Calling it ‘brain disease’ makes addiction harder to treat
AT LAST official count, in 2015, over 33,000 people have died from opioid painkillers, heroin, and fentanyl — twice the number killed by guns — and the number of fatalities is rising. Health officials, police chiefs, employers, welfare workers, and politicians at all levels of government are desperately calling for more effective drug treatment, better prevention, smarter opioid prescribing, and improved pain management.
Urgent attention is being devoted to every facet of the epidemic except one: how to think about drug addiction itself. As the opioid crisis deepens, it’s time to examine whether current thinking about addiction limits our understanding of the epidemic and impedes our efforts to contain it.
Within the medical and research communities, the dominant narrative holds that that addiction is a “brain disease.” In a seminal article published 20 years ago in Science, “Drug Addiction is a Brain Disease and it Matters,” Alan Leshner, then director of the National Institute on Drug Abuse, or NIDA, proclaimed that addiction was a brain disease on the ground that “addiction is tied to changes in brain structure and function.”
Before Leshner and his NIDA colleagues designated addiction a disease of the brain — meaning that addiction is fundamentally a drug-induced disorder of disrupted brain function — doctors and much of the public regarded addiction as a vague sort of “disease” that manifested as an uncontrollable drive to use drugs or alcohol. Leshner coined a durable metaphor, writing that drugs “hijack” the brain’s motivational and reward circuitry thereby making the condition involuntary. The brain disease model of addiction soon became orthodoxy in academic and research circles, which are heavily dependent on NIDA funding for training and research, and was also adopted by politicians, drug czars, public health officials, and the treatment industry. “Addiction is a chronic disease of the brain,” then-Surgeon General Vivek Murthy asserted in a report last year, “and it’s one that we have to treat the way we would any other chronic illness: with skill, with compassion and with urgency.” This idea has by now filtered into mass culture. “Opioid Addiction Is a Brain Disease, Not a Moral Failing — and We Have to Stop Looking At It That Way,” declares a headline from a popular fashion and beauty magazine.
The formulation’s appeal is obvious: It is tidy. It signifies medical gravitas and neuroscientific sophistication. It also implies that suffers should not be subject to social stigma — another benevolent aim — even though most research shows that this kind of reframing is unlikely to reduce the public’s aversion to addicted individuals.
For its part, NIDA had high hopes that neuroscience would led to better treatments. “Groundbreaking discoveries about the brain [are] enabling us to respond effectively to the problem,” proclaimed Nora Volkow, who succeeded Leshner as head of NIDA in 2003. The truth, to date, is much less exhilarating. No new important biological treatments or medications for addiction have emerged since addiction was officially labeled a brain disease by NIDA. And the useful medications we do have — methadone (1939), buprenorphine (1966), the overdose “antidote” naloxone (1960), and the opioid blocker naltrexone (1963) — were all developed before the ascent of addiction neuroscience.
By making the brain the seat of addiction, its champions at NIDA hoped to elicit more funding from Congress for research and treatment. Laudable aims, to be sure, but they’re rooted in the dubious assumption that neurobiology is destiny. The “brain [of an addicted person] is no longer able to produce something needed for our functioning and that healthy people take for granted, free will,” Volkow claimed.
To be sure, neural circuits involved in motivation, pleasure, and impulsivity are altered in the course of addiction. Genes, too, play a role in how the brain reacts to short and long-term exposure to drugs, and the strength of such innate influence differs among individuals, making some more vulnerable to developing drug problems.
Yet although biological changes constrain some of the choices that addicts make, in no way do those changes preclude the capacity to make important decisions. That is why President Obama’s drug czar, Michael Botticelli, himself a former alcoholic, was able to change his behavior despite the alterations his brain had undergone. Back in 1988, he was charged with drunk driving on the Massachusetts Turnpike; a judge gave him the choice of going to jail or participating in a treatment program. Botticelli made a decision: He went to a church basement for help, joined Alcoholics Anonymous, and quit drinking. Yet on CBS’s “60 Minutes,” Botticelli contradicted the significance of his own story when he drew an analogy between having cancer and being addicted. “We don’t expect people with cancer to stop having cancer,” he said.
Botticelli’s analogy doesn’t work. No amount of reward or punishment can alter the course of, say, brain cancer. It is an entirely autonomous biological condition. Imagine threatening to impose a penalty on a brain cancer victim if her vision or speech continued to worsen or to offer of $1 million if she could stay well. It wouldn’t matter.
Addiction, by comparison, is a complex set of activities whose course can be altered when the user confronts foreseeable consequences. A vast research literature on contingency management intervention, familiar to psychologists for decades, bears out this claim: rewards, such as gift cards or movie tickets for clean urine screens improve outcomes. (NIDA actually supports contingency management research — not nearly as much as it should, mind you — and in doing so betrays something of a split between its misbegotten messaging and its duty to fund useful clinical research.)
Clearly, people who are addicted have some capacity for control, but why do they exercise it at certain times but not at others? The answer is the context in which the addict finds herself. How available is the drug, for example? How hopeless or isolated is she? Are there opportunities for help? Can she envision a more meaningful life and see a way to attain it? What are her reasons for using, and what will happen if she continues? Even the intensity of craving and the distress of opioid withdrawal can be modulated by her expectations of these experiences.
A swirl of circumstances surrounds the addicted individual. And when even a few of them change, quitting and recovery can look more attractive and achievable to her. That may happen spontaneously in the face of new rewards, say, when a new relationship comes along or a child is born, or new threats in the form of a spouse threatening to leave, for example. These shifting dynamics can motivate the addict to quit on her own, contrary to assertions that addicts cannot just stop. Still, many cannot quit unaided; in that case, treatment can become the necessary catalyst to help her deploy her intrinsic capacity for choice and control.
