Women with gestational diabetes (GD) have reduced antioxidant capacity; however, the relationship between maternal diet, maternal biochemical capacity, breast milk concentration, and infant intake has not been adequately explored in the literature. An exploration of underlying mechanism(s) is warranted, particularly for nutrient antioxidants impacted by maternal intake. These nutrients may provide a means for modifying maternal and infant antioxidant capacity. Oxygen radical absorbance capacity (ORAC), alpha-tocopherol, ascorbic acid, and beta-carotene concentrations were measured in breast milk of women with and without GD. Plasma, three-day diet records, and breast milk were collected at 6 to 8 weeks postpartum. Student’s t-test was used to compare breast milk ORAC, nutrient antioxidant concentration and plasma ORAC between women with and without GD. Pearson correlations were used to determine associations among antioxidant concentrations in breast milk and dietary antioxidant intake. Breast milk antioxidant concentrations were associated with maternal intake of beta-carotene (r = 0.629, p = 0.005). Breast milk and plasma ORAC and antioxidant vitamin concentrations were not significantly different between GD and NG women. Breast milk ORAC associated with breast milk alpha-tocopherol for NG (r = 0.763, p = 0.010), but not GD women (r = 0.385, p = 0.35), and with breast milk ascorbic acid for GD (r = 0.722, p = 0.043) but not NG women (r = 0.141, p = 0.70; interaction p = 0.041). In GD participants, breast milk ORAC was significantly associated with plasma ORAC (r = 0.780, p = 0.039). ORAC and antioxidant vitamin concentrations in breast milk in women with GD were comparable to women with NG; however, the relationships between breast milk ORAC and vitamin concentrations differed in GD versus NG women for alpha-tocopherol and ascorbic acid.

Low glycemic-index foods may reduce postprandial oxidative stress by reducing postprandial glucose excursions, but the evidence for this is limited by dietary confounders. To determine whether reducing postprandial glucose per se reduces postprandial oxidative stress, overnight-fasted participants (BMI 25.0–39.9 kg/m², n = 18) consumed four test meals in random order: 75 g dextrose solution (Dex) within 5 min (bolus/noC), Dex slowly over 3.25 h (sipping/noC), bolus with 1 g vitamin C (bolus/C) and sipping with 1 g vitamin C (sipping/C). Venous blood was taken at intervals over 6 h; a standard lunch was consumed at 4 h. Sipping flattened postprandial glucose and insulin and reduced free fatty acid rebound compared to bolus (p < 0.05). Vitamin C raised serum vitamin C from ~20 to ~55 μmol/L. The total peroxyl radical trapping antioxidant potential (TRAP) increments differed after lunch, with a main effect of vitamin C at 5 h (mean ± SEM; C 70 ± 23 vs. noC −29 ± 27; p = 0.016) and main effects of rate (sipping 57 ± 25 vs. bolus −71 ± 28; p = 0.0002) and vitamin C (C 58 ± 25 vs. noC −73 ± 28; p = 0.0003) at 6 h. By multiple regression analysis, the TRAP area under the curve (AUC) was positively associated with the insulin AUC (p < 0.001) and negatively with the glucose and vitamin C AUCs (p < 0.05). The oxidized LDL increments were higher 6 h after sipping than bolus (7 ± 7 vs. −20 ± 7, p = 0.005). The oxidized LDL AUC was negatively associated with the TRAP AUC (p < 0.001). These results support the hypothesis that reducing postprandial glucose reduces postprandial oxidative stress.