Most authors who discuss willpower assume that everyone knows what it is, but our assumptions differ to such an extent that we talk past each other. We agree that willpower is the psychological function that resists temptations – variously known as impulses, addictions, or bad habits; that it operates simultaneously with temptations, without prior commitment; and that use of it is limited by its cost, commonly called effort, as well as by the person's skill at executive functioning. However, accounts are (...) usually not clear about how motivation functions during the application of willpower, or how motivation is related to effort. Some accounts depict willpower as the perceiving or formation of motivational contingencies that outweigh the temptation, and some depict it as a continuous use of mechanisms that interfere with re-weighing the temptation. Some others now suggest that impulse control can bypass motivation altogether, although they refer to this route as habit rather than willpower.It is argued here that willpower should be recognized as either or both of two distinct functions, which can be calledresolveandsuppression. Resolve is based on interpretation of a current choice as a test case for a broader set of future choices, which puts at stake more than the outcome of the current choice. Suppression is inhibiting valuation of (modulating) and/or keeping attention from (filtering) immediate alternatives to a current intention. Perception of current choices as test cases for broader outcomes may result in reliable preference for these outcomes, which is experienced as an effortlesshabit– a successful result of resolve, not an alternative method of self-control. Some possible brain imaging correlates are reviewed. (shrink)

Technological artefacts have, in recent years, invited increasingly intimate ways of interaction. But surprisingly little attention has been devoted to how such interactions, like with wearable devices or household robots, shape our minds, cognitive capacities, and moral character. In this thesis, I develop an embodied, enactive account of mind--technology interaction that takes the reciprocal influence of artefacts on minds seriously. First, I examine how recent developments in philosophy of technology can inform the phenomenology of mind--technology interaction as seen through an (...) enactivist lens. Second, I show how an enactive account of remembering can improve operationalizations of the memory palace mnemonic through virtual reality devices. Third, I draw on virtue ethics to argue that an enactivist approach allows us to better grasp the morally shaping aspects of artefacts by looking at social robots. Fourth, I fend off an underlying metaphysical concern about enactivism by arguing that an embodied, enactive account is compatible with the multiple realization of cognitive processes. This principle is often seen as a crucial test favouring accounts such as extended functionalism over enactivism and I argue that some forms of enactivism pass this test as well. Finally, I conclude by considering what the future relationship between enactivism and functionalism may have in store for the study of mind--technology interaction. (shrink)

Background: Recent literature on addiction and judgments about the characteristics of agents has focused on the implications of adopting a ‘brain disease’ versus ‘moral weakness’ model of addiction. Typically, such judgments have to do with what capacities an agent has (e.g., the ability to abstain from substance use). Much less work, however, has been conducted on the relationship between addiction and judgments about an agent’s identity, including whether or to what extent an individual is seen as the same person after (...) becoming addicted. Methods: We conducted a series of vignette-based experiments (total N = 3,620) to assess lay attitudes concerning addiction and identity persistence, systematically manipulating key characteristics of agents and their drug of addiction. Conclusions: In Study 1, we found that US participants judged an agent who became addicted to drugs as being closer to ‘a completely different person’ than ‘completely the same person’ as the agent who existed prior to the addiction. In Studies 2-6, we investigated the intuitive basis for this result, finding that lay judgments of altered identity as a consequence of drug use and addiction are driven primarily by perceived negative changes in the moral character of drug users, who are seen as having deviated from their good true selves. (shrink)

It has recently been suggested that delusions be conceived of as symptoms on the harmful dysfunction account of disorder: delusions sometimes arise from dysfunction, but can also arise through normal cognition. Much attention has thus been payed to the question of how we can determine whether a delusion arises from dysfunction as opposed to normal cognition. In this paper, we consider another question, one that remains under-explored: which delusions warrant treatment? On the harmful dysfunction account, this question dissociates from the (...) question about dysfunction—there are a broad range of “treatable conditions” beyond mere harmful dysfunctions. As such, many conditions that arise from normal cognition are also eligible for medical intervention. We argue that some delusions that arise from normal cognition may well fall under the banner of treatable conditions. We examine the practical and ethical questions surrounding such treatment, including the issue of coercive and deceptive treatment options. (shrink)

This article uses Marc Lewis’ work as a springboard to discuss the socio-political context of the brain disease model of addiction (BDMA). 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)

I applaud Fenton and Wiers' attempt to find a demarcation point between cases of addiction that fall within the range of normal function and those that may count as disease. However, I argue that continua don't offer demarcation points, the mechanisms involved are not demonstrably different, and trying to pin down subjectivity doesn't help.

