New Study Casts Doubt on Current "Despair" Models of Addiction

The recent Hari/Hart/Lewis hypothesis that addiction is not primarily metabolic or genetic, but rather the result of "despair" or "sociological conditions" or "flawed learning," takes a major hit in a new report appearing in The National Bureau of Economic Research. The study suggests that "changes in economic conditions account for less than one-tenth of the rise in drug and opioid-involved mortality rates." 

Jason Schwartz at Addiction & Recovery News does a deep dive into the flawed thinking behind the new (old?) sociological views of addiction here.

Drug Craving, or How to Be Your Own Worst Enemy

Plus the disease model, warts and all.

Bielefeld, Germany—

The second in an irregular series of posts about a recent conference, Neuroplasticity in Substance Addiction and Recovery: From Genes to Culture and Back Again. The conference, held at the Center for Interdisciplinary Research (ZiF) at Bielefeld University, drew neuroscientists, historians, psychologists, philosophers, and even a freelance science journalist or two, coming in from Germany, the U.S., The Netherlands, the UK, Finland, France, Italy, Australia, and elsewhere. The organizing idea was to focus on how changes in the brain impact addiction and recovery, and what that says about the interaction of genes and culture. The conference co-organizers were Jason Clark and Saskia Nagel of the Institute of Cognitive Science at the University of Osnabrück, Germany.  Part One is here.

Marc Lewis, a developmental neuroscientist who is currently professor of human development and applied psychology at Radboud University in The Netherlands, and who spent five days discussing addiction with the Dalai Lama and a small group of scientists, scholars, and addiction specialists in Dharamsala, India, last year, was a late but welcome addition to the speaker list at the conference.

Author of Memoirs of an Addicted Brain, and a self-confessed “drug addict turned neuroscientist,” Dr. Lewis always brings a thought-provoking dual perspective to his work on addiction. (See my review of his book here.) He also blogs here.

In Bielefeld, Dr. Lewis offered up a wide-ranging view of what addiction is and is not, linking neuroscience, psychology, and Buddhism in the process. 

Craving is “the one condition all addicts agree is their worst enemy,” Lewis said. “This is one place where science and subjectivity have to come together. Scientists need to focus on this, because addicts are completely unanimous about it. This is the enemy. It’s not physical withdrawal symptoms, it’s not relief. It is craving.”

Buddhism teaches that “craving is the fundamental engine of personality development,” Lewis said. “It’s what keeps us going around and around.” But if you don’t much like the notion of the wheel of reincarnation, Lewis suggested, then you can contemplate “the cyclical nature of how we repeat patterns in life that lead to suffering.”

“Craving is such an unpleasant state, that after a while, you end up doing it, you get the drugs. I did opiates, and I would spend hours and hours trying to sit on my hands, trying to watch something on TV, trying to go for a walk, and finally, there’s this thing that keeps rising in the background, and it doesn’t go away. It was a constantly growing tension, an anxiety and discomfort, that came from very deep down. You spend most of your energy trying to hold this thing at bay, and according to the ego depletion literature, you can’t do that for very long. These cognitive control centers just give up. They are limited resources.”

Craving is not a steady state. It grows. “Neuroscience helps us understanding why craving is so nasty.” Enter “delay discounting,” a term from behavioral economics used by several speakers during the conference. Delay discounting is the proposition that the perceived value of something rises steeply as the reward gets closer in time. A variation of this idea is seen in the classic marshmallow test for children: One marshmallow now, or two if you wait until later?

“Craving traps you in delay discounting,” said Lewis. “Immediate reward is worth more than imagined future happiness. The job of dopamine in the striatum is to increase the attractiveness or value of one goal, and to reduce the attractiveness and value of all the other goals. This is a brain that is well designed for addiction. You get tons of dopamine rising up in anticipation of reward. So you’re really stuck in the immediate. At which point you’ve effectively lost contact with the rest of your life. In the narrative of who you are, you can’t even include next week, or the next morning.”

Nonetheless, Lewis finds serious problems with the standard disease model of addiction, as championed by NIDA’s Nora Volkow and other in the NIH, however brain-based he may be. As a developmental neuroscientist, Lewis is predisposed to viewing the brain as a locus of change by definition. “The disease model uses brain change as a foundational premise. But brains change with development, anyway. And in fact, brains are designed to change.”

Any proper model of addiction, he insisted, has to correspond with what we know about brain change. “But it also has to correspond with addicts’ experiences. I was a drug addict from about age 25 to 30. I was in really bad shape. And now I talk with a lot of drug addicts, and one of the things that I keep hearing is that scientists and clinicians don’t really know what they’re doing—they don’t know where to go with it. They know that addiction is really nasty, but they don’t know what it’s like, unless they’ve been there.”

Lewis offered a view of addiction that shifts the semantic focus from disease to development. The drug is not the culprit. By reconceptualizing addiction as a developmental disorder, he suggested, we can move the debate forward into the world, where the action is:

Addiction results from accelerated learning, the acquisition of thought patterns that rapidly self-perpetuate because of the brain’s tendency to become sensitized to highly attractive rewards. This is a developmental process, accelerated by a neurochemical feedback loop that is particular to strong attractions. Like other developmental outcomes, addiction isn’t easy to reverse, because it’s based on synaptic restructuring. Like other developmental outcomes, it arises from neural plasticity, and uses it up at the same time.

And the mechanisms responsible are the same ones responsible for many things that involve desire, learning, reward seeking, and compulsive behavior—including the so-called behavioral addictions like overeating and compulsive sex. However, “the severe consequences of addiction don’t make it a disease, any more than the consequences of violence make violence a disease.”

In an email exchange after the conference, I followed up with Dr. Lewis on some of these matters, and he sent me the following additional thoughts on the “diseasing” of addiction:

Proponents of the disease model argue that addiction changes the brain. And they're right: it does. But the brain changes anyway, at every level, from gene expression, to cell density, to the size and shape of the cortex itself. Of course, neuroscientists who subscribe to the disease model must know that brains change over development. Their take on pathological brain change would have to be very specific in order to be convincing. For example, they would have to show that the kind (or extent or location) of brain change characteristic of addiction is nothing like that observed in normal learning and development. But this they cannot do. The kind of brain changes seen in addiction also show up when people take up rock collecting, fall in love, learn how to cook, or become obsessed with their appearance. The brain contains only a few major traffic routes for learning and goal seeking. And, like the main streets of a busy city, they are often under construction.  Brain disease may be a useful metaphor for how addiction seems, but it's not a valid explanation for how it actually works.