Epigenetic changes in early life and future risk of obesity

Abstract

The rapid increase in incidence of obesity over the past two decades cannot be explained solely 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 obesity in later life. Initially, human studies showed that low birth weight was associated with an increased risk of obesity but increasingly there is evidence that overnutrition in the early life can also increase susceptibility to future obesity. These findings have now been replicated in animal models, which have shown that both maternal under-and overnutrition can induce persistent changes in gene expression and metabolism. The mechanism by which the maternal nutritional environment induces such changes is beginning to be understood and involves the altered epigenetic regulation of specific genes. In this review, we discuss the recent evidence that shows that early-life environment can induce altered epigenetic regulation leading to the induction of an altered phenotype. The demonstration of a role for altered epigenetic regulation of genes in the developmental induction of obesity opens the possibility that interventions, either through nutrition or specific drugs, may modify long-term obesity risk and combat this rapid rise in obesity.

An Early Feeding Practices Intervention for Obesity Prevention

“…1,2 In the fetal and early life periods, interactions between biology and environmental exposures produce epigenetic effects that influence the risk of childhood obesity. 3,4 Hence, early life interventions, when both behavior and biology are "plastic," have potential both to ameliorate epigenetic effects and increase resilience to the behavioral and metabolic challenges posed by an obesogenic environment. 1 Early feeding practices likely compound increased obesity risk conferred by genetic predisposition and prenatal factors such as excess gestational weight gain.…”

“…50 Established risk factors such as parent weight status, maternal nutrition, excess gestational weight gain, formula feeding, and rapid early weight gain may induce epigenetic processes that in turn increase susceptibility to obesity. 1,3,4 Emerging evidences suggest other heritable infant factors may also confer increased obesity risk. A recent twin study 51 has shown that exclusively breastfed infants at 3 months of age, identified by their mothers as having a big appetite (higher food responsiveness and lower satiety responsiveness), gained more weight from 0 to 15 months, with weight trajectory differences apparent as early as 3 months.…”

Obesity and eating behaviour in children and adolescents: Contribution of common gene polymorphisms

“…However the mechanisms by which these loci act on body weight are still largely unknown and may be complicated further by alterations in gene-expression via epigenetic events in specifi c genes (Lillycrop & Burdge, 2011), in addition to alterations to DNA sequence variation. Although a role in general neuronal development has been postulated (Willer et al, 2009), and current attempts to address this issue systematically in adults are largely underpowered, it will be important to evaluate their role in childhood eating behaviours using sophisticated and direct behavioural assessments (Blundell et al, 2009) across specifi c growth points.…”

Women’s reported health behaviours before and during pregnancy: A retrospective study

“…Over the last two decades overweight and obesity rates have reached epidemic proportions worldwide, with no evidence that these levels are abating (1)(2)(3) . Globally, obesity rates have almost doubled in adults (2,4,5) and children are also "getting fatter" (6,7) .…”