The eating disorders (EDs) anorexia nervosa (AN) and bulimia nervosa (BN) are severe psychiatric disorders that typically occur during adolescence and young adulthood and are associated with high mortality (1). Individuals with AN are severely underweight, and individuals with BN are normal weight to overweight and regularly binge and purge. Symptoms such as food restriction, episodic binge eating, purging, excessive exercise, and shape and weight preoccupations often overlap, and common biological mechanisms may be present (2). The EDs, especially AN, are often difficult to understand. On one hand, there are objective typical disease signs and symptoms such as suffering, altered drive to eat, and electrolyte abnormalities, and it has been shown that genetic factors play a role; on the other hand, there is a selfdestructive willfulness and treatment resistance to the point that EDs were not considered biologically based disorders in the past (3).What causes EDs, and how can we advance treatment development? Psychosocial factors have been explored such as conflicts relating to development, family functioning, high trait anxiety, and the stress to follow an ideal of thinness (1). However, most young people are exposed to similar stressors, and the question arises whether there are biological aspects that could make a person vulnerable to develop an ED. Genetic research has suggested that EDs are familial, but investigators are still searching for specific genetic patterns that characterize individuals prone to an ED. Various brain imaging methods are now widely used in psychiatry to understand the neurobiology of disorders better. Although these imaging methods are not perfect and typically cannot be as definitive as, for instance, single neuron recordings in basic neuroscience, they have greatly advanced understanding of brain function (4).In this issue of Biological Psychiatry, two studies used structural magnetic resonance imaging of the brain to explore cortical thickness in EDs. Marsh et al. (5) recruited a sample of 68 adolescent girls and women, half of them with current BN and the other half healthy control subjects. Subjects underwent magnetic resonance imaging, and for each brain voxel the distance between an individual subject's gray matter surface and a template image was measured. The data were corrected for age and illness duration, and post hoc regression analyses did not suggest effects from medication use or comorbidity.The group comparison of surface morphology showed that the individuals with BN had normal whole-brain volume but decreased localized cortical volumes across prefrontal and temporoparietal cortex and increased volumes in the inferior occipital and parietal lobes. Those volume alterations seemed to be largely driven by white matter underlying the gray matter.The more binge/purge episodes the subjects with BN had, the lower the cortical volume measure was. The cortical thickness analysis also showed scattered reduced values for the group with BN compared with controls in bilateral dors...