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Article

Industrial Bread Composition: Potential Implications for Patients with Inflammatory Bowel Disease

by
Shelly Shakhman
1,2,
Tamar Pfeffer-Gik
1,2,
Sarine Elial-Fatal
1,2,
Yelena Broitman
1,3,
Henit Yanai
1,3,
Uri Gophna
4,
Iris Dotan
1,3 and
Lihi Godny
1,2,*
1
Division of Gastroenterology, Rabin Medical Center, Petah Tikva 4941492, Israel
2
Nutrition Department, Rabin Medical Center, Petah Tikva 4941492, Israel
3
Faculty of Medical and Health Sciences, Tel Aviv University, Tel Aviv 6997801, Israel
4
The Shmunis School of Biomedicine and Cancer Research, Tel Aviv University, Tel Aviv 6997801, Israel
*
Author to whom correspondence should be addressed.
Nutrients 2025, 17(13), 2120; https://doi.org/10.3390/nu17132120
Submission received: 23 May 2025 / Revised: 23 June 2025 / Accepted: 23 June 2025 / Published: 26 June 2025
(This article belongs to the Special Issue Nutritional Strategies in Inflammatory Bowel Disease)
Browse Figures
Versions Notes

Abstract

Background: Ultra-processed food (UPF) intake, particularly that of industrial breads rich in food additives (FAs) like emulsifiers, has been linked to higher risk of inflammatory bowel diseases (IBD). Here, we screened the ingredients and FAs used in the bread industry and reviewed their potential biological effects. Methods: We consecutively screened breads available at supermarket and health food store chains in Israel. Bread products were analyzed by dietitians and categorized into three categories based on their composition: low processed (traditional ingredients), medium processed (additives like malt and fibers), and highly processed (FAs like emulsifiers and preservatives). We conducted a literature review to explore the links between the identified FAs, microbial composition and intestinal inflammation. Results: Of the 233 breads screened, 195 (84%) were highly processed, 9 (4%) medium-processed and 29 (12%) low-processed. We identified 37 different FAs and ingredients used. Most breads contained preservatives—189 (81%), and emulsifiers—178 (76%). Calcium propionate (E-282) was the most prevalent preservative present in 112 (48%) breads, while sodium-stearoyl-2-lactylate (SSL-E-481) was the most prevalent emulsifier present in 86 (37%) breads. The literature review revealed that 19 (51%) FAs used in the bread industry were associated with the exacerbation of inflammation or gut microbiome dysbiosis by increasing cytokine production and adversely affecting microbial composition. Conclusions: Most of the available breads in Israel are highly processed, containing FAs that may mediate intestinal inflammation. Low-processed breads are available and may be more recommended to patients with IBD. Further understanding of the role of FAs in IBD etiology may guide dietary recommendations.

1. Introduction

Inflammatory bowel disease (IBD), specifically Crohn’s disease (CD) and ulcerative colitis (UC), are chronic inflammatory conditions of the gastrointestinal tract. Over recent decades, the incidence and prevalence of IBD have increased, both in Western countries and newly industrialized countries [1,2,3]. One of the risk factors associated with this surge is the “Western diet” [4,5], characterized by a high intake of ultra-processed foods (UPFs), refined sugars, saturated fats, and food additives (FAs), such as preservatives and emulsifiers [6,7,8,9]. Notably, high emulsifier intake was previously documented in the habitual diet of patients with CD [10].
A central component of the Western diet is bread, accounting (together with cereals and pastries) for 2.2% of monthly food spending in Israel [11]. In the United States, bread is ranked amongst the most consumed grain products across all age groups [12]. Recent data from our group further support bread’s dietary relevance in patients with IBD: among 271 patients with newly diagnosed CD, the median intake of bread products was 1.85 servings/day (IQR: 0.71–3.51), with only few reports of no bread consumption at all. These findings emphasize the widespread intake of bread among patients with IBD [13].
Previous studies have linked a higher intake of ultra-processed breads—the largest contributors to overall UPF consumption—to an increased risk of CD. Specifically, individuals in the highest quartile of UPF intake had a significantly greater risk of CD, with ultra-processed breads showing one of the strongest associations [14]. Other findings suggest that ultra-processed breads are also associated with a higher probability of active disease among patients with IBD [15].
These studies relied on the NOVA classification system; NOVA is widely accepted as one of the few recognized food classifications systems [16]. Despite its prominence, NOVA may oversimplify the classification of certain foods. For example, most breads—except freshly made, unpackaged varieties—are classified as the 4th level ‘ultra-processed’, regardless of differences in FAs composition [17]. This broad categorization may obscure potential differences in the biological effects of different FAs.
Given how commonly bread is consumed, the frequent questions raised by patients with IBD, and earlier studies pointing to a possible link between industrial bread and IBD, we aimed to assess the availability of low-processed breads in Israel. This involved screening commercially available breads and categorizing them based on their composition and level of processing. Additionally, we sought to explore the existing literature on FAs found in industrial breads and their potential impact on inflammation and gut dysbiosis.

