Addressing Criticisms of the Disease Model

Volkow, Koob, and McLellan on the neurobiology of addiction.

The New England Journal of Medicine recently published a review article, “Neurobiologic Advances from the Brain Disease Model of Addiction,” authored by three prominent figures in the field of addiction research: Nora Volkow, the director of the National Institute of Drug Abuse (NIDA); George Koob, the director of the National Institute of Alcohol Abuse and Alcoholism (NIAAA); and Thomas McLellan, founder and chairman of the Treatment Research Institute in Philadelphia.  The article summarizes the research that has “increasingly supported the view that addiction is a disease of the brain,” and concludes that “neuroscience continues to support the brain disease model of addiction.”

The implications of this, say the authors, are straightforward: “As is the case in other medical conditions in which voluntary, unhealthful behaviors contribute to disease progression (e.g., heart disease, diabetes, chronic pain, and lung cancer), evidence-based interventions aimed at prevention, along with appropriate health policies, are the most effective ways of changing outcomes.”

And some of the implications are immediate: “A more comprehensive understanding of the brain disease model of addiction many help to moderate some of the moral judgement attached to addictive behaviors and foster more scientific and public health-oriented approaches to prevention and treatment.”

In a supplementary appendix, the authors address some of the common criticisms of the disease model of addiction, and offer counter-arguments. The quotes below are excerpted directly from the appendix.

—Most people with addiction recover without treatment, which is hard to reconcile with the concept of addiction as a chronic disease.

This reflects the fact that the severity of addiction varies, which is clinically significant for it will determine the type and intensity of the intervention. Individuals with a mild to moderate substance use disorder, which corresponds to the majority of cases, might benefit from a brief intervention or recover without treatment whereas most individuals with a severe disorder will require specialized treatment

—Addicted individuals respond to small financial rewards or incentives (contingency management), which is hard to reconcile with the notion that there is loss of control in addiction.

The demonstrated effectiveness of contingency management shows that financial cues and incentives can compete with drug cues and incentives – especially when those financial incentives are significant and relatively immediate; and when control has been simply eroded rather than lost. Contingency management is increasingly being utilized in the management of other medical disorders to incentivize behavioral changes (i.e., compliance with medications, diets, physical activity).

—Gene alleles associated with addiction only weakly predict risk for addiction, which is hard to reconcile with the importance of genetic vulnerabilities in the Brain Disease Model of Addiction.

This phenomenon is typical of complex medical diseases with high heritability rates for which risk alleles predict only a very small percentage of variance in contrast to a much greater influence of environmental factors (i.e., cirrhosis, diabetes, asthma, cardiovascular disease). This reflects, among other things, that the risk alleles mediate the response to the environment; in the case of addiction, the exposures to drugs and stressful environments.

Overlaps in brain abnormalities between people with addiction and control groups raises questions on the role that brain abnormalities have on addiction.

The overlap is likely to reflect the limitation of currently available brain imaging techniques (spatial and temporal resolutions, chemical sensitivity), our limited understanding of how the human brain works, the complexity of the neurobiological changes triggered by drugs and the heterogeneity of substance use disorders.

Treatment benefits associated with the Brain Disease Model of Addiction have not materialized.

Medications are among the most effective interventions for substance use disorders for which they are available (nicotine, alcohol and opiates). Moreover, progress in the approval of new medications for substance use disorders has been slowed by the reluctance of pharmaceutical companies to invest in drug development for addiction.

Benefits to policy have been minimal.

The Brain Disease Model of Addiction provided the basis for patients to be able to receive treatment for their addiction and for insurances to cover for it. This is a monumental advance in health policy. The Brain Disease Model of Addiction also provides key evidence-based science for retaining the drinking age at 21 years.

Drug Craving, or How to Be Your Own Worst Enemy

Plus the disease model, warts and all.

Bielefeld, Germany—

The second in an irregular series of posts about a recent conference, Neuroplasticity in Substance Addiction and Recovery: From Genes to Culture and Back Again. The conference, held at the Center for Interdisciplinary Research (ZiF) at Bielefeld University, drew neuroscientists, historians, psychologists, philosophers, and even a freelance science journalist or two, coming in from Germany, the U.S., The Netherlands, the UK, Finland, France, Italy, Australia, and elsewhere. The organizing idea was to focus on how changes in the brain impact addiction and recovery, and what that says about the interaction of genes and culture. The conference co-organizers were Jason Clark and Saskia Nagel of the Institute of Cognitive Science at the University of Osnabrück, Germany.  Part One is here.

Marc Lewis, a developmental neuroscientist who is currently professor of human development and applied psychology at Radboud University in The Netherlands, and who spent five days discussing addiction with the Dalai Lama and a small group of scientists, scholars, and addiction specialists in Dharamsala, India, last year, was a late but welcome addition to the speaker list at the conference.

Author of Memoirs of an Addicted Brain, and a self-confessed “drug addict turned neuroscientist,” Dr. Lewis always brings a thought-provoking dual perspective to his work on addiction. (See my review of his book here.) He also blogs here.

In Bielefeld, Dr. Lewis offered up a wide-ranging view of what addiction is and is not, linking neuroscience, psychology, and Buddhism in the process. 

Craving is “the one condition all addicts agree is their worst enemy,” Lewis said. “This is one place where science and subjectivity have to come together. Scientists need to focus on this, because addicts are completely unanimous about it. This is the enemy. It’s not physical withdrawal symptoms, it’s not relief. It is craving.”

Buddhism teaches that “craving is the fundamental engine of personality development,” Lewis said. “It’s what keeps us going around and around.” But if you don’t much like the notion of the wheel of reincarnation, Lewis suggested, then you can contemplate “the cyclical nature of how we repeat patterns in life that lead to suffering.”

