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Nora D. Volkow

Director, National Institute on Drug Abuse

It’s Not About Getting High: What Neuroscience Teaches Us About Addiction

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This editorial appears in the addictions issue of National Council Magazine.

By: Nora D. Volkow, Director, National Institute on Drug Abuse

Those on the front lines who study and address behavioral health have struggled for decades to remove the stigma that persists around mental illness and addictive disorders. In the addiction field, this has meant trying to educate the public that addiction is a multifaceted brain disease. One that transforms the world for a person with addiction into an environment of drug-related cues, inflicts painful punishment for not seeking and using the drug and, perhaps most importantly, reduces the ability to exert free choice over the impulse to take drugs.

It is difficult for people without addictions to understand that people with addictions are not just seeking to “get high” but suffer a medically rooted impairment in their autonomy that thwarts their best intentions to attain freedom from drugs. Despite the fact that for 20 years
addiction science has revealed vividly that this is the case, the stigma remains a major obstacle.

We have long understood that the euphoria of drug intoxication involves the neurotransmitter dopamine flooding the reward (pleasure) circuits in the brain’s limbic regions (specifically the nucleus accumbens and the dorsal striatum). But this acute intoxication (or binge) phase is just one part of the cycle of addiction. Recent advances in neuroimaging and genetics have given us deeper insight into changes across many other brain regions that characterize phases of the
addiction cycle, including the extreme suffering of withdrawal and the mental preoccupation that characterizes cravings. We now also have a clear understanding of how drug use compromises the brain circuits necessary to exert self-control or willpower over drug use.

In addition to the extreme “pull” of the drug caused by its direct or indirect effects on the reward circuits during intoxication, there is a “push” caused by another set of adaptations to circuitry in the basal forebrain areas known as the extended amygdala. These changes produce the highly stressful or even intolerable state of withdrawal. A person who has progressed from abuse to addiction no longer takes the drug to feel the euphoria of dopamine flooding the pleasure centers but to escape the stress of withdrawal. These separate systems of reward and what my colleague, National Institute on Alcohol Abuse and Alcoholism Director George Koob, calls “anti-reward” conspire to create an ensemble of physical need for the drug simply to
feel normal or functional, if only briefly.

In fact, because the addicted brain adapts to the recurring presence of the drug by reducing the number of dopamine receptors in the reward pathway, “reward” itself becomes so blunted that the drug no longer causes pleasure as much as it creates relief. Thus, the idea that people with addictions take drugs to “get high” (which implies euphoria) is extremely misleading. They take drugs mainly to stop feeling low.

If this were the whole story—that addicted people suffer in the absence of the drug—they still might be able to exert willpower to resist taking it because they understand the harm it is causing and are able to focus on the larger goal of well-being. This is the faulty assumption behind the stigma surrounding substance use disorders: Addicted people may suffer, but their drug use is still a choice and if they are resolute enough, they can refuse that choice.

Unfortunately, it is not that simple. We now know that the push/pull of withdrawal and relief involving the brain’s limbic regions are only part of a bigger story involving powerful learning mechanisms and changes to circuits in the prefrontal cortex that are necessary for exerting such choice. Over time, learned associations between the relief provided by drugs and various environmental cues transform an addicted person’s world into a landscape of cues and triggers. Everything reminds them of the drug or of its absence. This makes it difficult or impossible to stop thinking about the drug and how or when to obtain it next. Equally insidious are the changes to the person’s willpower capacity.

We now know that the dopamine desensitization that dulls the reward circuits’ sensitivity to pleasure also affects prefrontal circuits that are necessary to exert self-control. Impaired dopamine signaling in the prefrontal cortex seriously weakens the person’s ability to resist urges and follow through with decisions, including the decision to stop taking the drug. As a result of these processes, the world of an addicted person could be compared to a cunningly designed video-game environment. Challenges to sobriety are around every corner and the person is forced to navigate the environment using a game controller with buttons that are unresponsive or stuck, often steering the gameworld avatar in precisely the direction the player does not wish to go.

However, the result is far more devastating and consequential than any video game. Most people with addictions, in my experience, do not wish to use drugs. Because of the numerous troubles their addictions have caused, they consciously avoid drugs and the cues that lead them to drug use. But they repeatedly find themselves acting against their best intentions in the all-too-familiar cycle of relapse.

The good news is that addiction is not an inevitable outcome of drug use or even drug abuse. Many interacting genetic, environmental and developmental factors contribute to a person’s risk for developing an addiction. Addiction only affects a subset of people who try or use drugs, even in the most vulnerable years of adolescence. We also know from brain imaging that, in time, it is possible to at least partially restore the affected brain circuitry, including the normal density of dopamine receptors and the function of prefrontal brain regions. Preventing relapse during recovery may require behavioral interventions as well as medications. People with opioid use disorders may require agonist or partial agonist medications like methadone or buprenorphine to control withdrawal and cravings or antagonists like extended-release naltrexone to prevent intoxication from occurring. Naltrexone and other drugs can be used to treat alcohol use disorders and medications also exist for nicotine addiction.

Over the coming years, our increasingly clear picture of the brain mechanisms underlying disordered drug use and the transition to addiction will lead to new medications and improved treatment and prevention approaches. Because our society places so much value on freedom, many people still have trouble accepting that a medical condition could erode something as basic as a person’s ability to act freely in their own best interest. The very nature of addiction challenges society’s deeply held preconceptions about willpower and self-control. Thus, delivering effective treatments to those in need will require us to do a better job educating the public and policymakers that addiction is not a moral failing; it is a disease in which essential motivational and self-control systems of the brain are compromised. Medical intervention, not punishment or moral re-education, is required to restore this essential human birthright.

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