This volume brings together original papers by a number of the leading researchers on addiction, together with some contributions from others whose research has been less centrally concerned with addiction. Inevitably, much of the material covered will be familiar to those who are have been keeping up with the debate: the big names rehearse the theories for which they have come to be known. However even in those papers in which theories elaborated at greater length elsewhere are sketched, there is usually enough new material to make this volume essential reading for addiction researchers. For reasons of space, I will mention only some of the papers in this review, those that I found especially interesting. Other readers, with different aims, would select different papers for special attention.
The volume moves from neurobiology, through to behavior and then on to issues in philosophy and public policy. This format is a natural one, since the behavioral work often builds on the neurobiological work in its construction of theories, and the philosophical work interprets the scientific work. The first papers review the neurobiology of addiction. A great deal of material converges on two systems being centrally involved in addiction: a reward system which motivates seeking and consuming behavior and an executive system that allows the organism to pursue longer-term goals. Dopamine pathways are centrally involved in signaling reward value; the drugs and behaviors to which organisms become addicted all, in different ways, seem to hijack the dopaminergic signal so that the organism overvalues the object of its addiction (relative to the value placed on it by executive systems). At the same time as the object of addiction is overvalued, however, executive control is also weakened, so that the organism finds itself simultaneously less motivated and less able to resist. As Bickel and Yi point out, these changes also make treatment more difficult. For instance, a weakening of executive control might cause a myopia for reward and therefore an inability to tolerate the frustration involved in drug-treatment programs, or lead to a decrease in the kind of cognitive flexibility needed for implementing CBT strategies. This predicts that some addicts will have easier pathways to recovery than others, which is borne out by the evidence (Heyman claims that we may have a distorted view of addiction because the data tends to be drawn from studies of the clinical population, but people may enter clinical programs only because they suffer from addictions more resistant to recovery than most).
Bickel and Yi conclude their chapter with some fascinating speculations. They note that there is evidence that agents have discount functions that are sensitive to their environments: hunter/gatherers, for instance, discount the future far more sharply than do farmers. Presumably, this difference is the result of the fact that farming requires longer temporal horizons to be successful. Given the fact that our discount functions are sensitive to our environments, they argue that increasing rates of obesity, declining household savings and increased addiction might all be due to the rise of consumer culture, which makes people steeper discounters.
Is addiction one thing or many? Redish argues that though behaviorally it is one thing, differences in etiology are sufficient for us to regard it as a cluster of related disorders. There are (at least) eight vulnerabilities in decision-making processes that cause addiction; each vulnerability represents a distinct pathway to the syndrome. Addiction can be the product of alterations in the needs of the organism, of cognitive deficits leading to a reduced ability to properly categorize situations, of alterations of discounting rates, and so on. Though it is clear that the vulnerabilities Redish identifies are real, and that different addicts will exhibit different vulnerabilities to different extents, is not clear to me that these differences are sufficient to lead us to conclude that addiction is many things and not one. It remains plausible -- so far as I can see -- to think that the core of addiction involves a dysfunction in dopaminergic systems, with the vulnerabilities Redish identifies explaining how this dysfunction comes about or how it is maintained. Nevertheless, the differences he identifies will certainly be relevant to how treatment and prevention strategies ought to be tailored.
Ross argues for the view with which he has come to be associated, and which is diametrically opposed to Redish's: that addiction has a core, and that this core is best revealed by pathological gambling. Drugs of addiction alter the brain in various ways that obscure the central pathology involved in addiction. The core of addiction involves increases in dopamine in the nucleus accumbens --corresponding to the overvaluation of the object of addiction -- and a consequent decrease of serotonin in the frontal lobes, thereby leading to a decrease of executive control. This biases the organism toward a focus on the predictors of reward. Reward, here, is understood neurobiologically; the experienced reward -- the hedonic properties of the object of addiction -- may come to dissociate from its motivating power. Indeed, this is a predictable consequence of the fact that the dopamine signal comes to be attached not to what we think of as rewards, at the personal level (food, sex, drugs) but to surprises: to differences between expected and (neurobiologically) experienced reward. The reward signal peaks when the experience is better than expected and falls to baseline when the reward is just as expected. This makes us novelty seekers, and gambling is addictive because it is predictably surprising. Drugs of addiction influence the dopamine signal chemically; gambling does it via its unpredictable returns.
Gene Heyman's views are also familiar to those who keep up with the literature. Heyman works at the level of behavior rather than neurobiology. He argues that drug-seeking and consuming behavior is voluntary behavior, in the sense that it responds to positive and negative incentives. The mystery with regard to addiction is therefore the following: giving that addiction is voluntary, why do addicts continue to consume when the costs of consumption are greater than the rewards? The answer, he suggests, is the drugs of addiction undermine the value of competing goods, especially social interaction. This fact entails that consuming drugs is always more rewarding, in the short term, than engaging in such interactions, even though in the longer term social interactions would be more rewarding. This explanation is the only one he offered in his recent book, and seems unable to explain process addictions. Here Heyman supplements the explanation by noting some of the neural effects of drugs, which may be shared by process addictions.
Howard Rachlin notes the similarities between self-control problems and altruism. Both can be seen as involving forgoing a reward for the sake of another; the difference between them consists in the fact that in the former case the other is in fact one's future self. He suggests that addicts treat themselves at other times as nonaddicts treat other people. This is an interesting suggestion which deserves further exploration.
Other highlights of the volume include Ainslie's detailed exploration of three alternative explanations for inconsistencies in agents' valuations, Kincaid and Sullivan's examination of whether addiction should be understood on a medical model, and Schroeder's interpretation of the dopamine signal as implementing desire in agents, and his subsequent argument that in the case of addiction the signal misrepresents desire. All these papers, and others I have not mentioned, deserve more attention than I can give them here. Those people with a serious interest in addiction will want to read them all.
© 2011 Neil Levy
Neil Levy, Ph.D., University of Oxford & Melbourne University.