“Craving is such an unpleasant state, that after a while, you end up doing it, you get the drugs. I did opiates, and I would spend hours and hours trying to sit on my hands, trying to watch something on TV, trying to go for a walk, and finally, there’s this thing that keeps rising in the background, and it doesn’t go away. It was a constantly growing tension, an anxiety and discomfort, that came from very deep down. You spend most of your energy trying to hold this thing at bay, and according to the ego depletion literature, you can’t do that for very long. These cognitive control centers just give up. They are limited resources.”

Craving is not a steady state. It grows. “Neuroscience helps us understanding why craving is so nasty.” Enter “delay discounting,” a term from behavioral economics used by several speakers during the conference. Delay discounting is the proposition that the perceived value of something rises steeply as the reward gets closer in time. A variation of this idea is seen in the classic marshmallow test for children: One marshmallow now, or two if you wait until later?

“Craving traps you in delay discounting,” said Lewis. “Immediate reward is worth more than imagined future happiness. The job of dopamine in the striatum is to increase the attractiveness or value of one goal, and to reduce the attractiveness and value of all the other goals. This is a brain that is well designed for addiction. You get tons of dopamine rising up in anticipation of reward. So you’re really stuck in the immediate. At which point you’ve effectively lost contact with the rest of your life. In the narrative of who you are, you can’t even include next week, or the next morning.”

Nonetheless, Lewis finds serious problems with the standard disease model of addiction, as championed by NIDA’s Nora Volkow and other in the NIH, however brain-based he may be. As a developmental neuroscientist, Lewis is predisposed to viewing the brain as a locus of change by definition. “The disease model uses brain change as a foundational premise. But brains change with development, anyway. And in fact, brains are designed to change.”

Any proper model of addiction, he insisted, has to correspond with what we know about brain change. “But it also has to correspond with addicts’ experiences. I was a drug addict from about age 25 to 30. I was in really bad shape. And now I talk with a lot of drug addicts, and one of the things that I keep hearing is that scientists and clinicians don’t really know what they’re doing—they don’t know where to go with it. They know that addiction is really nasty, but they don’t know what it’s like, unless they’ve been there.”

Lewis offered a view of addiction that shifts the semantic focus from disease to development. The drug is not the culprit. By reconceptualizing addiction as a developmental disorder, he suggested, we can move the debate forward into the world, where the action is:

Addiction results from accelerated learning, the acquisition of thought patterns that rapidly self-perpetuate because of the brain’s tendency to become sensitized to highly attractive rewards. This is a developmental process, accelerated by a neurochemical feedback loop that is particular to strong attractions. Like other developmental outcomes, addiction isn’t easy to reverse, because it’s based on synaptic restructuring. Like other developmental outcomes, it arises from neural plasticity, and uses it up at the same time.

And the mechanisms responsible are the same ones responsible for many things that involve desire, learning, reward seeking, and compulsive behavior—including the so-called behavioral addictions like overeating and compulsive sex. However, “the severe consequences of addiction don’t make it a disease, any more than the consequences of violence make violence a disease.”

In an email exchange after the conference, I followed up with Dr. Lewis on some of these matters, and he sent me the following additional thoughts on the “diseasing” of addiction:

Proponents of the disease model argue that addiction changes the brain. And they're right: it does. But the brain changes anyway, at every level, from gene expression, to cell density, to the size and shape of the cortex itself. Of course, neuroscientists who subscribe to the disease model must know that brains change over development. Their take on pathological brain change would have to be very specific in order to be convincing. For example, they would have to show that the kind (or extent or location) of brain change characteristic of addiction is nothing like that observed in normal learning and development. But this they cannot do. The kind of brain changes seen in addiction also show up when people take up rock collecting, fall in love, learn how to cook, or become obsessed with their appearance. The brain contains only a few major traffic routes for learning and goal seeking. And, like the main streets of a busy city, they are often under construction.  Brain disease may be a useful metaphor for how addiction seems, but it's not a valid explanation for how it actually works.

Random Notes from the College on Problems of Drug Dependence

Opening day addresses at the annual meeting.

(These are notes on research in progress, not findings written in stone).

--NIDA director Nora Volkow talked up buspirone (Buspar) as a treatment for cocaine addiction, and referred to favorable results on buspirone for cocaine self-administration in monkeys in a large clinical trial. Also, different vaccine strategies are in the works, including different pharmacological approaches to blocking specific dopamine transporter molecules.

--Edward Sellers of DL Global Partners, a drug research consulting firm, emphasized the importance of enzyme variations in smoking. Variants of the CYP2A6 enzyme of metabolization allow us to identify “slow metabolizers” who respond well to placebo or nicotine patch therapy, and other smokers who don’t.

--Sherry McKee of the Yale University School of Medicine reminded everyone that cigarette smokers—even very light smoking “chippers”— are far more likely to have concurrent drinking problems than non-smokers. Smoking helps drinkers drink more and longer. To demonstrate such “potentiated reinforcement,” she showed a delightful video of her child eating cookies, then craving a glass of milk, then succumbing to another round of cookie consumption…

--Jack Henningfield of Pinney Associates, and former NIDA research chief, said that the reason the National Institute on Alcohol Abuse and Alcoholism (NIAAA) became an agency focused on “one molecule” is because Senator Harold Hughes, recovering alcoholic from Iowa, and Bill W., co-founder of Alcoholics Anonymous, wanted it that way.

--David Penetar of Harvard Medical School and McLean Hospital added more evidence of the link between alcohol and cigarettes, noting that “90 per cent of smokers drink,” and that smokers are three times as likely to be alcoholics than non-smokers. He pointed to research documenting a disturbing “increased desire to drink” when wearing a nicotine patch. With a patch, subjects reported feeling the effects of alcohol sooner and longer.

