SUN-055 Prenatal Exposure to Artificial Sweeteners

Introduction: In adults, epidemiologic studies consistently show negative health outcomes (e.g. insulin resistance, stroke) related to artificial (or non-nutritive) sweetener (NNS) intake. In children, NNS sweetened beverage consumption is associated with higher total energy and sugar intake. In infants, we documented the immediate appearance of NNS in breast milk after mothers consume diet soda. A positive association between prenatal NNS exposure and higher BMI at 1 year of life has been observed in infants whose mothers routinely consumed NNS during pregnancy. In mice, we recently reported marked changes in intestinal microbiome and hepatic detoxification pathways of pups that had been exposed to NNS via their mothers’ intake during pregnancy and lactation. Thus, we conducted a pilot project to determine whether there is direct evidence for prenatal NNS exposure in humans. In future studies, we will investigate effects on health outcomes. Methods: Concentrations of 3 NNS (acesulfame-potassium (ace-K), sucralose and saccharin) were measured with liquid chromatography-mass spectrometry in cord blood samples (n=15) and amniotic fluid samples (n=13). Aspartame cannot be measured because of its prompt metabolism into aspartic acid and phenylalanine. The cord blood samples were obtained from offspring of women enrolled in a sickle cell clinical trial at the NIH, while the amniotic fluid samples had been obtained for clinical purposes during the 3(rd) trimester. No dietary information was available other than 2 of 13 women were not in the fasting state when undergoing amniocentesis. Results: In the cord blood samples, ace-K and saccharin were present in 12/15 (80%) samples. None of the samples contained sucralose. In the 13 amniotic fluid samples, 10 (77%) samples contained at least one sweetener. One sample was positive for all 3 sweeteners. Maximum concentrations in cord blood were 6.5 ng/mL for ace-K and 2.7 ng/mL for saccharin, while maximum concentrations in amniotic fluid were 78.9 ng/mL for ace-K, 55.9 ng/mL for saccharin, and 30.6 ng/mL for sucralose (non-fasting sample). Most women were in the fasting state before undergoing amniocentesis or giving birth, thus NNS peak concentrations could not be determined in this pilot study. Discussion and Conclusion: 80% of cord blood samples (babies’ blood) and 77% of amniotic fluid samples (reflecting babies’ direct gastrointestinal/lung exposure) contained ace-K, saccharin and/or sucralose. We speculate that NNS exposure may influence in utero growth and development, e.g. sweet taste preference and metabolic pathways. Prospective studies are necessary to test these hypotheses. Results will determine whether current recommendations (or lack thereof) regarding NNS intake during pregnancy and lactation need to be revised.