Drugs and Disease: A Look Forward

First published 2/18/2014.

Former National Institute on Drug Abuse (NIDA) director Alan Leshner has been vilified by many for referring to addiction as a chronic, relapsing “brain disease.” What often goes unmentioned is Leshner’s far more interesting characterization of addiction as the “quintessential biobehavioral disorder.”

Multifactorial illnesses present special challenges to our way of thinking about disease. Addiction and other biopsychosocial disorders often show symptoms at odds with disease, as people generally understand it. For patients and medical professionals alike, questions about the disease aspect of addiction tie into larger fears about the medicalization of human behavior.

These confusions are mostly understandable. Everybody knows what cancer is—a disease of the cells. Schizophrenia? Some kind of brain illness. But addiction? Addiction strikes many people as too much a part of the world, impacted too strongly by environment, culture, behavior, psychology, to qualify. But many diseases have these additional components. In the end, the meaning of addiction matters less than the physiological facts of addiction.

One of the attractions of medical models of addiction is that there is such an extensive set of data supporting that alignment. Specifically, as set down in a famous paper by National Institute of Drug Abuse director Nora Volkow and co-author Joanna Fowler: “Understanding the changes in the brain which occur in the transition from normal to addictive behavior has major implications in public health…. We postulate that intermittent dopaminergic activation of reward circuits secondary to drug self-administration leads to dysfunction of the orbitofrontal cortex via the striato-thalamo-orbitofrontal circuit.” This cascade of events is often referred to as the “hijacking” of the brain by addictive drugs, but nothing is really being hijacked. Rather, the abusive use of drugs changes the brain, and that should come as no surprise, since almost everything we do in the world has the potential of changing the brain in some way. “Why are we so surprised that when you take a poison a thousand times, it makes some changes in your head?” said the former director of a chemical dependency treatment program at the University of Minnesota. “It makes sense that [addictive drugs] change things.”

Critics like Fernando Vidal object to a perceived shift from “having a brain” to “being a brain.” He is saying that he cannot see the point of “privileging” the brain as a locus for the study of human behavior. In “Addiction and the Brain-Disease Fallacy,” which appeared in Frontiers in Psychiatry, Sally Satel and Scott Lillienfeld write that “the brain disease model obscures the dimension of choice in addiction, the capacity to respond to incentives, and also the essential fact people use drugs for reasons (as consistent with a self-medication hypothesis).”

An excellent example of the excesses of the anti-brain discussions is an article by Rachel Hammer of Mayo Clinic and colleagues, in the American Journal of Bioethics-Neuroscience. “Many believed that a disease diagnosis diminishes moral judgment while reinforcing the imperative that the sick persons take responsibility for their condition and seek treatment.” But only a few paragraphs later, the authors admit: “Scholars have theorized that addiction-as-disease finds favor among recovering addicts because it provides a narrative that allows the person simultaneously to own and yet disown deviant acts while addicted.” Furthermore: “Addiction reframed as a pathology of the weak-brained (or weak-gened) bears just as must potential for wielding stigma and creating marginalized populations." But again, the risk of this potentially damaging new form of stigma “was not a view held by the majority of our addicted participants…”

And so on. The anti-disease model authors seem not to care that addicted individuals are often immensely helped by, and hugely grateful for, disease conceptions of their disorder, even though Hammer is willing to admit that the disease conception has “benefits for addicts’ internal climates.” In fact, it often helps addicts establish a healthier internal mental climate, in which they can more reasonably contemplate treatment. Historian David Courtwright, writing in BioSocieties, says that the most obvious reason for this conundrum is that “the brain disease model has so far failed to yield much practical therapeutic value.” The disease paradigm has not greatly increased the amount of “actionable etiology” available to medical and public health practitioners. “Clinicians have acquired some drugs, such as Wellbutrin and Chantix for smokers, Campral for alcoholics or buprenorphine for heroin addicts, but no magic bullets.” Physicians and health workers are “stuck in therapeutic limbo,” Courtwright believes.

