Dietary Emulsifiers Research Articles

Dietary emulsifiers impact mouse health.

Dietary emulsifiers impact mouse health.

The effect of dietary emulsifiers and thickeners on intestinal barrier function and its response to acute stress in healthy adult humans: A randomised controlled feeding study.

Although dietary emulsifiers are implicated in the pathogenesis of Crohn's disease, their effect has not been studied in humans. To determine the effects of high- and low-emulsifier diets (HED, LED) on intestinal barrier function in healthy subjects in unstressed and acutely stressed states. We conducted a single-blinded, cross-over, controlled feeding trial in 22 healthy adults. After recording 7 days of their habitual diet, we randomised participants to HED or LED with ≥3-week washout between diets. On dietary completion, acute stress was induced via intravenous corticotrophin-releasing hormone. We assessed dietary adherence, effects on 2-h urinary lactulose: rhamnose ratio (LRR), serum concentrations of lipopolysaccharide-binding protein, soluble-CD14 and markers of epithelial injury and inflammation. Dietary adherence was excellent. In an unstressed state, median (interquartile range) LRR during HED was 0.030 (0.018-0.042); on LED, this was 0.042 (0.029-0.078; p = 0.04). LPB concentrations were lower on HED than LED (p = 0.026), but no differences were observed for epithelial injury or inflammation. Under acute stress, LRR increased by 89% (-1% to 486%) on HED (p = 0.004), differing (p = 0.001) from 39% (1%-90%) decrease on LED (p = 0.009). Soluble-CD14 also increased (p < 0.001). The LED had a prolonged carry-over effect on suppressing HED-induced changes during stress. Similar changes in LRR and soluble-CD14 were observed when HED was used as the first diet (both p < 0.01). High intake of emulsifiers improved barrier function in the unstressed state, but increased intestinal permeability to stress, without evidence of inflammation. A LED was protective of the stress effect.

Common dietary emulsifiers promote metabolic disorders and intestinal microbiota dysbiosis in mice

Dietary emulsifiers are linked to various diseases. The recent discovery of the role of gut microbiota–host interactions on health and disease warrants the safety reassessment of dietary emulsifiers through the lens of gut microbiota. Lecithin, sucrose fatty acid esters, carboxymethylcellulose (CMC), and mono- and diglycerides (MDG) emulsifiers are common dietary emulsifiers with high exposure levels in the population. This study demonstrates that sucrose fatty acid esters and carboxymethylcellulose induce hyperglycemia and hyperinsulinemia in a mouse model. Lecithin, sucrose fatty acid esters, and CMC disrupt glucose homeostasis in the in vitro insulin-resistance model. MDG impairs circulating lipid and glucose metabolism. All emulsifiers change the intestinal microbiota diversity and induce gut microbiota dysbiosis. Lecithin, sucrose fatty acid esters, and CMC do not impact mucus–bacterial interactions, whereas MDG tends to cause bacterial encroachment into the inner mucus layer and enhance inflammation potential by raising circulating lipopolysaccharide. Our findings demonstrate the safety concerns associated with using dietary emulsifiers, suggesting that they could lead to metabolic syndromes.

Inulin protects against the harmful effects of dietary emulsifiers on mice gut microbiome.

The prevalence of inflammatory bowel diseases is increasing, especially in developing countries, with adoption of Western-style diet. This study aimed to investigate the effects of two emulsifiers including lecithin and carboxymethyl cellulose (CMC) on the gut microbiota, intestinal inflammation and the potential of inulin as a means to protect against the harmful effects of emulsifiers. In this study, male C57Bl/6 mice were divided into five groups (n:6/group) (control, CMC, lecithin, CMC+inulin, and lecithin+inulin). Lecithin and CMC were diluted in drinking water (1% w/v) and inulin was administered daily at 5 g/kg for 12 weeks. Histological examination of the ileum and colon, serum IL-10, IL-6, and fecal lipocalin-2 levels were analyzed. 16S rRNA gene V3-V4 region amplicon sequencing was performed on stool samples. In the CMC and lecithin groups, shortening of the villus and a decrease in goblet cells were observed in the ileum and colon, whereas inulin reversed this effect. The lipocalin level, which was 9.7 ±3.29 ng in the CMC group, decreased to 4.1 ±2.98 ng with the administration of inulin. Bifidobacteria and Akkermansia were lower in the CMC group than the control, while they were higher in the CMC+inulin group. In conclusion, emulsifiers affect intestinal health negatively by disrupting the epithelial integrity and altering the composition of the microbiota. Inulin is protective on their harmful effects. In addition, it was found that CMC was more detrimental to microbiota composition than lecithin.

