Marijuana Dependence and Legalization

Making best guesses about pot.

One essential question about state marijuana legalization continues to dog the debate:  Namely, as marijuana becomes gradually legal, how do we estimate how many people will become dependent? How can we estimate the number of cannabis users who will become addicted under legalization, and who otherwise would not have succumbed?

Back in 2011, neuroscientist Michael Taffe of the Scripps Research Institute in San Diego, writing on the blog TL neuro, referenced this common question, noting that “the specific estimate of dependence rate will quite likely vary depending on what is used as the population of interest… Obviously, changing the size of the underlying population is going to change the estimated rate….”

But change it how, and by how much? The truth is, we don’t know. We can’t know in advance. There are sound arguments for both positions: Legal marijuana will lead to increased rates of cannabis addiction because of lower price and greater availability. On the other hand, almost everybody likely to become addicted to marijuana has probably already been exposed to it, including teens.

What we can start attempting to find out with greater rigor, however, is this: How many chronically addicted marijuana users are out there right now?

In The Pathophysiology of Addiction  by George Koob, Denise Kandel, and Nora Volkow (2008), the base rate of cannabis dependence was estimated to be 10.3% for male users and 8.7% for female users. Their data came from the National Survey on Drug Use and Health, and the rate is similar to common estimates for prescription stimulant addiction. The dependence rate for cigarettes is at least three times as high. However, an overall dependence rate of 9.7%, when men and women smokers are combined, is the origin of the highly contested figure of 10%.

Since then, other databases have been tapped for estimates of existing cannabis dependence. In October of 2013, using the Global Burden of Disease database maintained by the World Bank, British and Australian researchers, along with collaborators at the University of Washington in the U.S., published revised estimates in the open-access journal PLOS ONE, based on numbers from 2010.  The scientists culled and pooled a series of epidemiological estimates and concluded that roughly 11 million cases of cannabis dependence existed worldwide in 1990, compared to 13 million cases in 2010. This boost can be accounted for in part by population increases.

Are these dependent users distributed evenly across the globe? They are not. The PLOS ONE paper demonstrates that marijuana use is markedly more prevalent in certain regions: “Levels of cannabis dependence were significantly higher in a number of high income countries including Australia, New Zealand, the United States, Canada, and a number of Western European countries including the United Kingdom.” High income equals high marijuana usage and dependence—“Cannabis dependence in Australasia was about 8 times higher than prevalence in Sub-Saharan Africa West.” But there may be major holes in the epidemiological database: “This is particularly the case for low income countries, where there is typically limited information on use occurring, even less on levels of use, and usually no data on prevalence of dependence.”

In conclusion, the researchers found an age and sex-standardized cannabis addiction prevalence of 0.2%. “Prevalence was not estimated to have changed significantly from 1990, although increased population size produced an increase in the number of cases of cannabis dependence over the period.”

In another 2008 study, this one published in the Journal of Clinical Psychiatry, scientists at Columbia University and the New York State Psychiatric Institute looked at a set of 2,613 frequent cannabis users, using the development of significant withdrawal symptoms as the leading indicator. About 44% of regular dope smokers experienced two or more cannabis withdrawal symptoms, while about 35% reported three or more symptoms. The most prevalent symptoms in this study were fatigue, weakness, anxiety, and depressed mood. “Over two-thirds smoked more than 1 joint/day on days they smoked during their period of heaviest use; mean joints smoked/day was 3.9. About one-fifth had primary major depression….”

Age of onset was not predictive of withdrawal symptoms in this large study. The investigators suggest that “irritability and anxiety may receive great clinical consensus as regular features of cannabis withdrawal because they are subjectively and clinically striking compared to fatigue and related symptoms.” The researchers also speculate that somatic symptoms of weakness and fatigue might be attributed to varying levels of THC, compared to the presence of other cannabinoids such as CBD. The study is further evidence supporting an “association of primary panic disorder or major depression with cannabis depression/anxiety withdrawal symptoms,” suggesting a “possible common vulnerability, meriting further investigation.”

