5%. This is comparable this website to a study in central Greece assessing 11-year-olds weight status where a total of 30.3% were reported

to be overweight and 6.7% obese [13]. The fact that parental BMI was positively associated with their child’s BMI highlights the importance of family history and environment in the development of obesity. The overweight and obese children in the current study had significantly higher arterial blood pressure, lower HDL-C levels, higher TG and increased insulin compared to their the normal weight counterparts. Higher Tanner scores and heights of the overweight and obese group also suggest earlier onset of puberty, which is often frequently observed in overweight and obese children [14]. GSK2126458 purchase Any interaction between sexual maturity and effects of allelic variation on lipid levels that may have occurred could be accounted for in analyses from the Tanner measures. Genetic factors are considered important determinants of plasma lipid levels in adults, demonstrated in several of the recent genome wide association studies (GWAS) in which a number of candidate genes have been confirmed [15] and [16]. The meta-analysis of 3 GWAS by Willer et al. (2008) identified strong associations with variants in APOA5/A4/C3/A1 cluster, APOE, CETP and LPL influencing plasma lipid concentrations. Although a number

of associations comparable to those seen in adults were confirmed in this study, the role of genetic factors in the heterogeneity of plasma lipid levels in children is less clear. Replication of these variants in cohorts of children is needed. In GENDAI, APOE genotypes were associated with differences in TC and LDL-C plasma levels and the TC: HDL-C ratio. The LDL-C and TC lowering

effect of the ɛ2 allele reported in the recent meta-analysis [17] was also observed in this cohort of young Greek children. Carriers of the ɛ4 allele had LDL-C and TC levels that were 19.9% and 12.2% higher than carriers of the ɛ2 allele and 2.8% and 1.3% higher than ɛ3/ɛ3 subjects. The results of a 21-year longitudinal study on changes in serum lipids in 1233 Finns followed from childhood to adulthood AZD9291 datasheet consistently observed the ɛ2 allele to be associated with lower LDL-C levels and the ɛ4 allele with higher TC and LDL-C levels (p < 0.001 for all associations) in childhood. The LDL-C-lowering effect of the ɛ2 allele was an association that was tracked through to adulthood, having a greater effect with increasing age (p = 0.039). The association of the APOE genotype with plasma TC and LDL-C has been reported in children as young as 3 years old [18]. The fact that differences in lipid levels cannot be detected in children at birth by the APOE genotype leads to the conclusion that lipid levels are influenced by genetic and environmental factors in a child’s very first years of life [18].