Photo Credit: http://www.thejournalshop.com/

Addiction Doctors Pick Top Ten Journal Articles

A screen for problem gambling, medications for insomniac alcoholics, and more.

A group of addiction doctors presented a Top Ten List of peer-reviewed articles from 2011 at the American Society of Addiction Medicine’s Annual Medical-Scientific Conference in Richmond, VA. Dr. Michael Weaver presented the findings, noting that the list was “reached by consensus, and articles were selected not only for their quality but also to represent different areas of addiction medicine.” Dr. Weaver stressed that “not all published studies were done really well, and some may not apply to the patients treated by a particular clinician.”

According to Dr. Edward Nunes, with the Department of Psychiatry at Columbia University, the journal articles provide a "nice mixture on epidemiology and clinical outcome or clinical trials research,” which represent “the type of evidence most relevant to patient care."

Thanks to Catharine Zivkovic (@ccziv) for drawing attention to this list. The summaries are my own. Disclaimer: In some cases, these brief summaries are based solely on a reading of the journal abstracts.

1. 

Hsueh-Han Yeh, M.S. et al. (2011). Five-Year Trajectories of Long-Term Benzodiazepine Use by Adolescents: Patient, Provider, and Medication Factors. Psychiatric Services 62(8): 900–907.

 A Taiwanese study analyzing benzodiazepine prescription records came up with a simple solution: “Prescribers can reduce the risk of long-term use by assessing whether pediatric patients have received benzodiazepines from multiple doctors for various medical conditions.” Huh. Who’d have thought of that one, eh? But for various reasons, such checks, and the open records required to make them possible, are the exception rather than the rule in current health care systems. The study group found that for long-term users under 21, defined as anyone in receipt of a benzodiazepine prescription for 31 or more days in a calendar year, one in four patients fell into the categories of “accelerating or chronic users.” Specifically, “A history of psychosis or epilepsy, prescription by providers from multiple specialties, and receipt of benzodiazepines with a long half-life or mixed indications significantly increased one's risk of becoming a chronic or accelerating user.”

2. 

McBride, O, and Cheng, Hui G. (2011) Exploring the emergence of alcohol use disorder symptoms in the two years after onset of drinking: findings from the National Surveys on Drug Use and Health. Addiction 106(3): 555-563.

This study looked for clinical features of alcohol dependence and socially maladaptive drinking patterns during the first 24 months of alcohol use, based on stats from the 2004-2007 National Surveys on Drug Use and Health (NSDUH). Result: New alcohol users “frequently experienced problems relating to self-reported tolerance, spending a great deal of time recovering from the effects of alcohol and unsuccessful attempts at cutting down on drinking. The likelihood of experiencing the clinical features increased steadily in the first 9 months after use, but appeared to plateau or only gradually increase thereafter.” The researchers suggest there may be a window of opportunity during the 2nd year of drinking.

3.

Volberg, Rachel A., et al. (2011) A Quick and Simple Screening Method for Pathological and Problem Gamblers in Addiction Programs and Practices. The American Journal on Addictions. 20(3): 220-227.

Doctors, as these researchers point out, don’t often screen their patients for pathological gambling. To combat this, the investigators offer health professionals brief computer screenings they have developed for use in identifying problem gambling. “Given the high rates of comorbidity, routine and accurate identification of gambling-related problems among individuals seeking help for substance abuse and related disorders is important.” 

4.

Alford, Daniel. P., et al. (2011). Collaborative Care of Opioid-Addicted Patients in Primary Care Using Buprenorphine: Five-Year Experience. Archives of Internal Medicine 171(5):425-431.

Buprenorphine remains an underused but often effective treatment for opiate addiction, the authors of this study maintain. The cohort being studied was a group of addicted patients under the dual care of general physicians and nurse care managers. “Of patients remaining in treatment at 12 months, 154 of 169 (91.1%) were no longer using illicit opioids or cocaine based on urine drug test results,” the investigators report. However, dropout rates were high. The researchers did find that the nurse-doctor model was workable: “Collaborative care with nurse care managers in an urban primary care practice is an alternative and successful treatment method for most patients with opioid addiction that makes effective use of time for physicians who prescribe buprenorphine.”

5. 

Kolla, B.P., et. al. (2011) Pharmacological Treatment of Insomnia in Alcohol Recovery: A Systematic Review. Alcohol and Alcoholism 46: 578-585.

In this Mayo Clinic review of drugs used for sleep problems in alcohol recovery, the authors combed through more than 1,200 articles and reported that, of all the old and new drugs being used, an old and rarely used medication—trazadone—improved sleep measures as reliably as anything else that was tested. Gabapentin got good but equivocal marks due to questions about testing and inclusion criteria. Topiramate and carbamazepine helped in some cases. Furthermore, “in single, small, mostly open-label studies, quetiapine, triazolam, ritanserin, bright light and magnesium have shown efficacy, while chlormethiazole, scopolamine and melperone showed no difference or worsening. Conclusion: Trazodone has the most data suggesting efficacy.”

6.

Bohnert, A.S., et. al. (2011). Association between opioid prescribing patterns and opioid overdose-related deaths. Journal of the American Medical Association 305: 1315-1321.

