Online research in philosophy

There is a growing consensus among neuroscientists that people can become addicted to food, and that at least some cases of obesity have addiction as their cause. By contrast, the rest of the world continues to see obesity as either a disease of the metabolism, or as a reckless case of self-harm. Among obesity researchers, there has been a lively debate on the issue of whether obesity ought to be considered a disease. Few researchers, however, have suggested that obesity is a disease in the same sense as addiction is usually claimed to be a disease—that is, a disease of behaviour with a neurological cause. In this piece, I review what is now a compelling body of evidence for food addiction, to establish that many or most cases of obesity have addiction at their foundation. I then argue that in spite of this, obesity ought not to be considered a neurobehavioural disease in the sense usually attributed to drug addiction. Given the link between addiction and obesity, this implies that the disease conception of addiction must be abandoned. I conclude by assessing some of the implications this move has for policy and ethics, with regard to both obesity and drug addiction.

This essay investigates the tensions produced by the categorization of different forms of excessive desire under the singular model of addiction, and it challenges the increasing acceptance of addiction as an all-purpose explanation for unruly desires through a comparison of the different forms of disordered desire in sex addiction and alcoholism. Moreover, it argues for a broad understanding of addictive processes to undermine the normative and moralizing assumptions of addiction discourses. Refiguring addiction as a kind of intimacy is one way of making sense of the intense relationships people can develop with substances and with activities.

Leading addiction researchers survey the latest findings in addiction science, countering the simplistic cultural stereotypes of the addict.

Biomedical science has been remarkably successful in explaining illness by categorizing diseases and then by identifying localizable lesions such as a virus and neoplasm in the body that cause those diseases. Not surprisingly, researchers have aspired to apply this powerful paradigm to addiction. So, for example, in a review of the neuroscience of addiction literature, Hyman and Malenka (2001, p. 695) acknowledge a general consensus among addiction researchers that “[a]ddiction can appropriately be considered as a chronic medical illness.” Like other diseases, “Once addiction has taken hold, it tends to follow a chronic course.” (Koob and La Moal 2006, p. ?). Working from this perspective, much effort has gone into characterizing the symptomology of addiction and the brain changes that underlie them. Evidence for involvement of dopamine transmission changes in the ventral tegmental area (VTA) and nucleus accumbens (NAc) have received the greatest attention. Kauer and Malenka (2007, p. 844) put it well: “drugs of abuse can co-opt synaptic plasticity mechanisms in brain circuits involved in reinforcement and reward processing”. Our goal in this chapter to provide an explicit description of the assumptions of medical models, the different forms they may take, and the challenges they face in providing explanations with solid evidence of addiction. <br>.

Neuroscience has substantially advanced the understanding of how changes in brain biochemistry contribute to mechanisms of tolerance and physical dependence via exposure to addictive drugs. Many scientists and mental health advocates scaffold this emerging knowledge by adding the imprimatur of disease, arguing that conceptualizing addiction as a brain disease will reduce stigma amongst the folk. Promoting a brain disease concept is grounded in beneficent and utilitarian thinking: the language makes room for individuals living with addiction to receive the same level of compassion and access to healthcare services as individuals living with other medical diseases, and promotes enlightened social and legal policies. However such claims may yield unintended consequences by fostering discrimination commonly associated with pathology. Specifically, the language of neuroscience used to describe addiction may reduce attitudes such as blame and responsibility while inadvertently identifying addicted persons as neurobiological others. In this paper, we examine the merits and limitations of adopting the language of neuroscience to describe addiction. We argue that the reframing of addiction in the language of neuroscience provides benefits such as the creation of empowered biosocial communities, but also creates a new set of risks, as descriptive neuroscience concepts are inseparable from historical attitudes and intuitions towards addiction and addicted persons. In particular, placing emphasis on the diseased brain may foster unintended harm by paradoxically increasing social distance towards the vulnerable group the term is intended to benefit.

Neuroscience has substantially advanced the understanding of how changes in brain biochemistry contribute to mechanisms of tolerance and physical dependence via exposure to addictive drugs. Many scientists and mental health advocates scaffold this emerging knowledge by adding the imprimatur of disease, arguing that conceptualizing addiction as a brain disease will reduce stigma amongst the folk. Promoting a brain disease concept is grounded in beneficent and utilitarian thinking: the language makes room for individuals living with addiction to receive the same level of compassion and access to healthcare services as individuals living with other medical diseases, and promotes enlightened social and legal policies. However such claims may yield unintended consequences by fostering discrimination commonly associated with pathology. Specifically, the language of neuroscience used to describe addiction may reduce attitudes such as blame and responsibility while inadvertently identifying addicted persons as neurobiological others. In this paper, we examine the merits and limitations of adopting the language of neuroscience to describe addiction. We argue that the reframing of addiction in the language of neuroscience provides benefits such as the creation of empowered biosocial communities, but also creates a new set of risks, as descriptive neuroscience concepts are inseparable from historical attitudes and intuitions towards addiction and addicted persons. In particular, placing emphasis on the diseased brain may foster unintended harm by paradoxically increasing social distance towards the vulnerable group the term is intended to benefit.

To cite this Article: , 'Affective Neuroscience and Addiction', The American Journal of Bioethics, 7:1, 20 - 21 To link to this article: DOI: 10.1080/15265160601064066 URL: http://dx.doi.org/10.1080/15265160601064066..

Addiction neuroethics has emerged as a field that underscores the public orientation of addiction neuroscience. The goal of this chapter is to suggest a social epistemology of neuroscience, with special attention to the communication of addiction neuroscience. It aims to set social epistemology in a complementary relation to neuroethics, as part of this important interdisciplinary space, but one where issues of knowledge circulation and science communication are foregrounded. This focus demonstrates the difficulties of seeing science communication as an instrumental means to fulfilling a wide variety of epistemic ends. The chapter also examines the roles of communication optimism and pessimism in framing the communication work that needs to be achieved for a successful publicly oriented field of addiction neuroethics.

This book, a member of the Series in Affective Science, is a unique interdisciplinary sequence of articles on the cognitive neuroscience of emotion by some of ...