Can an addiction be treated with a drug? Imagine: a simple pill to satisfy all of one’s cravings for drugs or alcohol, and to avoid the ravages of this disease. It would revolutionize our treatment of addiction. And since we’re constantly told that addiction is a brain disease, it only makes sense that, once we understand the underlying biology, we’ll be able to create just such a pill, right? Countless researchers, labs, and pharmaceutical companies are indeed trying to do this, as we speak.
The addict struggling to get clean might scramble to be first in line to receive this magic pill. The recovered addict, on the other hand, would probably argue that a chemical solution, a “drug to end all drugs,” so to speak, is far too simplistic. Addictions are behavioral, psychological, social, and spiritual problems (and, yes, they also have some underlying neurochemical factors, too). A pill may treat withdrawal symptoms, or help to reduce the complications of intoxication, or to minimize craving, but even if that pill is 99% effective in reducing cravings, or preventing the intoxicating effect of a drug, the addict will always look to achieve that 1%. It’s how the disease works.
I mention this not only because I am familiar with the recovery process (including the twelve-step approach, which is decidedly not pharmacological but is probably the closest thing we have to an “effective treatment”), but I am also familiar with how well-meaning professionals often trivialize addiction and recovery. Our own biases sometimes keep us from recognizing what should be obvious.
A good example is in the January 2011 American Journal of Psychiatry, which contains a letter to the editor suggesting that disulfiram (commonly known as Antabuse) ought to be investigated for its “anticraving” properties. They point out that disulfiram may increase levels of dopamine in the brain, and since dopamine is “involved” in reward (and addicts sometimes have decreased dopamine activity in the reward pathways), it may reduce craving for addictive drugs and behaviors.
For those of you who don’t know about Antabuse, it has been around since the 1940s and is known as an “aversive” agent. When a person drinks alcohol while taking Antabuse, the drug impairs one of the key steps in alcohol metabolism, leading to the build-up of acetaldehyde in the blood, which causes sweating, nausea, vomiting, flushing, and headache. By itself, Antabuse has no effect on drinking or the desire to drink, but when an alcoholic drinks on Antabuse, the reaction is so uncomfortable that the person learns this association with alcohol and avoids it in the future. (Good old-fashioned classical conditioning at work.)
My reaction to the letter in the journal is not that the authors were factually incorrect, or that we shouldn’t study disulfiram and its properties, but that their argument misses the point. Despite decades of experience with Antabuse, we still have alcoholism and other addictive behaviors, so obviously it’s not a magic bullet. And people who take Antabuse still crave alcohol, so it doesn’t reduce craving to any meaningful degree (in fact, one of the arguments against using Antabuse is that people who want to drink– which is, unfortunately, most alcoholics– simply stop taking it.) The authors cite a case study in which a patient’s desire to gamble “disappeared completely” after taking Antabuse, but as with most everything in psychiatry, how do we know this had anything to do with the drug?
It’s quite naive to think that a simple pill will work in an addiction when addictions are far more complex entities. It reminds me of the doctor who chooses Wellbutrin instead of a different antidepressant for a depressed patient “because she smokes” (the active compound in Wellbutrin, bupropion, also sold as Zyban, has been shown to be effective in smoking cessation). Or the doctor who prescribes Suboxone for the daily Oxycontin and Vicodin addict. Or the doctor who adds Topamax to the regimen of the obese bipolar patient (because some studies show a modest decrease in food craving).
These are not bad ideas (and yes, I’ve seen them all), but again they miss the point. The depressed smoker isn’t going to give up nicotine because she’s all of a sudden taking Wellbutrin. The opiate addict won’t unlearn his addictive behaviors and mindset because he’s now taking Suboxone.
If science continues to look at addictions through the lens of neurotransmitters and “reward pathways” in the brain, and to use animal models to study substance dependence (it goes without saying that a rat in a cage is quite different from the homeless crack-addicted prostitute, or the high-powered alcoholic CEO), then we will achieve nothing more than partial success in treating substance dependence. The clinical trials for “anticraving” drugs like Campral and naltrexone themselves show how limited they are; they measure their effects in terms of “number of drinking days” or “time until first heavy drinking day.” Not in binary terms like “drinking” or “not drinking.”
I know that none of the experts in the addiction field would ever suggest that a medication will solve any individual’s (much less society’s) addiction problem. But I’m concerned about the non-expert clinician, who has neither experienced nor witnessed true addiction. I’m also concerned about the addict, who sees a news headline about some new anti-alcoholism or anti-obesity pill and believes that the wonders of modern science will cure his addiction (so he doesn’t have to look at his own problems).
We in the field also need to be careful about what we promise our patients, and understand the limits of our science. Perhaps we should go one step further and scrap the science altogether, and instead focus on other ways to understand what drives our patients to drink or use drugs, and emphasize a more comprehensive approach to recovery– and yes, one that will require the addict to do a lot more than just take a pill.