“If the brain disease model ever yields a pharmacotherapy that curbs craving, or a vaccine that blocks drug euphoria, as some researchers hope,” Courtwright says, “we should expect the rapid medicalization of the field. Under those dramatically cost-effective circumstances, politicians and police would be more willing to surrender authority to physicians.” The drug-abuse field is characterized by, “at best, incomplete and contested medicalization.” That certainly seems to be true. If we are still contesting whether the brain has anything essential to do with addiction, then yes, almost everything about the field remains “incomplete and contested.”

Sociologists Nikolas Rose and Joelle M. Abi-Rached, in their book Neuro, take the field of sociology to task for its “often unarticulated conception of human beings as sense making creatures, shaped by webs of signification that are culturally and historically variable and embedded in social institutions that owe nothing substantial to biology.”

And for those worried about problems with addicts in the legal system, specifically, over issues of free will, genetic determinism, criminal culpability, and the “diseasing” of everything, Rose and Abi-Rached bring good news: “Probabilistic arguments, to the effect that persons of type A, or with condition B, are in general more likely to commit act X, or fail to commit act Y, hold little or no sway in the process of determining guilt.” And this seems unlikely to change in the likely future, despite the growing numbers of books and magazine articles saying that it will.

Opponents of the disease model of addiction and other mental disorders are shocked, absolutely shocked, at the proliferation of “neuro” this and “neuro” that, particularly in the fields of advertising and self-improvement, where neurotrainers and neuroenhancing potions are the talk of the moment. Sociologists claim to see some new and sinister configuration of personhood, where a journalist might just see a pile of cheesy advertising and a bunch of fast-talking science hucksters maneuvering for another shot at the main chance. When has selling snake oil ever been out of fashion?

For harm reductionists, addiction is sometimes viewed as a learning disorder. This semantic construction seems to hold out the possibility of learning to drink or use drugs moderately after using them addictively. The fact that some non-alcoholics drink too much and ought to cut back, just as some recreational drug users need to ease up, is certainly a public health issue—but one that is distinct in almost every way from the issue of biochemical addiction. By concentrating on the fuzziest part of the spectrum, where problem drinking merges into alcoholism, we’ve introduced fuzzy thinking with regard to at least some of the existing addiction research base. And that doesn’t help anybody find common ground.

Graphics Credit: http://www.docslide.com/disease-model/

Addicts and Disease

Commentary.

Former National Institute on Drug Abuse (NIDA) director Alan Leshner has been vilified by many for referring to addiction as a chronic, relapsing “brain disease.” What often goes unmentioned is Leshner’s far more interesting characterization of addiction as the “quintessential biobehavioral disorder.”

Multifactorial illnesses present special challenges to our way of thinking about disease. Addiction and other biopsychosocial disorders often show symptoms at odds with disease, as people generally understand it. For patients and medical professionals alike, questions about the disease aspect of addiction tie into larger fears about the medicalization of human behavior.

These confusions are mostly understandable. Everybody knows what cancer is—a disease of the cells. Schizophrenia? Some kind of brain illness. But addiction? Addiction strikes many people as too much a part of the world, impacted too strongly by environment, culture, behavior, psychology, to qualify. But many diseases have these additional components. In the end, the meaning of addiction matters less than the physiological facts of addiction.

One of the attractions of medical models of addiction is that there is such an extensive set of data supporting that alignment. Specifically, as set down in a famous paper by National Institute of Drug Abuse director Nora Volkow and co-author Joanna Fowler: “Understanding the changes in the brain which occur in the transition from normal to addictive behavior has major implications in public health…. We postulate that intermittent dopaminergic activation of reward circuits secondary to drug self-administration leads to dysfunction of the orbitofrontal cortex via the striato-thalamo-orbitofrontal circuit.” This cascade of events is often referred to as the “hijacking” of the brain by addictive drugs, but nothing is really being hijacked. Rather, the abusive use of drugs changes the brain, and that should come as no surprise, since almost everything we do in the world has the potential of changing the brain in some way. “Why are we so surprised that when you take a poison a thousand times, it makes some changes in your head?” said the former director of a chemical dependency treatment program at the University of Minnesota. “It makes sense that [addictive drugs] change things.”

