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


  • We will share all data and coding information with those wishing to replicate the study. The project described was supported by Grant R01 DA14577 from the National Institute on Drug Abuse and the National Human Genome Research Institute. We thank Marguerite Robinson and Ashley Hicks for their thoughtful comments on this article.

Direct correspondence to Molly J. Dingel, University of Minnesota Rochester, Center for Learning Innovation, 300 University Sq., 111 S. Broadway, Rochester, MN 55904 〈〉.



In this article, we seek to better understand how a genomic vision of addiction may influence drug prevention and treatment. Though social influences on substance use and abuse (e.g., peer and family influence, socioeconomic status) are well documented, biomedical intervention is becoming increasingly technoscientific in nature. We wish to elucidate how emphasizing biological influences on substance use may lead to a vision of addiction as a phenomenon isolated within our bodies and neurochemistry, not lived daily within a complex social web of relationships and a particular political economy, including the tobacco industry, which aggressively markets products known to cause harm.


We explore the emerging view of addiction as a “disease of the brain” in open-ended interviews with 86 stakeholders from the fields of nicotine research and tobacco control. Interview data were analyzed using standard qualitative techniques.


Most stakeholders hold a medicalized view of addiction. Though environmental variables are understood to be a primary cause of smoking initiation, the speed and strength with which addiction occurs is understood to be a largely biological process. Though stakeholders believe that an increased focus on addiction as a disease of the brain is not likely to lead to widespread unrealistic expectations for cessation therapies, they remain concerned that it may reinforce teenagers’ expectations that quitting is not difficult. Finally, stakeholder responses indicate that genetic and neuroscientific research is unlikely to increase or decrease stigmatization, but will be used by interest groups to buttress their existing views of the stigma associated with smoking.


We argue that the main potential harms of focusing on biological etiology stem from a concept of addiction that is disassociated from social context. Focusing on genetic testing and brain scans may lead one to overemphasize pharmaceutical “magic bullet cures” and underemphasize, and underfund, more traditional therapies and public health prevention strategies that have proven to be effective. Genetic research on addiction may fundamentally change our conception of deviance and our identities, and may thus transform our susceptibility to substance use into something isolated in our biology, not embedded in a biosocial context.