2. Methods

2.1. Breads Screening

This work was conducted as part of the IBDMED study (NCT05536544), which investigates the role of the Mediterranean diet in patients with IBD. Given that bread is a widely consumed staple food and included in the whole grains category of the Mediterranean diet, we examined the availability of low-processed bread options as preferable choices.
Commercially available breads were screened by IBD dietitians for their ingredient composition and FAs content, based on data retrieved from the online websites of two national chain stores during January–March 2023. The two chains are among the most prominent in their respective sectors and hold a big share of Israeli grocery markets, with significant national reach, multiple stores nationwide, and a broad product selection. One chain represents a large, mainstream supermarket with wide distribution across Israel, while the other is a health food store that caters to a more niche, health-conscious consumer base. Both chains operate online platforms with detailed product information, allowing for consistent and reliable ingredient extraction.
All bread products including buns and pita breads with a detailed product description and ingredient list were included in the analysis and coded. Data extracted included their brand names, weight, and prices in Israeli Shekels (ILS). The products were also divided into three groups according to the store they were available in—general/health food/both. Bread prices and weights were summarized using basic descriptive statistics, including means and standard deviations (SD±).

2.2. Ingredients Analysis

After mapping all ingredients, FAs were cross-referenced against the Food and Agriculture Organization of the United Nations (FAO)/World Health Organization (WHO) Codex of general standards for FAs (GSFA) [18] and against the food industry guidelines of the Ministry of Health in Israel [19]. We excluded flour and salt, which are part of the basic bread recipe, as well as nuts and seeds, which are unprocessed by nature.
Each of the FAs identified within the bread products was first assigned to its functional group (emulsifier/preservative/stabilizer/acidity regulator, etc.). In addition to Codex-defined FAs, our classification included certain technological ingredients—such as added gluten, palm oil, or added fibers—that are not formally categorized as FAs under the Codex but are widely used in industrial processing and are generally not used in home-baking. These ingredients are being referred to as FAs based on their relevance to food processing levels. Then, the different ingredients and FAs used in the breads were assigned into three categories. The green category included ingredients typically used in home-made breads such as yeast, sourdough, sugar, and olive or canola oil; the orange category included FAs and technological ingredients that extend beyond the basic bread recipe like malt, enzymes, and added fibers whose health implications are generally considered less concerning; the red category included FAs and technological ingredients used in the food industry, reflecting higher levels of processing like emulsifiers, preservatives, sweeteners, or added gluten, as detailed in Table 1 [20].
Each bread was then categorized into one of three categories according to the next rule—if it contained at least one ‘red’ ingredient, it was categorized as highly processed; if it contained no ‘red’ ingredients but at least one ‘orange’ ingredient, it was categorized as medium-processed; and if it did not contain ‘red’ or ‘orange’ FAs or ingredients, it was categorized as low-processed. The price for 100 g of bread was calculated from the total weight and price of each product. The Kruskal–Wallis test was used in order to compare differences across the three bread categories.

2.3. Literature Review

We conducted a literature review using PubMed to explore links between the identified FAs and IBD, inflammation, or gut dysbiosis. Key terms included “inflammation,” “gut microbiome,” “IBD,” and “dysbiosis,” combined with the FAs found in industrial breads. For each FA, we searched using both its E-number and common name, limiting results to English-language publications. To minimize bias, we prioritized peer-reviewed, recent studies and included both positive and negative findings. This ensured a comprehensive evaluation of potential associations or mechanisms linking these FAs to the targeted health outcomes. To ensure relevance to the field of IBD, we included studies with implications for gut inflammation, dysbiosis, or barrier dysfunction. Studies were excluded if they focused on non-human models with limited applicability to IBD, or investigated outcomes beyond the scope of gut inflammation. We excluded from the literature review ingredients from the green category as well as FAs that belonged to the red category where ingredient specificity was lacking, like ‘flavorings’ or ‘baking improver’.

