The notion of addiction as a “chronic, relapsing brain disease” — which frames addiction as a dysfunction of normal brain systems involved in reward, motivation, learning and choice — has gained tremendous traction over the past fifteen or so years.  This model, strongly advocated by the past two directors of the National Institute on Drug Abuse (NIDA), Alan Leshner and Nora Volkow, emerged both from research conducted since the 1970s on the neurochemical underpinnings of craving and pleasure and work carried out with the powerful imaging technologies which became available during the 1980s and 90s.  This is a terribly important development for social scientists interested in medicine and health.  While the model has gained increasing ubiquity outside of scientific domains in the English-speaking world, promoted by highly visible media productions (such as HBO’s 2007 “Addiction“), it diverges in significant ways from the understandings of addiction which have been prevalent in these countries for decades (for example, the “disease model” of 12 step programs).

One of the nice things about the latest issue of BioSocieties, devoted to “Drugs, addiction, and society” and guest edited by Deanne Dunbar, Howard Kushner and Scott Vrecko, is that it addresses issues emerging from the “chronic, relapsing brain disease” model of addiction, without simply writing the model off as yet another example of neurobiological reductionism.  Rather, the editors have made an impressive effort to get social scientists and biological or clinical researchers talking to one another in novel and substantive ways.  As they write in their Introduction to the issue:

“Contributors to this special issue were invited to consider aspects of the shift in addiction studies towards physiological models and therapies as a development not only of theoretical interest, but also one with a broad range of potential personal, therapeutic and governmental reorientations. As the reader will see, the articles by social scholars presented here have endeavored to imbue their analysis with practical significance, to acknowledge the physical in addition to the socially constructed, and perhaps to slightly relax their total suspicion of the claims of neuroscience. Meanwhile, scientists’ articles included here and presented at the conference have acknowledged the importance of ‘the social’ to their work, and have made efforts to consider the intended (though perhaps not the unintended) impact of their laboratory findings on social policy,” (Dunbar, Kushner and Vrecko 2010).

Addressing the issues examined in the introduction, this article suggests an integrative ‘cultural biology of addiction’, which aims at encouraging a continuing dialogue between neuroscientists and those engaged in social studies of addiction. This cultural biology of addiction provides an alternative framework that brings together seemingly contradictory social-constructionist and biologically reductionist claims about addictions.

Discoveries in basic science have helped us understand the drug abuse/dependence/addiction brain disorder. One can view this brain disorder as a long-lasting, relapsing pattern of drug seeking and taking with adverse consequences. Drug self-administration studies in animals have revealed brain circuits and neurotransmitters that underlie drug-induced reward and reinforcement. Moreover, studies of effects of drugs on receptors have shown us how drugs can change gene expression and how drugs can change the biochemical makeup of the brain. Drug-induced changes in the brain are very long lasting, which presumably can explain why drug addiction is a chronic and relapsing disease. Also, drugs exert their actions at least partly through evolved brain circuits that serve functions critical for survival such as feeding and sex. Thus, drugs can harness our strongest instincts and the desire to use them can become very powerful. These findings should influence research, treatment and policy towards the disorder of drug addiction and abuse.

This article contributes to cultural theorizations of the regulation of deviant forms of thought and behaviour through an analysis of scientific accounts of, and approaches to, managing ‘behavioural addictions’. Much cultural analysis assumes that biomedical formulations of addiction simply provide a scientific façade for forms of social control, and hence, that such formulations are unworthy of serious consideration. I argue that critical inquiries into processes of social change and social regulation could be strengthened by carefully considering, and engaging with, contemporary addiction medicine; and provide an example of such an approach by examining some of the new descriptions of people, emotions and behaviours – as well as new means of acting on individuals, feelings and conduct – that have begun to emerge within theories, therapies and popular science representations that frame behavioural addictions as brain diseases. Although recognizing the validity of some biomedical claims – for example, that there are physiological components to behavioural compulsions, and that effective addiction therapies may act on the bodies of patients – I argue against conceptualizing behavioural compulsions as diseases, and against conceptualizing therapeutic interventions for such compulsions as ‘treatments’. Instead, I make the case that, according to biomedical discourses themselves, it is more accurate to describe addiction interventions – which are used to produce better citizens, rather than to cure biological diseases – as ‘civilizing technologies’.