Dietary emulsifier consumption accelerates type 1 diabetes development in NOD mice

The rapidly increasing prevalence of type 1 diabetes (T1D) underscores the role of environmental (i.e. non-genetic) determinants of T1D development. Such factors include industrialized diets as well as the intestinal microbiota with which they interact. One component of industrialized diets that deleteriously impact gut microbiota is dietary emulsifiers, which perturb intestinal microbiota to encroach upon their host promoting chronic low-grade intestinal inflammation and metabolic syndrome. Hence, we investigated whether 2 dietary emulsifiers, carboxymethylcellulose (CMC) and polysorbate-80 (P80), might influence the development of T1D in NOD mice, which spontaneously develop this disorder. We observed that chronic emulsifier exposure accelerated T1D development in NOD mice, which was associated with increased insulin autoantibody levels. Such accelerated T1D development was accompanied by compositional and functional alterations of the intestinal microbiota as well as low-grade intestinal inflammation. Moreover, machine learning found that the severity of emulsifier-induced microbiota disruption had partial power to predict subsequent disease development, suggesting that complex interactions occur between the host, dietary factors, and the intestinal microbiota. Thus, perturbation of host–microbiota homeostasis by dietary emulsifiers may have contributed to the post-mid-20th-century increase in T1D.

Vaccination against microbiota motility protects mice from the detrimental impact of dietary emulsifier consumption.

Dietary emulsifiers, including carboxymethylcellulose (CMC) and polysorbate 80 (P80), perturb gut microbiota composition and gene expression, resulting in a microbiota with enhanced capacity to activate host pro-inflammatory gene expression and invade the intestine's inner mucus layer. Such microbiota alterations promote intestinal inflammation, which can have a variety of phenotypic consequences including increased adiposity. Bacterial flagellin is a key mediator of emulsifiers' impact in that this molecule enables motility and is itself a pro-inflammatory agonist. Hence, we reasoned that training the adaptive mucosal immune system to exclude microbes that express flagellin might protect against emulsifiers. Investigating this notion found that immunizing mice with flagellin elicited an increase in mucosal anti-flagellin IgA and IgA-coated microbiota that would have otherwise developed in response to CMC and P80 consumption. Yet, eliciting these responses in advance via flagellin immunization prevented CMC/P80-induced increases in microbiota expression of pro-inflammatory agonists including LPS and flagellin. Furthermore, such immunization prevented CMC/P80-induced microbiota encroachment and deleterious pro-inflammatory consequences associated therewith, including colon shortening and increased adiposity. Hence, eliciting mucosal immune responses to pathobiont surface components, including flagellin, may be a means of combatting the array of inflammatory diseases that are promoted by emulsifiers and perhaps other modern microbiota stressors.

Maternal emulsifier consumption programs offspring metabolic and neuropsychological health in mice.

Modern lifestyle is associated with a major consumption of ultra-processed foods (UPF) due to their practicality and palatability. The ingestion of emulsifiers, a main additive in UPFs, has been related to gut inflammation, microbiota dysbiosis, adiposity, and obesity. Maternal unbalanced nutritional habits during embryonic and perinatal stages perturb offspring's long-term metabolic health, thus increasing obesity and associated comorbidity risk. However, whether maternal emulsifier consumption influences developmental programming in the offspring remains unknown. Here, we show that, in mice, maternal consumption of dietary emulsifiers (1% carboxymethyl cellulose (CMC) and 1% P80 in drinking water), during gestation and lactation, perturbs the development of hypothalamic energy balance regulation centers of the progeny, leads to metabolic impairments, cognition deficits, and induces anxiety-like traits in a sex-specific manner. Our findings support the notion that maternal consumption of emulsifiers, common additives of UPFs, causes mild metabolic and neuropsychological malprogramming in the progeny. Our data call for nutritional advice during gestation.

Mechanisms of gut epithelial barrier impairment caused by food emulsifiers polysorbate 20 and polysorbate 80.

