There is a debate about the nature of addiction, whether it is a result of brain damage, brain dysfunction, or normal brain changes that result from habit acquisition, and about whether it is a disease. I argue that the debate about whether addiction is a disease is much ado about nothing, since all parties agree it is “unquestionably destructive.” Furthermore, the term ‘addiction’ has disappeared from recent DSM’s in favor of a spectrum of ‘abuse’ disorders. This may be a good (...) thing indicating more nuance in typing the heterogeneous phenomena we used to call ‘addiction’. (shrink)

The current dominant perspective on addiction as a brain disease has been challenged recently by Marc Lewis, who argued that the brain-changes related to addiction are similar to everyday changes of the brain. From this alternative perspective, addictions are bad habits that can be broken, provided that people are motivated to change. In that case, autonomous choice or “free will” can overcome bad influences from genes and or environments and brain-changes related to addiction. Even though we concur with Lewis that (...) there are issues with the brain disease perspective, we also argue that pointing to black swans can be important, that is: there can be severe cases where addiction indeed tips over into the category of brain disease, but obviously that does not prove that every case of addiction falls into the disease category, that all swans are black. We argue that, for example, people suffering from Korsakoff’s syndrome, can be described as having a brain disease, often caused by alcohol addiction. Moreover, the brain changes occurring with addiction are related to choice-behaviour, habit formation and insight, hence essential mental abilities to break the addiction. We argue for a more graded perspective, where both black swans and white swans are rare, and most cases of addiction come as geese in different shades of gray. (shrink)

A modest opposition to the brain disease concept of addiction has been mounting for at least the last decade. Despite the good intentions behind the brain disease rhetoric – to secure more biomedical funding for addiction, to combat “stigma,” and to soften criminal approaches – the very concept of addiction as a brain disease is deeply conceptually confused. We question whether Lewis goes far enough in his challenge, robust as it is, of the brain disease concept. For one thing, the (...) notion that addiction is a disease is challenging to refute or confirm because the disease concept itself is poorly defined in medical and psychological nosology. More important, quibbling over what kind of disease addiction is unlikely to be productive. The rational response to adjudicating whether addiction is a brain disease is not to engage in potentially fruitless debates over the question of disease classification but rather to view addiction as an enormously complex set of behaviors that operate on several dimensions, ranging from molecular function and structure and brain physiology to psychology, the psychosocial environment, and social and cultural relations. (shrink)

In his target article and recent interesting book about addiction and the brain, Marc Lewis claims that the prevalent medical view of addiction as a brain disease or a disorder, is mistaken. In this commentary we critically examine his arguments for this claim. We find these arguments to rest on some problematical and largely undefended assumptions about notions of disease, disorder and the demarcation between them and good health. Even if addiction does seem to differ from some typical brain diseases, (...) we believe contrary to Lewis, that there are still good reasons to maintain its classification as a mental or behavioral disorder. (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)

I review the brain disease model of addiction promoted by medical, scientific, and clinical authorities in the US and elsewhere. I then show that the disease model is flawed because brain changes in addiction are similar to those generally observed when recurrent, highly motivated goal seeking results in the development of deep habits, Pavlovian learning, and prefrontal disengagement. This analysis relies on concepts of self-organization, neuroplasticity, personality development, and delay discounting. It also highlights neural and behavioral parallels between substance addictions, (...) behavioral addictions, normative compulsive behaviors, and falling in love. I note that the short duration of addictive rewards leads to negative emotions that accelerate the learning cycle, but cortical reconfiguration in recovery should also inform our understanding of addiction. I end by showing that the ethos of the disease model makes it difficult to reconcile with a developmental-learning orientation. (shrink)

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.