Hanna Pickard1. 1. William H. Miller III Department of Philosophy & Berman Institute of Bioethics, Johns Hopkins University, 281 Gilman Hall, 3400 N. Charles Street, Baltimore, MD, 21218, USA. h.pickard@jhu.edu.
Abstract
RATIONALE: Although increasingly subject to criticism, the brain disease model of addiction (BDMA) remains dominant within addiction science. Yet few advocates or critics of the BDMA have provided an account of what a brain disease is. The aim of this review is to conceptually clarify what it would mean for the BDMA to be true, rather than to argue decisively for or against it. OBJECTIVES: Conceptual clarification of the BDMA requires consideration of possible models of disease and their relationship to the BDMA. A barrier to such consideration is belief that the BDMA is necessary to combatting addiction stigma. To address this barrier, I begin with discussion of what we know about the effects of the brain disease label on addiction stigma, and why labelling effects should have no bearing on the validity of the BDMA. I then distinguish strong, minimal, network, and mismatch models of disease, and I argue that the BDMA aligns with a strong disease model. This means that underlying brain pathology is hypothesized to be the cause of the personal-level observable signs and experienced symptoms characteristic of addiction. Evaluation of the BDMA therefore requires analysis of the concepts of brain dysfunction and causation, and their application to addiction science. RESULTS: Brain dysfunction cannot be analyzed merely as brain changes or brain differences; nor can it be inferred merely from the presence of personal-level signs and symptoms. It is necessary to have an account of normal brain function by which to measure it. The theoretical and empirical challenges to developing such an account are not insurmountable, but they are substantial. Although there exist competing analyses of causation, there is a relatively standard method used to establish it within experimental science: intervention. Using this method, the causal significance of brain states, such as, e.g., extensive gray matter loss and/or neuroadapations in the mesocorticolimbic dopamine system, is not yet fully demonstrated. Further studies are necessary to determine their effect compared with other possible variables, such as, e.g., alternative reinforcers. CONCLUSIONS: Conceptual clarification and preliminary empirical assessment of the BDMA recommends agnosticism about its validity and an openness to heterogeneity; in some cases addiction may be a brain disease, in others not. Either way, addiction stigma can be combatted by fighting moralism about drugs and moralistic drug policies directly, as opposed to resting hopes on the brain disease label.
RATIONALE: Although increasingly subject to criticism, the brain disease model of addiction (BDMA) remains dominant within addiction science. Yet few advocates or critics of the BDMA have provided an account of what a brain disease is. The aim of this review is to conceptually clarify what it would mean for the BDMA to be true, rather than to argue decisively for or against it. OBJECTIVES: Conceptual clarification of the BDMA requires consideration of possible models of disease and their relationship to the BDMA. A barrier to such consideration is belief that the BDMA is necessary to combatting addiction stigma. To address this barrier, I begin with discussion of what we know about the effects of the brain disease label on addiction stigma, and why labelling effects should have no bearing on the validity of the BDMA. I then distinguish strong, minimal, network, and mismatch models of disease, and I argue that the BDMA aligns with a strong disease model. This means that underlying brain pathology is hypothesized to be the cause of the personal-level observable signs and experienced symptoms characteristic of addiction. Evaluation of the BDMA therefore requires analysis of the concepts of brain dysfunction and causation, and their application to addiction science. RESULTS: Brain dysfunction cannot be analyzed merely as brain changes or brain differences; nor can it be inferred merely from the presence of personal-level signs and symptoms. It is necessary to have an account of normal brain function by which to measure it. The theoretical and empirical challenges to developing such an account are not insurmountable, but they are substantial. Although there exist competing analyses of causation, there is a relatively standard method used to establish it within experimental science: intervention. Using this method, the causal significance of brain states, such as, e.g., extensive gray matter loss and/or neuroadapations in the mesocorticolimbic dopamine system, is not yet fully demonstrated. Further studies are necessary to determine their effect compared with other possible variables, such as, e.g., alternative reinforcers. CONCLUSIONS: Conceptual clarification and preliminary empirical assessment of the BDMA recommends agnosticism about its validity and an openness to heterogeneity; in some cases addiction may be a brain disease, in others not. Either way, addiction stigma can be combatted by fighting moralism about drugs and moralistic drug policies directly, as opposed to resting hopes on the brain disease label.
Authors: Rita Z Goldstein; A D Bud Craig; Antoine Bechara; Hugh Garavan; Anna Rose Childress; Martin P Paulus; Nora D Volkow Journal: Trends Cogn Sci Date: 2009-08-27 Impact factor: 20.229
Authors: Jillian L Seiler; Caitlin V Cosme; Venus N Sherathiya; Michael D Schaid; Joseph M Bianco; Abigael S Bridgemohan; Talia N Lerner Journal: Curr Biol Date: 2022-02-07 Impact factor: 10.900