One of the reasons this matters is because of the very tight relationship between marijuana addiction and major depressive disorder. A 2008 study of young adults in the journal Addictive Behaviors  found that participants with comorbid cannabis dependence and major depressive disorder, the most commonly dependence symptom was withdrawal, reported by more than 90% of the subjects in the study. 73% of the subjects experienced four symptoms or more. After that, the most common symptoms were irritability (an underreported but significant behavioral problem), restlessness, anxiety, and a variety of somatic symptoms, including gastrointestinal problems, loss of appetite, and sleep disturbances, including night sweats and vivid dreaming. The authors, affiliated with University of Pittsburgh School of Medicine, concur with the conclusion of earlier researchers:  “Given the weight of evidence now supporting the clinical significance of a cannabis withdrawal syndrome, the burden of proof must rest with those who would exclude the syndrome….”

Clearly, cannabis does not contribute to the world disease burden in the same way that alcohol, nicotine, and opiods do. However, it’s fair to say that for a minority of users, cannabis dependence causes disabilities and liabilities that are not always trivial.

Mark A. R. Kleiman, a Professor of Public Policy at UCLA and a consultant to the state of Washington on marijuana legalization, told PBS:

The couple of million who stay stoned all day, every day, account for the vast bulk of the total marijuana consumed, and thus the total revenues of the illicit marijuana industry. That's typical. The money in any drug, including alcohol, is in the addicts, not the casual users. There was a big fuss during the 80s about how much casual middle-class drug use there was and how respectable folks were supporting the markets. It's certainly true that most people who are illicit drug users are employed, stable respectable citizens. But it doesn't follow that if we could get the employed, stable respectable citizens to stop using illicit drugs, the problem would mostly go away.

Tips For Dating a Person in 12 Step Recovery

Would you let your daughter go out with an addict?

In the title of her book, Girlfriend of Bill, author Karen Nagy riffs on the time-honored public code for mutual AA recognition: “Are you a friend of [AA co-founder] Bill?” Nagy says she was unable to find any material written “specifically for someone who is new to such a relationship or who is thinking about dating someone in recovery.” So she wrote one, and the publishing arm of Hazelden brought it out. People in Hazelden-style recovery (Nagy calls them “PIRs”) can present challenges, since, as Nagy learned by dating several of them, stopping drinking or using is not necessarily the end of the matter.

Readers should know that the book is written from the perspective of a member of Al-Anon, who is also a firm believer in the 12 Steps. But if dating people who participate in AA or NA is not your thing, than Nagy suggests dating people from SMART recovery, Secular Organizations for Sobriety, church, mental health peer support programs, therapy groups, and so on. Her own experience, however, appears mainly limited to men in and out of 12-Step recovery programs.

While the controversial disease model of addiction continues to provoke heated debate, Nagy discovered that “knowing addiction is a disease has helped me to confront and get over my past prejudices about alcoholics and drug addicts, and to better understand why they might think, act, and react the way they do.”

“Change is tough for all of us,” says Nagy, “but it can be especially hard for an addict” because of the strong tendency to rationalize and resist needed change. Addicts, she adds, “are also known for ‘wanting it now,’ a trait that could be related to their brain chemistry and addictive cravings.” (Or, as non-practicing addict Carrie Fisher memorably put it, “instant gratification takes too long.”)

Her summation of the notion behind the AA/NA concept of a higher power is a common one these days: “Some might call their Higher Power God; others might define it as nature, the positive energy of their group, or an unnamed sense of spirit.” While that may sound naïve to some, what the addict must grasp is that white-knuckle notions of triumph through personal will may have to be abandoned along the way, if we are talking about chronic, active addiction. And she correctly points out that the AA Big Book is “written in an old-fashioned style that hearkens back to the 1930s,” when the amateur self-help group known as AA was founded.

