Anorexia nervosa (AN) represents an eating disorder, which features the highest rate of mortality among all psychiatric disorders. The disease prevalence is increasing steadily, and an effective cure is missing. The neurobiology of the disease is largely unknown, and only a few studies were designed to disclose specific brain areas, where altered neural transmission may occur. In AN behavioral alterations surpassing altered feeding are present, which often involve archaic behaviors finalized to the survival of the species. In fact, alterations of sleep and reward-driven behavior accompany the eating disorder, where a disruption of peripheral and central circadian rhythms occurs along with effortful behaviors, aberrant learning and mild cognitive impairment. Abnormal behavior often co-exists with a number of metabolic alterations in peripheral organs. The present article wishes to analyze the potential role of altered brain circuitry within the brainstem reticular formation during AN. In fact, this brain area contains neuronal nuclei and pathways, which are pivotal in connecting eating pattern with archaic behaviorsand autonomic activity within peripheral organs. A number of reticular nuclei releasing catecholamine and non-catecholamine neurotransmittersare evidenced in relationship with altered behavioral states and vegetative control to produce this psycho-metabolic disorder. The relevance of the reticular formation in sustaining the disorder is discussed in the light of developing effective therapeutic strategies.