3. Results

3.1. Most Breads Are Highly Processed and Contain Multiple FAs

We screened a total of 240 different bread products; of these, seven were excluded due to insufficient information or duplicate products listed under different names. Overall, 233 breads were included in the final analysis. Of these, 160 (68%) were available at the supermarket, 56 (25%) at the health food store, and 17 (7%) were available in both.
The bread composition analysis showed that most breads—195 (84%)—were classified as highly processed, 9 (4%) as medium-processed, and 29 (12%) as low-processed (Figure 1A). Across these breads, we identified 37 different types of FAs and ingredients used in the bread industry in Israel, in addition to wheat flour, salt, nuts and seeds, which were excluded from this analysis since they form the basic bread recipe. While salt was not included in the FAs classification—given its role in the basic bread recipe—it was quantified separately due to its nutritional relevance, particularly its contribution to dietary sodium intake. Notably, it was present in 230 (99%) of breads.
The number of FAs and functional ingredients varied significantly across bread processing levels. Median FA counts in low-, medium-, and highly processed breads were 1 (IQR: 1–2), 3 (IQR: 3–4), and 8 (IQR: 6–10), respectively (p < 0.001) (Figure 1B). Notably, all highly processed breads contained more than one red ingredient, reflecting how breads within this category often include multiple FAs. The most common FA in the low-processed category was yeast, present in 199 (85%) of breads.
Bread prices were comparable across the three processing level groups. The median weight of a loaf of bread was 556 g (IQR: 530–631 g). When calculated per 100 g, the median prices for low-, medium-, and highly processed breads were 2.98, 2.78, and 3.09 ILS/100 g, respectively (p = 0.434) (Figure 1C).

3.2. Preservatives and Emulsifiers Are Dominant in Industrial Breads

Next, we analyzed the prevalence of different FAs and technological ingredients used. Most breads contained preservatives—89 (81%), and emulsifiers—178 (76%). Enzymes were found in 159 (68%) and added gluten in 148 (64%). The other commonly used FAs were malt in 109 (47%), added fiber in 88 (38%), soy flour in 60 (26%), and vegetable oils in 46 (20%) breads. Some of the FAs recognized were found in less than 10% of breads, like corn starch or wheat starch used in 14 (6%) and 11 (5%) breads, respectively (Figure 2A).
As preservatives and emulsifiers were the most prevalent FAs used, we further analyzed their different types (Figure 2B). A total of five preservatives were identified; of them, the most common was calcium propionate (E-282) found in 112 (48%) breads. Another two common preservatives were potassium sorbate (E-202) found in 42 (18%) breads and acetic acid (E-260) in 33 (14%) breads. The other two preservatives, calcium sorbate (E-203) and sodium diacetate [E-262(ii)], were rarely used, present only in one product each. A total of four emulsifiers were identified; the most used emulsifier was sodium stearoyl-2-lactylate (SSL, E-481) present in 86 (37%) breads, exclusively used in breads sold in supermarkets, with none detected in health food store breads. Alongside SSL (E-481), there were three other emulsifiers used; mono- and diglycerides of fatty acids (MDGs, E-471), previously reported as the largest contributor to emulsifier exposure in patients with IBD and healthy controls [21], were found in 22% of breads, while diacetyl tartaric acid esters of mono- and diglycerides (DATEM, E-472e) were present in 16% breads. Interestingly, carboxymethyl cellulose (CMC, E-466), extensively researched in IBD and related to the induction of gut dysbiosis and reduced α-diversity [10,22,23], was found in only 2% of industrial breads (Table 2).
We next compared the use of the two most common leavening agents, both considered low-processed, yeast and sourdough. Most breads utilized yeast or a combination of yeast and sourdough as leavening agents. Breads leavened using yeast were more prominent—119 (51%), followed by products which used both yeast and sourdough—80 (34%). A small number of 30 (13%) breads used only sourdough, and 4 (2%) breads did not use any leavening agent (Figure 2C).

