How might genes contribute to obesity? Currently, there are quite a few theories that (the thrifty gene hypothesis, the fetal programming hypothesis, the predation release hypothesis, the sedentary lifestyle hypothesis, the ethnic shift hypothesis, the increased reproductive fitness hypothesis, the assortative mating hypothesis, and the complex hypothesis) intend to explain the genetic basis of human obesity [9, 10]. However, an acceptable consensus in the field is still lacking, probably due to the fact that complex genetic interactions influence the development of obesity. One of the intriguing explanations for the rapid rise in obesity is the mismatch between today's environment and “energy thrifty genes” that multiplied in the past under different environmental conditions when food sources were rather scarce. In other words, according to the “thrifty genotype” hypothesis, environments in which food is plentiful year around are now challenging the same genes that helped our ancestors survive occasional famines. It has been argued that the thrifty genotype is just part of a wider spectrum of ways in which genes can favor fat accumulation in a given environment. These ways include the
