The Obese Species congress, featuring a multidisciplinary approach to obesity, was held in Erice October 21–26, 2011, organized by the International School of Ethology of the Majorana Foundation. The introductory lecture by John Blundell provided an overview of the development of the research field of obesity, going from the model of energy expenditure with homeostatic control of appetite to environmental interaction defining susceptible and resistant human phenotypes. He presented an example of phenotypes, noting that while 80% of the obese population loses body weight under physical exercise, as would be expected, a full 20% gains weight. A genetic approach to brain control of appetite was described by Bradford Lowell. Using Cre/Lox technology, he showed the importance of the antiobesity effect of the leptin-gabaergic system, the Agouti related peptide and glutamatergic brain system in food-seeking activity. The brain and gut communication has been the target of study for treatment of obesity for several years with little success. Matthias Tschop showed that concomitant injection of gut peptides such as GLP1, GIP and glucagone can decrease food intake in humans, suggesting that polydrug therapy should be the basis for treating an obese person. The first day concluded with Daniele Piomelli speaking of the ‘‘cannabinoid fiasco’’ of rimonabant in the control of human obesity; he indicated that the naturally occurring amide of ethanolamide and oleic acid could reduce feeding through a brain oxitocinergic mechanism. Saverio Cinti discussed the role of brown and white fat tissue in the control of energy intake. Two considerations emerged. First, brown is a good fat and low temperature can increase its mass. Second, there is evidence that obesity is the consequence of adipose tissue inflammation. Brown and white adipocytes are in equilibrium depending by environmental factor in particular food and temperature. The temperature can increase the BAT mass by a transdifferentiation process. On the other hand, the necessity to energy storage following to excessive energy intake moves the BAT towards WAT. Moreover when WAT is too much due to its hypertrophy up to the critical death size inflammation could arise. Visceral adipocytes have a critical death size smaller than subcutaneous adipocytes, thus explaining the higher inflammation and higher morbidity of visceral fat. According to the hypothesis of Cinti, the smaller critical death size of visceral adipocytes is due to their main origin from brown adipocytes transformed into small white adipocytes less expansible that white ones. Antonio Vidal-Puig described the Insig1/SREBP1/ SCD1 network, an allostatic regulatory loop designed to preserve white adipose tissue lipid omeostasis. Down regulation of this system leads to obesity-induced insulin resistance. The importance of early stress events in the control of depressive-like disorders as a contribution to eating disorders was discussed by Anna Moles. The role of stress in obesity was also pointed out by Zofia Zukowska and Alessandro Bartolomucci, who gave us a behavioral model to study new drugs that can interfere with hypothalamus-pituitary-adrenal axis function. The role of membrane lipids as components of cell membrane, serving S. G. Sukkar (&) Dir. Resp.le U.O.D. Dietetica e Nutrizione Clinica, Az. Ospedale-Universita San Martino di Genova, Universita di Genova, Pad. VII piano 2 , Largo R. Benzi 10, 16132 Genoa, Italy e-mail: samir.sukkar@hsanmartino.it