3.3. Prevalent FAs May Have Implications on Inflammation or Gut Microbiome

Finally, to assess the potential implications of FAs used in bread industry, we conducted a literature review to explore the association between FAs, intestinal inflammation and gut microbiome. The review included 53 articles, all experimental studies using different models. The largest group comprised animal studies (n = 29), including various mouse models (DSS-induced colitis, IL-10 knockout, Rag1 knockout, and Casp8ΔIEC mice). Human studies or human samples (n = 14) included clinical trials with IBD patients, healthy subjects, and studies using human microbiota in specialized systems. In vitro studies (n = 11) utilized various models including cell cultures (Caco-2 cells, RAW 264.7 macrophages) and fecal microbiota cultures. These experimental studies examined how FAs affect inflammation and gut microbiome, while others investigated mechanisms by which specific FAs influence intestinal integrity and immune function. The literature review revealed that 19 FAs were associated with negative effects on inflammation or the gut microbiome. However, a closer examination showed that only 14 of these had consistently negative findings, while the remaining 5 demonstrated mixed outcomes. Ten ingredients showed potentially beneficial effects.
Preservatives, which were the most prominent FAs, like calcium propionate (E-282) and potassium sorbate (E-202) prevalent in 48% and 18% of products, respectively, exhibit immunological effects, including increased serum IgG and inflammatory cytokines [29]. Emulsifiers, including SSL (E-481), MDGs (E-471), and DATEM (E-472e), have been linked to alterations in gut microbiome diversity and composition, as well as increases in circulating lipopolysaccharides (LPS) and pro-inflammatory cytokines (e.g., IL-1β, IL-6, and TNF-α) [23,24,25]. Additionally, CMC (E-466), though present in only 2% of the products screened, demonstrates a potent effect on microbial gene expression, bacterial adherence, and inflammatory responses in various models [10,22,23,26,36]. These FAs contribute to an altered gut environment, which may exacerbate inflammatory conditions.
In addition to preservatives and emulsifiers, other FAs have shown similar effects. Palm oil, for example, has been reported to disrupt tight junction proteins and increase LPS translocation in Caco-2 cells, while also increasing flare risk in patients with UC in remission [37,38]. Animal studies have further demonstrated that palm oil can shift the microbiome toward increased Proteobacteria with decreased Firmicutes in the small intestine [39,40]. Some thickeners like maltodextrin increased biofilm formation of adherent-invasive E. coli and enhanced IL-1β production. Artificial sweeteners, like acesulfame potassium (E-950), have been linked to increased pro-inflammatory markers and microbial dysbiosis [41,42].
On the other hand, some FAs exhibit mixed effects. Guar gum (E-412), for instance, has demonstrated varied outcomes across different models—it reduced colonic inflammation and increased beneficial short-chain fatty acids in colitis models, yet also modified intestinal T cell responses in an immunosuppressed model and increased specific bacterial populations including Clostridium groups and Bacteroides fragilis [43,44]. In contrast, components of soy, including lunasin, phosphatidylcholine, and phytosterols, may support remission in IBD patients by promoting apoptosis via the NF-κB pathway, improving clinical responses and reducing colitis symptoms. Phytosterols, specifically, have been shown to inhibit the NF-κB pathway in intestinal epithelial cells and experimental murine colitis models. Additionally, phosphatidylcholine has demonstrated efficacy in increasing histological remission rates in patients with UC refractory to mesalazine [45,46,47,48]. Other compounds, such as citric acid (E-330) and ascorbic acid (vitamin C, E-300), provide potential benefits by promoting beneficial gut bacteria and exhibiting anti-inflammatory properties, respectively [49,50]. Lactic acid has been found to delay LPS-induced monocyte activation and inhibit TNF-α secretion, partially through interference with key signaling pathways, suggesting a role in modulating inflammatory responses [51]. These findings highlight the complex and often opposing effects of different FAs on gut health and inflammation, suggesting careful consideration is needed when evaluating their use, particularly in the context of IBD (Supplementary Materials, Table S1).

