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.

What Do We Mean When We Talk About Craving?

An essay on drug addiction and need.

For years, craving was represented by the tortured tremors and sweaty nightmares of extreme heroin and alcohol withdrawal. Significantly, however, the one symptom common to all forms of withdrawal and craving is anxiety. This prominent manifestation of craving plays out along a common set of axes: depression/dysphoria, anger/irritability, and anxiety/panic. These biochemical states are the result of the “spiraling distress” (George Koob’s term) and “incomprehensible demoralization” (AA’s term) produced by the addictive cycle. The mechanism driving this distress and demoralization is the progressive dysregulation of brain reward systems, leading to biologically based craving. The chemistry of excess drives the engine of addiction, which in turn drives the body and the brain to seek more of the drug.

Whatever the neuroscientists wanted to call it, addicts know it as “jonesing,” from the verb “to jones,” meaning to go without, to crave, to suffer the rigors of withdrawal. Spiraling distress, to say the least—a spiraling rollercoaster to hell, sometimes. Most doctors don’t get it, and neither do a lot of the therapists, and least of all the public policy makers. Drug craving is ineffable to the outsider.

As most people know, behavior can be conditioned. From maze-running rats to the “brain-washed” prisoners of the Korean War, from hypnotism to trance states and beyond, psychologists have produced a large body of evidence about behavior change—how it is accomplished, how it can be reinforced, and how it is linked to the matter of reward.

It is pointless to maintain that drug craving is “all in the mind,” as if it were some novel form of hypochondria. Hard-core addicts display all the earmarks of the classical behavioral conditioning first highlighted almost a century ago by Ivan Pavlov, the Russian physiologist. Pavlov demonstrated that animals respond in measurable and repeatable ways to the anticipation of stimuli, once they have been conditioned by the stimuli. In his famous experiment, Pavlov rang a bell before feeding a group of dogs. After sufficient conditioning, the dogs would salivate in anticipation of the food whenever Pavlov rang the bell. This conditioned response extended to drugs, as Pavlov showed. When Pavlov sounded a tone before injecting the dogs with morphine, for example, the animals began to exhibit strong physiological signs associated with morphine use at the sound of the tone alone. Over time, if the bell continued to sound, but no food was presented, or no drugs were injected, the conditioned response gradually lost its force. This process is called extinction.

Physical cravings are easy to demonstrate. Abstinent heroin addicts, exposed to pictures of syringes, needles, or spoons, sometimes exhibit withdrawal symptoms such as runny noses, tears, and body aches. Cravings can suddenly assail a person months—or even years—after discontinuing abusive drug use. Drug-seeking behavior is a sobering lesson in the degree to which the human mind can be manipulated by itself. The remarkable tenacity of behavioral conditioning has been demonstrated in recent animal studies as well. When monkeys are injected with morphine while recorded music is played, the music alone will bring on withdrawal symptoms months after the discontinuation of the injections.  When alcoholics get the shakes, when benzodiazepine addicts go into convulsions, when heroin addicts start to sweat and twitch, the body is craving the drug, and there is not much doubt about it. But that is not the end of the matter.

“Craving is a very misunderstood word,” said Dr. Ed Sellers, now with the Centre for Addiction and Mental Health in Toronto. “It’s a shorthand for describing a behavior, but the behavior is more complicated and interesting than that. It’s thought to be some intrinsic property of the individual that drives them in an almost compulsive, mad way. But in fact when you try to pin it down—when you ask people in a general context when they’re exposed to drugs about their desire to use drugs, they generally give rather low assessments of how important it really is.”

While cravings can sometimes drive addicts in an almost autonomic way, drug-seeking urges are often closely related to context, setting, and the expectancy effect. It has become commonplace to hear recovering addicts report that they were sailing through abstinence without major problems, until one day, confronted with a beer commercial on television, or a photograph of a crack pipe, or a pack of rolling papers—or, in one memorable case of cocaine addiction, a small mound of baking powder left on a shelf—they were suddenly overpowered by an onrush of cravings which they could not successfully combat. “If you put them in a setting where the drug is not available, but the cues are,” said Sellers, “it will evoke a conditioned response, and you can show that the desire to use goes up.” Most people have experienced a mild approximation of this phenomenon with regard to appetite. When people are hungry, a picture of a cherry pie, or even the internal picture of food in the mind’s eye, is enough to cause salivation and stomach rumblings. Given the chemical grip which addiction can exert, imagine the inner turmoil that the sight of a beer commercial on television can sometimes elicit in a newly abstinent alcoholic.

When addicts start to use drugs again after a period of going without, they are able to regain their former level of abuse within a matter of days, or even hours. Some sort of metabolic template in the body, once activated, seems to remain dormant during abstinence, and springs back to life during relapse, allowing addicts to escalate to their former levels of abuse with astonishing speed. This fact, and no other, is behind the 12-Step notion of referring to oneself as a “recovering,” rather than recovered, addict—a semantic twist that infuriates some people, since it seems to imply that an addict is never well, never cured, for a lifetime.

Relapse sometimes seems to happen even before addicts have had a chance to consciously consider the ramifications of what they are about to do. In A.A., this is often referred to as forgetting why you can’t drink. It sounds absurd, but it is a relatively accurate way of viewing relapse. Addiction, as one addict explained, “is the only disease that tells you you ain’t got it.”

Graphics Credit: http://www.aapsj.org/

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Neurobiology of Addiction

Book Review




By George F. Koob and Michel Le Moal.
Academic Press
(Elsevier), London, 2006.

Over the past twenty-five years, the neurobiology of addiction has become established as an important arena of scientific study. In particular, the molecular adaptations the brain makes in response to addictive drugs has placed addiction squarely in the forefront of modern brain science.

Dr. George F. Koob, a respected American alcoholism researcher of long standing, has put together an academic treatise beyond the expertise and the pocketbooks of most laypersons, but the book is of crucial importance in the burgeoning
field of addiction science.

In Neurobiology of Addiction, Koob and co-worker Michel Le Moal review the neural and molecular mechanisms responsible for the effects of individual addictive drugs in five categories--psychostimulants, opium, alcohol, nicotine,and cannabis.

Particularly well documented is the “anti-reward” system, by which the abuse of addictive drugs leads to a net decrease in dopamine and serotonin in the nucleus accumbens,the brain structure associated with withdrawal and craving. Thus, the
pursuit of artificial pleasure becomes, through the process of addiction, a state of chronic depletion of the brain neurotransmitters associated with states of joy, happiness and well-being.

The authors also do a good job of putting forth their theory of “allostasis,” defined as a “state of chronic deviation of the regulatory system from its normal (homeostatic) operating level.” The addicted brain is constantly attempting to normalize through counteradaptions at the neural level, as well as by switching on the body’s stress responses. Craving and anxiety are among the behavioral results.

[For more on George Koob,
The Chemical Carousel: What Science Tells Us About Beating Addiction © Dirk Hanson 2008, 2009.

Sources:

--Koob, George, and Le Moal, Michel. “Drug Abuse: Hedonic Homeostatic
Dysregulation.” Science. October 3, 1997. 278: 55.

--Everitt, Barry J. “From the Dark Side to the Bright Side of Drug Addiction.”
Science 314 p. 59, 6 October 2006.