Accidental prescription overdose deaths are on the rise, and this group of university researchers in Ann Arbor and Indianapolis thinks it may have something to do with how the dosing instructions are usually worded.  They set out to investigate “the association of maximum prescribed daily opioid dose and dosing schedule (“as needed,” regularly scheduled, or both) with risk of opioid overdose death among patients with cancer, chronic pain, acute pain, and substance use disorders.” They found from VHA hospital records that “the frequency of fatal overdose over the study period among individuals treated with opioids was estimated to be 0.04%.” The risk for overdose was directly related to the “maximum prescribed daily dose of opioid medication.” And patients who stuck with regular dosages, or took opioids “as needed,” were not at any elevated risk for overdose. Another obvious but frequently overlooked conclusion: “Among patients receiving opioid prescriptions for pain, higher opioid doses were associated with increased risk of opioid overdose death.”

7. 

Allsop, D.J. et al. (2011). The Cannabis Withdrawal Scale development: patterns and predictors of cannabis withdrawal and distress. Drug and Alcohol Dependence 19(1-2):123-9.

Rates of treatment for marijuana abuse and addiction are increasing, say these Australian authors, along with relapse rates. They have devised a Cannabis Withdrawal Scale that measures such withdrawal effects as associated distress, strange dreams, trouble sleeping, and angry outbursts—common manifestations of withdrawal from weed. The scientists maintain that their “Cannabis Withdrawal Scale can be used as a diagnostic instrument in clinical and research settings where regular monitoring of withdrawal symptoms is required.”

8.

West, R., et al. (2011) Placebo-Controlled Trial of Cytisine for Smoking Cessation. New England Journal of Medicine 365: 1193-1200.

This important study assessed the effectiveness of the drug cytisine in smoking cessation programs, and a potential star was born. In a single-center, randomized, double-blind, placebo-controlled trial, the journal paper concluded that “cytisine was more effective than placebo for smoking cessation. The lower price of cytisine as compared with that of other pharmacotherapies for smoking cessation may make it an affordable treatment to advance smoking cessation globally.”

9. 

Elkashef A., et al. (2011) Topiramate for the treatment of methamphetamine addiction: a multi-center placebo-controlled trial. Addiction Published online 12/16.

Conducted at eight medical centers across the U.S., this study found that for most of the 140 methamphetamine-dependent adults under scrutiny, use of topiramate produced “abstinence from methamphetamine during weeks 6-12.” That’s the good news. Unfortunately,  “secondary outcomes included use reduction versus baseline, as well as psychosocial variables… topiramate did not increase abstinence from methamphetamine during weeks 6-12.” That’s the bad news. And here’s the silver lining, as far as the investigators are concerned: “Topiramate does not appear to promote abstinence in methamphetamine users but can reduce the amount taken and reduce relapse rates in those who are already abstinent.”

10.

Levina. A., et al. (2011). Molecular Mechanism for a Gateway Drug: Epigenetic Changes Initiated by Nicotine Prime Gene Expression by Cocaine. Science Translation Medicine 3(107) 107-109.

There really is s a gateway drug. In fact, there are two of them in our culture. Almost every potential addict starts out with alcohol or cigarettes or both. Because they are legal and easily available. So is cocaine and marijuana, once you get the hang of it, but in the beginning, and all around us, it’s booze and cigs. The amazing premise of this final study is this: “Pretreatment of mice with nicotine increased the response to cocaine, as assessed by addiction-related behaviors and synaptic plasticity in the striatum, a brain region critical for addiction-related reward.” Nicotine primes subjects for cocaine addiction, in effect. “These results from mice prompted an analysis of epidemiological data, which indicated that most cocaine users initiate cocaine use after the onset of smoking and while actively still smoking, and that initiating cocaine use after smoking increases the risk of becoming dependent on cocaine, consistent with our data from mice. If our findings in mice apply to humans, a decrease in smoking rates in young people would be expected to lead to a decrease in cocaine addiction.”

Photo Credit: www.flickr.com/

From Their Mouth to Your Ear: Researchers Talk Drugs

A collection of five-question interviews.

I’ll be away from the Addiction Inbox office this week, attending the big TEDMED health and medicine powwow in Washington, D.C.

In the meantime, here’s a summation (with links) of the interviews I’ve been doing recently in the “five-question interview” series. I’ve been very lucky to nab some state-of-the-art thinkers, working at the top of their fields, from psychiatry to pharmacology to neuroscience.

See below for the story thus far:



David Kroll, former Professor and Chair of Pharmaceutical Science at North Carolina Central University in Durham, is now Science Communications Director for the Nature Research Center at the North Carolina Museum of Natural Sciences.

“The attraction to users was, until recently, that Huffman cannabis compounds (prefixed with "JWH-" for his initials) could not be detected in urine by routine drug testing. Hence, incense products containing these compounds have been called ‘probationer's weed.’" MORE

Vaughan Bell is a Senior Research Fellow at the Institute of Psychiatry, King’s College, London. He is also honorary professor at the Universidad de Antioquia in Medellín, Colombia.

"I was very struck by the appearance of classic Kluver form constants [after taking ayahuasca], geometric patterns that are probably caused by the drug affecting the visual neurons that deal with basic perceptual process (e.g. line detection)." MORE

Jon Simons, a cognitive neuroscientist, is a lecturer in the Department of Experimental Psychology at the University of Cambridge, UK, and principal investigator at the University’s Memory Laboratory.

“If you’re at a party and happen to drunkenly strike up conversation with Angelina Jolie (or Brad Pitt, if you prefer) and, bowled over by your charm and witty repartee, she tells you her phone number, you may well not remember it when you wake up sober the next morning. However, the evidence suggests that you would have a better chance of recalling the number if you got drunk again." MORE

Bankole Johnson is professor and chairman of the University of Virginia’s Department of Psychiatry and Neurobehavioral Sciences.