4. Discussion

Here, we provide an assessment of the composition of industrial breads available in Israel, alongside a review of the potential implications of their ingredients in IBD. Among the 233 breads analyzed, 84% were classified as highly processed, with an average of eight FAs, including FAs associated with inflammation and gut dysbiosis.
Given the large quantities of bread consumed, the rise in mass production has led to a shift away from traditional baking methods toward breads that more closely resemble the UPFs characteristic of the Western diet [9,52]. These changes raise concerns about potential long-term health impacts. Research indicates that the Western diet and high consumption of UPFs can induce gut dysbiosis and promote inflammation, contributing to the development of IBD [8,53,54,55]. Importantly, previous epidemiological observations have linked the consumption of highly processed bread with an increased risk of IBD, specifically CD development, disease relapse, and IBD-related complications [14,15,56].
The characterization of the screened industrial breads revealed notable differences in their ingredient lists compared to traditional breads. The industrial breads analyzed were primarily highly processed, with extensive use of FAs. FAs are often used in bread to improve shelf life and texture, yet they have been linked to negative health outcomes, such as gut microbiome dysbiosis and chronic inflammation [57,58,59]. Although we also identified low-processed breads in grocery stores/supermarkets, their availability was considerably lower than that of the highly processed ones.
The most common FAs used in industrial breads were preservatives and emulsifiers, many of which are primarily synthetic, such as SSL (E-481) and CMC (E-466). While some, like propionate, acetate, and mono- and diglycerides (MDGs, E-471), resemble naturally occurring metabolites, they may exert different effects. For example, orally ingested propionate has shown distinct metabolic impacts compared to microbiota-derived propionate and does not replicate its beneficial effects [60,61].
The literature review revealed that FAs found in most breads, particularly preservatives and emulsifiers, have been previously associated with inflammation and microbiome alterations. This was reflected by increased levels of LPS, IL-1β, IL-6, and TNF-α in serum, as well as increased intestinal epithelial barrier permeability [22,29,35,62]. Multiple studies have shown impact on the microbiome, including changes in bacterial load and composition, such as a decrease in members of Akkermansia, Bifidobacterium, Lactobacillus, and Lupinus luteus [23,24,63]. SSL, the most prominent emulsifier, found only in breads sold in the supermarket, was linked to microbiome alterations in vitro, including reduction in the relative abundance of Clostridiaceae, Lachnospiraceae, and Ruminococcaceae and increase in LPS [24]. Of note, calcium propionate (E-282) and potassium sorbate (E-202), used as preservatives, previously showed an increase in cytokine production such as TNF-α [29]. Interestingly, acetic acid (E-260), which was also commonly used in breads, showed mixed effects. While it has been used to induce colitis and oral inflammation in animal models [33], high concentrations of acetate demonstrated protective effects in a patient-derived human epithelial cell culture model, including improved epithelial resistance and reduced expression of IL8 and TNFα [34] (Table 2).
In addition, leavening agents may also affect inflammation. Dietary yeast was previously shown to alter T cell responses in ASCA-positive CD patients and increase IgA levels [64,65]. In Casp8ΔIEC mice, yeast-leavened bread exacerbated colitis [66]. Conversely, sourdough bread has been associated with increased production of short-chain fatty acids [67]. As yeast is commonly used in homemade bread, it was initially included in the green category. However, considering the potential adverse effect of yeast on inflammation, sourdough might be a preferable leavening agent in a subset of patients with IBD.
Added gluten and dietary fiber are common technological ingredients present in 68% and 38% of breads, respectively. Both FAs have complex effects on gut health and inflammation. Current evidence does not support specific recommendations to restrict gluten in IBD management; however, some therapeutic diets, such as the Crohn’s Disease Exclusion Diet (CDED), CD-Treat, and The Specific Carbohydrate Diet (SCD), incorporate gluten avoidance as part of their protocol [68,69,70,71]. Gluten increases intestinal permeability via MyD88-dependent zonulin upregulation and reduces microbial α-diversity, particularly Firmicutes, in gluten-sensitive models [72,73,74]. In contrast, dietary fibers generally support gut health and IBD management, and their effects vary by subtype, solubility, and fermentation profile. In dysbiotic conditions, the inappropriate fermentation of fibers may exacerbate inflammation, underscoring the need for targeted research on these dietary components [75,76].
A noteworthy finding from our analysis is that salt was present in 230 (99%) of the breads examined, highlighting its widespread use in industrial bread manufacturing. Additionally, vitamin C, considered an antioxidant, was found in 137 (59%) of the breads, while no bread samples contained artificial food colorings. These components contribute to the overall nutritional and FA profiles of the breads and warrant further consideration in relation to health outcomes.
