Is Fructose Linked to Adiposity in Babies? (FLAB)
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.
|Study Design:||Observational Model: Cohort
Time Perspective: Prospective
|Official Title:||Is Fructose Linked to Adiposity in Babies?|
- % adiposity (DEXA) [ Time Frame: After delivery, neonatal adiposity will be measured using DEXA. This part of the protocol takes place 4-5 months after recruitment. ] [ Designated as safety issue: No ]After delivery, neonatal adiposity will be measured using DEXA.
- cord blood insulin (corrected by cord blood glucose) [ Time Frame: At delivery (in the OR): 4-5 months after recruitment ] [ Designated as safety issue: No ]
- cord blood triglycerides [ Time Frame: At delivery (in the OR): 4-5 months after recruitment ] [ Designated as safety issue: No ]
- cord blood leptin [ Time Frame: At delivery (in the OR): 4-5 months after recruitment ] [ Designated as safety issue: No ]
- anthropometric measurements on the newborn [ Time Frame: After delivery (4-5 months after recruitement) ] [ Designated as safety issue: No ]birth weight, arm, thigh, and abdominal circumference, subscapular skinfolds
- fetal fractional thigh volume obtained by fetal ultrasound [ Time Frame: At 32 weeks gestation (4 months after recruitment) ] [ Designated as safety issue: No ]The fetal fractional thigh volume will me measured in addition to routine fetal measurements at 32 weeks estimated gestation age. This measurement is a measure of neonatal adiposity.
- cord blood uric acid [ Time Frame: At delivery (in the OR): 4-5 months after recruitment ] [ Designated as safety issue: No ]
|Study Start Date:||January 2011|
|Study Completion Date:||January 2013|
|Primary Completion Date:||June 2012 (Final data collection date for primary outcome measure)|
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.
Please refer to this study by its ClinicalTrials.gov identifier: NCT01262781
|United States, California|
|San Francisco General Hospital|
|San Francisco, California, United States, 94110|
|Principal Investigator:||Robert Lustig, MD||University of California, San Francisco|
|Study Director:||Anjali Jain, MD||University of California, San Francisco|