“With growing and clear acceptance of the neurobiological underpinnings of addiction, our work on pharmacogenetics promises to provide effective medications—such as ondansetron—that we can deliver to an individual likely to be a high responder, based on his or her genetic make up." MORE

Michael Farrell is the director of the National Drug and Alcohol Research Centre (NDARC) at the University of New South Wales in Sydney, Australia. Before that, he was Professor of Addiction Psychiatry at the Institute of Psychiatry at Kings College, London.

“The near complete absence of methadone or buprenorphine treatment in American prisons is hard to understand, when you see what a great contribution US research and treatment with methadone and buprenorphine has had globally. Now there are over 300,000 people on methadone in China as part of HIV and AIDS prevention." MORE

Deni Carise is a clinical psychologist who serves as senior vice president and chief clinical officer at Phoenix House, a leading U.S. non-profit drug treatment organization with more than 100 programs in 10 states.

“Those in recovery see the disease of alcoholism or addiction as a moral obligation to get well. If you know you have this disease and the only way to keep it under control is not to use alcohol or drugs, then that’s what you have to do." MORE


Keith Laws is professor of cognitive neuropsychology and head of research in the School of Psychology at the University of Hertfordshire, UK.

"Some may tolerate 100s or even 1000s of E tablets, but for others far fewer may lead to memory problems. We can predict that 3 in 4 users will develop memory problems, but not which 3 or after how many tablets." MORE

photo credit: http://www.startawritingbusiness.co.uk

Interview with Deni Carise, Chief Clinical Officer of Phoenix House

Why addiction treatment works—if you let it.

This time around, our “Five-Question Interview” series features clinical psychologist Deni Carise, senior vice president and chief clinical officer at Phoenix House, a leading non-profit drug treatment organization with more than 100 programs in 10 states. Chances are, you may have seen or heard her already: Dr. Carise has been a guest commentator about drugs and addiction for Nightline, ABC’s Good Morning America, Fox News, and local New York media outlets. She is frequently quoted in US News and World Report and other periodicals, blogs at Huffington Post, and has also consulted for the U.N. Office on Drugs and Crime.

Dr. Carise earned her doctorate at Drexel University, and served as a post-doctoral fellow at the Center for Studies of Addiction at the University of Pennsylvania. Currently, she is also adjunct clinical professor in the University of Pennsylvania’s Department of Psychiatry. She has been involved with drug abuse treatment and research for more than 25 years, and has worked extensively in developing countries to integrate science-based drug treatments into local programs. She has worked with adults and adolescent populations including dually diagnosed clients, Native Americans, and with medical populations (including spinal cord-injured, cardiac care and trauma patients).

1. As chief clinical officer for Phoenix House Foundation, what's your job description?

Deni Carise: My main responsibility is to ensure that we provide the highest possible standard of care. This means making sure that treatment methods across our programs are consistent with the latest research, represent a variety of evidence-based practices, and are delivered with fidelity. I also collaborate on the implementation and evaluation of Phoenix House’s national and regional strategies to achieve clinical excellence. My home base is New York, but I work directly with all of our programs and regularly travel to our California, New England, Mid-Atlantic, Texas, and Florida regions. I also oversee the activities of our Family Services, Quality Assurance, Research, Workforce Development, and Training initiatives. Finally, I help Phoenix House spread awareness to the public about the need to reduce the stigma of addiction and to increase access to treatment services.

2. As a clinical psychologist, how did you become involved in drug and alcohol treatment and recovery?

Deni Carise: I actually became involved in the Substance Abuse Treatment (SAT) field prior to becoming a clinical psychologist. When I decided that I wanted to get sober, I got some help from a counselor. This counselor was so helpful to my recovery that I decided to become an SA counselor so that I could assist others on this journey. I was working as a model at that time, and there were a few aspects of that career that I didn’t like: First, it was very clear that I would become less valuable in my career as I got older; secondly, my value was exclusively based on appearance, not knowledge or skills; and finally, my work didn’t contribute to the greater good—that is, no one benefitted by my work. I wanted a new career where I would become more valuable as I got older and more experienced, and where my knowledge and skills would be of value. I also wanted to do something I felt was contributing to society. The SAT field seemed to fit all these criteria.

3. What makes it so difficult for people to accept the disease components of serious drug addiction?

Deni Carise: People have difficulty accepting the disease concept of addiction for three reasons. First, people believe addiction is self-induced; you wouldn’t have it if you didn’t use drugs, right? There is some truth to this, but of all those who try drugs, an estimated 5 to 10% (depending on the drug) will become addicted. There’s a reason why the other 90 to 95% don’t become addicted.

That brings us to reason #2: People generally don’t believe there is a genetic cause. It is now very clear that there is a genetic component to substance use disorders. For example, if a father is an insulin-dependent diabetic, the heritability estimates range from 70 to 90% likelihood that the man’s son will also be diabetic. For hypertension, the heritability estimates are from 25 to 50%, depending which study we look at. For alcohol, the estimates are 55 to 65% likelihood that a young man will be alcohol dependent if his father is. For opiate dependence, it’s 35 to 50%.

The third and probably most important reason is that people think calling addiction a disease absolves the substance abuser of responsibility for his or her actions. Nothing could be further from the truth. Those in recovery see the disease of alcoholism or addiction as a moral obligation to get well. If you know you have this disease and the only way to keep it under control is not to use alcohol or drugs, then that’s what you have to do.

4. Overall, treatment doesn't seem to be that effective. What's missing?

Deni Carise: I believe treatment is effective. We’re just expecting the wrong results. Substance abuse has the same characteristics as any chronic medical disorder. The problem is that we (society, families, even me) want addiction to respond to treatment as though it’s an acute medical problem, like a broken leg or appendicitis. If it were an acute problem, we could send our kids, loved ones, even ourselves to treatment for a set number of days (maybe 7, maybe 28) and leave the hospital or treatment facility with the condition cured—as we would after surgery for an appendicitis! I would love that.

