Reward and inhibition in obesity and cigarette smoking: Neurobiological overlaps and clinical implications

•Obesity and cigarette smoking frequently co-occur, but little is known about the effect on neurocognitive function.•Both obesity and smoking lead to the dysregulation of dopamine reward circuits and hypoactivation in inhibitory control-associated brain regions.•Individuals comorbid for both obesity and smoking show altered function in inhibitory control neurobiology and differences in how this translates to behavior as compared to lean smokers.•The potentially complicating neurocognitive influence of increasing body mass index may make quitting smoking more difficult. Cigarette smoking and obesity are the leading causes of premature morbidity and mortality and increase the risk of all-cause mortality four-fold when comorbid. Individuals with these conditions demonstrate neurobiological and behavioral differences regarding how they respond to rewarding stimuli or engage in inhibitory control. This narrative review examines the role of reward and inhibition in cigarette smoking and obesity independently, as well as recent research demonstrating an effect of increased body mass index (BMI) on neurocognitive function in individuals who smoke. It is possible that chronic smoking and overeating of highly palatable food, contributing to obesity, dysregulates reward neurocircuitry, subsequently leading to hypofunction of brain networks associated with inhibitory control. These brain changes do not appear to be specific to food or nicotine and, as a result, can potentiate continued cross-use. Changes to reward and inhibitory function due to increased BMI may also make cessation more difficult for those comorbid for obesity and smoking.