Critics like Fernando Vidal object to a perceived shift from “having a brain” to “being a brain.” He is saying that he cannot see the point of “privileging” the brain as a locus for the study of human behavior. In “Addiction and the Brain-Disease Fallacy,” which appeared in Frontiers in Psychiatry, Sally Satel and Scott Lillienfeld write that “the brain disease model obscure the dimension of choice in addiction, the capacity to respond to incentives, and also the essential fact people use drugs for reasons (as consistent with a self-medication hypothesis).”

An excellent example of the excesses of the anti-brain discussions is an article by Rachel Hammer of Mayo Clinic and colleagues, in the American Journal of Bioethics-Neuroscience. “Many believed that a disease diagnosis diminishes moral judgment while reinforcing the imperative that the sick persons take responsibility for their condition and seek treatment.” But only a few paragraphs later, the authors admit: “Scholars have theorized that addiction-as-disease finds favor among recovering addicts because it provides a narrative that allows the person simultaneously to own and yet disown deviant acts while addicted.” Furthermore: “Addiction reframed as a pathology of the weak-brained (or weak-gened) bears just as must potential for wielding stigma and creating marginalized populations." But again, the risk of this potentially damaging new form of stigma “was not a view held by the majority of our addicted participants…”

And so on. The anti-disease model authors seem not to care that addicted individuals are often immensely helped by, and hugely grateful for, disease conceptions of their disorder, even though Hammer is willing to admit that the disease conception has “benefits for addicts’ internal climates.” In fact, it often helps addicts establish a healthier internal mental climate, in which they can more reasonably contemplate treatment. Historian David Courtwright, writing in BioSocieties, says that the most obvious reason for this conundrum is that “the brain disease model has so far failed to yield much practical therapeutic value.” The disease paradigm has not greatly increased the amount of “actionable etiology” available to medical and public health practitioners. “Clinicians have acquired some drugs, such as Wellbutrin and Chantix for smokers, Campral for alcoholics or buprenorphine for heroin addicts, but no magic bullets.” Physicians and health workers are “stuck in therapeutic limbo,” Courtwright believes.

“If the brain disease model ever yields a pharmacotherapy that curbs craving, or a vaccine that blocks drug euphoria, as some researchers hope,” Courtwright says, “we should expect the rapid medicalization of the field. Under those dramatically cost-effective circumstances, politicians and police would be more willing to surrender authority to physicians.” The drug-abuse field is characterized by, “at best, incomplete and contested medicalization.” That certainly seems to be true. If we are still contesting whether the brain has anything essential to do with addiction, then yes, almost everything about the field remains “incomplete and contested.”

Sociologists Nikolas Rose and Joelle M. Abi-Rached, in their book Neuro, take the field of sociology to task for its “often unarticulated conception of human beings as sense making creatures, shaped by webs of signification that are culturally and historically variable and embedded in social institutions that owe nothing substantial to biology.”

And for those worried about problems with addicts in the legal system, specifically, over issues of free will, genetic determinism, criminal culpability, and the “diseasing” of everything, Rose and Abi-Rached bring good news: “Probabilistic arguments, to the effect that persons of type A, or with condition B, are in general more likely to commit act X, or fail to commit act Y, hold little or no sway in the process of determining guilt.” And this seems unlikely to change in the likely future, despite the growing numbers of books and magazine articles saying that it will.

Opponents of the disease model of addiction and other mental disorders are shocked, absolutely shocked, at the proliferation of “neuro” this and “neuro” that, particularly in the fields of advertising and self-improvement, where neurotrainers and neuroenhancing potions are the talk of the moment. Sociologists claim to see some new and sinister configuration of personhood, where a journalist might just see a pile of cheesy advertising and a bunch of fast-talking science hucksters maneuvering for another shot at the main chance. When has selling snake oil ever been out of fashion?

For harm reductionists, addiction is sometimes viewed as a learning disorder. This semantic construction seems to hold out the possibility of learning to drink or use drugs moderately after using them addictively. The fact that some non-alcoholics drink too much and ought to cut back, just as some recreational drug users need to ease up, is certainly a public health issue—but one that is distinct in almost every way from the issue of biochemical addiction. By concentrating on the fuzziest part of the spectrum, where problem drinking merges into alcoholism, we’ve introduced fuzzy thinking with regard to at least some of the existing addiction research base. And that doesn’t help anybody find common ground.