Unfortunately, we’ve been measuring treatment success the same way we would for a surgical problem, even though substance abuse and dependence are, in fact, chronic problems. Think about this—substance abuse treatment success is often measured by symptoms, drug use, and life problems prior to treatment and again six months after treatment ends. Imagine if we measured success of diabetes treatment the same way. We would measure their blood sugar levels, weight, number of diabetic crises, and other related problems before treatment. Then we’d send them off to a treatment program where we would prescribe medications, maybe give them insulin, teach them about a good diet, discharge them (take away that treatment), and measure their blood sugar levels, weight, etc. six months after we stopped the medication. Do we really think that would work with diabetes? Then why would we think it would work with addiction?

As with all chronic disorders, there are no prolonged, symptom-free periods without continued attention and self-management of the illness. Just as some people with diabetes can manage their illness with behavioral changes such as making healthy decisions when offered cakes or cookies, or starting an exercise program, some people with substance abuse problems can control their symptoms by changing their behaviors. This means not being around others who use, making the right decisions when offered alcohol or drugs, etc. For those who can’t do this alone, there’s treatment to teach them how to manage their disease and there are medications to assist them. And I’m talking about the diabetic and the substance abuser.

So treatment can work, but, just like any chronic disease, there’s no quick fix.

5. You're committed to working with developing countries to bring scientifically valid treatment within reach of poorer populations. How is the effort going?

Deni Carise: I’ve been really lucky to be able to consult for numerous treatment systems, universities, and countries around the world—including training clinicians from Nigeria, Thailand, Egypt, Greece, Iran, Singapore, Brazil, China, Iraq, India, and other countries. It’s fascinating to see how different countries approach local substance abuse problems. Some countries have historically asserted that substance abuse is not a problem in their communities, so for them to offer treatment of any kind means they need to change their socipolitical stance. That doesn’t happen quickly. For one country, the diagnosis of AIDS among 7 substance abusers who had shared needles was the impetus to providing treatment.

Much of what I’ve done internationally involves cultural adaptations of standardized instruments or clinical tools (such as the Addiction Severity Index assessment tool) for use within various cultures. To do this, I typically meet with numerous staff who deliver direct services in the country. We go over each assessment question or worksheet item looking at what would make sense in their culture. Types of things that frequently need adapting are questions about education (not everyone has “high schools”), employment and income, demographic questions such as race categories, and all manner of expressions used to describe drugs and clinical symptoms. Then we pilot the new interview or service with some local clients and get their perspective and make a final version.

Much of this work has been funded by the United Nations Office on Drug Use and Crime, the National Institute on Drug Abuse and Office of National Drug Control Policy.

NIDA'S Updated Guide Book Emphasizes Science

Drug addiction treatment trends.

Favoring objective medicine over moral exhortation, the National Institute on Drug Abuse (NIDA) has updated one of its primary research guides, continuing the trend toward focusing on the scientific aspects of drug and alcohol addiction.

In the preface to the updated 2nd Edition of Principles of Drug Addiction Treatment, available here, NIDA Director Nora D. Volkow writes:

“Addiction affects multiple brain circuits, including those involved in reward and motivation, learning and memory, and inhibitory control over behavior. Some individuals are more vulnerable than others to becoming addicted, depending on genetic makeup, age of exposure to drugs, other environmental influences, and the interplay of all these factors.”

Looking toward the future, Volkow writes that “we will harness new research results on the influence of genetics and environment on gene function and expression (i.e., epigenetics), which are heralding the development of personalized treatment interventions.”

Here are excerpts from a section of the updated guide titled “Principles of Effective Treatment.”

--No single treatment is appropriate for everyone.

“Matching treatment settings, interventions, and services to an individual's particular problems and needs is critical to his or her ultimate success in returning to productive functioning in the family, workplace, and society.”

--Treatment needs to be readily available.

“Potential patients can be lost if treatment is not immediately available or readily accessible. As with other chronic diseases, the earlier treatment is offered in the disease process, the greater the likelihood of positive outcomes.”

-- Remaining in treatment for an adequate period of time is critical.

“Research indicates that most addicted individuals need at least 3 months in treatment to significantly reduce or stop their drug use and that the best outcomes occur with longer durations of treatment. Recovery from drug addiction is a longterm process and frequently requires multiple episodes of treatment.”

-- Medications are an important element of treatment for many patients, especially when combined with counseling and other behavioral therapies.

“For example, methadone and buprenorphine are effective in helping individuals addicted to heroin or other opioids stabilize their lives and reduce their illicit drug use. Naltrexone is also an effective medication for some opioid-addicted individuals and some patients with alcohol dependence. Other medications for alcohol dependence include acamprosate, disulfiram, and topiramate.”

-- Many drug-addicted individuals also have other mental disorders.

“Because drug abuse and addiction—both of which are mental disorders—often co-occur with other mental illnesses, patients presenting with one condition should be assessed for the other(s). And when these problems co-occur, treatment should address both (or all), including the use of medications as appropriate.”

-- Treatment programs should assess patients for the presence of HIV/ AIDS, hepatitis B and C, tuberculosis, and other infectious diseases as well as provide targeted risk-reduction counseling to help patients modify or change behaviors that place them at risk of contracting or spreading infectious diseases.

“Typically, drug abuse treatment addresses some of the drug-related behaviors that put people at risk of infectious diseases. Targeted counseling specifically focused on reducing infectious disease risk can help patients further reduce or avoid substance-related and other high-risk behaviors.”

