Sweeteners and Liver Health: Evaluating Hepatotoxic Risks and Herbal Countermeasures

With rising health consciousness and the global epidemic of obesity and diabetes, there has been a marked shift toward the consumption of low-calorie sweeteners (LCSs) as substitutes for refined sugars. While these sweeteners—both artificial (such as aspartame, sucralose, and saccharin) and natural (like stevia and monk fruit extracts)—are widely used and generally regarded as safe, growing evidence raises concerns about their long-term effects on liver health. This review critically examines the hepatotoxic potential of commonly consumed LCSs by exploring molecular mechanisms of liver injury, including oxidative stress, mitochondrial dysfunction, inflammation, and disruption of gut-liver axis signaling. Histopathological alterations such as steatosis, hepatocellular ballooning, and fibrosis are also discussed, alongside metabolic disturbances like dyslipidemia and insulin resistance. In parallel, the review evaluates emerging data on hepatoprotective interventions derived from medicinal plants and dietary phytochemicals—such as curcumin, silymarin, and resveratrol—that may counteract sweetener-induced hepatic damage. Traditional herbal formulations and integrative therapeutic strategies are also considered. By synthesizing current preclinical and clinical findings, this review highlights critical knowledge gaps and proposes future research directions to ensure safe dietary practices and inform the development of effective, evidence-based strategies for liver protection in the context of increasing sweetener use. Keywords: sweeteners, hepatotoxicity, liver injury, herbal remedies, phytochemicals, oxidative stress, histopathology.

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Publication Details

Journal
IAA Journal of Applied Sciences
Published
2025-06-21
DOI
https://doi.org/10.59298/iaajas/2025/515600
Citations
1
Primary Topic
Diet, Metabolism, and Disease
Type
article
Field-Weighted Citation Impact
1.29
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article

Sweeteners and Liver Health: Evaluating Hepatotoxic Risks and Herbal Countermeasures

Kibibi Wairimu H.
1 citations
IAA Journal of Applied Sciences
Diet, Metabolism, and Disease
1.29
article

Sweeteners and Liver Health: Evaluating Hepatotoxic Risks and Herbal Countermeasures

Kibibi Wairimu H.
article en
1 citations

Abstract

With rising health consciousness and the global epidemic of obesity and diabetes, there has been a marked shift toward the consumption of low-calorie sweeteners (LCSs) as substitutes for refined sugars. While these sweeteners—both artificial (such as aspartame, sucralose, and saccharin) and natural (like stevia and monk fruit extracts)—are widely used and generally regarded as safe, growing evidence raises concerns about their long-term effects on liver health. This review critically examines the hepatotoxic potential of commonly consumed LCSs by exploring molecular mechanisms of liver injury, including oxidative stress, mitochondrial dysfunction, inflammation, and disruption of gut-liver axis signaling. Histopathological alterations such as steatosis, hepatocellular ballooning, and fibrosis are also discussed, alongside metabolic disturbances like dyslipidemia and insulin resistance. In parallel, the review evaluates emerging data on hepatoprotective interventions derived from medicinal plants and dietary phytochemicals—such as curcumin, silymarin, and resveratrol—that may counteract sweetener-induced hepatic damage. Traditional herbal formulations and integrative therapeutic strategies are also considered. By synthesizing current preclinical and clinical findings, this review highlights critical knowledge gaps and proposes future research directions to ensure safe dietary practices and inform the development of effective, evidence-based strategies for liver protection in the context of increasing sweetener use. Keywords: sweeteners, hepatotoxicity, liver injury, herbal remedies, phytochemicals, oxidative stress, histopathology.

IAA Journal of Applied SciencesVol. 13(2)
Good health and well-being
Openalex Percentile: Top 18%
Diet, Metabolism, and Disease
1.29
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