It’s easy to forget that there are common experiences that most recovering addicts are heir to. “We who care about a Person in Recovery are also powerless over alcohol and drugs,” Nagy writes. “Try as we might—we can’t control whether or not the PIR uses them.” And non-addicts who are dating them might usefully be forewarned about such things, Nagy believes. In addition, “It can take months for an addict’s body to adjust to abstinence,” she writes. “Aches and pains are common in withdrawal, and so are digestive problems that can include constipation, diarrhea, and loss of appetite… sleep disorders can be a huge problem….”

Nagy also tips boyfriends and girlfriends to the widening and primarily generational dispute over the use of medications for craving or associated mental health disorders. “Believing ‘a drug is a drug is a drug,’ many old-timers in recovery resist taking medications, whereas younger People in Recovery are more open to taking them if they need them.”

Addicts new to recovery may be coming off a period of social isolation, and a sense of being cut off from others. Nagy advises that a summary knowledge of the 12 Steps can be helpful, in particular the business about “making amends” to people one has harmed. Forgiveness is a touchy and ongoing bit of business. It never hurts to say you’re sorry, if in fact you are. Or to say it again.

Perhaps the single most common complaint takes the form of jealousy or irritation: Why is the Person in Recovery spending so much time with those other people, rather than with me? Aren’t I “supportive” enough? Nagy views the essence of AA/NA as a “spirituality of companionship—friends accompanying friends, helping, sharing, daring, celebrating, or grieving.” In the end, Nagy believes, “it’s not about religion; it’s about connection.”

Does Strong Marijuana Cause Addiction?

Strong pot matters, but maybe not the way we think.

Colorado, Washington, and some 20 additional states have now made various provisions for legal transactions involving marijuana. And since time immemorial, there has been an illegal market for marijuana. But try getting your hands on some marijuana straightforwardly, through appropriate channels, for purposes of medical research, and, well, most researchers have just said forget it.

Because in the U.S., a bizarre system of drug classification has led to the ludicrous situation of a virtual government monopoly on cannabis for experimental purposes. Can’t researchers just walk around this roadblock and procure pot in some manner that is legal in their state? No, they cannot—not if they want any serious research grants, or publication in refereed journals. Without the federal government imprimatur, marijuana research isn’t kosher, and could put researchers at legal risk. Researchers who go through channels report frequent and unpredictable delays, and this has been true for decades. Yet millions of recreational marijuana users can secure a supply of the drug, often accompanied by specific genetic information, often with relatively little effort.

The Drug Enforcement Administration (DEA) has refused to budge on its opposition to petitions for reclassification of cannabis. A recent Washington Post article  attributed the problem to “stigma associated with the drug, lack of funding and legal issues…. Scientists say they are frustrated that the federal government has not made any efforts to speed the process of research.”

However, as almost everyone knows, things are different in The Netherlands. It isn’t a big problem for researchers at the University of Amsterdam and elsewhere in that country to engage in behavioral studies of actual marijuana smokers. Participants in a recent study, the results of which appear in Addiction, were even allowed to use their own weed. (Thanks to Ivan Oransky for bringing this study to my attention.) The thesis being tested by Peggy van der Pol and colleagues is a familiar one: Do marijuana smokers “titrate” very strong pot—that is, do they modify their smoking/dosing behavior accordingly, in order to reduce overall THC exposure? If so, just because a cannabis user is ingesting high-THC plant material doesn’t mean that his or her THC blood levels are that much higher than smokers of less potent weed. But if this is NOT true—if smokers of strong pot are boosting their THC exposure significantly, the results could conceivably include impaired driving and greater rates of marijuana addiction.

Most studies that attempt to estimate the risk of cannabis dependence in pot smokers rely on a familiar yardstick—the number of days a smoker smokes per month. Dosing behavior, and other behavioral aspects of marijuana smoking that affect THC exposure, are usually ignored. The Dutch researchers found that, in a group of 600 frequent cannabis users, some smokers did in fact show “shorter puff duration and inhaled lower smoke volumes when joints with a higher THC concentration were used.” So, yes, users did engage in partial titration when they smoked stronger marijuana. However, this did not translate into the expected results. In a final sample of 98 participants, the scientists discovered that “users of stronger cannabis generally used larger amounts of cannabis to prepare their regular joint.” (The study participants smoked marijuana European-style, mixing their marijuana with tobacco.) And even though subjects smoking joints with higher THC levels did inhale at slightly lower volumes and at a slower pace, the average user of pot with THC levels of 12% or higher definitely inhaled more liters of smoked THC per month than users of less potent pot. But just to confound matters, total THC exposure over a month’s time turned out to be “a weak predictor of dependence severity, and did not remain significant after adjustment for baseline dependence severity.”

