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)

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)

People struggling with addiction are neither powerless over their addiction, nor are they fully in control. Lewis vigorously objects to the brain disease model of addiction, because it makes people lose belief in their self-efficacy, and hence hinders their recovery. Although he acknowledges that there is a compulsive state in addiction, he objects to the claim that this compulsion is carved in stone. Lewis argues that the BDMA underestimates the agency of addicted people, and hence hinder their recovery. Lewis’s work (...) offers us a very much to be welcomed neurobiology of recovery. It offers addicted people a hopeful and respectful narrative for their recovery that treats them as agents rather than as damaged brains. However, I argue that overestimating people’s agency can also result in people losing belief in their self-efficacy. Lewis’s strong focus on the agency of addicted people might not match their experiences of struggle, hence reinforcing their feelings of guilt when they fail to control their use. I propose to replace the notion of addiction as a disease with a notion of a disease-like stage in addiction. I call this stage the duress stage in addiction, in which the addictive behaviour is largely impervious to the agent’s values and to available techniques of self-control. However, the agent can overcome this stage by developing new techniques of self-control, by building on their self-concept and belief in self-efficacy, by changing their environments and habits, and by engaging in projects that are meaningful to the agent. (shrink)

A modest opposition to the brain disease concept of addiction has been mounting for at least the last decade. Despite the good intentions behind the brain disease rhetoric – to secure more biomedical funding for addiction, to combat “stigma,” and to soften criminal approaches – the very concept of addiction as a brain disease is deeply conceptually confused. We question whether Lewis goes far enough in his challenge, robust as it is, of the brain disease concept. For one thing, the (...) notion that addiction is a disease is challenging to refute or confirm because the disease concept itself is poorly defined in medical and psychological nosology. More important, quibbling over what kind of disease addiction is unlikely to be productive. The rational response to adjudicating whether addiction is a brain disease is not to engage in potentially fruitless debates over the question of disease classification but rather to view addiction as an enormously complex set of behaviors that operate on several dimensions, ranging from molecular function and structure and brain physiology to psychology, the psychosocial environment, and social and cultural relations. (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)

Marc Lewis argues that addiction is not a disease, it is instead a dysfunctional outcome of what plastic brains ordinarily do, given the adaptive processes of learning and development within environments where people are seeking happiness, or relief, or escape. They come to obsessively desire substances or activities that they believe will deliver happiness and so on, but this comes to corrupt the normal process of development when it escalates beyond a point of functionality. Such ‘deep learning’ emerges from consumptive (...) habits, or ‘motivated repetition’, and although addiction is bad, it ferments out of the ordinary stuff underpinning any neural habit. Lewis gives us a convincing story about the process that leads from ordinary controlled consumption through to quite heavy addictive consumption, but I claim that in some extreme cases the eventual state of deep learning tips over into clinically significant impairment and disorder. Addiction is an elastic concept, and although it develops through mild and moderate forms, the impairment we see in severe cases needs to be acknowledged. This impairment, I argue, consists in the chronic automatic consumption present in late stage addiction. In this condition, the desiring self largely drops out the picture, as the addicted individual begins to mindlessly consume. This impairment is clinically significant because the machinery of motivated rationality has become corrupted. To bolster this claim I compare what is going on in these extreme cases with what goes on in people who dissociate in cases of depersonalization disorder. (shrink)

Addiction appears to be a deeply moralized concept. To understand the entwinement of addiction and morality, we briefly discuss the disease model and its alternatives in order to address the following questions: Is the disease model the only path towards a ‘de-moralized’ discourse of addiction? While it is tempting to think that medical language surrounding addiction provides liberation from the moralized language, evidence suggests that this is not necessarily the case. On the other hand non-disease models of addiction may seem (...) to resuscitate problematic forms of the moralization of addiction, including, invoking blame, shame, and the wholesale rejection of addicts as people who have deep character flaws, while ignoring the complex biological and social context of addiction. This is also not necessarily the case. We argue that a deficit in reasons responsiveness as basis for attribution of moral responsibility can be realized by multiple different causes, disease being one, but it also seems likely that alternative accounts of addiction as developed by Flanagan, Lewis, and Levy, may also involve mechanisms, psychological, social, and neurobiological that can diminish reasons responsiveness. It thus seems to us that nondisease models of addiction do not necessarily involve moralization. Hence, a non-stigmatizing approach to recovery can be realized in ways that are consistent with both the disease model and alternative models of addiction. (shrink)

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)

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)

