Brain Change in Addiction as Learning, Not Disease.

Abstract

During the past 30 years, the assumption that addiction is a disease or pathology has crystallized into the “brain disease model of addiction.”1 This trend was driven by the convergence of 12-step thinking with residential treatment approaches in the latter half of the 20th century,2 the explosion of neuroimaging technologies that began in the 1990s, and promotion by professional organizations3 and community groups.4 According to the brain disease model, addiction is a chronic disease brought about by changes in the brain systems that mediate the experience and anticipation of reward and in higher-order systems that underlie judgment and cognitive control.1,5 The proponents of the model propose that these changes are driven by exposure to drugs of abuse or alcohol, though links with behavioral addictions have also been explored.6 The brain disease model is the most prevalent model of addiction in the western world. Particularly in the United States, it dominates professional and public discourse on prevention, treatment, research agendas, and policy issues. Because the disease model focuses on brain change, it has helped explain why persons with addictions find it difficult to change their thoughts and behaviors quickly or easily.6 Because it focuses on biologic factors rather than moral arguments, it has helped reduce the stigma faced by those with addictions and their families, at least in some respects. (See Table 1 for a broader discussion of stigma.) The brain disease model has also legitimized the role of doctors and other medical professionals in addiction treatment and driven research on new drugs to combat addiction, and it has been used to advocate for access to treatment and care rather than segregation and punishment. These aims and outcomes are well intended, and they have been beneficial in some contexts, but the narrow focus of the disease model on the neurobiologic substrates of addiction has diverted attention (and research funding) from other models.10 Alternatives to the brain disease model often highlight the social and environmental factors that contribute to addiction, as well as the learning processes that translate these factors into negative outcomes.11-15 For example, it has been shown repeatedly that adverse experiences in childhood and adolescence increase the probability of later addiction.13,14 Also, exposure to physical, economic, or psychological trauma greatly increases susceptibility to addiction.14-17 Learning models propose that addiction, though obviously disadvantageous, is a natural, context-sensitive response to challenging environmental contingencies, not a disease.18,19 Yet the brain disease model construes addictive learning in terms of pathologic brain changes triggered mainly by substance abuse. Learning models also favor individual solutions for overcoming addiction, facilitated by cognitive modifications and personal agency. (See Table 2 for a discussion of empowerment.) Learning models can include multiple levels of analysis: societal, social, psychological, and biologic. According to experts both inside and outside the medical From the University of Toronto, Toronto. Address reprint requests to Dr. Lewis at Klingelbeekseweg 24, 6812DH Arnhem, the Netherlands, or at m . lewis@ psych . ru . nl.