Uncontrollable chronic stressors include periods of drought, earthquake, hurricane and famine which demand searching for new territory and the drive and energy to support the search. Glucocorticoids (GC), secreted during stress, appear to adapt the organism perfectly to find a new, more hospitable site to live while maintaining metabolic energy for the search. In the brain, GC act to increase stimulus salience or motivation; the valence of the behaviour emitted depends on the conditions and state of the animal and available outlets. In rats, GC facilitate search and running behaviours, freezing, aggression, anxiety- and fear-like behaviours; they also stimulate ingestion of palatable fat and sugar, but not plain (boring) chow [1-4]. However, GC do stimulate chow intake in diabetic rats in a dose-related fashion, but insulin, acting through the hepatic vagus, stimulates lard ingestion while decreasing chow intake in diabetic rats [5-7]. In the periphery, GC are catabolic and mobilize substrates for hepatic gluconeogenesis, but they also stimulate insulin secretion, which, in turn determines which foods will be eaten. Together these hormones shift caloric stores from the periphery to central fat depots. However, there is a metabolic feedback signal to the hypothalamic-pituitary-adrenal axis as well as the well-known acute GC-mediated feedback at hypothalamus and pituitary. Central fat mass is inversely related to the magnitude of hypothalamic corticotropin-releasing factor expression [4], and voluntary lard ingestion by rats markedly reduces the amplitude of ACTH and corticosterone responses to acute restraint [7], suggesting that stressor-induced eating may serve as self-medication for protection against the central effects of stress. In current civilizations, where perceived stressors abound and palatable foods are readily available with minimum exertion, this evolutionarily brilliant set of actions of stress-induced GC almost certainly contributes to the current epidemic of obesity and the pathophysiologic association between abdominal obesity and the metabolic syndrome.