Is Fructose Linked to Adiposity in Babies?

The "fetal origins hypothesis" suggests that an individual's risk for obesity and metabolic disorders begins in utero; that fetal or early postnatal exposure to environmental factors, such as maternal nutrition or endocrine disrupting chemicals, adversely influences early development and results in permanent changes affecting energy storage and expenditure. Most studies on "fetal origins" of obesity in the offspring have focused on maternal high-fat diets; yet dietary fat consumption has not changed appreciably in the last two decades. One chemical exposure in both pregnant mothers and newborns that has been steadily increasing worldwide is fructose. Although ostensibly a carbohydrate, fructose is a potent lipogenic substrate, and in the hypercaloric state, as much as 30% of an ingested fructose load undergoes de novo lipogenesis to form triglyceride thus the effects of high-fat and high-fructose diets in terms of physiology and outcome are comparable. Substituting sucrose (fructose + glucose) for glucose alone increases visceral adiposity, insulin resistance, and dyslipidemia in adult animals and humans. For humans, fructose is ubiquitous in the food environment, especially for pregnant mothers, who are often counseled to drink juice during pregnancy, as it is deemed to be healthier than soda. The effects of fructose consumption during pregnancy on infant birth weight and adiposity has not yet been studied.