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)

The addiction literature is fraught with conceptual confusions, stalled debates, and an unfortunate lack of clear and careful attempts to delineate the phenomenon of addiction in a way that might lead to consensus. My dissertation has two overarching aims, one metaphysical and one practical. -/- The first aim is to defend an account of addiction as the systematic disposition to fail to control one’s desires to engage in certain types of behaviors. I defend the inclusion of desires and impaired control (...) in the definition, and I flesh out the notion of systematicity central to my dispositionalist framework. I engage the so-called ‘disease vs. choice’ debate, criticizing its presupposition that we are dealing here with a dichotomy and arguing that the movement towards a middle ground is the right track to take. I explain how the dispositionalist account can capture this middle ground and how it serves to expand upon existing views, in particular by filling in the metaphysical details. -/- The second aim is to show how the account I defend can help to unify the extant views and disciplinary perspectives in the literature. Both the dispositionalist aspect of my framework and the methodology adopted (applied ontology and systematic metaphysics) can move the literature towards both substantive and methodological unification. This will help to clear up conceptual confusions, resolve (or sometimes dissolve) apparently intractable disputes, situate different research perspectives with respect to each other, facilitate interdisciplinary dialogue, and help to frame important questions about addiction. Finally, I offer the beginnings of an ontology of addiction, which will provide a terminologically well-structured guide to the addiction literature in a way that will facilitate more effective and efficient communication and data management across disciplines. (shrink)

Addicts are often portrayed as compelled by their addiction and thus as a paradigm of unfree action and mitigated blame. This chapter argues that our best scientific theories of addiction reveal that, psychologically, addicts are not categorically different from non-addicts. There is no pairing of contemporary accounts of addiction and of prominent theories of moral responsibility that can justify our intuitions about the mitigation of addicts but not non-addicts. Two conclusions are advanced. First, we should either treat addicts as we (...) normally treat non-addicts (as fully culpable) or embrace the skeptical conclusion that everyone is less responsible than we thought—perhaps not responsible at all. Second, we should be doubtful that theorizing about responsibility will be advanced by focusing on particular kinds of psychopathologies. (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)

Substance addiction affects millions of individuals worldwide and yet there is no consensus regarding its conceptualisation. Recent neuroscientific developments fuel the view that addiction can be classified as a brain disease, whereas a different body of scholars disagrees by claiming that addictive behaviour is a choice. These two models, the Brain Disease Model and the Choice Model, seem to oppose each other directly. This article contends the belief that the two models in the addiction debate are polar opposites. It shows (...) that it is not the large amount of addiction research in itself what sets the models apart, but rather their extrapolated conclusions. Moreover, some of the most fiercely debated aspects - for instance, whether or not addiction should be classified as a disease or disorder - are irrelevant for the conceptualisation of addiction. Instead, the real disagreement is shown to revolve around capacities. Discussing addiction-related capacities, especially regarding impaired control, rather than the assumed juxtaposition of the two models can be considered the true addiction debate. More insight into the extent to which the capacities of the addicted individual were affected would be highly useful in various other areas, especially legal responsibility. (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)

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)

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)

Love, sex, and physical intimacy are some of the most desired goods in life and they are increasingly being sought on dating apps such as Tinder, Bumble, and Badoo. For those who want a leg up in the chase for other people’s attention, almost all of these apps now offer the option of paying a fee to boost one’s visibility for a certain amount of time, which may range from 30 min to a few hours. In this article, I argue (...) that there are strong moral grounds and, in countries with laws against unconscionable contracts, legal ones for thinking that the sale of such visibility boosts should be regulated, if not banned altogether. To do so, I raise two objections against their unfettered sale, namely that it exploits the impaired autonomy of certain users and that it creates socio-economic injustices. (shrink)

Substance addiction has been historically conceived and widely researched as a brain disease. There have been ample criticisms of brain-centred approaches to addiction, and this paper aims to align with one such criticism by applying insights from phenomenology of psychiatry. More precisely, this work will apply Merleau-Ponty’s insightful distinction between the biological and lived body. In this light, the disease model emerges as an incomplete account of substance addiction because it captures only its biological aspects. When considering addiction as a (...) brain disorder, it will be shown that research fails to account for the contextual, functional, and emotional aspects inherent to subjective health. It is concluded that, while the disease model is fundamental to our understanding of what happens in the brain, its brain-centred approach is cure-oriented. Instead, we suggest a care-orientated approach, which understands and treats the psychological feel as bodily experience situated in an environment, allowing for a more encompassing therapeutic perspective. (shrink)

Bianchi and colleagues have written an important article that proposes a harm reduction approach to eating disorders that mediates the ethical tension in the l...

