Artificial Sweeteners in Breast Milk: A Clinical Investigation with a Kinetic Perspective

Stampe, Sofie; Leth-Møller, Magnus; Greibe, Eva; Hoffmann-Lücke, Elke; Pedersen, Michael; Ovesen, Per

doi:10.3390/nu14132635

Cited by 4 publications

(2 citation statements)

References 34 publications

(42 reference statements)

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“…These authors also described the presence of acesulfame-K and saccharin in 100% and 80% of 15 cord blood samples, with maximum concentrations of 6.5 and 2.7 ng/ml, respectively, while sucralose and steviol glucuronide were not detected (55). A similar study (56) in 49 lactating mothers after the ingestion of acesulfame-K, saccharin, cyclamate, and sucralose, detected their appearance in breast milk at 240-300 min, with maximum concentrations of 936, 81.5 and 2.56 ng/ml Again, these results were independent of the weight and metabolic status of the mothers. The presence of saccharin, acesulfame K, steviol glucuronide and/or sucralose has also been reported in 77% of amniotic fluid (n = 13) samples (55).…”

Section: Nnss In Breast Milk and Amniotic Fluidmentioning

confidence: 70%

Maternal consumption and perinatal exposure to non-nutritive sweeteners: should we be concerned?

et al. 2023

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The context for this review is the rapid increase in the use of non-nutritive sweeteners (NNSs) instead of sugar in foods and beverages, a situation so prevalent in some countries that consumers are finding it increasingly challenging to access foods without NNSs. The benefits of consuming NNSs on obesity and diabetes are now being questioned, and studies have shown that they may exert physiological activities, sometimes independently of sweet taste receptor stimulation. Few studies, limited mainly to North American and European countries, have described the consumption of NNSs by pregnant or lactating women and infants. Most focus on beverages rather than foods, but all agree that consumption levels have increased dramatically. Although some studies report a negative impact of NNSs on the risk of preterm birth, increased birth weight and decreased gestational age, the level of evidence is low. Several studies have also reported increased weight gain in infancy, associated with maternal NNS intake. Interestingly, several NNSs have been detected in amniotic fluid and breast milk, usually (but not always) at concentrations below their established detection limit in humans. Unfortunately, the impact of chronic exposure of the fetus/infant to low levels of multiple NNSs is unknown. In conclusion, there is a stark contrast between the galloping increase in the consumption of NNSs and the small number of studies evaluating their impact in at-risk groups such as pregnant and lactating women and infants. Clearly, more studies are needed, especially in Latin America and Asia, to fill these gaps and update recommendations.

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Section: Nnss In Breast Milk and Amniotic Fluidmentioning

confidence: 70%

Maternal consumption and perinatal exposure to non-nutritive sweeteners: should we be concerned?

et al. 2023

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“…Most likely, women with a high intake of diet drinks may continue this intake during breastfeeding. We have, in a previous study, shown that ASs ingested by breastfeeding women are transferred to the milk, possibly affecting the nursing infant [21].…”

Section: Potential Mechanisms and Explanationsmentioning

confidence: 95%

Transplacental Transport of Artificial Sweeteners

et al. 2023

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The prevalence of obesity is increasing, and the origins of obesity and metabolic dysfunction may be traced back to fetal life. Currently, overweight pregnant women are advised to substitute sugar-sweetened beverages with diet drinks containing artificial sweeteners. Recent evidence suggests that the consumption of artificial sweeteners during pregnancy increases the risk of obesity in the child, but the mechanism is unknown. We hypothesized the transportation of artificial sweeteners across the placenta into the fetal circulation and the amniotic fluid. We included 19 pregnant women who were given an oral dose of acesulfame, cyclamate, saccharin, and sucralose immediately before a planned caesarean section. Nine women were included as controls, and they refrained from an intake of artificial sweeteners. The maternal and fetal blood and amniotic fluid were collected during the caesarean section, and concentrations of artificial sweeteners were measured using mass spectrometry. We found a linear relationship between the fetal plasma concentrations of artificial sweeteners and the maternal plasma concentrations, with adjusted coefficients of 0.49 (95% CI: 0.28–0.70) for acesulfame, 0.72 (95% CI: 0.48–0.95) for cyclamate, 0.51 (95% CI: 0.38–0.67) for saccharin, and 0.44 (95% CI: 0.33–0.55) for sucralose. We found no linear relationship between amniotic fluid and fetal plasma concentrations, but there were positive ratios for all four sweeteners. In conclusion, the four sweeteners investigated all crossed the placenta and were present in the fetal circulation and amniotic fluid.

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Hepatic P53 upregulation and the genotoxic potential of acesulfame-K treatment in rats with a special emphasis on in vitro lymphocyte and macrophage activity testing

Mohammed,

Abdelrazik,

Anwar

et al. 2024

Hum Exp Toxicol

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Acesulfame-k (Ace-k) is a widely used artificial sweetener in various products, and long-term cumulative and multisource exposure is possible despite inadequate toxicological data confirming its safety. Ninety male rats were divided into two main groups according to their body weight into immature and mature rats. Each group was subdivided into 3 subgroups: control untreated, 30 and 90 mg/kg b. w of Ace-k via gastric intubation. The treatment was performed daily 5 days per week for 12 weeks. At the end of the experimental period, blood samples were collected for in vitro testing of lymphocyte proliferation rate, comet assay, and macrophage activity about nitric oxide (NO) production. In addition, the collection of liver specimens was performed for P53 gene expression and histopathological evaluation. The results revealed that Ace-k induced modulation in lymphocyte proliferation rate and affected the production of NO by macrophages while increasing in tail moment in a dose-dependent manner that varied among different age groups. The upregulation of P53 in the liver was correlated with increased polyploidization and necro apoptotic reaction and various histopathological hepatic alterations. The present data revealed that chronic treatment of rats with Ace-k affects lymphocyte proliferation and macrophage activity in a dose-dependent manner. In addition, the genotoxic and hepatotoxic potential of Ace-k were confirmed.

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Artificial Sweeteners in Breast Milk: A Clinical Investigation with a Kinetic Perspective

Cited by 4 publications

References 34 publications

Maternal consumption and perinatal exposure to non-nutritive sweeteners: should we be concerned?

Maternal consumption and perinatal exposure to non-nutritive sweeteners: should we be concerned?

Transplacental Transport of Artificial Sweeteners

Hepatic P53 upregulation and the genotoxic potential of acesulfame-K treatment in rats with a special emphasis on in vitro lymphocyte and macrophage activity testing

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