Neuronal activity and its role in adiposity and food intake

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Using positron emission scanning and brain MRI, neuroanatomical correlates of hunger and satiety have been investigated. Importantly, analyses of this collected data has indicated that the left dorsolateral prefrontal cortex, an area of the brain important in reward processing, may be a satiety center. Neuronal activation in the left dorsolateral prefrontal cortex following a meal is consistently lower in this area in obese versus lean individuals, in both men and women. Moreover, we demonstrated that in subjects with Prader-Willi there is actual deactivation of this same area. Prader-Willi patients have uncontrolled hunger due to failure of meals to suppress satiety, so this deactivation (as opposed to only lesser activation in obese individuals) is further evidence of an important role for the prefrontal cortex in appetite control. We then conducted a parallel design study of active anodal stimulation to the left dorsolateral prefrontal cortex versus sham in obese individuals. We again measured ad libitum energy intake, but also had a follow-up 4 week outpatient follow-up in which tDCS was continued three times per week. In addition to measuring ad libitum energy intake, we also measured hunger scores and conducted post meal snack food tests. In the parallel design study, we were not able to replicate the lower ad libitum energy intake or weight loss in the active treatment group, but we found a steady decrease in hunger and urge to eat scores and lower intake of snack foods after 4 weeks of treatment. These results indicate it may take weeks for the effect of tDCS to be manifest. We have begun a longer 9 week outpatient study which will include functional MRI of the brain prior to and following the first and final tDCS session to investigate the acute and chronic effects of tDCS on the pre-frontal cortex and other brain regions.