Over the past decade, brain imaging has helped to better define eating disorder–related brain circuitry. Brain research on gray matter (GM) and white matter (WM) volumes had been inconsistent, possibly due to the effects of acute starvation, exercise, medication, and comorbidity, but newer studies have controlled for such effects. Those studies suggest larger left medial orbitofrontal gyrus rectus volume in ill adult and adolescent anorexia nervosa after recovery from anorexia nervosa, and in adult bulimia nervosa. The orbitofrontal cortex is important in terminating food intake, and altered function could contribute to self-starvation. The right insula, which processes taste but also interoception, was enlarged in ill adult and adolescent anorexia nervosa, as well as adults recovered from the illness. The fixed perception of being fat in anorexia nervosa could be related to altered insula function. A few studies investigated WM integrity, with the most consistent finding of reduced fornix integrity in anorexia and bulimia nervosa—a limbic pathway that is important in emotion but also food intake regulation. Functional brain imaging using basic sweet taste stimuli in eating disorders during the ill state or after recovery implicated repeatedly reward pathways, including insula and striatum. Brain imaging that targeted dopamine-related brain activity using taste-reward conditioning tasks suggested that this circuitry is hypersensitive in anorexia nervosa, but hyporesponsive in bulimia nervosa and obesity. Those results are in line with basic research and suggest adaptive reward system changes in the human brain in response to extremes of food intake—changes that could interfere with normalization of eating behavior.