The rising prevalence of many chronic diseases related to gut barrier dysfunction coincides with the increased global usage of dietary emulsifiers in recent decades. We therefore investigated the effect of the frequently used food emulsifiers on cytotoxicity, barrier function, transcriptome alterations, and protein expression in gastrointestinal epithelial cells. Human intestinal organoids originating from induced pluripotent stem cells, colon organoid organ-on-a-chip, and liquid-liquid interface cells were cultured in the presence of two common emulsifiers: polysorbate 20 (P20) and polysorbate 80 (P80). The cytotoxicity, transepithelial electrical resistance (TEER), and paracellular-flux were measured. Immunofluorescence staining of epithelial tight-junctions (TJ), RNA-seq transcriptome, and targeted proteomics were performed. Cells showed lysis in response to P20 and P80 exposure starting at a 0.1% (v/v) concentration across all models. Epithelial barrier disruption correlated with decreased TEER, increased paracellular-flux and irregular TJ immunostaining. RNA-seq and targeted proteomics analyses demonstrated upregulation of cell development, signaling, proliferation, apoptosis, inflammatory response, and response to stress at 0.05%, a concentration lower than direct cell toxicity. A proinflammatory response was characterized by the secretion of several cytokines and chemokines, interaction with their receptors, and PI3K-Akt and MAPK signaling pathways. CXCL5, CXCL10, and VEGFA were upregulated in response to P20 and CXCL1, CXCL8 (IL-8), CXCL10, LIF in response to P80. The present study provides direct evidence on the detrimental effects of food emulsifiers P20 and P80 on intestinal epithelial integrity. The underlying mechanism of epithelial barrier disruption was cell death at concentrations between 1% and 0.1%. Even at concentrations lower than 0.1%, these polysorbates induced a proinflammatory response suggesting a detrimental effect on gastrointestinal health.

Physiology of lipid digestion and absorption in poultry: An updated review on the supplementation of exogenous emulsifiers in broiler diets.

Lipids are a concentrated source of energy with at least twice as much energy as the same amount of carbohydrates and protein. Dietary lipids provide a practical alternative towardincreasing the dietary energy density of feeds for high-performing modern broilers. However, the digestion and absorption of dietary lipids are much more complex than that of the other macronutrients. In addition, young birds are physiologically limited in their capacity to utilise dietary fats and oils effectively. The use of dietary emulsifiers as one of the strategies aimed at improving fat utilisation has been reported to elicit several physiological responses including improved fat digestibility and growth performance. In practical terms, this allows for the incorporation of lipids into lower-energy diets without compromising broiler performance. Such an approach may potentially lower feed costs and raise revenue gains. The current review revisits lipids and the different roles that they perform in diets and whole-body metabolism. Additional information on the process of dietary lipid digestion and absorption in poultry; and the physiological limitation brought about by age on lipid utilisation in the avian gastrointestinal tract have been discussed. Subsequently, the physiological responses resulting from the dietary supplementation of exogenous emulsifiers as a strategy for improved lipid utilisation in broiler nutrition are appraised. Suggestions of nascent areas for a better understanding of exogenous emulsifiers have been highlighted.

P007 Paradoxical effects of high and low emulsifier diets on intestinal permeability in unstressed and stressed states in healthy human adults: a pilot randomised controlled feeding trial.

Abstract Background In preclinical models, high doses of specific emulsifiers induce intestinal inflammation. How these findings translate to Crohn’s disease (CD) is unclear, but the effects of dietary emulsifiers in the context of our food supply are needed before safe evaluation in a CD population. Aims To develop novel trial healthy diets matched for all dietary components, except emulsifiers; and to evaluate their suitability for study in patients with CD by defining, in healthy subjects, tolerance, blinding and adherence to the diets and their impact on intestinal permeability with and without stress. Methods In a pilot single-blinded, cross-over, randomised study, healthy subjects were fed for 4 weeks with ≥3-week washout between diets. Acute stress was induced via 100 mg intravenous corticotrophin-releasing hormone (CRH) on day 28 of each diet. Intestinal permeability was analysed directly with urinary lactulose to rhamnose ratio (LRR) before and at 2 weeks; fasting serum biomarkers reflecting barrier function (intestinal fatty acid binding protein, lipopolysaccharide binding protein [LBP], soluble CD14 and syndecan-1) were measured before and during each diet. All markers were also measured 2 h post CRH. Tolerance was assessed by gastrointestinal symptoms daily using a 100-mm visual analogue scale. Success of blinding was assessed by direct questioning and adherence (defined &amp;gt;95% consumption of only food provided) with food diaries. Results 18 of 20 participants enrolled [median age: 34 IQR 23-46 y; 75% female] finished both diets. The diets were well tolerated with minimal overall symptoms (low: mean 9.9 (SD 8.3) vs high: 9.5 [5.5] mm). Adherence was excellent (&amp;gt;95%). Blinding was reasonable with 30% of participants either not knowing or choosing a high emulsifier diet as the therapeutic diet. In the unstressed state (Fig 1), LRR reduced on the HIGH diet compared to baseline (p=0.016), but no difference between diets was seen. LPB concentrations were lower in the HIGH than LOW diet (p=0.039). Under acute stress (Fig 2), LRR increased by 49% during the HIGH diet (p=0.034), but fell by 41% during the LOW diet (p=0.027). The paired CRH-induced LRR was reduced on LOW vs HIGH diet in acute stress (p=0.043). No difference in concentrations of other biomarkers were seen between diets. Conclusion Novel low and high emulsifier trial diets were well tolerated, achieved good adherence and reasonable blinding. Paradoxically, intestinal permeability reduced with the HIGH diet in the unstressed state, but the LOW diet protected from stress-induced increase in permeability. These diets are suitable to evaluate the effects of emulsifiers on intestinal permeability and inflammation in patients with CD.

