Anorexia nervosa (AN) carries the highest mortality rate of any psychiatric disorder, with relapse rates of 30-50% following weight restoration. The persistence of the condition despite aggressive refeeding remains unexplained. Monteleone et al. (2015) demonstrated that endocannabinoid responses to hedonic eating remain abnormal in weight-restored AN patients, indicating that the physiological disruption outlasts the caloric deficit. This paper applies the biochemical computer framework (Craddock, 2026a; 2026b) to propose that AN represents a stuck program mode in which the organism Candida albicans has locked host feeding behavior into a substrate restriction phase through sustained modulation of endocannabinoid tone, serotonin precursor availability, and satiety signaling. The restriction phase serves the organism's program requirements for specific metabolic conditions, but the transition signal to resume normal feeding fails to arrive. The framework resolves the persistence problem, explains the pubertal-onset female predominance through documented organism sensitivity to estrogen and luteinizing hormone, and generates testable predictions linking organism colonization density to endocannabinoid disruption severity and treatment response. The net effect is directly dependent on colonization density.
Jim Craddock (Tue,) studied this question.