1 Given the challenges of studying physiological changes in children, scientists and policy makers often rely on human clinical and/or animal studies to improve their understanding of physical adaptations that may support potential mechanisms of DOHaD. The article by

Alves et al., 2 in this edition of the Jornal de Pediatria, is an excellent example of the research needed to advance the field. Still, it is important to place the results presented within a proper methodological and scientific context for a clear understanding of their learn more impact on nutrition science and policy, as well as on pediatric practices. Growth retardation severe enough to cause stunting (height for age less than two standard deviations of a reference population, HAZ < -2.0) is the primary outcome of chronic undernutrition and most often occurs in utero

and/or during the first two years of life, the “critical window” of growth. 3 During the first 30 months of growth and development, specific cells, organs, and systems may be differentially affected by undernutrition, depending on the specific point and extent of nutrient and/or energy restriction. Indeed, the nutritional environment during this “critical window” is the primary determinant of growth, while the nutritional environment after the age of 2 years primarily www.selleckchem.com/products/epz-6438.html influences body composition more than parameters of growth and development. Essentially, a child at age 2 years meets a juncture at which energy and nutrients that were previously directed towards growth are now directed toward weight and body composition, thereby creating the dietary environment that will allow potential adaptations from past energy restriction

to become manifest. Studies on the relationship between stunting and chronic diseases began in the mid-1990s, when Popkin et al.4 either reported that adults who were stunted as adolescents were more likely to be overweight than their normal height peers. Data from two longitudinal cohort studies suggest that growth retardation early in life predisposes a child to obesity or overweight later in childhood or in adulthood.5 and 6 However, some studies have demonstrated that stunting is not associated with adiposity later in life.7 and 8 Despite these apparently contradictory studies, it is important to consider that biological adaptations do not always become manifest without some environmental cue, such as increased refined sugar intake or chronic positive energy balance, conditions most often associated with the “nutrition transition” that accompanies economic development.9 Differences in the level of socio-economic development that give rise to an “obesigenic” environment may limit physiological adaptations to manifest as excess fat mass or obesity.