Akkermansia muciniphila counteracts the deleterious effects of dietary emulsifiers on microbiota and host metabolism

BackgroundAccumulating evidence indicates that some non-absorbed food additives, including emulsifiers carboxymethylcellulose (CMC) and polysorbate 80 (P80), can negatively impact intestinal microbiota, leading to microbiota encroachment, chronic low-grade intestinal inflammation and,...

Dietary Emulsifiers Exacerbate Food Allergy and Colonic Type 2 Immune Response through Microbiota Modulation

The significant increase in food allergy incidence is correlated with dietary changes in modernized countries. Here, we investigated the impact of dietary emulsifiers on food allergy by employing an experimental murine model. Mice were exposed to drinking water containing 1.0% carboxymethylcellulose (CMC) or Polysorbate-80 (P80) for 12 weeks, a treatment that was previously demonstrated to induce significant alterations in microbiota composition and function leading to chronic intestinal inflammation and metabolic abnormalities. Subsequently, the ovalbumin food allergy model was applied and characterized. As a result, we observed that dietary emulsifiers, especially P80, significantly exacerbated food allergy symptoms, with increased OVA-specific IgE induction and accelerated type 2 cytokine expressions, such as IL-4, IL-5, and IL-13, in the colon. Administration of an antibiotic regimen completely reversed the emulsifier-induced exacerbated susceptibility to food allergy, suggesting a critical role played by the intestinal microbiota in food allergy and type 2 immune responses.

Effects of Dietary Exogenous Hydrophilic Emulsifier Supplementation on Growth Performance and Carcass Traits in Broilers

The effects of dietary exogenous hydrophilic emulsifiers on the growth, nutrient digestibility, and carcass characteristics of broilers were evaluated. A total of 200 one-day-old broilers (Ross 308) were allotted to one of four treatment groups in a randomized complete block design in five replicates with 10 birds per pen during a 5-week growth experimental period. Birds were fed a corn-soybean meal-based diet with or without the addition of 0.025, 0.050, or 0.075% exogenous hydrophilic emulsifiers. The diets contained 3,025 and 3,075 metabolizable energy/kg for Phases 1 and 2, respectively. For each phase and the overall experimental period, body weight gain (linear, <i>P</i>&lt;0.05) and feed conversion ratio (linear, <i>P</i>&lt;0.05) improved in proportion to the dietary exogenous hydrophilic emulsifier level, while the average daily feed intake was not affected by dietary treatment. Improvement in growth performance by dietary treatments was observed during the last two weeks rather than the first three weeks of the growth phase. In carcass traits, abdominal fat content increased as dietary exogenous hydrophilic emulsifier level increased (linear, <i>P</i>&lt;0.05), whereas dietary emulsifier level did not affect the relative weight of the liver, breast, and leg muscles. In conclusion, addition of dietary exogenous hydrophilic emulsifiers from 0 to 0.075% in broiler diets improved the growth rate and feed efficiency of broilers without any deleterious effects on nutrient digestibility, although a corn-soybean meal-based diet had less energy content (3,025 and 3,075 metabolizable energy/kg) for 0-3 weeks and 3-5 weeks, respectively.