Although the specific FAs identified in breads are regulated in terms of permitted levels by national authorities such as the Ministry of Health [19], the actual exposure from daily consumption is not routinely monitored or well quantified. Notably, patients with IBD in Israel consume bread daily, and it may serve as a constant contributor to FAs exposure. While our study did not assess intake levels of FAs directly, their cumulative effects on gut microbiome and mucosal immunity remain a concern for both the prevention and maintenance of remission in IBD [13,15,21,56,71,77].
The majority of breads were highly processed, yet low-processed bread options were identified at both the supermarket and health food stores, though their selection was limited. In the low-processed category, we included products with minimal ingredients listed, considering them the closest alternatives to homemade bread with only 12% of the products meeting this criterion. The scarcity of low-processed breads highlights the need for future initiatives, such as encouraging the food industry to develop improved alternatives. Notably, we identified variability in the reported effects of different ingredients and FAs. For example, phosphatidylcholine, a component in soy flour, which is used as an emulsifier, was previously shown to improve clinical and histological scores in patients with UC [46]. This may serve as a better alternative to other emulsifiers like MDGs (E-471), which were shown to increase pro-inflammatory cytokines in animal models [25]. As presently the consumption of UPFs is practically inevitable, the inclusion of options with “safer” FAs is warranted.
In contrast to the Western diet, the Mediterranean diet emphasizes whole grains, fresh fruits, and vegetables, legumes, and healthy fats, particularly from olive oil, while limiting the consumption of UPFs [7,78]. It is characterized by minimally processed, nutrient-dense foods that support overall health and benefit the microbiome [79,80,81]. The Mediterranean diet is one of the recommended approaches for patients with IBD management globally and in Israel specifically [13,82,83,84,85,86,87,88]. As bread is a common and accessible source of whole grains in the Mediterranean diet, selecting minimally processed bread should be emphasized in nutritional recommendations and patient education regarding grocery shopping habits [81,82,89,90].
Notably, low-processed bread, which is usually perceived as having health benefits, is often priced competitively, counterintuitive to the prevalent assumption that healthier food options are generally more expensive.
The strength of our study lies in its comprehensive screening of all ingredients used in industrial breads in Israel. Study researchers, including dietitians trained in IBD, meticulously registered and categorized FAs into three distinct categories, noting their reported relation to IBD based on a literature review. This process and detailed categorization address the limitations of the NOVA classification system, which aggregates all FAs into the 4th ‘ultra-processed’ category without distinguishing between different ingredients. Although UPFs are prevalent in the Western diet, no universally accepted classification system exists. Frameworks like NOVA categorize foods based on their extent of processing but often fail to account for the specific health impacts of individual FAs [17,91]. Our study suggests a more “IBD-relevant” categorization should be considered, based on evidence from animal and human studies of IBD, and highlights the need for a more nuanced analysis of these FAs.
We acknowledge that our study has several limitations. First, bread categorization was based on broad nutritional criteria, and the associations between FAs, inflammation, and gut microbiome were based on basic science studies rather than clinical trials in patients with IBD. In the absence of screening methodologies to assess the immunological safety of FAs, translating basic science into nutritional recommendations may serve as a bridge for tailored and population-targeted recommendations. Second, our study focused on industrial breads in Israel, potentially reflecting a local phenomenon. Yet, our results align with findings from other Western populations. A recent Australian analysis categorized products from a packaged-food database and found that only 31.5% of 238 breads were free from emulsifiers or thickeners. Interestingly, the emulsifiers used in Australian breads were similar to those used in Israel, such as MDGs (E-471), SSL (E-481), and DATEM (E-472e), underscoring common practices in the bread industry across Western societies [77]. Finally, while we mapped the FAs used in industrial bread, we did not assess the actual quantities to which individuals are exposed. For instance, acetic acid (E-260) is regulated in bread, with levels lower than a tablespoon of vinegar per loaf. While this suggests minimal exposure per serving, the actual intake may vary depending on individual consumption patterns. Moreover, we cannot quantify the cumulative effect of daily bread consumption over time. Given bread’s ubiquity in diets and data from a recent cohort of patients with newly diagnosed CD, showing that its consumption among patients with IBD is prominent, further assessment is needed to evaluate the long-term impact of such exposures. Additionally, our analysis relied on product label declarations, which may not capture all FAs present in trace amounts below regulatory thresholds. As a result, the presence of certain FAs may be underreported, and our dataset likely reflects a conservative estimate of FAs exposure. Still, from a clinical and consumer perspective, these limitations are consistent with the level of information available to health professionals and the public in real-life decision making.

