Severe reductions in the brain's cortical gray matter thickness (CT) have repeatedly been reported in anorexia nervosa (AN). The underlying mechanisms of these drastic changes remain unclear. Associations with potential underlying neurochemical and metabolic features have not been evaluated. In this study, we investigated whether CT alterations, across the cortical surface, in AN (n = 114) compared to healthy controls (HC; n = 114 age-matched, range 12-29 years old) might be associated with the spatial distribution of neurotransmitter receptors, transporters and/or metabolic glucose uptake (i.e., "chemoarchitecture", based on data from PET binding studies in healthy individuals, as implemented by neuromaps). First, the correlation between CT alterations in AN and chemoarchitecture was evaluated at the group-level. Second, chemoarchitecture was leveraged to compute per-participant correlations of neuroreceptor maps with CT alterations at the individual-level. Correlations with psychiatric symptoms and associations with early weight gain (30-days after admission) were tested. Group-level results were replicated in an external sample. Regions showing substantial cortical thinning in AN were also characterized by higher AChN receptor density and higher glucose metabolism uptake. While CT was comparatively preserved in AN at the group-level in regions with higher HT1a and SERT receptor density, individual participants who exhibited cortical thinning in these regions also reported more severe symptoms (depression and body dissatisfaction) and showed less treatment-related weight gain. These associations may help to define a biological risk signature for AN, possibly allowing for future applications in treatment stratification and/or personalization.