Neural correlates of changing food choices while bypassing values.

Current theories suggest that altering choices requires value modification. To investigate this, normal-weight female participants' food choices and values were tested before and after an approach-avoidance training (AAT), while neural activity was recorded during the choice task using functional magnetic resonance imaging (fMRI). During AAT, participants consistently approached low- while avoiding high-calorie food cues. AAT facilitated low-calorie food choices, leaving food values unchanged. Instead, we observed a shift in indifference points, indicating the decreased contribution of food values in food choices. Training-induced choice shifts were associated with increased activity in the posterior cingulate cortex (PCC). In contrast, the medial PFC activity was not changed. Additionally, PCC gray matter density predicted individual differences in training-induced functional changes, suggesting anatomic predispositions to training impact. Our findings demonstrate neural mechanisms underlying choice modulation independent of valuation-related processes, which has substantial theoretical significance for decision-making frameworks and translational implications for health-related decisions resilient to value shifts.

Eating to dare - Nutrition impacts human risky decision and related brain function.

Macronutrient composition modulates plasma amino acids that are precursors of neurotransmitters and can impact brain function and decisions. Neurotransmitter serotonin has been shown to regulate not only food intake, but also economic decisions. We investigated whether an acute nutrition-manipulation inducing plasma tryptophan fluctuation affects brain function, thereby affecting risky decisions. Breakfasts differing in carbohydrate/protein ratios were offered to test changes in risky decision-making while metabolic and neural dynamics were tracked. We identified that a high-carbohydrate/protein breakfast increased plasma tryptophan/LNAA (large neutral amino acids) ratio which mapped to individual risk propensity changes. The nutrition-manipulation and tryptophan/LNAA fluctuation effects on risk propensity changes were further modulated by individual differences in body fat mass. Using fMRI, we further identified activation in the parietal lobule during risk-processing, of which activities 1) were sensitive to the tryptophan/LNAA fluctuation, 2) were modulated by individual's body fat mass, and 3) predicted the risk propensity changes in decision-making. Our results provide evidence for a personalized nutrition-driven modulation on human risky decision and its metabolic and neural mechanisms.