Graphics Credit: http://www.docslide.com/disease-model/

Does Brain Research Obscure Addiction’s Root Causes?

Did Dickens Get It Right?

Breathe the polluted air, foul with every impurity that is poisonous to health and life; and have every sense, conferred upon our race for its delight and happiness, offended, sickened and disgusted, and made a channel by which misery and death alone can enter. Vainly attempt to think of any simple plant, or flower, or wholesome weed, that, set in this foetid bed, could have its natural growth, or put its little leaves forth to the sun as God designed it. And then, calling up some ghastly child, with stunted form and wicked face, hold forth on its unnatural sinfulness, and lament its being, so early, far away from Heaven—but think a little of its having been conceived, and born, and bred, in Hell!

That’s how Charles Dickens chose to put the generational question, in his 1848 novel, Dombey and Son. Poverty and bad mothering (there was hardly any fathering) stunted a child’s “natural” inclinations toward normalcy and love. As the reed is bent, and so on. It is a forceful and memorable literary case for the debilitating effects of childhood deprivation, illness, and trauma. And quite timely, given the ongoing backlash against the “disease model” of addictions and mental illnesses. Did Dickens have it right, more than 150 years ago? Has the research associated with the disease model—the brain breakthroughs, the MRI scans, and the neurotransmitter studies—all been giant detours away from root causes?

You would think so, listening to the cacophony of voices seeking to discredit the notion of addictions and mental illnesses as medical diseases. Medical and psychiatric opinion appear to be revolving away from a strict study of mechanisms of the brain, and back toward the study of society and the environment as root causes of conditions like schizophrenia and drug addiction.

Assuming that we avoid the drastic road of looking beyond the brain entirely for addiction causes—which would represent a true return to the past—what seems to be called for is some sort of “third way” of threading between the determinism of DNA and the fuzzy humanism surrounding the question of social causation, even as many researchers and commentators have become frustrated with the pace of new drug discovery for treating addictive disease, and are threatening to throw out the baby with the bathwater.

Recently, during a lively dinner in Amsterdam, I raised some of these questions with neuroscientist Marc Lewis, Professor of Human Development and Applied Psychology at Radboud University in Nijmegen, The Netherlands, and author of Memoirs of an Addicted Brain: A Neuroscientist Examines his Former Life on Drugs.

“Addictive drugs convert the brain to recognize only one face of God, to thrill to only one suitor,” Lewis wrote in that excellent book. Dopamine becomes “specialized, stilted, inaccessible through the ordinary pleasures and pursuits of life, but gushing suddenly when anything associated with the drug comes into awareness…. I wish this were just an exercise in biological reductionism, or neuro-scientific chauvinism, but it’s not. It’s the way things really work.”

Nonetheless, even Dr. Lewis is unhappy with the idea of calling drug addiction a “disease.” But why? Dopamine, says Lewis, is about craving and attraction, and not just about pleasure. There is too much going on with addictive behavior to fit neatly into the disease category, Lewis believes. Lewis doesn’t argue that brain structure is not causal—much of his book is devoted to proving that it is—but rather that the early brain, in the first two years of life, is so malleable that parent-child experiences shape the style of that young brain, so to speak. “There must be neural correlates to addiction,” he said, “ but this can occur in early childhood, and not from innate genetics.”

This idea has sweeping ramifications. It suggests that a person could become a drug addict entirely independent of his or her inborn genetic predilections. It suggests that a biological propensity for addiction may not need to be innate in order for the disorder to develop. The neurobiological preconditions may develop in early childhood, or even in the womb, and an individual’s basic chromosomal endowment may not be as predictive or protective as we have previously concluded.

I am not yet convinced on this point. Certainly there is evidence that addicted people have often had traumatic childhoods. Or, as we now refer to them: ACEs, or adverse childhood experiences. But should we be spotlighting parents and social setting, as we did for most of the 20th Century, or should we be paying attention to the disordered central nervous system, with associated behavioral traits such as impulsivity, low harm avoidance, and difficulty imaging future consequences, that characterize the behavior and cause much of the frustration in dealing with chronically “bad” children?