Nonetheless, even with some degree of titration, “a positive association between total puff volume and withdrawal/craving was found, indicating that a larger inhaled volume may increase the THC exposure sufficiently to result in significant effects on clinical outcomes.” (Here is the UK National Health Service take on the research.) 

It is always difficult to say for certain in a prospective, cross-sectional study of behavior whether participants are acting the way they would act in “real life,” although efforts were made to allow smoking at home, or in Dutch coffee shops, as well as the laboratory. Interestingly, the one behavior that seemed to predict dependence in post-hoc analyses was a simple one. Smokers were allowed to mix a joint however they wished, and smoke however much of it they wanted to. Smokers who finished their joints, rather than leaving a portion of it for later, were the smokers more likely to be associated with dependence in the follow-up studies. In fact, “percentage of the joint smoked may be a simple proxy for risky smoking behavior.”

In addition, certain withdrawal symptoms correlated with dependence: “Increased somatic withdrawal symptoms are predictive of relapse, and…. increased physical tension is a significant predictor of relapse.”

As with alcohol, it seems that it is not necessarily how much you smoke or drink. It is how you smoke or drink. Strong marijuana doesn't cause addiction. The way certain people use strong pot can result in addiction, however.

Earlier research has shown that higher levels of cannabis dependence are associated with greater functional impairment, and that "the average level of impairment caused by cannabis, while mild for most users, can rise to the level of tobacco withdrawal which is of well established clinical significance.”

 Physical distress, a “somatic” variable, often matters more, in terms of relapse, than the amount of marijuana smoked, or any other symptom on the roster of functional impairments—including mood and other negative affect variables.  In an earlier study published in PLOS ONE,  investigators found that “cannabis withdrawal is clinically significant because it is associated with elevated functional impairment to normal daily activities, and the more severe the withdrawal is, the more severe the functional impairment is. Elevated functional impairment from a cluster of cannabis withdrawal symptoms is associated with relapse in more severely dependent users.”

van der Pol P., Liebregts N., Brunt T., van Amsterdam J., de Graaf R., Korf D.J., van den Brink W. & van Laar M. (2014). Cross-sectional and prospective relation of cannabis potency, dosing and smoking behaviour with cannabis dependence: an ecological study, Addiction,   n/a-n/a. DOI: 10.1111/add.12508

The Escalating Debate Over E-Cigarettes

Follow the bouncing ping-pong ball.

“E-cigarettes are likely to be gateway devices for nicotine addiction among youth, opening up a whole new market for tobacco.”

—Lauren Dutra, postdoctoral fellow at the UCSF Center for Tobacco Control Research and Education.

“You’ve got two camps here: an abstinence-only camp that thinks anything related to tobacco should be outlawed, and those of us who say abstinence has failed, and that we have to take advantage of every opportunity with a reasonable prospect for harm reduction.”

—Richard Carmona, former U.S. Surgeon General, now board member of e-cigarette maker NJOY. 

“Consumers are led to believe that e-cigarettes are a safe alternative to cigarettes, despite the fact that they are addictive, and there is no regulatory oversight ensuring the safety of the ingredients in e-cigarettes.”

—From a letter to the Food and Drug Administration (FDA) signed by 40 state attorneys general.

“E-cigarettes need more time to develop and to out-compete deadly conventional cigarettes, but they have the potential to end the tobacco epidemic. So if regulators decide to ban them or submit them to stricter regulations than conventional cigarettes, this would be detrimental to public health.”

—Professor Peter Hajek, director of the Tobacco Dependence Research Unit at the Wolfson Institute of Preventive Medicine. 

