Obesity induces a low grade chronic inflammatory state since childhood, who favors the subsequent appearance of insulin resistance and increases the risk of atherogenesis, among other co-morbidities. This state of subclinical inflammation can be evaluated through quantification of various biomarkers such as C-reactive protein (CRP), the tumor necrosis factor alpha and interleukins. Thus, these biomarkers are elevated in obese subjects. In our study we determined the levels of high sensitivity CRP (hs-CRP) in children, specifically in two cohort, children of age prepubertal (6-8 years-old) and adolescents (12-16 years-old), and we have studied its association with variations in the degree of obesity, as well as with plasma levels of lipids and other Adipokine leptin as. On the other hand, we analyzed possible genetic determinants of levels of hs-CRP and evaluated the role of diet as a modulator of blood values of hs-CRP. Our results show that the passage of a state of excess weight in the prepubertal age to normal weight in adolescence, is associated with a considerable improvement in the hs-CRP values against the highest levels observed in children who are obese at both ages. On the other hand, low levels of CRP are associated with levels higher HDL-c and Apo-A1 in the two age groups of our study. Another result is the significant association of the hs-CRP levels with the levels of leptin, independent of BMI. With respect to genetic factors associated with levels of hs-CRP, our population shows an association of polymorphisms in different regions of the PCR gene (rs1205, rs1130864, rs2794521 and rs1800947) and their haplotypes with plasma levels of hs-CRP. In addition, we have found an interesting association of levels of hs-CRP with SNPs of leptin and leptin receptor genes, supporting the idea that other loci may influence these levels. Finally, our data highlight the influence of diet on levels of hs-CRP, a diet rich in fruits and vegetables, high fiber content, is associated with values lower than hs-CRP. In conclusion, our data support the reversibility of the state of chronic inflammation associated with childhood obesity after weight normalization. Also, the data obtained in our study are running to the participation of the leptin in the state of inflammation chronic observed in the obesity. Finally, our data have led to the conclusion that a healthy diet seems to influence positively the attenuation of cardiovascular risk, so that preventive measures during childhood can help improve the inflammatory state of low-grade observed in children.