The Third Way could well be epigenetics, defined as the study of how gene expression can be modified without making direct changes to the DNA. Writing in Science News, Tina Hesman Saey explains that "epigenetic mechanisms alter how cells use genes but don't change the DNA code in the genes themselves.... The ultimate effect is to finely tune to what degree a gene is turned on or off. Often the fine tuning is long-lasting, setting the level of a gene's activity for the lifetime of the cell."  From a scientific point of view, epigenetics opened the door for a new way of thinking about addiction.

 An addict, as Lewis told me, “is like a starving animal.” You cannot talk that animal out of stalking it prey. However, Lewis believes it is time to do away with the dominant role that the chase for specific genes has played in addiction science. The endeavor resembles a classic needle-in-the-haystack kind of search, and is unlikely to come up with something simple but significant. Lewis believes that in many cases “womb trauma and infant trauma during the first two years” is sufficient to create the innate biological architecture responsible for addiction. Is this true in every case? The research pictures strongly suggests that it isn’t—sorry, Dr. Maté. It seems clear that some people are hardwired for addiction in a way that transcends family environment and social circumstances. We have all heard of the perfect young man or woman, with every advantage, and a loving home life, who succumbs, mysteriously, to the lure of addictive drugs.

We also discussed an article Lewis wrote for Perspectives on Psychological Science, called “Dopamine and the Neural Now,” in which he argues that “the disease-versus-choice debate creates a false dichotomy: Neuroscience does not have to frame addiction as a disease. Rather, it can help explain how addicts make impulsive choices in the moment and distort appraisal and decision-making habits in the long run…. repeated dopamine enhancement modifies brain structures to maximize the appeal of addictive activities, minimize the appeal of competing rewards, and undermine the cognitive capacities necessary to choose between them. I conclude that addiction is not a monolithic state but a recurrent series of choices that permit negotiation, and sometimes cooperation, between immediate and long-range goals.”

Despite the growing popularity of ACE hypotheses for explaining addiction, Lewis insists that addiction is neither a disease of choice nor a genetic imperative. In some ways, it is a meta-disease, calling into question, as all “mental” illnesses do, the very notions of personhood and autonomy. But a Third Way of thinking about addiction; one that incorporates both the innate propensities of our genetic endowment and the many ways early experience can shape the expression of our DNA, may help draw the addiction field out of the “either/or” thinking that continues to shape many of the debates.

 As Saey wrote in Science News: “Such findings suggest that medicines that interrupt or reverse epigenetic changes… could one day prevent or cure addiction." Drugs to treat drug addiction are going to be a central feature of future addiction research, no matter how we rejuggle the relationship between nature and nurture.

Graphics Credit: http://news4geeks.net/

Ivan Oransky on the Disease Model at TEDMED 2012

What we think about when we think about “disease.”

It’s a safe bet that the number of M.D.s who have made a mid-career switch to journalism is rather small. And when Dr. Ivan Oransky did it, he didn’t go in for half measures. The former online editor of Scientific American, and the former deputy editor of The Scientist, Oransky now serves as Executive Editor of Reuters Health. He teaches medical journalism at New York University, where he also holds an appointment as clinical assistant professor of medicine—while maintaining three, yes three, separate blogs. He is well known for two innovative blogs known as Retraction Watch and Embargo Watch. And he recently kicked off a personal blog, the Oransky Journal.

So clearly, he’s a very lazy man. Nonetheless, he found time to give a very popular talk on the shortcomings of the disease model of medicine at last week’s TEDMED conference in Washington, D.C. And he found additional time to grant me an interview afterwards, with some interesting thoughts on how the mania for medicalization could affect addiction treatment.

Speaking at the Kennedy Center for the Performing Arts, Oransky compared patients in the nation’s current medical system to baseball coach Billy Beane, a once-promising player who washed out in the minors and was recently portrayed by Brad Pitt in the movie Moneyball. “Our medical system is just as bad at predicting what’s happening to patients as baseball scouts were at predicting what would happen to Billy Beane,” Oransky told the audience of 1,500.