“There is no scientific evidence that e-cigarettes are a safe substitute for traditional cigarettes or an effective smoking cessation tool. In fact, they may entice young people into trying traditional cigarettes.”

—Russ Sciandra, New York State Director of Advocacy, American Cancer Society.

“I firmly believe that the [New York] City Council’s bill restricting e-cigarettes is a major blow to people who are trying to stop smoking and will end up accomplishing the opposite of advocates’ intended goals of improving people’s health and reducing smoking-related deaths.”

—Tony Newman, director of media relations for the Drug Policy Alliance.

“Once a young person gets acquainted with nicotine, it’s more likely that they’ll try other tobacco products. E-cigarettes are a promising growth area for the tobacco companies, allowing them to diversify their addictive and lethal products with a so-called ‘safe cigarette.’”

—Alexander Prokhorov, head of the Tobacco Outreach Education Program, University of Texas.

“What would constitute a final victory in tobacco control? Must victory entail complete abstinence from e-cigarettes as well as tobacco? To what levels must we reduced the prevalence of smoking? What lessons should be drawn from the histories of alcohol and narcotic-drug prohibition?”

—Amy L. Fairchild, professor of sociomedical sciences, Mailman School of Public Health, Columbia University. 

Photo Credit: St. Paul Pioneer Press (Chris Polydoroff).

Hey, Wake Up, It’s Brain Awareness Week

Your brain doesn’t come with an instruction manual.

The Dana Foundation’s annual Brain Awareness Week (BAW), March 10-16, seems particularly appropriate and useful this time around, after a year in which brain-based disease models of human behaviors came under fire from social scientists and neuroscientists alike.

A recent analysis of the coverage of neuroscience in the popular press showed that the number of news articles using the terms "neuroscience" or "neuroscientist" had increased by a factor of 30 between 1985 and 2009. Moreover, the NIH's massive Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative, designed to speed up our understanding of the neural workings of the human brain in the years ahead, is in progress.

Brain Awareness Week, which takes place each year during the third week of March, is the global campaign to increase public awareness about the progress and benefits of brain research. The Federation of European Neuroscience Societies (FENS) administers a BAW grants program for European partners.

During the week, campaign partners around the world organize activities to educate their communities about the brain and brain research. A product of the Dana Alliance for Brain Initiatives, Brain Awareness Week “unites the efforts of partner organizations worldwide in a celebration of the brain for people of all ages. Activities are limited only by the organizers’ imaginations and include open days at neuroscience labs; exhibitions about the brain; lectures on brain-related topics; social media campaigns; displays at libraries and community centers; classroom workshops; and more.”

In league with hundreds of governmental and private partner institutions around the world, BAW’s enormous calendar of events testifies to the success of this outreach. The week kicks off with an interview with Kelley Remole, Ph.D., the director of neuroscience outreach at Columbia University and the co-president of the Greater NYC Chapter of the Society for Neuroscience. 

Here you will find a pile of publications and resources.

And here is a bunch of downloadable brain stuff for kids.

Six Writers Who Battled the Bottle

Book review.

In The Trip to Echo Spring: On Writers and Drinking, author Olivia Laing’s stated goal is “to know why writers drink, and what effect this stew of spirits has had upon the body of literature itself.” To which I can only say, best of luck. The goal is impossibly ambitious; the book itself a bit digressive and loosely organized. But Laing has harvested a satisfying litany of literary anecdotes related to drinking, and throws out a few of her own.

The writers she submits to scrutiny are F. Scott Fitzgerald, Ernest Hemingway, Tennessee Williams, John Cheever, John Berryman, and Raymond Carver—all of them unambiguously alcoholic and, for most of their lives, resolutely in denial. Only two of them—Carver and Cheever—attained some measure of sobriety in their later lives. Fitzgerald died of a heart attack at 44, Hemingway and Berryman committed suicide, and Tennessee Williams either choked on a bottle cap or died of an overdose of pills. If any of that sounds deliciously romantic, than this is a book you need to read. “People don’t like to talk about alcohol,” Laing flatly states. “They don’t like to think about it, except in the most superficial of ways. They don’t like to examine the damage it does and I don’t blame them.”