Graphics Credit: NIDA

The CYP2D6 Factor

Enzymes And Drug Abuse

Different drugs effect different people differently.

Drugs are broken down into their constituent waste products by specific sets of enzymes. A subset of the human population, variously estimated at 3% to 7%, are categorized as “poor metabolizers.” For them, a drug’s recommended dosage is often far too high. The culprit is a gene variant that codes for a liver enzyme called cytochrome P450 isoenzyme 2D6, known in shorthand as CYP2D6. Poor metabolizers produce less of this crucial enzyme, which means that drugs are broken down and excreted at a much slower pace. In these people, the recommended dose results in higher drug concentrations. This obviously can make a crucial difference in how a person reacts to the drugs.

About one out of 20 people has a mutation in the 2D6 gene that causes a lack of the enzyme, according to UC-San Francisco biochemist Ira Herskowitz. “Those people are really getting a whopping dose”(New York Times, registration required). In addition, if a person with normal CYP2D6 levels is taking several drugs that are broken down by CYP2D6, then the enzyme’s ability to degrade one drug can greatly inhibit its ability to degrade the others. This increases the possibility of adverse drug interactions, particularly among the elderly, who may already be suffering from liver disease or impaired renal function.

Drugs of abuse severely complicate these enzymatic issues, since addicts and alcoholics are not known for volunteering information about their condition to medical or hospital personnel. Poor metabolizers often have little or no reaction to codeine-based medications. Screening tests for CYP2D6 variations are becoming cheaper and more widely available.

Enzyme interactions can work the other way, too. St. John’s Wort, for example, is suspected of activating another drug breakdown enzyme, CPY3A, thereby accelerating, rather than retarding, the destruction of other drugs. The herb can alter the metabolization of Phenobarbital, tamoxifen, oral contraceptives, and antiviral medications (Science, subscription required). Drugs must be combined with caution, and people need to monitor dosages, because of the tremendous degree of metabolic variation that exists.

“Start low and go slow” is still the best advice. A 2002 report from Georgetown University’s Center for Drug Development Science found that the dosage recommendations of 21 per cent of the drugs coming to market from 1980 to 1999 were later revised. Fully 80 per cent of those revisions involved a reduction in the original recommended dose. A related survey undertaken in Europe by the World Health Organization obtained similar results. “It’s long been known that for individual subjects the dosage listed on a drug label is not necessarily the right one,” said one of the authors of the Georgetown study. Typically, the recommended dosage is set early in the testing process, after analyzing results from a limited number of volunteer subjects (New York Times, registration required.) A more rigorous analysis of initial data would help get the dosage right the first time. Metabolic profiles that screen for CYP2D6 mutations will greatly assist this process.

Fearing Medicine

By Dirk Hanson

Have Americans become afraid of their doctors?

Once upon a time, Americans went to their doctors to get pills. Doctors complained that patients believed competent medical care consisted of being handed a prescription. In the absence of that piece of paper with the unintelligible signature, a patient was apt to claim that the doctor’s visit had been a waste of time. What was the point of seeing a doctor if the doctor didn’t give you anything that would cure what ailed you?

That was then. Patients now demand that doctors and pill makers come clean about the safety of the products they offer (long overdue), and that the pills themselves be absolutely benign in their effects (utterly impossible). In ever-greater numbers, Americans are coming to fear prescription drugs. This condition, in extremis, is a phobia with a recognized set of diagnostic criteria: pharmacophobia—an abnormal fear of medicine.

Today, Americans go to their doctors to be healthy and “drug-free.” If they are taking prescription medications, their goal is to get off them. Yesterday, patients demanded pills for conditions they didn’t have, or for which pills were ineffective. Today, patients are routinely filing lawsuits, demanding to know why their doctor gave them pills. Ironically, one of the major hindrances to health care, from a doctor’s point of view, is “patient non-compliance”—sick people often don’t take their pills properly. (This may be a good place to note that I do not work for, or with, or against Big Pharma, as the drug companies are now called. I don’t work for anybody.)

The drug industry, one of the most tightly regulated industries in America, is the kind of corporate villain Americans understand. What particularly rankles many critics is that the drug companies advertise.

“Presumably,” Joseph Davis concedes in his jeremiad against drug advertising in the journal Hedgehog Review, “some percentage of those who identify their face and their feelings with those signified in the ads actually suffer from a debilitating condition. So much to the good.”

But of little significance, it seems. The central issue for Davis is: What if people who don’t need those pills are exposed to those ads? Normal people might think they need those pills—and they don’t! And very soon, as you can easily see, you’ve got trouble in River City. In the same issue of Hedgehog Review, biomedical ethics professor Leigh Turner professes similar shock, recounting with indignation “a world where a host of marketing strategies are used to package tidy, authoritative, and often profoundly misleading claims” about the safety and effectiveness of products. You can imagine how I felt when I learned that commercial advertisers were capable of doing that.

For lack of a better term, we will have to settle for calling it the real world, where soap, life insurance, housing, cars, psychiatric care, and legal advice are all marketed in misleading ways, to people who don’t always need them. And so it is with pills. However, where once patients desired this, they now resent the offer. Writing in the May 2007 issue of Harper’s, Gary Greenberg declares that “Under the agreement we’ve made—that they are doctors, that I am sick, that I must turn myself over to them so they can cure me—the medicine must be treated with the reverence due a communion wafer.”

Previously, patients wanted their communion wafers, and doctors were often accused of withholding them. Now, as Greenberg makes clear, patients fear doctors will drag them to the altar and force the holy wafers down their throats. One cannot help wondering what manner of pact Greenberg would like to arrive at with his treating physicians. His approach does not seem like a particularly promising step forward in doctor-patient relations.

