Ainslie’s contribution offers a useful refinement of his powerful model of intertemporal bargaining. However, he focuses mostly on the cognitive mechanisms of choice. I suggest that these interact with emotional, personality, and developmental dynamics that cannot be ignored, either psychologically or neurally.

Although these authors sometimes resort to medical terminology, we strongly agree that addiction is not a disease and that the Brain Disease Model of Addiction captures only one part of the story and distorts the big picture. Yet Satel and Lilienfeld continue to conflate a neurobiological model with a disease model. They also complain that my modeling of addiction reveals a hidden “neurocentric” bias, despite my integration of multiple levels of analysis, exactly as they recommend.

Despite its historical contribution, Heather sees the Brain Disease Model of Addiction as failing to relieve stigma, increasing fatalism, and fundamentally wrong. He also sees “choice” as partly volitional and partly unconscious, implying no moral violation. I agree on all counts. Heather then presents a disorder-of-choice model of addiction, highlighting the failure of self-regulation with respect to immediate goals. Not only do I endorse such modeling, but the neural mechanisms I describe may help to explicate it more thoroughly.

Pickard’s contribution reminds me that conceptualizing choice is no simple matter. Pickard sees choice as entirely voluntary, while I argue that choice is only partially voluntary. Choices are based on appraisals of situations, which fluctuate due to external circumstances and internal states such as emotion and mood. Habit itself competes with volition, and all these parameters vary with development. Psychological factors such as delay discounting and especially one's belief in one's agency are critical for volitional choice as well.