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.

Origins of the Disease Model of Addiction

Roger Williams and “deranged cellular metabolism.”

                                                  (with Linus Pauling, 1974-------------->)

The idea of addiction as a disease first began to gain a tentative foothold in scientific and government circles in the early 1960s, after the publication of E.M. Jellinek’s The Disease Concept of Alcoholism. Jellinek may not have invented the “alcohol science movement,” as he called it, and he may not have been much of a scientist himself (the evidence suggests that he faked his doctorate), but he was the first to describe the “disease syndrome” of alcoholism—chronic relapse leading to death by liver failure. A salesman by nature, Jellinek ardently presented the disease model of alcoholism to the world of the social sciences just as zealously as he had previously done banana research in Honduras for United Fruit, and biostatistics work for Worcester State Hospital in Massachusetts. The trouble was that the “science” part of alcohol science was murky at best. No real progress was made in loosening the grip that traditional psychology exerted upon the prevailing public view of addiction.

A few years earlier, in 1959, a colorfully maverick dissenter named Roger J. Williams, professor of chemistry at the University of Texas, had proposed a specific disease model of his own; one that went all but unnoticed at the time. The late Roger Williams was best known as the biochemist who discovered vitamin B-5, commonly known as pantothenic acid, one of the so-called “anti-stress” vitamins. This discovery produced a nice revenue stream for Williams’ home university through the patents he took out on various processes for synthesizing B-5.

 One of the problems with traditional theories of alcoholism, Williams believed, was that it was very difficult to identify the specific psychosocial pathologies psychiatrists insisted were behind alcoholism—such things as infantile regression and oral fixation. Those few researchers who did pay attention to alcoholism, he asserted, “have been so diverted by the rather vague and ill-defined personality disorders that alcoholics allegedly have that they have failed to concentrate upon the one thing that all alcoholics have—whether they are rich or poor... introverts or extroverts, dominant or submissive, repulsive or charming—namely, an excessive appetite for alcohol.”  The idea of appetite was, for Williams, the essential semantic shift. As Williams insisted in his book, Alcoholism: The Nutritional Approach:

“Alcohol is a physiological agent and the urge which the initial drink produces, in my opinion, arises because of deranged cellular metabolism. Except for the fact that derangement is involved, the urge is fundamentally similar to the urge we have for water when our tissues become dehydrated, for salt when our tissues become salt-hungry... or the unfortunate craving some diabetics have for sugar....”

Dr. Williams was saying that after a certain point, the burning urge for alcohol, or the insatiable craving for heroin became, for “addiction-prone” people, indistinguishable from the primal drives of food, thirst, or sex. “This is something that it is impossible to understand unless we take into account the tremendous biochemical individuality that exists.” If alcohol and addictive drugs didn’t effect you that way, well then, they just didn’t, and you thanked your lucky stars for it, the way you would be thankful for not having allergies or diabetes. Blood composition, enzyme levels, endocrine activities, excretion patterns, and nutritional needs all vary from person to person, argued Williams, and the effect of any given addictive drug was going to vary widely from person to person. This neglect of biochemical individuality, Williams was convinced, was the reason physicians had no medical treatment to offer. They had the wrong paradigm—they were focusing on the drugs themselves, and not on the bodies and brains of the users.

There were, Williams insisted, periodic references in the literature to what he called the “X” factor—some particular defect, or excess, or absence, that was present in alcoholics, but absent in moderate drinkers and abstainers. The hunt for the X Factor, for Substance H, was fast becoming the Holy Grail of addiction research.

Williams thought the X factor was genetic.

Photo Credit: http://bioinst.cm.utexas.edu