Obesity is an important medical and civilization problem due to health consequences and increasing incidence. The development of obesity is influenced by genetic and environmental factors. Despite intensive research the results of which allowed to identify genetic variants predisposing to the development of obesity, the knowledge about the genetic basis of this metabolic disease still remains incomplete. Furthermore, the contribution of single polymorphic gene variants to shaping the obesity phenotype is minimal and accounts for a small part of body weight variability. The need for further research in the field of obesity etiology has increased the interest in the role of epigenetics as a mediator of gene-environment interactions, underlying the development of obesity and related comorbidities. Epigenetics deals with changes in gene expression that are not related to changes of the nucleotide sequence in DNA. Epigenetic modifications include DNA methylation, post-translational modifications of histone proteins and synthesis of non-coding microRNA (miRNA). There is growing evidence indicating that environmental exposures (among others the influence of nutrients) in prenatal and early postnatal development may induce permanent changes in the epigenome, predisposing to an increased risk of obesity in later life. Epigenome-Wide Association Study (EWAS) allowed to indicate differences in the methylation pattern of genes in obese people compared to healthy subjects with normal body weight as well as to identify the first epigenetic markers of obesity in humans. EWAS also allowed to recognize epigenetic changes under the influence of nutrients, during weight loss and occurring during exercise interventions. Significant progress in epigenetic studies on the causes of obesity will allow to predict the risk for this metabolic disease already at a young age and it gives the possibility of introducing targeted prevention strategies.