Previous discussions of addiction have often focused on the question of whether addiction is a disease. This discussion distinguishes that question – the disease question – from the question of whether addiction is a disability. I argue that, however one answers the disease question, and indeed on almost any credible account of addiction, addiction is a disability. I then consider the implications of this view, or why it matters that addiction is a disability. The disease model of addiction has led (...) many to see addiction as primarily a medical problem, and to make medical treatment of the addicted person the first priority in addressing addiction. Once addiction is viewed as a disability, different concerns are foregrounded. The problem of addiction resides not only in the addicted person, but also in the social environment in which the addicted person finds herself. The fundamental ethical question about addiction is not how addicted persons can be treated or otherwise changed, but how a just society can make reasonable accommodations for addicted persons. (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)

Previous studies suggest that psychopathic traits commonly present as comorbid with substance use disorders. Moreover, neuroimaging and psychometric findings suggest that psychopathic traits may predispose individuals to a sensitized reward response to drugs. Given that substance use disorders are characterized by a neurocognitive bias toward drug-reward relative to non-drug reward, it is possible that heightened psychopathic characteristics may further predispose to this processing bias. To evaluate this possibility, we assessed psychopathic traits (measured using the PCL-R; Hare, 2003 ) in 105 (...) probationers/parolees and evaluated the relationship between PCL-R scores, lifetime duration of drug use, and biases in neural response to drug- compared to food-related videos. Psychopathic traits (potentially driven by interpersonal/affective traits) were positively correlated with drug > food reactivity within the right insula and left amygdala. In addition, psychopathic traits modulated the relationship between drug use and drug > food reactivity within the left dorsomedial prefrontal cortex, right insula, and left caudate nucleus. Specifically, lifetime duration of drug use correlated positively with drug > food reactivity in participants with lower levels of psychopathic traits and correlated negatively with drug > food reactivity in individuals with higher levels of psychopathic traits. These results help reconcile prior studies on psychopathy and drug-stimulus processing and provide neurocognitive support for the notion that psychopathic traits serve as an underlying risk factor for substance use disorders. These results suggest that different treatment regimens for substance abuse for individuals with higher or lower levels of psychopathy may be beneficial and suggest that reduction of neurocognitive biases to drug-related stimuli may offer useful targets for future treatment protocols. (shrink)

Cannabis use in some individuals can meaningfully introduce de novo risk for the initiation of opioid use and development of opioid use disorder. These risks may be particularly high during adolescence when cannabis use may disrupt critical periods of neurodevelopment. Current research studying the combination of genetic and environmental factors involved in substance use disorders is poorly understood. More research is needed, particularly to identify which adolescents are most at risk and to develop effective interventions addressing contributing factors such as (...) trauma and psychiatric comorbidity. (shrink)

The brain disease model of addiction is widely endorsed by agencies concerned with treating behavioral disorders and combatting the stigma often associated with addiction. However, both its accuracy and its effectiveness in reducing stigma have been challenged. A proposed alternative, the “choice” model, recognizes the residual rational behavior control capacities of addicted individuals and their ability to make choices, some of which may cause harm. Since harmful choices are ordinarily perceived as blameworthy, the choice model may inadvertently help justify stigma. (...) This paper seeks to fully naturalize the choice model by highlighting the determinants of voluntary action and thus increase its potential for destigmatizing addiction. In light of a deterministic understanding of behavior, it is unreasonable to suppose that addicted individuals could have made different choices in becoming addicted and in subsequent situations. To the extent that stigma is motivated by the supposition that addicted individuals could have chosen otherwise in actual situations, a deterministic understanding of addictive behavior promises to mitigate blame and stigma. (shrink)

