ReviewInternational journal of women's health2026
Effect of High Intensity Sweeteners on the Reproductive System: From the Onset of Puberty to Menstrual Health: A Comprehensive Review of Human and Animal Evidence.
Review in International journal of women's health, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
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Authors and funding
3 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Introduction: High-Intensity Sweeteners (HISs) are widely consumed as calorie-free sugar substitutes, particularly among girls and women of reproductive age. Despite their regulatory approval, growing evidence suggests potential endocrine-disrupting properties that may negatively impact women's reproductive health. Objective: This narrative review synthesizes human and animal evidence on the Potential Pathological Effects of AS on puberty onset and menstrual health, while elucidating the underlying biological mechanisms. Methods: A structured search of references in PubMed, Scopus, Web of Science, and Embase up to 2025 was conducted, prioritizing studies from 2015 onwards. Inclusion criteria required quantitative measurements of AS exposure and reproductive endpoints in non-pregnant, non-lactating women, or relevant animal models. Seventeen studies (12 animals, 5 humans) were thematically synthesized. Results: Chronic exposure to AS specifically aspartame, sucralose, saccharin, and acesulfame-K-disrupts female reproductive physiology through composition-dependent and developmentally timed mechanisms. These mechanisms include (1) suppression of the hypothalamic-pituitary-gonadal (HPG) axis through downregulation of Kiss1; (2) ovarian mitochondrial dysfunction, oxidative stress, and follicular atresia; and (3) reduced estrogen production by the gut microbiota through disruption of the estrobulum. Importantly, these effects often occur independently of body weight or metabolic changes. Human data have linked maternal and prepubescent AS consumption to premature thelarche, menstrual irregularities, and altered rate of puberty, particularly in carriers of TAS1R2/TAS1R3 polymorphisms. It is noteworthy that not all sweeteners pose the same risk: advantame and glycyrrhizin show neutral or protective profiles. Conclusion: Artificial sweeteners may not be harmless, especially above the acceptable daily intake (ADI), and they could act as bioactive endocrine disruptors. However, given that much of the current evidence derives from animal studies and limited observational human data, further well-designed human studies are needed to confirm these associations and clarify their clinical significance.
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