It has been easy to demonstrate, both in humans and animals, that the stresses which disturbed either the physiological homeostasis, the behavioural homeostasis or both simultaneously, induced the modifications of the food intake; these disorders often found expression in the inappropriate eating or, less frequently, in temporary anorectic phases. The most relevant hypotheses localized, in the anterior and median hypothalamus (paraventricular nuclei, ventral median nuclei, lateral hypothalamic area), the neurobiological mechanisms which were involved in this stress/eating behaviour relationship. In the brain, both aminergic and peptidergic systems were concerned; the stress-induced hyperphagia required the functionality of the dopamine, dorsal noradrenergic bundle and endogenous opioids of the central nervous system. The dramatic stress-induced anorexia was based upon the reciprocal actions of serotonin, norepinephrine and CRF systems. Other peptides, which some of them belonged to the brain-gut peptide group, could interfere with these mechanisms. The neuropeptides being common in the stress and eating physiological systems, the regulatory mechanisms were most coherent; nevertheless, the precise nervous structures and neurochemical circuits that produced the stress-induced hyperphagia or stress-induced anorexia, remain unknown.