Nicotine addiction is a manifold process involving dysregulated brain circuitry subserving reward and motivation (i.e. corticostriatal). Despite extant cross-species models in the literature, there is a gap in the human literature concerning the role of corticostriatal pathways that regulate appetitive processes, whether cognitive training may restructure circuitry function, and whether neuroplasticity in self-regulatory mechanisms alter appetitive behaviors, in particular cigarette smoking. Preliminary data from our laboratory provide initial support for our published model positing that cognitive control training via Mindfulness Oriented Recovery Enhancement (MORE), to enhance valuation of non-drug related reward relative to drug reward may remediate maladaptive appetitive behaviors, craving, and affective deficits by restructuring reward processing. The goal of this proposal is to examine the effects of MORE on corticostriatal mediated regulation of appetitive responding and smoking. Smokers (N=100) will be randomized to 4-weeks of MORE or CBT, undergo fMRI pre/post training, complete a laboratory-based smoking relapse analog task, and be followed for 2-weeks to assess relations between neural function, lab behavior and real-world smoking.
Nicotine addiction is a chronic, relapsing brain disorder and although it is the leading cause of preventable premature death in the US, ~20% of adults smoke and among those that try to quit, the majority relapse. Preclinical and Human models suggest that nicotine addiction disrupts neural function in a corticostriatal network involved in motivation and reward. The overarching goal of this proposal is to utilize clinical neuroscience to investigate the effects of Mindfulness Oriented Recovery Enhancement (MORE) on corticostriatal circuitry function, regulation of appetitive processes and determine the value of this cognitive training for treating nicotine addiction.
