Editorial

Substance dependencies and behavioral addictions are increasingly considered to be acquired neurological disorders by many healthcare professionals and researchers in the field.^1,2 For example, the American Society of Addiction Medicine defines addiction as a “primary, chronic disease of brain reward, motivation, memory, and related circuitry.” ³ Although few scientists question the importance of addiction-related neurobiological research, a controversy has arisen in recent months regarding the “brain disease model of addiction” (BDMA).⁴ Hall, Carter, and Forlini define the BDMA as “the popular simplification of work in this specialty [i.e., neuroscience-based explanations of addiction] that has had a major influence on popular discourse on addiction in scientific journals and mainstream media.” ⁴

Hall et al. contend that leaders of the U.S. National Institute on Drug Abuse (NIDA) have exaggerated the level of empirical support for the BDMA and directed too much of the agency's resources to neurobiological research (in 2014, 41.4% of NIDA's budget was devoted to basic and clinical neuroscience). Further, Hall and colleagues argue that the BDMA has, to date, largely failed to deliver effective new treatments for addiction; has made only a limited contribution to pertinent public policies; and has appeared not to reduce the stigma associated with addiction (by replacing the “moral model” of addiction with a brain disease-based conceptualization).^4-7

Worse, according to Hall et al., adoption of the BDMA has led NIDA to pursue new and expensive treatments for addiction, such as deep brain stimulation, when it might have instead focused on increasing access to available therapies or promoting cost-effective population-based prevention interventions (e.g., taxation and regulatory policies). Finally, Hall et al. cite very limited evidence^5-7 that suggests the BDMA may in some cases diminish substance misusers’ feelings of self-efficacy over their compulsive behaviors. Research examining brain disease conceptualizations of other psychiatric disorders, such as schizophrenia, does not appear to support their stigma-reducing effects.^8-9

The directors of the U.S. National Institute on Drug Abuse and National Institute on Alcohol Abuse and Alcoholism have vigorously countered Hall et al.'s assessment of the BDMA.^10,11 They contend there is substantial preclinical and clinical evidence for the BDMA, that the model has already contributed to the development of effective treatments (e.g., buprenorphine-naloxone treatment for opioid addiction, varenicline for tobacco addiction), that key policy developments such as the Affordable Care Act and 2008 Paul Wellstone and Pete Domenici Mental Health Parity and Addiction Equity Act (that increased access to addiction treatment) were backed by the BDMA, and that the BDMA “significantly diminishes the stigma attached with addiction and gives hope to those fighting this devastating disease.”¹⁰

What are we to make of these assertions and counter-assertions? We believe there is little evidence, at present, to suggest that promulgation of the BDMA will reduce the stigma of addictive disorders and that it may, in actuality, reduce perceived self-efficacy in individuals tackling their addictions. Until such time as there is evidence, the purported stigma-reducing effects of the BDMA should be viewed with significant caution and not touted as one of its virtues. Likewise, an excessive emphasis on the BDMA may have contributed to diminished interest in population-based prevention policies and programming, with only 23.8% of NIDA's 2014 budget being dedicated to epidemiological, health service, and prevention research. Consideration needs to be given to how the BDMA contributes to policy development in the United States and elsewhere in the world, to ensure that this model supports, and does not hinder, access to effective addiction treatment.

Whilst the BDMA's role in understanding addictions should be considered carefully, we believe it has the potential to play an important part of the wider work in this field. Expectations that the BDMA would lead to more effective new treatments by now may be unreasonably optimistic, and it is reasonable to expect that such developments may still materialize in the middle-to-long term. In this vein, Volkow, Koob, and McLellan commented that “So why is it that, despite all the scientific evidence, the BDMA is so frequently singled out for criticism? Maybe because of people's expectations that science should immediately translate into transforming solutions, which have not materialized for addiction, nor for most of the other brain diseases..”¹⁰

The arguments proposed by Hall et al. and the counter arguments from NIDA, NIAAA and others have sparked a debate that will provide an opportunity to consider how best any particular etiological model of addiction should be incorporated into our wider understanding of this complex and multifaceted discipline.