This contextual alchemy gets lost when the brain looms so large in the explanation of addiction. And when the brain takes center stage, medical approaches assume greater promise than they actually have.
Consider the story of buprenorphine, or “bupe.” Like methadone, bupe (trade name: Suboxone) is an opioid and so can prevent withdrawal and blunt cravings. It can also produce euphoria in high enough doses. Unlike methadone, however, bupe’s chemical structure makes it less dangerous if taken in excess. Thus, bupe can be prescribed out of a doctor’s office — methadone cannot — as long as the doctor has passed an eight-hour test.
NIDA promoted buprenorphine as a medication that primary care doctors could use to treat heavy opioid addiction. More precisely, it could help reverse the brain changes of addiction, and therefore resolve the addict’s problem. But it turned out that many busy primary care doctors were not up to the time-consuming job of treating complicated patients. Early in their treatment, patients need close monitoring along with counseling, and observed urine collection. Bupe simply can’t be administered like antibiotics or blood pressure pills. The evidence? By 2015, buprenorphine became the third most diverted prescription opioid in the country: patients abuse it and sell it. In many prisons, bupe is both abused by inmates and used for barter; all the medication originally dispensed by well-meaning doctors to patients who divert it. Now bupe mega-clinics, resembling notorious pill mills, are cropping up in some states. These developments are giving buprenorphine a bad name, which is a shame, because it can be enormously helpful when administered properly to motivated individuals.
Another problem with a heavily biological perspective is that it undervalues the powerful social and psychological engines of addiction. The much-publicized “deaths of despair” among poorly educated, low-income white Americans attest poignantly to this reality. Volumes of social science research confirm that addiction breeds in communities where opportunities are scarce, pessimism is rife, and drug use is normalized. Still, one need not hail from a Rust Belt town that is “hemorrhaging jobs and hope,” as in J.D. Vance’s “Hillbilly Elegy,” to seek a good numbing agent.
No matter how wealthy they might be, people discover that opioids are an excellent short-term balm for existential maladies like self-loathing, emptiness, erosion of purpose, and isolation. Years of heavy use condition people to desire drugs at the first stab of distress. After so much time spent damaging themselves, their families, and their futures, a new layer of anguish has formed over the original bedrock of misery, urging onward the cycle of misery-and-relief. Surely, people don’t chose to be addicts, but that is not what they are choosing: what they want is relief.
That people use drugs for reasons — a notion the brain disease model can’t accommodate — helps explain why people are so ambivalent about giving up opioids, why they drop out of treatment at high rates, and why many don’t even take advantage of treatment when it is offered. The link between psychic pain and addiction explains why some people are more vulnerable to abusing opioid prescriptions than others, contrary to the popular trope that we are all at risk.
Meanwhile, those who advance a brain disease model are left to explain persistent drug use in purely biological terms, pointing to dopamine surges in the reward circuitry that underlie drug cravings and to damage induced in brain regions important to self-control. To be sure, biology is involved, but it is only one part of the story, and often not the most important. Perhaps we should think about addiction as a symptom of pre-existing problems, not a distinct disease in its own right.
The unidimensional brain disease model has not delivered on its therapeutic promises because its explanatory reach is too limited. What good, then, can come of abandoning a strictly neuroscientific view of addiction? For one, we would view addiction as a set of behaviors powered by multiple intersecting causes across several dimensions — biological, psychological, social, and cultural. For any given user at any given time, one or several of these factors may be more or less influential.
A more nuanced view would also expose the false choice that experts often put to us — namely, that addiction is a disease and not a moral matter. Granted, this rhetoric is intended to shift attitudes toward compassion and treatment over blame and punishment. This is a worthy goal, to be certain. But the price of shaming us into to endorsing “disease” (or “brain disease”) lest we pick the palpably offensive alterative — “moral failing” — is the loss of crucial knowledge about addiction.
What we need to know is this: Addicted individuals have the capacity to make choices. The most effective treatment programs for addiction rely not on medications alone, but on sanctions and incentives to shape more healthy behaviors. Engagement in treatment is key to recovery, because the longer a patient remains, the better he or she fares.
In light of the marked ambivalence that besets so many users, any intervention that sways their decision to remain in care is constructive. Methods include, for example, the creative use of incentives in treatment programs, and diversion programs within the criminal justice system. Anti-addiction medication may sometimes be necessary to stabilize patients while they embark on the ambitious journey of rebuilding themselves, their relationships, and their futures.
There is little that NIDA can do for those “dying of a broken heart,” as President Bill Clinton described white Americans who lack diplomas and face diminished life expectancies. That kind of renewal is a daunting cultural project. At the very least, however, NIDA should stop promoting rhetoric that needlessly narrows our thinking about addiction.
In grim tandem, the currency of the brain disease model grew alongside the opioid epidemic. Flawed thinking about addiction by no means caused the problem, but a neurocentric orientation obscures vital truths. For one, it downplays the fact that addicts retain the capacity for choice. The brain disease model also fosters an unrealistic medication campaign. Lastly, it distracts us from the crucial reality that excessive drug use serves a psychological function, no matter how self-destructive it is.
If there’s a dark gift of the drug epidemic, it’s that we are forced to become more thoughtful about why we have one.
Dr. Sally Satel is a resident scholar at the American Enterprise Institute. She works, part time, in a methadone clinic in Washington DC. Scott O. Lilienfeld is the Samuel Candler Dobbs Professor of Psychology at Emory University.