The Neural Implications of Eating Disorders: A Narrative Review on the Intersections of Evolutionary Mechanisms and Modern Mismatch Environments

Anorexia nervosa (AN) carries one of the highest mortality rates among psychiatric illnesses, yet sociocultural and psychological models leave its persistence and its resistance to weight restoration incompletely explained. Starvation itself reorganizes neural, endocrine, and immune function through mechanisms conserved across species. Previous work has considered these changes as consequences of illness rather than mechanisms that maintain it, rarely connecting them to the evolutionary logic of neurological survival. This review questions how prolonged starvation—and the evolutionary mechanisms shaping starvation and malnutrition—impact the neural profile of eating disorders, with AN examined as the principal case. This review proposes that core features of AN reflect an “evolutionary echo”: primitive starvation-response systems, activated under contemporary social pressures, that persist even when they cease to be adaptive. This narrative synthesis of peer-reviewed studies from 2000 to 2026 integrates human PET and MRI findings, experimental starvation physiology, and cognitive research on reward learning using animal models. Three findings recur. Starvation shifts cerebral metabolism and reduces gray matter in the prefrontal cortex, insula, and cingulate, which is partly reversed by refeeding. Shift from goal-directed choice to habit is accompanied by blunted striatal reward signaling and reduced set-shifting. Deficits in implicit learning are more pronounced in adults with longer illness than in adolescents, consistent with accumulation under starvation rather than a fixed premorbid trait. These findings support a model portraying AN as a consequence of interactions between metabolic, neural, and immune adaptations originally conditioned to survive famine, thereby linking neurological and psychological explanations.