Framing Nicotine Addiction as a “Disease of the Brain”: Social and Ethical Consequences†

In November 2010, the Director of the National Institutes of Health (NIH), Francis Collins, announced the creation of a taskforce to help move all substance use, abuse, and addiction research programs within the NIH into a single, new institute (Collins, 2010). This transition would force a merger of the National Institute on Drug Abuse (NIDA), the National Institute on Alcohol Abuse and Alcoholism (NIAAA), and the drug-related research portfolios from other institutes such as the National Cancer Institute (NCI) (Seffrin et al., 2010). Supporters justify the new institute’s creation by highlighting an emerging body of scientific findings: recent research in neuroscience suggests that a single mechanism underlies compulsive behavior and addiction, regardless of the particular substance or drug of abuse. Similar brain reward pathways are thought to be involved in the development and maintenance of addiction, raising the possibility of common risk factors and the hope for novel prevention and treatment strategies across substances. In addition, supporters argue that many would be better served by a single institute combining all substance use, including patients with comorbid drug use, as well as the general population, which would benefit from comprehensive early prevention efforts (Scientific Management Review Board, 2010). Collins stated that this new institute “makes scientific sense and would enhance NIH’s efforts to address the substance abuse and addiction problems that take such a terrible toll on our society” (Collins, 2010). However, the merger remains contentious; others express concern that the merger will result in less funding for drug or substance-specific research portfolios focused on prevention, as well as decreased support for psychological and social research. One concern is that an overly reductionist vision of addiction is fueling the merger in ways that may narrow the research focus, minimizing approaches that situate addiction within a complex biopsychosocial context. One coalition of tobacco prevention groups complained: “We believe that the proposed reorganization could also narrow the focus of tobacco-related research to issues related to addiction when such research, however significant, is only one of several areas in which innovation research is necessary to expand the evidence base” (Seffrin et al., 2010:2–3). Similarly, Caryn Lerman, President of the Society for Research on Nicotine and Tobacco, advised NIH director Francis Collins that if “tobacco use research is to be moved from other NIH institutes to a new Institute, retain tobacco policy and product research within NCI, consistent with the relevance of this subset of the portfolio to medical consequences of drug use” (Lerman, 2010:3, emphasis in original). In other words, there is a concern that addiction’s etiology will be reduced to biology alone, to a “disease of the brain.” No decisions have been announced regarding this possible merger. Framing addiction as a disease of the brain with common mechanisms is one driving force behind the proposed merger, which is of special concern since NIDA claims that it alone “supports more than 85 percent of the world’s research on the health aspects of drug abuse and addiction” (National Institute on Drug Abuse, 2004). Although NIDA funds prevention and environmental influences on drug initiation, maintenance, and cessation, the bulk of NIDA research funding ($519.497 million) goes to “Basic and Clinical Neuroscience,” which includes work to “expand the understanding of the neurobiological, genetic/epigenetic, and behavioral factors underlying drug abuse and addiction” (National Institute on Drug Abuse, 2011). Another $116.017 million goes to “Pharmacotherapies and Medical Consequences” research, which is responsible for “medications development aimed at helping people recover from drug abuse and addiction and sustain abstinence” (National Institute on Drug Abuse, 2011). By contrast, research in “Epidemiology, Services and Prevention Research,” which seeks to “promote integrated approaches to understand and address the interactions between individuals and environments that contribute to the continuum of drug abuse-related problems,” receives less funding ($260.465 million). Cutting-edge research that seeks to “elucidate the nature of the addictive process; to determine the potential use of new therapies for substance abuse, both pharmacological and psychosocial; and to decipher the long-term consequences of drug abuse on brain development, maturation, function, and structure, and on other organ systems,” funded through the intramural research program,” receives $90.368 million (National Institute on Drug Abuse, 2011).NIAAA similarly privileges biomedical research (Midanik, 2004). Clearly, though prevention and gene- and brain-environment interaction is important to these funding institutions, genetic and neuroscience research are prioritized, suggesting the discursive power of reductionist, biological views of addiction. Important social consequences arise from the way neuroscience and genetic research is subtly, and at times not so subtly, constructing a new understanding of addiction as a disease of the brain or as a “genetic” or biological disorder. In this article, we use nicotine addiction as a case study through which to understand the changing nature of our perceptions of addiction and to anticipate how new frameworks will be integrated into existing public health and clinical programs at the federal, state, and local levels. Indeed, the issues and concerns we raise are not limited to the study of one phenomenon, nicotine addiction, but are relevant to a range of complex behaviors that involve substance use for which researchers seek to locate genetic underpinnings. Tobacco serves as an illustrative case because the medicalization of smoking/tobacco addiction has occurred more recently than for other substances, for example, alcoholism. It is also an arena where both social programs (e.g., clean air laws and higher taxes) and pharmaceutical interventions (e.g., nicotine replacement therapies) have been successful. In this article we draw on in-depth interviews with 86 experts in tobacco control, nicotine addiction research, or smoking cessation to examine how genetic research on addiction (and addiction more broadly) shapes the meaning ascribed to smoking and thus affects the scope and structure of tobacco control policy. This article is organized around four key questions raised by critical analyses of this body of research. First, will genetic research change how we understand addiction? We argue that most stakeholders hold a medicalized view of addiction, though a cultural shift that would locate addiction solely within the body, especially with regard to initiation, has not occurred. However, biology is widely understood to be a factor in the strength and speed with which one becomes addicted after initiation. Second, will increased focus on addiction as a disease of the brain lead to unrealistic expectations for treatment? Our data suggests that this is not likely, but for teenagers, it may reinforce expectations that quitting smoking is not difficult. Third, will it change the way people understand cessation, cessation options, and their personal responsibility for or ability to quit smoking? We argue that this research will change what people understand to be the most effective cessation techniques, with increased emphasis on pharmaceuticals and decreased emphasis on “willpower” and modification of behaviors and environments. Finally, will it increase or decrease stigmatization of smoking? We predict that it is unlikely this research will either increase or decrease smoking stigma, but that individuals will utilize the research to buttress their existing view of stigmatization and smoking. Because of the complex nature of smoking and addiction, we join the voices of those from a wide variety of disciplines studying addiction who are calling for an interdisciplinary understanding of addiction as a biosocial or biocultural phenomenon (Acker, 2010; Courtwright, 2010; Keane and Hamill, 2010; Kushner, 2010; Vrecko, 2010; Windle, 2010).