This article critically examines two versions of addiction, the neuroscientific model of addiction as a brain disease and the behavioural model of addiction developed by pain medicine. By juxtaposing these different ways of seeing and acting on addiction, the article challenges the assumption that addiction is a constant and singular entity that can be identified outside a particular context. It also highlights the uses, limitations and tensions of each approach. The molecular gaze of the chronic relapsing brain disease model has the potential to undermine the stigmatization of addicts, while the therapeutic gaze of pain medicine recognizes that changes in the brain produced by long-term drug use are not in themselves pathological. The article suggests that the brain disease model is limited in its scope because it removes addiction from the social context in which it is experienced. On the other hand, the molecular knowledge produced by brain-based research is likely to challenge the ability of pain medicine to maintain clear-cut distinctions between dependence, the drug-seeking behaviour of pain patients and addiction.

Although neuroscience has produced elegant models of addiction as a brain process, it does not address the incidence and prevalence of conditions like addiction in populations. As incidence and prevalence are the measures of a condition in a society, understanding rates of social problems is critical to controlling them. Nevertheless, not all upsurges in drug use in a population constitute true emergencies. It is useful to distinguish drug eras, new patterns of drug use that emerge in a population and then stabilize or decline from epidemics of drug-related harm. A historical epidemiology of drug-related harm draws from history, science and social science to examine the conditions that produce such epidemics. Compulsive crack use concentrated in American urban neighborhoods characterized by poverty and cultural isolation in the 1980s and the object of lurid media coverage, can be better understood through the lens of the historical epidemiology of drug-related harm. This model holds that serious upsurges in harmful drug use result from the introduction of powerful new drugs or drug forms to populations that lack experience with them and that suffer from multiple dimensions of structural disadvantage.

Early to mid-twentieth century studies on the neurophysiology of the role of conditioned cues in relapse, conducted at the Addiction Research Center in Lexington, Kentucky, were the historical antecedents to today’s neuroimaging studies. Attempts in the 1940s to see ‘what’s going on in the brains of these addicts’ were formative for the field, as was foundational work done in the 1940s and 1950s by Abraham Wikler on conditioned cues, the role of what he called the ‘limbic system’ in relapse, and possible uses of narcotic antagonists to prevent relapse by extinguishing cues. This article sketches the historical context in order to situate continuities between historical antecedents and a current ethnographic case study focused on current neuroimaging studies of the role of ‘craving’ – and neural processes that precede conscious ‘craving’ and occur ‘outside awareness’ – in relapse conducted by Anna Rose Childress at the Treatment Research Center in Philadelphia, Pennsylvania. The article showcases the incommensurability between claims that ‘addiction’ is a matter of individual choice, and claims that it is a neurochemical disorder disruptive of volition. Neuroscientists offer scientific vocabulary and imagery that both shape and respond to the social experience of addiction. The conclusion considers the value of moving toward a critical neuroscience more cognizant of the social worlds in which ‘addiction’ occurs, not in the restricted sense of ‘social factors’ but through awareness of the social–situational contexts and relationships within which ‘addictions’ are experienced and studied.

From about 1930 to the late 1960s a definition of addiction dominated in the United States that made opiate-style abstinence reactions essential, and distinguished sharply between true addiction and merely psychological drug habituation. This definition was so narrow that it left all stimulants out of the addictive category, and it was not uncontested. By looking at the postwar efforts of one of the chief architects of this definition, pharmacologist Maurice Seevers, to defend his conception of addiction in both scientific and policy realms, I demonstrate the contingency of this construction of addiction upon methodological commitments and industrial interests related to amphetamines and tobacco.

Emerging technological advances in genetics and neuroscience have spawned innovative or elaborated conceptual models in the field of addiction science, as well as contributed to the mushrooming of new knowledge. By addictions, reference is made to chronic, often relapsing disorders typified by obsession, compulsion or physical or psychological dependence. In this article it is proposed that a multilevel developmental contextual approach to substance use and addictions provides a useful framework for integrating existing studies across disciplines and serving as a generative guide to intriguing novel research questions. The multilevel developmental contextual approach emphasizes multiple-factor influences on substance use and addiction, the conjoint influence of variables from different levels of analysis (for example, genetic, biochemical, physiological, cognitive, social, neighborhood, societal), and dynamic, probabilistic behavior-outcome relations (that is, the occurrence as well as the nature of expression of substance problems and addiction depend on a range of emerging, interactive factors that may vary across individuals and over time). The approach is illustrated with a long-term prospective study of predictors of binge drinking from adolescence to young adulthood and a description of the role of brain processes and mechanisms involved in the development and expression of alcohol use during adolescence.

This article examines ‘the NIDA paradigm’, the theory that addiction is a chronic, relapsing brain disease characterized by loss of control over drug taking. I critically review the official history of the National Institute on Drug Abuse (NIDA) paradigm and analyze the sources of resistance to it. I argue that, even though the theory remains contested, it has yielded important insights in other fields, including my own discipline of history.