Online research in philosophy

There continues to be a debate on whether addiction is best understood as a brain disease or a moral condition. This debate, which may influence both the stigma attached to addiction and access to treatment, is often motivated by the question of whether and to what extent we can justly hold addicted individuals responsible for their actions. In fact, there is substantial evidence for a disease model, but the disease model per se does not resolve the question of voluntary control. Recent research at the intersection of neuroscience and psychology suggests that addicted individuals have substantial impairments in cognitive control of behavior, but this "loss of control" is not complete or simple. Possible mechanisms and implications are briefly reviewed.

Deep brain stimulation (DBS) has been proposed as a potential treatment of drug addiction on the basis of its effects on drug self-administration in animals and on addictive behaviours in some humans treated with DBS for other psychiatric or neurological conditions. DBS is seen as a more reversible intervention than ablative neurosurgery but it is nonetheless a treatment that carries significant risks. A review of preclinical and clinical evidence for the use of DBS to treat addiction suggests that more animal research is required to establish the safety and efficacy of the technology and to identify optimal treatment parameters before investigating its use in addicted persons. Severely addicted persons who try and fail to achieve abstinence may, however, be desperate enough to undergo such an invasive treatment if they believe that it will cure their addiction. History shows that the desperation for a cure of addiction can lead to the use of risky medical procedures before they have been rigorously tested. In the event that DBS is used in the treatment of addiction, we provide minimum ethical requirements for clinical trials of its use in the treatment of addiction. These include: restrictions of trials to severely intractable cases of addiction; independent oversight to ensure that patients have the capacity to consent and give that consent on the basis of a realistic appreciation of the potential benefits and risks of DBS; and rigorous assessments of the effectiveness and safety of this treatment compared to the best available treatments for addiction.

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.

During the past 200 years, Soviet scientists have extensively investigated and evaluated the effects of psychoactive drugs in humans. An examination of the resultant literature provides insight into the four distinct periods that comprise this era of research.

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.

We are unlikely to stop seeking pleasure, as this would prejudice our health and well-being. Yet many psychoactive substances providing pleasure are outlawed as illicit recreational drugs, despite the fact that only some of them are addictive to some people. Efforts to redress their prohibition, or to reform legislation so that penalties are proportionate to harm have largely failed. Yet, if choices over seeking pleasure are ethical insofar as they avoid harm to oneself or others, public health strategies should foster ethical choice by moving beyond current risk management practices embodied in the harm reduction movement. The neuroscience of pleasure has much to offer neuroethics and public health strategies. Distinguishing between ‘wanting’ and ‘liking’ fosters new understandings of addiction. These hold promise for directing the search for pharmacotherapies which prevent addiction and relapse or disrupt associated neuromechanisms. They could inform new research into creating lawful psychoactive substances which give us pleasure without provoking addiction. As the health and well being of human and other animals rests upon the experience of pleasure, this would be an ethical objective within public health strategy. Were ethical and neurobiological obstacles to ending addiction to be overcome, problems associated with excessive consumption, the lure of unlawful psychoactive substances and the paucity of lawful means to achieve pleasurable altered states would remain. Non-addictive designer drugs, which reliably provided lawful access to pleasures and altered states, would ameliorate these public health concerns insofar as they fostered citizens’ informed, ethical choices according to a neurobiological taxonomy of pleasures.

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.

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>.