Neuroscience has substantially advanced the understanding of how changes in brain biochemistry contribute to mechanisms of tolerance and physical dependence via exposure to addictive drugs. Many scientists and mental health advocates scaffold this emerging knowledge by adding the imprimatur of disease, arguing that conceptualizing addiction as a brain disease will reduce stigma amongst the folk. Promoting a brain disease concept is grounded in beneficent and utilitarian thinking: the language makes room for individuals living with addiction to receive the same level (...) of compassion and access to healthcare services as individuals living with other medical diseases, and promotes enlightened social and legal policies. However such claims may yield unintended consequences by fostering discrimination commonly associated with pathology. Specifically, the language of neuroscience used to describe addiction may reduce attitudes such as blame and responsibility while inadvertently identifying addicted persons as neurobiological others. In this paper, we examine the merits and limitations of adopting the language of neuroscience to describe addiction. We argue that the reframing of addiction in the language of neuroscience provides benefits such as the creation of empowered biosocial communities, but also creates a new set of risks, as descriptive neuroscience concepts are inseparable from historical attitudes and intuitions towards addiction and addicted persons. In particular, placing emphasis on the diseased brain may foster unintended harm by paradoxically increasing social distance towards the vulnerable group the term is intended to benefit. (shrink)

Supervised injectable opioid assisted treament prescribes injectable opioids to individuals for whom other forms of addiction treatment have been ineffective. In this article, we examine arguments that opioid-dependent people should be assumed incompetent to voluntarily consent to clinical research on siOAT unless proven otherwise. We agree that concerns about competence and voluntary consent deserve careful attention in this context. But we oppose framing the issue solely as a matter of the competence of opioid-dependent people and emphasize that it should be (...) considered in the context of inequities in access to siOAT as a medical treatment. Consequently, we suggest that bioethics literature on nonexploitation, which focuses on clinical research in low-income countries, is helpful due to locating ethical issues within systemic social conditions. Finally, we consider the implications of our argument for the ethics of clinical research on siOAT. (shrink)

Free will has been the object of debate in the context of addiction given that addiction could compromise an individual’s ability to choose freely between alternative courses of action. Proponents of the brain-disease model of addiction have argued that a neuroscience perspective on addiction reduces the attribution of free will because it relocates the cause of the disorder to the brain rather than to the person, thereby diminishing the blame attributed to the person with an addiction. Others have worried that (...) such displacement of free will attribution would make the person with a drug addiction less responsible. Using the paradigmatic literature on the seductive allure of neuroscience explanations, we tested whether neuroscience information diminishes attributions of free will in the context of addiction and whether respondent characteristics influence these attributions and modulate the effect of neuroscience information. We performed a large-scale, web-based experiment with 2,378 German participants to explore how attributions of free will in the context of addiction to either alcohol or cocaine are affected by: (1) a text with a neurobiological explanation of addiction, (2) a neuroimage showing effects of addiction on the brain, and (3) a combination of a text and a neuroimage, in comparison to a control group that received no information. Belief in free will was measured using the FAD-Plus scale and was, subsequent to factor analysis, separated into two factors: responsibility and volition. The investigated respondent characteristics included gender, age, education, self-reported knowledge of neuroscience, substance-use disorder (SUD), and having a friend with SUD. We found that attributions of volition (in the cocaine-subsample) were reduced in the text and neuroimage-treatment compared to the control group. However, respondent characteristics such as education and self-reported knowledge of neuroscience were associated with lower attributions of responsibility for both substances, and education was associated with lower attribution of volition for the alcohol sub-sample. Interaction analyses showed that knowledge of neuroscience was found to generally decrease attribution of responsibility. Further research on attribution of free will should consider the effects of context and respondent characteristics, which appeared surprisingly larger than those induced by experimental treatments. (shrink)

To deepen understanding of efforts to consider addiction a “brain disease,” we review critical appraisals of the disease model in conjunction with responses from in-depth semistructured stakeholder interviews with (1) patients in treatment for addiction and (2) addiction scientists. Sixty-three patients (from five alcohol and/or nicotine treatment centers in the Midwest) and 20 addiction scientists (representing genetic, molecular, behavioral, and epidemiologic research) were asked to describe their understanding of addiction, including whether they considered addiction to be a disease. To examine (...) the NIDA brain disease paradigm, our approach includes a review of current criticism from the literature, enhanced by the voices of key stakeholders. Many argue that framing addiction as a disease will enhance therapeutic outcomes and allay moral stigma. We conclude that it is not necessary, and may be harmful, to frame addiction as a disease. (shrink)