The obesity epidemic has reached down into the infant and toddler age group. Dietary indiscretion during pregnancy, particularly in our current food environment, is a major risk factor for both gestational diabetes and neonatal macrosomia (>4kg newborns), which is itself a risk factor for obesity and metabolic syndrome in the offspring, possibly even during childhood. Temporal increases in fructose consumption in the last two decades coincide with temporal increases weight gain during pregnancy and with increased birth weight, including a higher prevalence of macrosomic newborns. Our central hypothesis is that higher fructose consumption during pregnancy is a risk factor for infant obesity and metabolic syndrome.

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.

Inclusion Criteria:

• Agreement to participate in all measurements
• Plans to remain in the area through delivery
• Ability to understand and give informed consent in either English or Spanish.

Exclusion Criteria:

• Presence of diabetes prior to the index pregnancy
• Presence of gestational diabetes during a previous pregnancy
• Presence of diabetes or of other chronic metabolic disease such as cardiovascular disease, active thyroid disease, liver disease, pulmonary or psychiatric disorders, HIV
• Any disorder requiring diet therapy (i.e., renal insufficiency)
• Multiple gestation
• Prior history of intrauterine growth retardation
• Use of substances known to cause intrauterine growth retardation (e.g., smoking or drug use). -
• Once recruited, any ultrasonographic evidence of intrauterine growth retardation during the course of the pregnancy would also lead to exclusion.

Pregnant women between 18 to 40 years of age are eligible for this study