endorphin production, since they share common receptor sites. But the model is an idealized one based on neurochemical research, like all Alan Leshner’s theorizing about addiction. The model has not been related to epidemiologic data (who gets addicted), to clinical data (withdrawal symptoms), or even to biological data (how opiate use affects endorphin levels).
And an examination of actual addiction experiences—their social, situational, and life-span variability—shows that these proposed endorphin-based and other neurochemical and brain-behavior models can have only the most inexact relationship to experienced addiction. You let me know when you find one study that establishes the relationship between a measure of endogenous opiate production, reception, or residual levels and an independent measure of addict behavior or reported withdrawal stress—it isn’t going to happen, and Leshner’s traveling road show is selling snake oil.
The fact that methadone patients claim this model explains why they can’t withdraw is an argument against methadone for me, as much as I welcome methadone as a harm-reduction technique. Addicts all the time explain why they can’t change, and ironically this experiential data is—as you use it—the evidence used to support the most hard-wired biological claims about addiction! It is an irony worth pondering.