Abstract

Lewis’ neurodevelopmental model provides a plausible alternative to the brain disease model of addiction that is a dominant perspective in the USA. We disagree with Lewis’ claim that the BDMA is unchallenged within the addiction field but we agree that it provides unduly pessimistic prospects of recovery. We question the strength of evidence for the BDMA provided by animal models and human neuroimaging studies. We endorse Lewis’ framing of addiction as a developmental process underpinned by reversible forms of neuroplasticity. His view is consistent with epidemiological evidence of addicted individuals ‘maturing out’ and recovering from addiction. We do however hold some reservations about Lewis’ model. We do not think that his analysis of the neurobiological evidence is clearly different from that of the BDMA or that his neurodevelopmental model provides a more rigorous interpretation of the evidence than the BDMA. We believe that our understanding of the neurobiology of drug use is too immature to warrant the major role given to it in the BDMA. Our social research finds very mixed support for the BDMA among addicted people and health professionals in Australia. Lewis’ account of addiction requires similar empirical evaluation of its real-world implications.