Start with John Cheever, author of The Wapshot Chronicle, Bullet Park, The Falconer, and short stories, including “The Swimmer,” which begins: “It was one of those mid-summer Sundays when everyone sits around saying, ‘I drank too much last night.’”

“I cannot remember my meanness,” Cheever wrote poignantly, “because my recollections are damaged by alcohol.” It may have been literally true. Cheever suffered from aphasia, hallucinations, and seizures.  On the basis of a CAT scan from 1975, Laing makes the argument that Cheever suffered from diffuse cerebral atrophy, and possible Korsakoff syndrome, a neurological disorder seen almost exclusively in alcoholics.

Tennessee Williams, Pulitzer Prize-winning author of plays such as A Streetcar Named Desire and The Night of the Iguana, also suffered a litany of medical problems directly related to alcohol, including peripheral neuritis in his feet. “Of course I would love to believe the good doctor,” Williams wrote, “but I don’t quite believe him.”

The title of Laing’s book comes from Tennessee Williams’s Cat on a Hot Tin Roof, in which Brick, the alcoholic son, frequently takes “a little short trip to Echo Spring,” referring to the liquor cabinet containing his favorite brain of bourbon. But awareness has a way of creeping in around the edges. In an early story that foreshadowed the play, the character of Brick says, “A man that drinks is two people, one grabbing the bottle, the other one fighting him off it, not one but two people fighting each other to get control of a bottle.” 

Williams endured years of psychoanalysis and spent time in mental hospitals. He dutifully kept detailed notebooks: “Two Scotches at bar. 3 drinks in morning. A daiquiri at Dirty Dick’s, 3 glasses of red wine at lunch and 3 of wine at dinner—Also two Seconals so far, and a green tranquilizer whose name I do not know and a yellow one I think is called reserpine or something like that.” Now think of making it through a single day under that load of intoxicants.

F. Scott Fitzgerald, best known for his novel The Great Gatsby, wrote to his editor, Maxwell Perkins, in 1934: “I have drunk too much and that is certainly slowing me up. On the other hand, without drink I do not know whether I could have survived this time.” Laing notes that this ambivalence “could be interpreted as a refusal to see alcohol as a cause rather than a symptom of his troubles,” and in this Fitzgerald was by no means alone. For Fitzgerald, as for many others of the day, being “on the wagon” often meant restricting oneself to beer and the occasional glass of champagne. Fitzgerald, on the wagon at the rate of 30 beers a day, said that “when I swell up I switch to cokes.”

Laing provides us with a litany of these “excuse notes” from her writers: “I drink because it improves my work. I drink because I am too sensitive to live in the world without it. There are hundreds more of these,” she writes. In Ernest Hemingway’s A Moveable Feast, she finds “an example of someone flat-out denying their own disease….” My own personal favorite is Hemingway’s letter in which he claims to be amazed and chagrined that alcohol, something “I could not have lived without many times; or at least would have cared to live without; was a straight poison to Scott instead of a food.”

John Berryman, poet, Pulitzer Prize Winner, National Book Award winner, and author of The Dream Songs, also battled depression and a tendency to fall down stairs, breaking arms, legs, and wrists. He served a stint as a creative writing instructor at the University of Iowa writing program, as would John Cheever and Raymond Carver. He ended up at the University of Minnesota, where he dried out repeatedly at Hazelden and other local clinics. Even Berryman’s most ardent supporters gave up on him. His chairman at the university said of him: “I concluded that the only John one could love was a John with 2 or 3 drinks in him, no more & no less, & such a John could not exist.” Berryman killed himself by jumping off a bridge in Minneapolis.

Let’s let Raymond Carver—poet, short story writer, and legendary drunk— have the last word. In a 1982 poem, he wrote:

And then…something: alcohol—

What you’ve really done

And to someone else, the one

You meant to love from the start.

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/