Over the span of the last decades there has been an alarming worldwide increase in childhood obesity  , which tends to track into adulthood  . Childhood obesity is associated with a significant risk for the development of type 2 diabetes, hypertension, dyslipidemia, metabolic syndrome, and is also a risk factor for early cardiovascular events. The timing of the obesity epidemic is parallel to the increased availability of calorie-dense foods and a more sedentary lifestyle – the ‘obesogenic environment’  .
However, not all individuals become obese while living in the same environment.Therefore, variability among individuals is suspected to result from heritability of obesity susceptibility genes that interact with components in the ‘obesogenic environment’ to promote positive energy balance responsible for weight gain  . Recent evidence, primarily from animal studies and observational data in humans, suggests that the epigenome can be altered by maternal diet during the periconceptionalperiod and that these programming events may underlie later disease risk. In one of the works cited below it was demonstrated that the priconceptual micronutrients altered methylation at the differentially methylated regions of imprinted genes associated with obesity. These results may support the concept that nutrition in critical periods of life can permanently influence the development of chronic diseases. The ‘obesogenic environment’ is a complex of contributing factors that influence the dietary choice, physical activity, or metabolism responsible for maintaining energy balance. Both sedentary behavior and reduced physical activity promote the overconsumption of dietary macronutrients, particularly fats and refined carbohydrates  . It is widely accepted that high-fat diets, characterized by enhanced palatability and high-energy density, may be primarily responsible for the current obesity epidemic.
Also, increased consumption of carbohydrates, particularly refined carbohydrates and sugar-sweetened beverages, can contribute to the increased prevalence of obesity  . The dietary pattern, food frequency, and breakfast consumption may also have an impact on body weight and on markers of the metabolic syndrome. Finally, the connection between gut microbiota, energy homeostasis, and inflammation and its role in the pathogenesis of obesity-related disorders are emerging as a new break for intervention. Although current childhood obesity intervention programs have traditionally focused only on generalized population guidelines, further investigation and insight into gene-diet interactions may serve an important role in both the prevention and treatment of childhood obesity by using targeted nutritional and drug therapies. This chapter reviews a selection of important articles published between July 2012 and June 2013 focusing on the relation between nutrition, obesity and metabolic syndrome in the pediatric age group.