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)

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)

Skepticism about the limits of online learning is as old as online learning itself. As with other technologically-driven innovations in pedagogy, there are deep-seated worries that important educational goods might be effaced or obscured by the ways of teaching and learning that online methods allow. One family of such worries is inspired by reflections on the bodily basis of an important kind of understanding, and skepticism over whether this bodily basis can be inculcated in the absence of actual, flesh-and-blood, classroom (...) interactions. This paper focuses on the ways in which such worries arise in the influential work of Hubert Dreyfus. The negative conclusion for which I argue is that endorsing Dreyfus's Merleau-Pontian picture of the relationship between bodily skill and understanding does not commit us to his general pessimism concerning online learning—bodily, emotional, and interactive dimensions might be essential to learning, but we lack reasons to think that online learning necessarily lacks these dimensions. The negative argument motivates a positive claim: rather than giving up on online learning we should focus on designing courses and pedagogies that scaffold the bodily, affective and interactive dynamics constitutive of understanding in a particular domain. (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)

In this introduction we set out some salient themes that will help structure understanding of a complex set of intersecting issues discussed in this special issue on the work of Marc Lewis: conceptual foundations of the disease model, tolerating the disease model given socio-political environments, and A third wave: refining conceptualization of addiction in the light of Lewis’s model.

Can addiction be credibly invoked as an excuse for moral harms secondary to particular decisions to use drugs? This question raises two distinct sets of issues. First, there is the question of whether addiction is the sort of consideration that could, given suitable assumptions about the details of the case, excuse or mitigate moral blameworthiness. Most discussions of addiction and moral responsibility have focused on this question, and many have argued that addiction excuses. Here I articulate what I take to (...) be the best argument for this view, based on the substantial difficulty that people with severe addiction experience in controlling drug-related behavior. This, I argue, may in some cases be sufficient to ground a mitigating excuse, given the way in which addiction undermines agents’ responsiveness to relevant moral reasons to do otherwise. Much less attention has been devoted to a second set of issues that critically affect the possibility of applying this mitigating excuse in particular cases, derived from the ambivalent nature of agential control in addiction. In order to find a fitting response to moral harm, the person with the right standing to blame must make a judgment about the extent to which the agent possessed certain morally relevant capacities at the time of the act. In practice, this will often prove tremendously difficult to assess. The ethical challenge for the person with the right standing to blame is fundamentally one of making a judgment about matters that seem underdetermined by the available evidence. (shrink)

While some form of loss of control is often assumed to be a common feature of the diverse manifestations of addiction, it is far from clear how loss of control should be understood. In this paper, I put forward a concept of decrease in control in addiction that aims to fill this gap and thus provide a general framework for thinking about addictive behavior. The development of this account involves two main steps. First, I present a view of degrees of (...) control as the degree to which an agent would be responsive to potential or counterfactual sufficient reasons to do otherwise. Second, I sketch an account of the relevant control-undermining factors in addiction that is consonant with my proposed view of degrees of control. Being a high-level functional property, reasons-responsiveness is particularly well suited to frame an account of control-undermining factors that is doubly pluralistic: it encompasses the contribution of factors both internal and external to the agent, and it is consistent with various proposals as to the precise nature of the anomaly taking place in the psychology of addiction. (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)

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)

Flanagan asserts that my model of addiction would apply as well to sonnet writing. Yet his most interesting point is that “addiction” is an imprecise label for a cluster of distinct phenomena. I agree with him that we need to examine these distinctions, but that doesn’t negate their shared features. Neuroscience can play an important role in advancing our understanding of both commonalities and distinctions within the phenomena of addiction.

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.

Szalavitz’s model and mine share a good many components. Foremost among them is the conviction that addiction is a developmental trajectory, not a disease. Szalavitz is correct that we should consider controlled substance use an acceptable outcome, though I would like her to shift her terminology away from the medical mainstream. Finally, I suggest that Szalavitz's important idea of a "reset" in brain development might best be addressed by the notion of kindling.

Although these authors sometimes resort to medical terminology, we strongly agree that addiction is not a disease and that the Brain Disease Model of Addiction captures only one part of the story and distorts the big picture. Yet Satel and Lilienfeld continue to conflate a neurobiological model with a disease model. They also complain that my modeling of addiction reveals a hidden “neurocentric” bias, despite my integration of multiple levels of analysis, exactly as they recommend.

Frank and Nagel are very interested in the causes and consequences of moralizing about addiction. If addiction is a disease, moralistic concerns are sidelined. If it's a choice, we'd better identify clear reasons to absolve addicts from blame. While these are interesting considerations, they don't have much to do with the model of addiction I put forward in the target article.

Berridge's nuanced approach to the conceptualization of addiction as a disease is easier for me to accept than most others. In fact, Berridge and I agree on many core features of addiction, but still not on how to label it. When competing definitions reach a standoff on intellectual grounds, we should look at the clinical utility of each. And here I think that Berridge misses a critical insight. Yet, we end by agreeing to keep listening to each other.

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)

In 2022, an estimated 110,000 people died of an opioid-related drug overdose in the United States (Ahmad et al. 2024) primarily related to illicit fentanyl. However, fatal overdoses comprise only a...