Sucralose dominates the global sweetener market and comprises 30% of the United States sweetener market. Present in more than 4,500 foods and beverages, sucralose plays a fundamental role in the food industry and is unfortunately expected to strengthen its presence in the market.
Studies report that some factors cause the opposite of what we want to avoid obesity and diabetes. Recent research reports possible links with systemic inflammation, metabolic diseases, alterations in the intestinal microbiota, liver damage and toxic effects at the cellular level (Table 2, Figure 2 of the first link). Even the WHO has recently issued an alert indicating that sucralose consumption may be related to systemic inflammation and metabolic diseases. Sucralose, even in amounts considered normal for intake, while highlighting undesirable effects such as cytotoxicity, genotoxicity and immunomodulation. Research in humans indicates possible effects on thyroid function and connections with autoimmune thyroiditis, while animal studies provide histomorphological evidence of pancreatic toxicity and aggravation of the development of autoimmune diseases.
It has been reported that neurons activated by leptin are also stimulated by sucralose, suggesting that sucralose consumption could potentially alter the appetite-satiety axis and raise the threshold for feeling full. It also increased the expression of the dopaminergic nucleus, promoting food intake and suggesting a potential link between sucralose consumption and deregulation of the neuronal mechanisms that control food intake.
The inflammatory consequences of sucralose consumption can persist across generations. It has been shown that newborns of high sucralose intake (HSI) mothers showed a substantial increase in their percentage of inflammatory monocytes. Additionally, umbilical cord tissue from babies of HSI mothers showed higher levels of tumor and disease suppressive immune enhancers IL-1 beta and TNF-alpha and IL-10. This evidence shows that excessive sucralose ingestion during pregnancy affects the metabolic and inflammatory characteristics of newborns. Sucralose has the potential to alter the composition of the maternal gut microbiota and, consequently, this could affect breast milk during the bacterial transfer process. A previously established link connects the greater presence of this archaeon in the colastrum with obesity in children.
Sucralose may exacerbate intestinal inflammatory activity in mice at risk for Crohn's disease. Due to possible intestinal dysbiosis, it is believed that sucralose could be a major contributor to inflammatory bowel disease.
Studies in rats provide evidence that sucralose can deactivate hepatic ribosomes, causing cytokine-mediated inflammation in the liver Ad. The rats may develop liver fibrosis, hyperplasia and lymphocyte infiltration. Sucralose increased Hb1Ac levels, reduced red and white blood cells, and decreased hematocrit and hemoglobin levels. Subsequent histopathological studies revealed severe liver and kidney damage.
Sucralose dominates the global sweetener market and comprises 30% of the United States sweetener market. Present in more than 4,500 foods and beverages, sucralose plays a fundamental role in the food industry and is unfortunately expected to strengthen its presence in the market.
Studies report that some factors cause the opposite of what we want to avoid obesity and diabetes. Recent research reports possible links with systemic inflammation, metabolic diseases, alterations in the intestinal microbiota, liver damage and toxic effects at the cellular level (Table 2, Figure 2 of the first link). Even the WHO has recently issued an alert indicating that sucralose consumption may be related to systemic inflammation and metabolic diseases. Sucralose, even in amounts considered normal for intake, while highlighting undesirable effects such as cytotoxicity, genotoxicity and immunomodulation. Research in humans indicates possible effects on thyroid function and connections with autoimmune thyroiditis, while animal studies provide histomorphological evidence of pancreatic toxicity and aggravation of the development of autoimmune diseases.
It has been reported that neurons activated by leptin are also stimulated by sucralose, suggesting that sucralose consumption could potentially alter the appetite-satiety axis and raise the threshold for feeling full. It also increased the expression of the dopaminergic nucleus, promoting food intake and suggesting a potential link between sucralose consumption and deregulation of the neuronal mechanisms that control food intake.
The inflammatory consequences of sucralose consumption can persist across generations. It has been shown that newborns of high sucralose intake (HSI) mothers showed a substantial increase in their percentage of inflammatory monocytes. Additionally, umbilical cord tissue from babies of HSI mothers showed higher levels of tumor and disease suppressive immune enhancers IL-1 beta and TNF-alpha and IL-10. This evidence shows that excessive sucralose ingestion during pregnancy affects the metabolic and inflammatory characteristics of newborns. Sucralose has the potential to alter the composition of the maternal gut microbiota and, consequently, this could affect breast milk during the bacterial transfer process. A previously established link connects the greater presence of this archaeon in the colastrum with obesity in children.
Sucralose may exacerbate intestinal inflammatory activity in mice at risk for Crohn's disease. Due to possible intestinal dysbiosis, it is believed that sucralose could be a major contributor to inflammatory bowel disease.
Studies in rats provide evidence that sucralose can deactivate hepatic ribosomes, causing cytokine-mediated inflammation in the liver Ad. The rats may develop liver fibrosis, hyperplasia and lymphocyte infiltration. Sucralose increased Hb1Ac levels, reduced red and white blood cells, and decreased hematocrit and hemoglobin levels. Subsequent histopathological studies revealed severe liver and kidney damage.
https://www.frontiersin.org/journals/oncology/articles/10.3389/fonc.2020.00710/full (2020).--
https://www.mdpi.com/2075-1729/14/3/323 (2024).--
https://pubmed.ncbi.nlm.nih.gov/36979631/ (2023).—
https://journalmedicals.com/index.php/AJOAIMS/article/view/139 (2024).--