ESPE Abstracts

Obesity in humans represents a cumulative retention of a tiny fraction of total energy intake as fat, which is accompanied by growth of the metabolically active, energy demanding, lean body mass. Since the energy balance regulation operates irrespective of the excess fat storage, availability of the required energy supplies is a permissive condition for obesity development. It occurs predominantly among people genetically predisposed and/or living with social or mental challenges. This is usually attributed to increased food intake due to environmental cues and/or increased appetite. However, although experimentally induced excessive food intake may enlarge the fat mass, it does not produce the obesity phenotype, characterized by the resistance to being reduced. I propose a theory in which the body responds to social disruptions as threats of a future lack of food by an adiposity force building a reserve of energy independent of the regulation of the energy balance. It is based on the assumption that our evolutionary development required collaboration in gathering and sharing of food, combined with precautionary measures against anticipated failing food supplies. Social challenges are perceived as such threats, which activate the adiposity force through the brain to instigate the growth of fat and lean mass by neuro-hormonal signaling bypassing the appetite regulation. The signals may induce minor alterations in the balance between adipogenesis and apoptosis in the adipose tissue and between lipogenesis and lipolysis in the adipocytes. If both perceived social threats and food abundance continue, the adiposity force pushes the fat accretion process to continue without inhibition by feedback signals from the fat mass, eventually leading to more obesity, and more so among genetically predisposed. If the theory is right, the challenge is to find ways to reduce or interrupt the signals from the brain to the adiposity stores.