Dietary emulsifier consumption alters gene expression in the amygdala and paraventricular nucleus of the hypothalamus in mice

Dietary emulsifier consumption promotes systemic low-grade inflammation, metabolic deregulation, and possibly an anxiety-like phenotype. The latter finding suggests that dietary emulsifiers impact brain areas that modulate stress responses. The goal of the current study was to test whether emulsifier consumption is associated with changes in gene expression in the amygdala and the paraventricular nucleus of the hypothalamus (PVN), two brain areas that are involved in behavioral and neuroendocrine responses to stress. Using RNA-Seq, we compared groups consuming either carboxymethylcellulose or polysorbate 80 for 12-weeks. A total of 243 genes were differentially expressed in the amygdala and PVN of emulsifier-treated mice compared to controls. There was minimal overlap of differentially expressed genes in CMC- and P80-treated animals, suggesting that each emulsifier acts via distinct molecular mechanisms to produce an anxiety-like phenotype. Furthermore, gene ontology and pathway analysis revealed that various stress, metabolic, and immune terms and pathways were altered by emulsifiers. These findings are the first to demonstrate that emulsifier consumption changes gene expression in brain regions that are critical for stress responding, providing possible molecular mechanisms that may underly the previously observed anxiety-like phenotype.

Randomized Controlled-Feeding Study of Dietary Emulsifier Carboxymethylcellulose Reveals Detrimental Impacts on the Gut Microbiota and Metabolome

Epidemiologic and murine studies suggest that dietary emulsifiers promote development of diseases associated with microbiota dysbiosis. Although the detrimental impact of these compounds on the intestinal microbiota and intestinal health have been demonstrated in animal and invitro models, impact of these food additives in healthy humans remains poorly characterized. To examine this notion in humans, we performed a double-blind controlled-feeding study of the ubiquitous synthetic emulsifier carboxymethylcellulose (CMC) in which healthy adults consumed only emulsifier-free diets (n= 9) or an identical diet enriched with 15 g per day of CMC (n= 7) for 11 days. Relative to control subjects, CMC consumption modestly increased postprandial abdominal discomfort and perturbed gut microbiota composition in a way that reduced its diversity. Moreover, CMC-fed subjects exhibited changes in the fecal metabolome, particularly reductions in short-chain fatty acids and free amino acids. Furthermore, we identified 2 subjects consuming CMC who exhibited increased microbiota encroachment into the normally sterile inner mucus layer, a central feature of gut inflammation, as well as stark alterations in microbiota composition. These results support the notion that the broad use of CMC in processed foods may be contributing to increased prevalence of an array of chronic inflammatory diseases by altering the gut microbiome and metabolome (ClinicalTrials.gov, number NCT03440229).

Dietary emulsifier and antioxidant improved astaxanthin utilization and antioxidant capacity of rainbow trout ( Oncorhynchus mykiss )

This study investigated the effects of dietary emulsifiers and antioxidants on astaxanthin utilization and antioxidant capacity of rainbow trout. First, 50 and 100 mg kg−1 of synthetic astaxanthin (AST-50 and AST-100) were added to the control diet (Con), then 400 mg kg−1 sodium taurocholate (ST), 100 mg kg−1 tea polyphenols (TP) and 100 mg kg−1 surfactin (SUR) were added to the AST-50 diet. The six diets were fed to rainbow trout (6.69 ± 0.02) g for 6 weeks. No significant differences were found in weight gain and feed conversion ratio among all the diets (p > .05). The flesh redness (a*), yellowness (b*) and the astaxanthin content in flesh and liver were significantly increased in fish fed with ST, TP and SUR diets compared with the CON fish, but these values were lower than that in fish fed with AST-100 diet (p < .05). Diets involving TP and SUR significantly enhanced T-AOC in flesh, serum and liver, whereas T-SOD was decreased than those of AST-50 and ST diets (p < .05). In conclusion, the supplementation of tea polyphenols and surfactant in the diet effectively improved the astaxanthin deposition and antioxidant capacity of rainbow trout, and sodium taurocholate promoted the deposition of astaxanthin, rather than the antioxidant capacity.

The Emulsifier Carboxymethylcellulose Induces More Aggressive Colitis in Humanized Mice with Inflammatory Bowel Disease Microbiota Than Polysorbate-80.