The present dissertation starts from the general claim that neuroscience is not neutral, with regard to theoretical questions like the nature of consciousness, but it needs to be complemented with dedicated conceptual analysis. Specifically, the argument for this thesis is that the combination of empirical and conceptual work is a necessary step for assessing the significant questions raised by the most recent study of the brain. Results emerging from neuroscience are conceptually very relevant in themselves but, notwithstanding its theoretical sophistication, (...) neuroscience is not sufficient to provide a complete interpretation or an appropriate understanding of their impact. Consequently, the present thesis starts from the need for an interdisciplinary and hybrid field of research, i.e. fundamental neuroethics. Within this framework, the thesis takes consciousness and related disorders and the addicted brain as illustrative cases of the potential fruitful collaboration between empirical and conceptual investigations. The general goal of the thesis is to contribute to the overall development of bridging the gap between empirical and conceptual understandings of consciousness. The first paper sets the theoretical framework, providing an empirically-based description of the brain with significant philosophical implications for an understanding of consciousness. The last three papers of the thesis try to apply the theoretical framework to illustrative cases. Papers II and III analyse the possible application of science and technology for an easier detection and clinical care of patients with disorders of consciousness, with particular attention to communication mediated by neurotechnology and the simulation of the conscious brain, respectively; paper IV provides a potentially new ethical analysis of addiction within the elaborated general conceptual framework. The conclusion of the thesis is that the impact of neuroscientific results needs that a dedicated conceptual approach reveals and investigates their conceptual meaning. This conceptual analysis is not exclusive but integrative and complementary to the empirical science. The case of consciousness, analysed from both an ethical and conceptual point of view, is highly illustrative in this respect. In the end, a conceptual/linguistic work of clarification is urgently needed. (shrink)

Clinical fields of the “sciences of the mind” (psychotherapy, psychiatry, etc.) lack integrative conceptual frameworks that have explanatory power. Mainly descriptive-classificatory taxonomies like DSM dominate the field. New taxonomies such as Research Domain Criteria (RDoC) aim to collect scientific knowledge regarding “systems” for “processes” of the brain. These terms have a supradisciplinary” meaning if they are considered in context of Systems Science. This field emerges as a platform of theories like general systems theory, catastrophe theory, synergetics, chaos theory, etc. It (...) provides a lot of abstract concepts, constructs, methods and models. We assume that these tools also enable theoretical integration in the diversified field of clinical practice in the sciences of the mind. Additionally, systems thinking in clinical psychology improves conceptual links to currently network-oriented neurobiology. However, clear definitions of systemic terms are necessary to emerge from their mainly metaphorical use. Here we revise mainly terms like “structure”, “process” and “dynamics” as they are used already in psychology, psychoanalysis, psychopathology and psychiatry in an ill-defined way. For instance, affective-cognitive structures like “life space” or “object representations” can be seen as products of mental processing. These structures, in turn, modulate dynamics of mental processes. Additionally, we suggest a coupled network concept of emotions and motivations as the main subsystem that modulates mental dynamics that results in a qualitative systemic model of the mind. Finally, we assume that a revisited systemic approach could improve interdisciplinary understanding of the mental. ystem for mental dynamics. In this context, we assume that a revisited systemic approach could improve interdisciplinary understanding of the mental. (shrink)

Physicians who care for critically ill people with opioid use disorder frequently face medical, legal, and ethical questions related to the provision of life-saving medical care. We examine a complex medical case that illustrates these challenges in a person with relapsing injection drug use. We focus on a specific question: Is futility an appropriate and useful standard by which to determine provision of life-saving care to such individuals? If so, how should such determinations be made? If not, what alternative decisionmaking (...) framework exists? We determine that although futility has been historically utilized as a justification for withholding care in certain settings, it is not a useful standard to apply in cases involving people who use injection drugs for non-medical purposes. Instead, we are welladvised to explore each patient's situation in a holistic approach that includes the patient, family members, and care providers in the decision-making process. The scope of the problem illustrated demonstrates the urgent need to definitively improve outcomes in people who use injection drugs. Increasing access to high quality medication-assisted treatment and psychiatric care for individuals with opioid use disorder will help our patients achieve a sustained remission and allow us to reach this goal. (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)

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)

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...

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)

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)

This qualitative study, using content analysis, examines to what extent addiction, its causes, consequences, and prevention methods are covered and which types of addiction are discussed in Religious Culture and Moral Knowledge courses. The study focuses on how these topics are presented in RCMK textbooks, which primarily address substance addictions such as drugs, alcohol, and tobacco, while briefly mentioning behavioural addictions like overeating, gambling, and technology use. Addiction is portrayed as a moral issue affecting mental, physical, and spiritual health, as (...) well as an individual's self-control and sense of responsibility. Substance addictions receive greater emphasis, reflecting their association with religious texts and state anti-addiction policies, whereas behavioural addictions are given less consideration. The study concludes that addiction should be approached in a comprehensive and progressively deepening manner as students advance through grade levels in RCMK textbooks. In its current form, the information does not appear to effectively develop skills or serve a preventive function that encourages healthier choices. (shrink)