Extending the two-component model of delusion to substance use disorder etiology and recovery

Abstract

The brain disease model (BMDA) and psychosocial models of addiction attend to phenomena at different levels of biological organization, and evidence suggests neither is sufficient to explain substance use disorder (SUD). Here, we extend a Bayesian model of the emergence and persistence of delusions to SUD etiology and recovery, building upon efforts to link lower-level impacts of psychoactive compounds to higher-level phenomena such as attitudes, beliefs, and self-control. According to the resulting two-component model of SUD, psychoactive substances interact with genetic and environmental factors to produce delusions about the biological importance of substance use and its contexts by perturbating basic human affective systems. These delusions are most often revised or rejected based on individuals’ existing belief systems. But in some individuals, factors explaining the persistence of an array of delusions (e.g., lower levels of executive functioning) prevent the evaluation and revision system from rejecting or revising beliefs that attribute high salience to substance-related stimuli. This theory provides novel hypotheses regarding the potential roles of factors such as dichotomous thinking, positive illusions and self-deception, and denial or lack of awareness in SUD etiology and recovery. Furthermore, it provides an account of SUD that may result in less stigma than the BDMA.