“Every day, thousands of people across the country are diagnosed with pre-conditions,” he said. “We hear about pre-hypertension, we hear about pre-dementia and pre-anxiety. We also refer to sub-clinical conditions, like sub-clinical hardening of the arteries. One of my favorites is called sub-clinical acne. If you look up their website as I did, you’ll see that they say this is the easiest acne to treat. You don’t have any pustules or inflammation—you don’t actually have acne.  I have a name for preconditions—I call them preposterous.”

Every year, according to Oransky, “we are spending more than two trillion dollars on health care," and yet more than 100,000 people a year are dying from complications of the treatments they're getting, rather than from the conditions that are being treated. [Revised 4-15]. And most patient advocacy groups eventually learn to “expand the number of people who are eligible for a given treatment” for fundraising purposes, he said.

As evidence of this trend toward medicalization, Oransky pointed to the novel notion of a “previvor.” According to FORCE, the cancer research advocacy group that coined the term: "A previvor is a survivor of a predisposition to cancer.” The term is used to describe someone who, for example, has a genetic risk for breast cancer, but has not been diagnosed with the disease. “Previvor was coined in 2000 after a challenge from a community member who said she ‘needed a label,’” according to the group’s web site.

We are all previvors of some disorder, Oransky argues. In the spirit of giving everyone a precondition, Oransky coined the term “pre-death.” What is pre-death? “Every single one of you has it,” Oransky told the audience, “because you have the risk factor for it, which is being alive."

Using his favorite metaphor—baseball—Oransky explained the secret of Billy Beane’s revolutionary success as a coach: “The secret wasn’t to swing at every pitch, like the sluggers do. You had to find the guys who liked to walk, because getting on base by a walk is just as good. And in our health care system, we need to figure out, ‘is that really a good pitch, or do we need to let it go by, and not swing at everything?’ We all need to keep in mind that in medicine, sometimes less is more.”

After his talk, I asked Oransky how the theme of medicalization might apply to the disease of addiction. Medicalization, he said, is a matter of “taking advantage of people, manipulating them so they can’t make informed decisions.” In the case of addiction treatment, Oransky pointed to the “proliferation of ads for treatment in beautiful places. It’s all selling and self-diagnosis. They’re selling you on the fact that you need to be treated.” He also pointedly referred to the practice of “medical astro-turfing,” where a supposedly grass roots effort by patients or advocates is “usurped by interest group pressure.” Sometimes that usurpation is patently obvious, is in the case of many advocacy groups set in motion and funded by pharmaceutical companies or the liquor industry.

Sometimes, of course, you do need to be treated. And Oransky notes that in health areas such as addiction and mental illness—disorders where social stigma remains high, compared to, say, a blood infection—there are “fewer pressures to medicalize.” And possibly, too few pressures to medicalize. “There’s no quick and easy test, no MRI where you can point to the place in the brain that lights up and say, “you are an alcoholic.” The science of addiction, which has been moving by fits and starts into the medical mainstream, has a long way to go, compared with many other disease categories. And it has left a gap through which medical workers and treatment staff can march, chanting, “I have a system,” Oransky says.

Perhaps, then, the study of addiction to alcohol and other drugs requires both more medicalization of the research kind, and less of the “precondition” or “sub-clinical” kind. As for the second kind, Oransky believes we are already medicalizing binge drinking in a counterproductive way. In addition, “there are always attempts to widen the market. Look at how obesity has been made to overlap with addiction.” As for medications being used to combat craving among addicts in treatment, Oransky noted the tendency to “repurpose” drugs on the basis of soft data. “They took wellbutrin, an antidepressant that didn’t work very well, and offered it for smoking cessation. So I would want to see data that is really robust” before treating addicts with such medications.

On the other hand, Oransky noted, “We don’t have to worry about malaria, we don’t need to medicalize tuberculosis. But do diseases that have a strong stigma, like addiction, actually benefit from medicalization?  If we find out that they do, than we should do it.”

There’s something else Oransky believes is overdue for true medicalization: “The social determinants of health care—poverty, the way we build our suburban environments. Concentrate on stuff that we know kills people. Medicalize that.”

In the end, he said, “we need to use marketing strategies to effectively get treatment to the people who need it, not to the people who don’t.”

