Why Addiction is NOT a Brain Disease

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Addiction to substances (e.g., booze, drugs, cigarettes) and behaviors (e.g., eating, sex, gambling) is an enormous problem, seriously affecting something like 40% of individuals in the Western world. Attempts to define addiction in concrete scientific terms have been highly controversial and are becoming increasingly politicized. What IS addiction? We as scientists need to know what it is, if we are to have any hope of helping to alleviate it.

There are three main definitional categories for addiction: a disease, a matter of choice, and self-medication. There is some overlap among these meta-models, but each has unique implications for treatment, from the level of government policy to that of available options for individual sufferers.

The dominant party line in the U.S. and Canada is that addiction is a brain disease. For example, according to the National Institute on Drug Abuse (NIDA), “Addiction is defined as a chronic, relapsing brain disease that is characterized by compulsive drug seeking and use, despite harmful consequences.” In this post, I want to challenge that idea based on our knowledge of normal brain change and development.

Why many professionals define addiction as a disease.

The idea that addiction is a type of disease or disorder has a lot of adherents. This should not be surprising, as the loudest and strongest voices in the definitional wars come from the medical community. Doctors rely on categories to understand people’s problems, even problems of the mind. Every mental and emotional problem fits a medical label, from borderline personality disorder to autism to depression to addiction. These conditions are described as tightly as possible, and listed in the DSM (Diagnostic and Statistical Manual of Mental Disorders) and the ICD (International Classification of Diseases) for anyone to read.

I won’t try to summarize all the terms and concepts used to define addiction as a disease, but Steven Hyman, M.D., previous director of NIMH and Provost of Harvard University, does a good job of it. His argument, which reflects the view of the medical community more generally (e.g., NIMH, NIDA, the American Medical Association), is that addiction is a condition that changes the way the brain works, just like diabetes changes the way the pancreas works. Nora Volkow M.D. (the director of NIDA) agrees. Going back to the NIDA site, “Brain-imaging studies from drug-addicted individuals show physical changes in areas of the brain that are critical for judgment, decisionmaking, learning and memory, and behavior control.” Specifically, the dopamine system is altered so that only the substance of choice is capable of triggering dopamine release to the nucleus accumbens (NAC), also referred to as the ventral striatum, while other potential rewards do so less and less. The NAC is responsible for goal-directed behaviour and for the motivation to pursue goals.

Different theories propose different roles for dopamine in the NAC. For some, dopamine means pleasure. If only drugs or alcohol can give you pleasure, then of course you will continue to take them. For others, dopamine means attraction. Berridge’s theory (which has a great deal of empirical support) claims that cues related to the object of addiction become “sensitized,” so they greatly increase dopamine and therefore attraction — which turns to craving when the goal is not immediately available. But pretty much all the major theories agree that dopamine metabolism is altered by addiction, and that’s why it counts as a disease. The brain is part of the body, after all.

What’s wrong with this definition?

It’s accurate in some ways. It accounts for the neurobiology of addiction better than the “choice” model and other contenders. It explains the helplessness addicts feel: they are in the grip of a disease, and so they can’t get better by themselves. It also helps alleviate guilt, shame, and blame, and it gets people on track to seek treatment. Moreover, addiction is indeed like a disease, and a good metaphor and a good model may not be so different.

What it doesn’t explain is spontaneous recovery. True, you get spontaneous recovery with medical diseases…but not very often, especially with serious ones. Yet many if not most addicts get better by themselves, without medically prescribed treatment, without going to AA or NA, and often after leaving inadequate treatment programs and getting more creative with their personal issues. For example, alcoholics (which can be defined in various ways) recover “naturally” (independent of treatment) at a rate of 50-80% depending on your choice of statistics (but see this link for a good example). For many of these individuals, recovery is best described as a developmental process — a change in their motivation to obtain the substance of choice, a change in their capacity to control their thoughts and feelings, and/or a change in contextual (e.g., social, economic) factors that get them to work hard at overcoming their addiction. In fact, most people beat addiction by working really hard at it. If only we could say the same about medical diseases!

The problem with the disease model from a brain’s-eye view.

According to a standard undergraduate text: “Although we tend to think of regions of the brain as having fixed functions, the brain is plastic: neural tissue has the capacity to adapt to the world by changing how its functions are organized…the connections among neurons in a given functional system are constantly changing in response to experience (Kolb, B., & Whishaw, I.Q. [2011] An introduction to brain and behaviour. New York: Worth). To get a bit more specific, every experience that has potent emotional content changes the NAC and its uptake of dopamine. Yet we wouldn’t want to call the excitement you get from the love of your life, or your fifth visit to Paris, a disease. The NAC is highly plastic. It has to be, so that we can pursue different rewards as we develop, right through childhood to the rest of the lifespan. In fact, each highly rewarding experience builds its own network of synapses in and around the NAC, and that network sends a signal to the midbrain: I’m anticipating x, so send up some dopamine, right now! That’s the case with romantic love, Paris, and heroin. During and after each of these experiences, that network of synapses gets strengthened: so the “specialization” of dopamine uptake is further increased. London just doesn’t do it for you anymore. It’s got to be Paris. Pot, wine, music…they don’t turn your crank so much; but cocaine sure does. Physical changes in the brain are its only way to learn, to remember, and to develop. But we wouldn’t want to call learning a disease.

So how well does the disease model fit the phenomenon of addiction? How do we know which urges, attractions, and desires are to be labeled “disease” and which are to be considered aspects of normal brain functioning? There would have to be a line in the sand somewhere. Not just the amount of dopamine released, not just the degree of specificity in what you find rewarding: these are continuous variables. They don’t lend themselves to two (qualitatively) different states: disease and non-disease.

In my view, addiction (whether to drugs, food, gambling, or whatever) doesn’t fit a specific physiological category. Rather, I see addiction as an extreme form of normality, if one can say such a thing. Perhaps more precisely: an extreme form of learning. No doubt addiction is a frightening, often horrible, state to endure, whether in oneself or in one’s loved ones. But that doesn’t make it a disease.

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