The history of ideas about addiction often comes down to a history of debates over the use and meaning of language. Nowhere is this more clear than in the interminable “Is addiction a ‘disease’?” debate. In Marc Lewis’ excellent Biology of Desire and in his paper that centers this issue, there is far more agreement between his work and mine than there is disagreement on the “disease” question. Here, however, I make a case for greater compatibility between the “disease” view (...) and learning models of addiction than Lewis does, because I think the nuance is worth exploring. Indeed, if addiction science and ethics paid more attention to nuance in general, the whole field would be far better off. (shrink)

In his target article and recent interesting book about addiction and the brain, Marc Lewis claims that the prevalent medical view of addiction as a brain disease or a disorder, is mistaken. In this commentary we critically examine his arguments for this claim. We find these arguments to rest on some problematical and largely undefended assumptions about notions of disease, disorder and the demarcation between them and good health. Even if addiction does seem to differ from some typical brain diseases, (...) we believe contrary to Lewis, that there are still good reasons to maintain its classification as a mental or behavioral disorder. (shrink)

Where does normal brain or psychological function end, and pathology begin? The line can be hard to discern, making disease sometimes a tricky word. In addiction, normal ‘wanting’ processes become distorted and excessive, according to the incentive-sensitization theory. Excessive ‘wanting’ results from drug-induced neural sensitization changes in underlying brain mesolimbic systems of incentive. ‘Brain disease’ was never used by the theory, but neural sensitization changes are arguably extreme enough and problematic enough to be called pathological. This implies that ‘brain disease’ (...) can be a legitimate description of addiction, though caveats are needed to acknowledge roles for choice and active agency by the addict. Finally, arguments over ‘brain disease’ should be put behind us. Our real challenge is to understand addiction and devise better ways to help. Arguments over descriptive words only distract from that challenge. (shrink)

In this two-part analysis, I analyze Marc Lewis’s arguments against the brain-disease view of substance addiction and for a developmental-learning approach that demedicalizes addiction. I focus especially on the question of whether addiction is a medical disorder. Addiction is currently classified as a medical disorder in DSM-5 and ICD-10. It is further labeled a brain disease by NIDA, based on observed brain changes in addicts that are interpreted as brain damage. Lewis argues that the changes result instead from normal neuroplasticity (...) and learning in response to the intense rewards provided by addictive substances, thus that addiction is not a brain disease and by implication not a medical disorder at all. I argue that even if one accepts Lewis’s reinterpretation of the brain evidence, his conclusions do not follow. Relying on my harmful-dysfunction analysis of medical disorder, I defend the view that substance addiction is in fact a medical disorder and a brain disorder. In Part 1, I identify five arguments Lewis puts forward against the brain-disease view and evaluate them as arguments that addiction is not a disorder: Addiction is not a chronic, relapsing condition; There is no clear boundary between addiction and other strong desires; Negative consequences are not unique to disorders; The brain disease model does not account for behavioral addictions; and, Addiction is like love. I argue that Lewis’s arguments are invalid because they fail to take account of the context of addiction and its relation to biological design. (shrink)

In this two-part analysis, I analyze Marc Lewis’s arguments against the brain-disease view of substance addiction and for a developmental-learning approach that demedicalizes addiction. I focus especially on the question of whether addiction is a medical disorder. In Part 1, I argued that, even if one accepts Lewis’s critique of the brain evidence presented for the brain-disease view, his arguments fail to establish that addiction is not a disorder. Relying on my harmful dysfunction analysis of disorder, I defended the view (...) that addiction is a medical disorder and a brain disorder. In Part 2, I consider some broader philosophical issues raised by Lewis’s arguments: I consider a larger puzzle, at the heart of the neo-Kraepelinian program in contemporary psychiatry, that is raised by Lewis’s argument that addiction is not a disorder because the brain displays no damage but only normal learning: must all mental disorders be brain disorders, or can mental disorders occur in normal brains? I argue that mental disorders can occur in normal brains. I critique Lewis’s response to the evolutionary “novel environment” approach to explaining why addiction is a disorder. Lewis agrees with brain-disease proponents that interpreting addiction as brain disorder relieves addicts of moral censure, but I argue that moral defect and brain disease are not exclusive. Finally, I consider Lewis’s “developmental-learning” account of addiction that encourages positive and empowering narrativizing of addiction, but I argue that the developmental-learning view is vacuous due to use of an overly broad notion of “development.”. (shrink)

Drug use and drug addiction are severely stigmatised around the world. Marc Lewis does not frame his learning model of addiction as a choice model out of concern that to do so further encourages stigma and blame. Yet the evidence in support of a choice model is increasingly strong as well as consonant with core elements of his learning model. I offer a responsibility without blame framework that derives from reflection on forms of clinical practice that support change and recovery (...) in patients who cause harm to themselves and others. This framework can be used to interrogate our own attitudes and responses, so that we can better see how to acknowledge the truth about choice and agency in addiction, while avoiding stigma and blame, and instead maintaining care and compassion alongside a commitment to working for social justice and good. (shrink)

Although I reject neuronormativity -- an idea central to the Brain Disease Model of Addiction -- Henden and Gjelsvik argue that the disease definition might refer to normativity in nonneural domains. They profess that a cognitive dysfunction, or a mismatch of evolutionary intentions, could also qualify as norm violations, thus legitimizing the disease label. The need for dividing lines is questioned as well. I rebut these criticisms in turn, but I must admit they are thought provoking.

I review the brain disease model of addiction promoted by medical, scientific, and clinical authorities in the US and elsewhere. I then show that the disease model is flawed because brain changes in addiction are similar to those generally observed when recurrent, highly motivated goal seeking results in the development of deep habits, Pavlovian learning, and prefrontal disengagement. This analysis relies on concepts of self-organization, neuroplasticity, personality development, and delay discounting. It also highlights neural and behavioral parallels between substance addictions, (...) behavioral addictions, normative compulsive behaviors, and falling in love. I note that the short duration of addictive rewards leads to negative emotions that accelerate the learning cycle, but cortical reconfiguration in recovery should also inform our understanding of addiction. I end by showing that the ethos of the disease model makes it difficult to reconcile with a developmental-learning orientation. (shrink)

The current dominant perspective on addiction as a brain disease has been challenged recently by Marc Lewis, who argued that the brain-changes related to addiction are similar to everyday changes of the brain. From this alternative perspective, addictions are bad habits that can be broken, provided that people are motivated to change. In that case, autonomous choice or “free will” can overcome bad influences from genes and or environments and brain-changes related to addiction. Even though we concur with Lewis that (...) there are issues with the brain disease perspective, we also argue that pointing to black swans can be important, that is: there can be severe cases where addiction indeed tips over into the category of brain disease, but obviously that does not prove that every case of addiction falls into the disease category, that all swans are black. We argue that, for example, people suffering from Korsakoff’s syndrome, can be described as having a brain disease, often caused by alcohol addiction. Moreover, the brain changes occurring with addiction are related to choice-behaviour, habit formation and insight, hence essential mental abilities to break the addiction. We argue for a more graded perspective, where both black swans and white swans are rare, and most cases of addiction come as geese in different shades of gray. (shrink)