One potential mechanism, mentioned in the article by Alves et al.,2 is an adaptation in lipid metabolism. In 2000, we reported that stunted children from shantytowns in São Paulo, Brazil metabolized lipids at a lower rate than normal height children from the same socioeconomic environment, independent of dietary intake and other confounding factors.10 A similar study, conducted with male subjects from the Hertfordshire Cohort in England, observed that men who had suffered intrauterine growth restriction

had a lower rate of lipid oxidation when compared those born with normal weight.11 Finally, Selleck LY294002 an elegant study that blended human nutrition and anthropology was conducted with adults from Buryat tribes in Southern Siberia, who suffered seasonal undernutrition after the collapse of the Soviet Union.12 The repeated bouts of food insecurity and poor physical growth were so severe that the generation born in this period was shorter

at adulthood than their parents. Metabolic studies of this generation observed that adults who were significantly shorter than their peers had a lower rate of lipid oxidation, controlling for body composition. Thus, based on these three studies of humans from vastly different geographical and socio-economic areas, a consistent observation is that those DNA Synthesis inhibitor who experienced some degree of growth retardation in utero or during early development present with a metabolic profile that favors fat accumulation during times of dietary excess. In fact, stunted children with impaired fat oxidation gained more central fat during a four-year follow-up period, independent of total fat mass and pubertal status.

13 Regarding the relationship between poor growth and other aspects of lipid metabolism, epidemiological studies have reported that adults who experience intrauterine growth retardation are more likely to suffer from atherogenic lipid profiles and cardiovascular disease than those who developed normally.14 and 15 Perhaps the most significant finding much by Alves et al.2 was the fact that despite benefiting from an intensive treatment program, the children studied only experienced improvements in their lipid profiles for some, but not all, of the parameters assessed. It was also astutely hypothesized that the increased TG concentrations reported may be the result of low LPL expression. These observations warrant explicit attention and the data presented should be further studied in order to develop a more comprehensive assessment of the nature of the lipid profiles in the subjects, including a comparison with a healthy control group of children and/or including measures of dietary factors that may contribute to plasma lipid concentrations. Florencio et al.16 observed that short, obese women had significantly greater total cholesterol and low-density lipoprotein (LDL) concentrations compared to normal height, obese women.