Brain Mechanisms and the Disease Model of Addiction: Is it the Whole Story of the Addicted Self? A Philosophical-Skeptical Perspective

Contemporary scientific and philosophical debates on addiction center on two models. In the brain disease model, drug addiction is a “chronic and relapsing brain disease that results from the prolonged effects of drugs on the brain” (Leshner 1997: 45). In contrast, the self or person model individuates addiction in folk psychological terms, as a kind of behavior marked by he repeated use of a drug of choice (DoC) and the difficulty involved in quitting (Satel and Lilienfeld 2013; Flanagan 2013a; Tekin et al. 2017). On the one hand, the brain disease model promotes cellular-level understanding, painting the addict as a biological organism. It takes seriously recent advances in brain imaging methods and the increased sophistication in the neuroscientific modeling of the brain’s reward system—the mesolimbic dopamine system—and promotes pharmaceuticals to target and rebalance the chemical anomalies in it. On the other hand, the self model sees the addict as a person or intentional system (Dennett 1971) who acts according to beliefs and desires and responds to complex historical, environmental, and interpersonal aspects of life. It points to the personal-socio-cultural markers of addiction and promotes social, psychological, and behavioral intervention strategies, e.g., encouraging the addict to change the interpersonal environment that triggers and perpetuates addictive behavior, to receive intensive psychotherapy, to cultivate meditation, and so on. Although each model accepts the validity of the other, to a certain point, there is a prima facie tension between them. The brain disease model acknowledges the environmental, social, and cultural factors in the development of addiction, but its proponents often favor neuroscientific work in lieu of other research paradigms, e.g., social sciences and cognitive sciences. The self model acknowledges the importance of the cellular-level understanding of addiction, but its adherents warn of the dangers of neuro-enthusiasm (Satel and Lilienfeld 2013), i.e., the promotion of scientific and clinical approaches to target the person. In this chapter, I propose using Ken Schaffner’s framework for thinking about reductionism in science (Schaffner 2013) to resolve the issue. In this framework, the brain disease model moves in the direction of what Schaffner calls “sweeping reductionism,” with the self model moving towards “creeping reductionism.” Because of the virtues of creeping reductionism, I argue the self model has more promise for addiction research. I start the chapter with a brief overview of Schaffner’s framework for reduction in science, describing his notions of “sweeping” and “creeping” reductionism. I apply this framework to the brain disease and the self models, noting the epistemic advantages of committing to the latter. In my analysis, I draw on scientific research and clinical work on addiction; to this I add first-person accounts of those influenced by addiction, a seldom used but rich resource(Tekin 2016).