The Disease Model Reconsidered

Historian looks at resistance to the “NIDA paradigm.”

The history of addiction as a brain disease “looks a lot like the history of atoms or germs, insofar as these were older and controversial ideas for which scientific confirmation later became available,” writes historian David Courtwright, author of Forces of Habit: Drugs and the Making of the Modern World.

In a recent issue of the social science journal BioSocieties, Courtwright surveys the history of the disease paradigm of drug addiction, and, in doing so, brings into focus several key dilemmas related to what former National Institute on Drug Abuse (NIDA) director Alan Leshner once characterized as the “quintessential biobehavioral disorder.”

The scientific evidence available to us at present largely supports a statement like Leshner’s. Researchers have documented long-term changes in brain structure and function due to drug abuse, and neuroimaging technologies have resulted in maps of the abnormal neuronal activity addicts exhibit. Courtwright cites the discovery of the endogenous opioid system, the mapping of receptor pathways, and the growing understanding of the mesolimbic dopamine reward pathway as evidence of clinical confirmation of theories about addictive disease that has been floating around in one form or another for many years.

Why then, Courtwright asks, does the medical profession largely stay clear of issues having to do with our law enforcement-driven drug war? Why are clinical professionals not on the front lines of revolt over this issue? “If addiction was beyond the individual’s control, then criminal punishment was as inappropriate as jailing a schizophrenic who wandered into an emergency room,” the author writes.

The most obvious reason for this conundrum, says Courtwright, is that “the brain disease model has so far failed to yield much practical therapeutic value.” The disease paradigm has not greatly increased the amount of “actionable etiology” available to medical and public health practitioners. “Clinicians have acquired some drugs, such as Wellbutrin and Chantix for smokers, Campral for alcoholics or buprenorphine for heroin addicts, but no magic bullets.” Physicians and health workers are “stuck in therapeutic limbo,” Courtwright believes. “The drug-abuse field is characterized by, at best, incomplete and contested medicalization.”

Moreover, unlike the current situation in the case of, say, diabetes or schizophrenia, “at least four important groups continue to wrestle for control of the addiction field.” (Medical personnel, police, social scientists, and political officials.) Social scientists, in particular, are frequently skeptical about the NIDA disease paradigm “as part of a broader post-World War II pattern of resistance against biological explanations of behavior, genetic research and the neo-Darwinian renaissance.”

Social scientists and neuroscientists “still live in their own gated academic communities,” Courtwright alleges. “There is a lot more at stake in the brain disease debate than our understanding of addiction.”

However, these problems do not mean that valuable findings in one area--addictive disease theory--cannot produce innovations in other research fields as well. In fact, such spinoffs happen all the time. Courtwright points to advancements in our understanding of evolution: “Michael Kuhar has argued that, because the brain co-evolved with neurotransmitters, it can usually manage its internal chemistry quite well. But it did not co-evolve with drugs, understood as recently introduced and wholly exogenous super-neurotransmitters that can override the brain’s control mechanisms.”

The author also cites spinoffs in economic studies: “The permanent alteration of neurons and the development of addiction in some, but not all, users also helped explain the commercial and tax appeal of drugs, insofar as they were nondurable goods with relatively inflexible demand curves. Even non-addicted users tended to consume more over time, because of tolerance.”

In the end, it is just possible to contemplate some sort of fusion, or meeting of the minds, over the disease model. As Courtwright speculates, “it may turn out that the tension between the personality and brain disease models is more apparent than real.” He cites as evidence such connections as the fit between impulsive, thrill-seeking behavior and an associated paucity of dopamine D2 and D3 receptors in the midbrain region. The result? Such people “have less inhibition of dopamine, and experience more reward when stimulated by risky behavior.” A nice fit. And the number of nice fits between social science and brain science continues to accumulate.

“If the brain disease model ever yields a pharmacotherapy that curbs craving, or a vaccine that blocks drug euphoria, as some researchers hope,” Courtwright says, “we should expect the rapid medicalization of the field. Under those dramatically cost-effective circumstances, politicians and police would be more willing to surrender authority to physicians.”

Graphics Credit: http://alcoholanddrugabuse.org