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)

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.

The image of craving as a desire of unimaginable and irresistible force is poised to solve the puzzle of addiction: persistent drug use despite severe negative consequences. But the image is flawed. Drawing on science, philosophy, and first‐person testimony, I argue against irresistibility and develop a more nuanced, heterogeneous account of craving for drugs. Craving comes in three varieties, each corresponding to a kind of answer to the question why people crave drugs: cue‐induced, goal‐focused, and attachment‐based. This in turn grounds (...) an approach to addressing addiction that is humane and heterogeneous, moving beyond strategies that are fundamentally controlling. (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)

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 recent strand in the philosophical literature on addiction emphasizes problems with diachronic self-control. Hanna Pickard, for example, argues that an important aspect of addiction consists in inability to identify with a non-addicted future self. This literature sits alongside another that treats addiction as the product of neural changes that “hijack” mechanisms of reward prediction, habit formation decision making and cognitive control. This hijacking literature originates in accounts that treat the neural changes characteristic of addiction as a brain disease. This (...) paper provides a framework based on predictive processing accounts of self-awareness that integrates the hijacking and diachronic accounts. I discuss a hijacking account proposed to explain disruption of addiction following lesion to the anterior insula cortex. I show how insula activity contributes to the type of identification implicated in diachronic accounts and how deactivation of the anterior insula can disrupt addiction by alienating the subject from her addictive tendencies. This is consistent with neural evidence but also incorporates the personal level features of addiction that are opaque to neural level explanation. (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.

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.

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.