More on Satel and the Disease Model

Satel sent Lemonick a link to a longer article on the same subject:

My job is to help addicts quit heroin and not go back to it in the future. If this is a challenge for the clinician, it’s a monumental effort for the addict. Every so often a patient will ask me if I can “hypnotize” him out of his habit. One patient told me he wished there were an anti-addiction pill, “something to make me not want.” Indeed, that is the timeless quest of troubled addicts everywhere: not to want. It comes as no news to them, however, that recovery is very much a project of the heart and mind. Nor is it news that recovery is attainable.

This is why I chafe at the conventional scientific wisdom about addiction: namely, that it is “a chronic and relapsing brain disease.”[4] This view is much heralded by the National Institute on Drug Abuse, or NIDA, part of the National Institutes of Health. NIDA is funded at slightly over $1 billion a year and carries enormous authority on Capitol Hill, among grant-seeking scientists, and in medical schools. The “brain disease” idea is promoted at major rehab institutions such as the Betty Ford Center and Hazelden[5]; it is now a staple of anti-drug education in high schools and in counselor education. And, of course, lawyers play fast and loose with the brain disease rhetoric in courtrooms[6].

The brain disease concept sends a perilous public health message. First, it suggests that an addict’s condition is amenable to a medical cure (much as pneumonia is cleared with antibiotics). Second, it misappropriates language more properly used to describe conditions such as multiple sclerosis or schizophrenia—afflictions that are neither brought on by the sufferer himself nor modifiable by his desire to be well. Third, it carries a fatalistic theme, implying that users can never free themselves of their drug or alcohol problems.

The brain disease rhetoric also threatens to obscure the vast role of personal agency in perpetuating the cycle of use and relapse to drugs and alcohol. It sends a mixed message that undermines the rationale for therapies and policies that depend on recognizing the addict’s potential for self-governance.

We tend to think of the cocaine addict in the throes of a days-long binge. He frantically gouges himself with needles, jams a new rock into his pipe every 15 minutes, or hungrily snorts lines of powder. Or we think of the heroin junkie either nodding off or doubled over in misery from withdrawal, so desperate for the next hit that he’ll get the money any way he can. In the grip of such forces, an addict cannot be expected blithely to get up and walk away. These tumultuous states—with neuronal function severely disrupted—are the closest drug use comes to being beyond the user’s restraint.

Yet addicts rarely spend all of their time in conditions of such intense neurochemical siege. In the days between binges, for example, cocaine addicts make many decisions that have nothing to do with drug-seeking. Should they clean the apartment? Try to find a different job? Kick that freeloading cousin off their couch for good? Heroin-dependent individuals often function quite well as long as they have regular access to some form of opiate drug in order to prevent withdrawal symptoms[11]. Most of my own patients even hold jobs while pursuing their heroin habits, which typically entail use about every six to eight hours.

In other words, there is room for other choices. These addicts could go to a Narcotics Anonymous meeting, for example, or enter treatment if they have private insurance, or register at a public clinic if they don’t. And yes, they could even stop cold turkey. I’ve interviewed scores of opiate addicts who have done it. They take lots of Valium-type drugs to handle withdrawal and suffer through a few days of vomiting, diarrhea, and cramping.

I am a clinician. I treat real-life patients. As a pragmatist, I can’t see the advantage of conceptualizing addiction as a “chronic and relapsing brain disease.” At the same time, no reasonable person would disagree that addiction is mediated through the dopamine system of the brain. Or that intense activation of the dopamine system makes it more difficult for users to quit. Or that genetic factors influence the intensity of the effect that users derive from substances, the rapidity with which they develop compulsive use, the potency of their cue-related craving, and the severity of withdrawal symptoms.

I prefer the language of self-agency because it is the one that translates best into efforts to prevent, treat, and overcome addiction. Perhaps one day discoveries unearthed by brain science will oblige me to reconsider, and talking about addiction in the idiom of neurobiology will be more fruitful in the clinical domain. But for now, people like me must engage a patient in a consideration of himself—his anxieties and aspirations—not his brain.

It’s worth reading the whole thing. She does a good job articulating the arguments against the disease model, which are worth knowing if you have any interest in defending it.

What I find especially ironic is that she works in a methadone clinic. First, if there’s not a brain disease, why is preventing withdrawal important? Why not just detox them? Second, she’s concerned about the disempowering effects of the disease model but works in a methadone clinic? It may work for some, but as long as we’re using anecdotes, I hear from scores of methadone recipients who describe it as slavery.

Lemonick’s response is here.