This article uses Marc Lewis’ work as a springboard to discuss the socio-political context of the brain disease model of addiction. The claim that promotion of the BDMA is the only way the general public can be persuaded to withhold blame and punishment from addicts is critically examined. After a discussion of public understandings of the disease concept of addiction, it is pointed out that it is possible to develop a scientific account of addiction which is neither a disease nor (...) a moral model but which the public could understand. Evidence is reviewed to suggest that public acceptance of the disease concept is largely lip-service and that the claim the BDMA removes stigma among the public and professionals is unsupported by evidence. Further, there is good evidence that biogenetic explanations of mental/behavioural disorders in general have been counterproductive in the attempt to ally stigma. A model of addiction as a disorder of choice may attract special problems in public-facing communications and risks being misunderstood. However, ways of presenting this model to the public are suggested that may avoid such risks. Lastly, the claim that the BDMA is the only way of ensuring access to treatment and of maintaining research funding for addiction is disputed and a way in which these benefits can be retained under a disorder-of-choice model proposed. The article concludes by enthusiastically endorsing Lewis’ call for a third stage in the governing image of addiction. (shrink)

Lewis’ neurodevelopmental model provides a plausible alternative to the brain disease model of addiction that is a dominant perspective in the USA. We disagree with Lewis’ claim that the BDMA is unchallenged within the addiction field but we agree that it provides unduly pessimistic prospects of recovery. We question the strength of evidence for the BDMA provided by animal models and human neuroimaging studies. We endorse Lewis’ framing of addiction as a developmental process underpinned by reversible forms of neuroplasticity. His (...) view is consistent with epidemiological evidence of addicted individuals ‘maturing out’ and recovering from addiction. We do however hold some reservations about Lewis’ model. We do not think that his analysis of the neurobiological evidence is clearly different from that of the BDMA or that his neurodevelopmental model provides a more rigorous interpretation of the evidence than the BDMA. We believe that our understanding of the neurobiology of drug use is too immature to warrant the major role given to it in the BDMA. Our social research finds very mixed support for the BDMA among addicted people and health professionals in Australia. Lewis’ account of addiction requires similar empirical evaluation of its real-world implications. (shrink)

Addiction appears to be a deeply moralized concept. To understand the entwinement of addiction and morality, we briefly discuss the disease model and its alternatives in order to address the following questions: Is the disease model the only path towards a ‘de-moralized’ discourse of addiction? While it is tempting to think that medical language surrounding addiction provides liberation from the moralized language, evidence suggests that this is not necessarily the case. On the other hand non-disease models of addiction may seem (...) to resuscitate problematic forms of the moralization of addiction, including, invoking blame, shame, and the wholesale rejection of addicts as people who have deep character flaws, while ignoring the complex biological and social context of addiction. This is also not necessarily the case. We argue that a deficit in reasons responsiveness as basis for attribution of moral responsibility can be realized by multiple different causes, disease being one, but it also seems likely that alternative accounts of addiction as developed by Flanagan, Lewis, and Levy, may also involve mechanisms, psychological, social, and neurobiological that can diminish reasons responsiveness. It thus seems to us that nondisease models of addiction do not necessarily involve moralization. Hence, a non-stigmatizing approach to recovery can be realized in ways that are consistent with both the disease model and alternative models of addiction. (shrink)

There is a debate about the nature of addiction, whether it is a result of brain damage, brain dysfunction, or normal brain changes that result from habit acquisition, and about whether it is a disease. I argue that the debate about whether addiction is a disease is much ado about nothing, since all parties agree it is “unquestionably destructive.” Furthermore, the term ‘addiction’ has disappeared from recent DSM’s in favor of a spectrum of ‘abuse’ disorders. This may be a good (...) thing indicating more nuance in typing the heterogeneous phenomena we used to call ‘addiction’. (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)

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)

Lewis ascribes the stubborn persistence of addictions to habit, itself a normal process that does not imply lack of responsiveness to motivation. However, he suggests that more dynamic processes may be involved, for instance that “our recurrently focused brains inevitably self-organize.” Given hyperbolic delay discounting, a reward-seeking internal marketplace model describes two processes, also normal in themselves, that may give rise to the “deep attachment” to addictive activities that he describes: People learn to interpret current choices as test cases for (...) how they can expect to choose in the future, thus recruiting additional incentive against a universal tendency to temporarily prefer smaller, sooner to larger, later rewards. However, when this incentive is not enough, the same interpretation creates incentive to abandon the failed area, leading to the abstinence violation effect and a localized weak will. Normal human value does not come entirely, or even mainly, from expectation of external rewards, but is generated endogenously in imagination. Hyperbolic discounting provides an account of how we learn to cultivate the hedonic importance of occasions for endogenous reward by building appetite. In this account, expectations of the far future have to be rewarded endogenously if they are be as important as currently rewarded alternatives; and this importance is prone to collapse. Both will and hedonic importance are recursive and thus hard to study by controlled experiment, but do represent modelable, reward-based hypotheses about the dynamic nature of habit. (shrink)