Anorexia nervosa (AN) is a severe and potentially life-threating condition that typically emerges in the teenage years. While AN is a complex disorder with myriad symptoms, caloric restriction is the central behavioral disturbance, and is characterized by a specific restriction of dietary fat. Converging data indicate that AN is associated with disturbances in the dopamine system. The dopamine system develops considerably during adolescence, and adequate nutrition plays a role in healthy brain development. Yet the effects of dietary restriction and the associated starved state that is an inherent feature of AN is poorly understood. Individuals with AN typically initiate dietary restrictions that accelerate, with mounting caloric reductions and weight loss and associated symptoms including anxiety and depression. This cascading pattern most commonly unfolds during adolescence and can lead to life-long struggles with eating, body image, and mood disturbance, if not unremitting AN. The restrictive eating pattern leads to decreased availability of many nutrients, some of which are particularly important in adolescent brain development. Here, we focus on polyunsaturated fats (PUFAs) and tyrosine which are specifically known to be critical for the functioning and development of the dopamine system. Our proposal aims to test the overarching hypothesis that among teens who develop AN, dietary restriction which is intrinsic to illness negatively impacts the dopamine (DA) system during a critical window of brain development, with enduring effects. We predict that these nutritional deficits will be associated with structural and functional disturbances in the DA system (baseline MRI scans with tractography, neuromelanin-MRI, and prediction error-fMRI). We predict that these nutritional deficits have enduring effects on the DA system even when weight restoration is successful, as evidenced by repeat MRI at 1 year. To assess the impact of being underweight, we will include individuals with atypical AN, who show all clinical features of AN but are not underweight, and 1-year longitudinal assessments will measure the enduring impact of these nutritional deficits. The proposed research has direct translational therapeutic implications – such as augmenting current treatments (including refeeding) with nutrient supplementation, thereby protecting the developing brain and curtailing the long-term negative sequelae of adolescent AN. With extant knowledge, such trials would be premature as the specific nutrients underlying AN-related starvation effects on brain development are unknown. We aim to close this gap by examining whether PUFAs and tyrosine mediate abnormalities in the DA system in adolescents with AN and atypical AN.