Epigenetics Lights Up the Obesity Field

Blundell et al. [1] in a recent Obesity Facts’ editorial challenges the reader with an interesting open question: ‘What is the part of epigenetics and other ‘omics’ in obesity research?’ The current editorial takes up the gauntlet thrown down by these authors and attempts to define the state of the art of this topic. ‘Omics’ tools have become essential to gain a more integrated and functional knowledge of the workings of cells as well as entire organisms, and the current evidence suggests that these advances will provide new opportunities for prevention, diagnosis, treatment and monitoring of obesity. So far, most of the ‘omics’ efforts in the obesity arena have been devoted to characterize the mechanisms of obesity onset [2–6]. This process started back in the 1990s with the development of experimental models of obesity and the microarray technologies and continues today with the addition of more advanced ‘omics’ technologies, but above all with more experienced researchers in the use and interpretation of these technologies. The human component of the ‘omics’ revolution started in 2006 thanks to the widespread availability of genome arrays and the subsequent proliferation of genome wide association studies [7–9]. These efforts have resulted in the identification of about 40 loci related to human obesity. Of those, FTO has been the most replicated and the one showing the highest statistical significance. However, despite these advances, the combined effect of all loci identified so far account for about 2–3% of the inherited contribution to obesity risk (40–70%). These humbling statistics confirm the complex nature of obesity and the need to identify additional factors including interactions between multiple genes and environmental factors [10–12]. Moreover, epigenetic modifications may be responsible for a significant proportion of the apparent missing heritability as well as the mechanisms by which the environment could induce metabolic changes with lasting effects.