Aspartame

Pregnancy

EFSA's 2013 scientific opinion used human phenylalanine modeling and concluded that intake up to its 40 mg/kg body weight per day ADI would not raise modeled phenylalanine above the clinical fetal threshold in people without PKU. The opinion is a risk assessment, not a pregnancy outcome trial. Halldorsson et al. (2010) studied 59,334 Danish pregnancies and Englund-Ögge et al. (2012) studied 60,761 Norwegian pregnancies; both reported associations between artificially sweetened beverages and preterm birth, but neither measured aspartame alone. Gjørup et al. (2025) reported that 72,821 women completed a pregnancy food-frequency questionnaire; the full analysis included 66,668 with artificially sweetened beverage data within a cohort that enrolled 101,042 pregnancies. Daily artificially sweetened beverage intake was associated with overweight at later childhood ages, but the study reported no association at birth or infancy and could not identify the sweetener. Ho et al. (2025) reported changes in lung metabolic and redox markers in mouse pups after maternal aspartame exposure; Andriichuk et al. (2026) found no measured changes in selected cortex features in newborn mice. These animal studies do not establish human pregnancy outcomes. Venegas Silva et al. (2026) found modest, mostly transient early effects in rat offspring exposed to maternal aspartame together with an obesogenic diet. Human evidence does not provide trimester-specific outcome estimates for aspartame alone.

Breastfeeding

LactMed's January 2024 review says intact aspartame is not detectable in breast milk and that very high intake can slightly raise milk phenylalanine. Sylvetsky et al. (2015) tested milk from 20 lactating volunteers and did not detect aspartame; the study did not measure infant health outcomes. LactMed states, "Although it is prudent to avoid the use of aspartame in women who are nursing an infant with phenylketonuria (PKU), amounts that are typically ingested in aspartame-sweetened foods and beverages do not result in any additional risk to breastfed infants with phenylketonuria." FSA guidance also identifies aspartame as a phenylalanine source relevant to people with PKU. Huang et al. (2021) analyzed 682 mother-infant pairs at three months postpartum. Estimated exposure to low-calorie sweeteners from maternal diet beverages was associated with higher odds of vomiting only in the lowest exposure category; higher exposure was not associated, and a complete-case analysis found no association across exposure categories. The cross-sectional study could not identify which sweetener was involved. Fowler et al. (2023) used retrospective maternal reports from 356 offspring and combined gestational and breastfeeding exposure. Male-specific associations were reported for autism, but the design could not separate exposure timing or establish a cause. The 2024 critique and author reply document substantial disagreement about the study's interpretation.

What was tested

EFSA's 2013 assessment included animal exposure studies and human phenylalanine modeling, while its pregnancy conclusion was not based on an aspartame-only pregnancy trial. Halldorsson, Englund-Ögge and Gjørup studied reported artificially sweetened beverages, not isolated aspartame. Sylvetsky et al. measured sweeteners in human milk; Huang et al. estimated infant exposure from maternal diet beverages; Fowler et al. retrospectively assessed maternal diet-soda and aspartame intake during pregnancy and breastfeeding. Recent animal studies measured mouse lung redox markers, newborn mouse cortex histology and rat offspring metabolism; these do not establish clinical effects in human pregnancies or nursing infants.