Virtuous actions seem to be both habitual and rational. But if we combine an intuitive understanding of habituality with the currently predominant paradigm of rational action, these two features of virtuous actions are hard to reconcile. Intuitively, acting habitually is acting as one has before in similar contexts, and automatically, that is, without thinking about it. Meanwhile, contemporary philosophers tend to assume the truth of what I call the reasons theory of rational action, which states that all rational actions are (...) actions for reasons. Whilst interpretations of this phrase are disputed, I argue that neither of the two leading views – which I call reasons internalism and reasons externalism – makes room for habitual actions to count as actions for reasons; by the reasons theory, they cannot be rational either. I suggest one way of effecting the reconciliation which, whilst it allows us to keep the reasons theory, requires us to conceive of reasons as even more radically external than current externalists believe them to be. (shrink)

Normative thinking about addiction has traditionally been divided between, on the one hand, a medical model which sees addiction as a disease characterized by compulsive and relapsing drug use over which the addict has little or no control and, on the other, a moral model which sees addiction as a choice characterized by voluntary behaviour under the control of the addict. Proponents of the former appeal to evidence showing that regular consumption of drugs causes persistent changes in the brain structures (...) and functions known to be involved in the motivation of behavior. On this evidence, it is often concluded that becoming addicted involves a transition from voluntary, chosen drug use to non-voluntary compulsive drug use. Against this view, proponents of the moral model provide ample evidence that addictive drug use involves voluntary chosen behaviour. In this paper we argue that although they are right about something, both views are mistaken. We present a third model that neither rules out the view of addictive drug use as compulsive, nor that it involves voluntary chosen behavior. -/- . (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)

The claim that addiction is a brain disease is almost universally accepted among scientists who work on addiction. The claim’s attraction rests on two grounds: the fact that addiction seems to be characterized by dysfunction in specific neural pathways and the fact that the claim seems to the compassionate response to people who are suffering. I argue that neural dysfunction is not sufficient for disease: something is a brain disease only when neural dysfunction is sufficient for impairment. I claim that (...) the neural dysfunction that is characteristic of addiction is not sufficient for impairment, because people who suffer from that dysfunction are impaired, sufficiently to count as diseased, only given certain features of their context. Hence addiction is not a brain disease (though it is often a disease, and it may always involve brain dysfunction). I argue that accepting that addiction is not a brain disease does not entail a moralizing attitude toward people who suffer as a result of addiction; if anything, it allows for a more compassionate, and more effective, response to addiction. (shrink)

Where does normal brain or psychological function end, and pathology begin? The line can be hard to discern, making disease sometimes a tricky word. In addiction, normal ‘wanting’ processes become distorted and excessive, according to the incentive-sensitization theory. Excessive ‘wanting’ results from drug-induced neural sensitization changes in underlying brain mesolimbic systems of incentive. ‘Brain disease’ was never used by the theory, but neural sensitization changes are arguably extreme enough and problematic enough to be called pathological. This implies that ‘brain disease’ (...) can be a legitimate description of addiction, though caveats are needed to acknowledge roles for choice and active agency by the addict. Finally, arguments over ‘brain disease’ should be put behind us. Our real challenge is to understand addiction and devise better ways to help. Arguments over descriptive words only distract from that challenge. (shrink)