Interestingly, Americans have shown little interest in a thorough examination of the adverse side effects of non-pharmaceutical approaches to health. Talk therapists and holistic practitioners of every stripe operate in a virtually regulation-free environment. Where, for example, can one find a list of common side effects associated with the practice of various forms of psychotherapy, from post-Freudian talk therapy to, say, the increasingly popular varieties of cognitive therapy? Where, I would like to know, is the list of unwanted side effects that can occur as the result of an on-air encounter with that manipulative bruiser, Dr. Phil?

Science writer Sharon Begley, in a June 18 Time column entitled “Get Shrunk at Your Own Risk,” declares: “What few patients seeking psychotherapy know is that talking can be dangerous, too—and therapists have not exactly rushed to tell them so.”

Among many other examples, Begley reminds us of the “recovered memory” therapies that tore families apart and sent innocent people to prison for the alleged sexual abuse of children. And “stress debriefing,” a method of re-experiencing traumatic events in an effort to eliminate Post Traumatic Stress Disorder, sometimes leads to increased stress and higher levels of anxiety, compared to PTSD victims who do not undergo such therapy. I’ll privilege an upset stomach and occasional loose stools from pills over that kind of deep-seated trauma any day.

Begley also cites a 2000 study of professional grief counseling which concluded that four out of ten people grieving for the death of a loved one through formal therapy would have been better off with no therapy at all. Compared to a control group, 40 per cent of mourners in professional therapy experienced increased depression and grief. (In some cases, the most benign contraindication is when the treatment doesn’t do anything at all.)

The side effects associated with talk therapies remain shrouded in mystery. “The number of people undergoing potentially risky therapies reaches into the tens of thousands,” Begley concludes. “Vioxx was yanked from the market for less.”

Drug Rehab in China

After two years of a nationwide “people’s war” against drug addiction in China, government authorities are claiming major accomplishments—but treatment, which is mostly compulsory, remains limited and largely ineffective, Chinese doctors say.

The Chinese surge against drugs was credited with numerous successes almost before it had begun. Zhou Yongkang, Minister of Public Security, told the official news agency Xinhua that officials had seized more than two tons of methamphetamine, and three million “head-shaking pills”--otherwise known as Ecstasy tablets.

Two years later, in June of 2007, Minister Yongang, claimed that the number of drug abusers in China had been cut from 1.16 million to 720,400 due to compulsory rehabilitation measures. “The effort has yielded remarkable results,” Yongang told the China Daily. (Other drug experts estimate the number of Chinese drug addicts to be 3 million or more.)

However, a recent paper co-authored by several Chinese physicians, published in the Journal of Substance Abuse Treatment, suggests that things are not so rosy. The report, titled, “Attitudes, Knowledge, and Perceptions of Chinese Doctors Towards Drug Abuse,” paints a dismal picture: Less than half the Chinese doctors working in drug abuse had any formal training in the treatment of drug addicts, the report found. Moreover, less than half of the treatment physicians believed that addiction was a disorder of the brain. (One cannot help wondering whether the percentage for American doctors would be any higher.)

The study could find no coherent doctrine or set of principles for drug rehabilitation being employed in China, beyond mandatory detox facilities. In the Chinese government’s White Paper on “Narcotics Control in China,” the practice of “reeducation-through-labor” is considered to be the most effective form of treatment. Another name for this form of treatment would be: prison.

There are perhaps as many as 200 voluntary drug treatment centers as well. These centers emphasize treating withdrawal symptoms, and feature more American-style group interaction and education, but observers say such centers are often used by people evading police or running from their parents.

In addition, the lack of formal support from the Chinese government has led to the closing of several such facilities after only a few months. The American origins of such treatment modalities have not helped sell such programs to government officials. Pharmaceutical treatments for craving remain unavailable in China.

SOURCES:

--Fan, Maureen. “U.S.-Style Rehabs Take Root in China as Addiction Grows.” Washington Post Foreign Service, A14, January 19, 2007.

--Yi-Lang Tang, et. al. “Attitudes, Knowledge, and Perceptions of Chinese Doctors Towards Drug Abuse.” Journal of Substance Abuse Treatment. vol. 29 no. 3. 215-220.

--“Anti-Drug Campaign Yields Result.” China Daily. June 16, 2007. http://www.china.org.cn.

--“With Prohibition Failing, China Calls for ‘People’s War’ on Drugs.” Drug War Chronicle. vol. 381. 4/8/05 http://stopthedrugwar.org

Speed Causing Strokes?

During the cocaine boom of the 1980s, addiction researchers learned that cocaine was sometimes capable of setting off serious seizures in users. Now, a related effect has been tentatively identified in two methamphetamine abusers-- strokes caused by microscropic tears in major arteries of the neck.

Although the study, published in the journal Neurology by researchers at the University of Texas Southwestern Medical Center, documented only the two cases, both young subjects-- women aged 29 and 36--were free of other risk factors. Stroke neurologists took note. Neurologist Steven Cramer at the University of California, Irvine, quoted at scientificamerican.com, said: “If I ever see any young person with a stroke--that is, anyone under 65--I’ll be sure now to do a toxicology screen.”

Stimulants like speed and cocaine markedly increase blood pressure while constricting blood vessels. According to Wengui Yu, one of the authors of the study, such work may help doctors “to better diagnose, treat, and prevent stroke in young adults.”

Sources:

--Choi, Charles Q. “Strokes in Young People Could be Due to Meth.” scientificamerican.com. December 26, 2006.

--McIntosh A., Hungs M., Kostanian V., Yu W. “Carotid artery dissection and middle cerebral artery stroke following methamphetamine use.” Neurology. 2006 Dec 26;67(12):2259-60.