THE BLOG
07/02/2015 02:11 pm ET Updated Jul 02, 2016

Addiction Is Not a Brain Disease, and That's Good News

In a recent article in HuffPost, Nora Volkow argued that addiction is a brain disease. She has been making this point forcefully for years, based on evidence that brain structure and function change with addiction, presumably as a consequence of drug use. The "disease model" is the currently accepted definition of addiction, endorsed by the mainstream medical, scientific, and treatment communities. And by governmental and institutional policy-makers. And by the families of addicts, who use its logic to usher their loved ones into residential rehabs. The disease model is enormously influential. And, as the director of NIDA (National Institute on Drug Abuse) and a renowned neuroscientist herself, Dr. Volkow is one of its most powerful advocates.

Yet not everyone agrees with her.

The comments following Dr. Volkow's post indicate a very different perspective, converging among nonbiologists: addiction isn't caused by drugs but by stress or trauma in early life, social exclusion or alienation in adolescence or adulthood, or the thwarting of life goals, such as reduced employment opportunities, e.g., for minorities. From this perspective, calling addiction a disease that requires medical care not only erodes individual empowerment -- often seen as the lynch-pin of recovery -- but justifies a rehab industry with dismal success rates and astronomical costs.

So the question of how to define addiction has become a heated debate; but it's more than just a semantic issue: It's a springboard to radically different approaches to treatment and prevention. Yet it's a debate that cannot be resolved by the butting of heads between humanists and neuroscientists. They don't speak the same language. The disease model thrives on biological data. It can only be dislodged when its biological foundations are shown to be flawed. My new book is The Biology of Desire: Why Addiction is Not a Disease, and that's what it sets out to do:

Like the general public, most of those arguing against the disease model assume that "brain change" automatically implies a disease process; then they change the subject. Others tune out (or get mad) when the brain is even mentioned in regard to addiction, because they assume that a neuroscientific description will somehow replace a more psychological or humanistic perspective, rather than complement it...

Whether we construe addiction as a disease, a choice, a complex sociocultural process, self-medication, or a string of bad-hair days, we only have one brain, and it's central to everything we do, everything we are. So a very important question is simply this: what does the brain do in addiction?

But before trying to answer that question, we need to understand how brains change normally. In fact, brains are supposed to change. Brain change--or neuroplasticity--is the fundamental mechanism by which infants grow into toddlers, who grow into children, who grow into adults, who continue to grow...Brain change is necessary for language acquisition and impulse control in early childhood, and for learning to drive a car, play a musical instrument, or appreciate opera later in life...

Of course, neuroscientists who subscribe to the disease model must know that brains change with learning and development. So they must view the brain change that accompanies addiction as extreme or pathological. In fact, they would have to show exactly that in order to be convincing. They would have to show that the kind (or extent or location) of brain change characteristic of addiction is nothing like what we see in normal learning and development, or even in the more extreme transitions people go through when they fall in love or have children. But that's where they step onto thin ice. The kind of brain changes seen in addiction [e.g., surges of dopamine in the regions highlighted by Volkow] also show up when people become absorbed in a sport, join a political movement, or become obsessed with their sweetheart or their kids. The brain contains only a few major traffic routes for goal seeking. Like the main streets of a busy city, the same routes get dug up and paved over time and time again, no matter who's in charge.

My book includes detailed biographical portraits of five people as they make their way from severe addiction to lasting recovery. These stories are combined with depictions of the brain changes that, science tells us, must have been going on simultaneously. But I also confront the question most often sidestepped by those who oppose the disease model: how does addictive learning differ from other learning? What makes it so hard to quit?

We know that synaptic patterns get reinforced with each repetition of the same kind of experience, whether it's playing the piano, baking bread, or smoking crack. And we know that repetition boosted by strong motivation is the strongest driver of synaptic shaping. Every time desire initiates another run for drugs, drink, porn, or gambling, it refines the network of synapses that anchor the addiction. So imagine the potency of a longed-for reward that only lasts a few hours. In its wake it leaves loss, disappointment, and often depression. Then desire naturally flares again, in the form of longing or craving, and the cycle is very likely to repeat itself.

In this way, addictions are based on false advertising. The striatum [or nucleus accumbens -- the goal-pursuit region of the brain] responds with eager anticipation to the glitter bestowed by our wishes and fantasies. But the high is never as good as promised and, worse, it doesn't last. For Brian, it was sparkling crystals of methamphetamine in a brimming pipe--tipping toward exhaustion. For Johnny, a glass of rum crackling around ice cubes--then the fadeout to unconsciousness... With these and other addictions, enjoyment fades quickly as drugs wear off, drinking sedates, the money's spent, or sexual pyrotechnics become boring. And then...there it is again, calling to us, a few hours later or the following day. Fragments of reward are tasted repeatedly, followed each time by loss and renewed craving. With the flame of desire rekindled so often, the same neural passages get dredged again and again. The result is accelerated learning.

The disease model of addiction has made its contribution, but it's time to move on. We don't have to ignore the biology of addiction to appreciate its psychology and to approach those who suffer humanistically rather than moralistically. So I end my book with a new approach to intervention, built on neuroscientific knowledge but also sifted through the first-hand experience of how addiction feels. Biology can bring us back to the most intimate insights about who we are and how we change.