Commonly used synthetic dietary emulsifiers, including carboxymethylcellulose (CMC) and polysorbate-80 (P80), promote intestinal inflammation. We compared abilities of CMC vs. P80 to potentiate colitis and impact human microbiota in an inflammatory environment using a novel colitis model of ex-germ-free (GF) IL10−/− mice colonized by pooled fecal transplant from three patients with active inflammatory bowel diseases. After three days, mice received 1% CMC or P80 in drinking water or water alone for four weeks. Inflammation was quantified by serial fecal lipocalin 2 (Lcn-2) and after four weeks by blinded colonic histologic scores and colonic inflammatory cytokine gene expression. Microbiota profiles in cecal contents were determined by shotgun metagenomic sequencing. CMC treatment significantly increased fecal Lcn-2 levels compared to P80 and water treatment by one week and throughout the experiment. Likewise, CMC treatment increased histologic inflammatory scores and colonic inflammatory cytokine gene expression compared with P80 and water controls. The two emulsifiers differentially affected specific intestinal microbiota. CMC did not impact bacterial composition but significantly decreased Caudoviricetes (bacteriophages), while P80 exposure non-significantly increased the abundance of both Actinobacteria and Proteobacteria. Commonly used dietary emulsifiers have different abilities to induce colitis in humanized mice. CMC promotes more aggressive inflammation without changing bacterial composition.

Small animal Review

Summary: In this month's Small Animal Review three published papers relating to animal gut health from other veterinary journals are summarised. The papers for this issue focus on the canine microbiome in gastrointestinal disease and the microbiota-related changes that occur as a result of canine diabetes mellitus, as well as a literature review on the impact of exposure to dietary emulsifiers on bowel and metabolic health.

Direct impact of commonly used dietary emulsifiers on human gut microbiota

BackgroundEpidemiologic evidence and animal studies implicate dietary emulsifiers in contributing to the increased prevalence of diseases associated with intestinal inflammation, including inflammatory bowel diseases and metabolic syndrome. Two synthetic emulsifiers in particular, carboxymethylcellulose and polysorbate 80, profoundly impact intestinal microbiota in a manner that promotes gut inflammation and associated disease states. In contrast, the extent to which other food additives with emulsifying properties might impact intestinal microbiota composition and function is not yet known.MethodsTo help fill this knowledge gap, we examined here the extent to which a human microbiota, maintained ex vivo in the MiniBioReactor Array model, was impacted by 20 different commonly used dietary emulsifiers. Microbiota density, composition, gene expression, and pro-inflammatory potential (bioactive lipopolysaccharide and flagellin) were measured daily.ResultsIn accordance with previous studies, both carboxymethylcellulose and polysorbate 80 induced a lasting seemingly detrimental impact on microbiota composition and function. While many of the other 18 additives tested had impacts of similar extent, some, such as lecithin, did not significantly impact microbiota in this model. Particularly stark detrimental impacts were observed in response to various carrageenans and gums, which altered microbiota density, composition, and expression of pro-inflammatory molecules.ConclusionsThese results indicate that numerous, but not all, commonly used emulsifiers can directly alter gut microbiota in a manner expected to promote intestinal inflammation. Moreover, these data suggest that clinical trials are needed to reduce the usage of the most detrimental compounds in favor of the use of emulsifying agents with no or low impact on the microbiota.EqoZ3FdEtmPoxYqtdfAGbnVideo abstract

Consumption of Select Dietary Emulsifiers Exacerbates the Development of Spontaneous Intestinal Adenoma.

Inflammation is a well-characterized critical driver of gastrointestinal cancers. Previous findings have shown that intestinal low-grade inflammation can be promoted by the consumption of select dietary emulsifiers, ubiquitous component of processed foods which alter the composition and function of the gut microbiota. Using a model of colitis-associated cancer, we previously reported that consumption of the dietary emulsifiers carboxymethylcellulose or polysorbate-80 exacerbated colonic tumor development. Here, we investigate the impact of dietary emulsifiers consumption on cancer initiation and progression in a genetical model of intestinal adenomas. In APCmin mice, we observed that dietary emulsifiers consumption enhanced small-intestine tumor development in a way that appeared to be independent of chronic intestinal inflammation but rather associated with emulsifiers’ impact on the proliferative status of the intestinal epithelium as well as on intestinal microbiota composition in both male and female mice. Overall, our findings further support the hypothesis that emulsifier consumption may be a new modifiable risk factor for colorectal cancer (CRC) and that alterations in host–microbiota interactions can favor gastrointestinal carcinogenesis in individuals with a genetical predisposition to such disorders.