Thrifty genotype: how applicable is it to obesity and type 2 diabetes?

The "thrifty genotype" hypothesis of Neel (Neel JV,Weder AB, Julius S: Type II diabetes, essential hypertension, and obesity as "syndromes of impaired genetic homeostasis": the "thrifty genotype" hypothesis enters the 21(st) century. Perspect Biol Med 42:44-74, 1998) explains persistence of genes fo r obesity and type 2 diabetes in humans by their historic advantages: when food supply was scarce and unstable, "thrifty" individuals were better able to conserve energy and, withstand famine, In today's Westernized society, this advantage is lost but the tendency to these "diseases of civilization" remains. The "thrifty genotype" is universal and may be explained by asymm etric regulation of appetite resulting in a strong defense against weight l oss and a quite weak one against weight gain. For most of human history, it was better to be moderately obese than slim, and potential late deleteriou s effects of obesity were irrelevant when life was short, Therefore, it is unlikely that any miracle cure will ever be found for obesity, and early ap petite training remains the most promising approach. Diabetes, however, is not universal, and its frequency is enormously different between population s, Neither for survival nor for fecundity is there any evolutionary advanta ge to being diabetic. Diabetes is a syndrome and not a disease and may be c aused by a great many different genes even within the same population,It is suggested that the preservation of diabetogenes is explainable by mutation accumulation. It is more frequent in isolated communities and the least fr equent in Europe with ifs history of many migrations and conquests, making the (recessive) diabetogenes more,widespread but decreasing the chances of their conquests, making the (recessive) homozygosity. Therefore, obesity ma y provoke diabetes in genetically predisposed individuals only and as an ep igenetic phenonmenon.