Early nutrition and programming of childhood obesity

The rapid increase in the incidence of obesity and metabolic syndrome over the past two decades cannot be explained only by genetic and adult lifestyle factors. There is now considerable evidence that the fetal and early postnatal environments also strongly influence the risk of developing metabolic syndrome later in life. There is considerable evidence for the induction of different phenotypes by variations in the early life environment, including nutrition, which in man is associated with a risk of metabolic disease: the "nutritional programming". Initially, human studies showed that low birth weight was associated with an increased risk of pbesity but increasingly there is evidence that overnutrition in the early life and early rapid growth can also increase susceptibility to future obesity. Moreover in the postnatal period, an excessive protein intake early in life has been associated with not eligible negative consequences from a digestive-metabolic point of view with negative effects later in life, in particular with an increased risk of developing obesity and thereby non-communicable diseases. It is likely that the induction of persistent changes to tissue structure and function by differences in the early life environment involves life-long alterations to the regulation of gene transcription. The mechanism which underlies such changes to gene expression is now beginning to be understood. The demonstration of altered epigenetic regulation of genes in phenotype induction suggests the possibility of interventions to modify long-term disease risk associated with unbalanced nutrition in early life.