5. Conclusions

This study provides an analysis of the composition of industrial breads in Israel, revealing that the majority are highly processed and contain multiple FAs previously associated with gut microbiome alterations and inflammatory responses. Our findings emphasize the importance of considering dietary factors such as industrial bread composition in the dietary management of patients with IBD. While further research is needed to establish definitive conclusions, particularly regarding the cumulative effects of FAs consumption, we suggest that dietary choices should prioritize low-processed foods. Additionally collaborative efforts with the food industry to explore the use of FAs with no previously reported immunological effects could be a step toward improving the nutritional quality of industrial breads. The data collected and tabulated may be used by health care practitioners and patients alike for making dietary choices. As findings from longitudinal studies incorporating comprehensive dietary assessments and clinical outcomes are reported, this categorization can be updated. Such information may be essential to clarify the potential role of industrial bread consumption in the development and management of IBD.

Supplementary Materials

The following supporting information can be downloaded at: https://www.mdpi.com/article/10.3390/nu17132120/s1, Table S1: FAs present in industrial breads, organized from the most to the least prevalent ingredient and their possible effects on microbiome or inflammation. ↓—decrease, ↑—increase. References [91,92,93,94,95,96,97,98,99,100,101,102,103,104,105,106,107,108] are cited in the Supplementary Materials.

Author Contributions

Conceptualization, S.S., I.D. and L.G.; data curation, S.S.; formal analysis, S.S. and L.G.; funding acquisition, I.D.; investigation, S.S.; methodology, S.S., T.P.-G., S.E.-F. and L.G.; supervision, I.D. and L.G.; writing—original draft, S.S. and L.G.; writing—review and editing, S.S., T.P.-G., S.E.-F., Y.B., H.Y., U.G., I.D. and L.G. All authors have read and agreed to the published version of the manuscript.

Funding

The study was partially supported by a generous grant from The Leona M. and Harry B. Helmsley Charitable Trust.

Institutional Review Board Statement

Not applicable.

Data Availability Statement

The original contributions presented in the study are included in the article/Supplementary Materials, further inquiries can be directed to the corresponding author.

Conflicts of Interest

These authors disclose the following: Lihi Godny: Takeda, Ferring, Altman; Tamar Pfeffer-Gik: Janssen, Danone, Altman; Henit Yanai: Pfizer, Abbvie, Janssen, Takeda, Bristol Myers Squibb, Eli-Lilly; Iris Dotan: Abbvie, Arena, Gilead/Galapagos, Genentech/Roche, Athos, Janssen, Pfizer, Takeda, Altman research, Celgene/BMS, Celltrion, Eli-Lilly, Dr. Falk Pharma, Ferring, Sandoz, and Harp diagnostics. The remaining authors disclose no conflicts.

References

  1. Ng, S.C.; Shi, H.Y.; Hamidi, N.; Underwood, F.E.; Tang, W.; Benchimol, E.I.; Panaccione, R.; Ghosh, S.; Wu, J.C.Y.; Chan, F.K.L.; et al. Worldwide incidence and prevalence of inflammatory bowel disease in the 21st century: A systematic review of population-based studies. Lancet 2017, 390, 2769–2778. [Google Scholar] [CrossRef] [PubMed]
  2. Wang, R.; Li, Z.; Liu, S.; Zhang, D. Global, regional and national burden of inflammatory bowel disease in 204 countries and territories from 1990 to 2019: A systematic analysis based on the Global Burden of Disease Study 2019. BMJ Open 2023, 13, e065186. [Google Scholar] [CrossRef]
  3. Alatab, S.; Sepanlou, S.G.; Ikuta, K.; Vahedi, H.; Bisignano, C.; Safiri, S.; Sadeghi, A.; Nixon, M.R.; Abdoli, A.; Abolhassani, H.; et al. The global, regional, and national burden of inflammatory bowel disease in 195 countries and territories, 1990–2017: A systematic analysis for the Global Burden of Disease Study 2017. Lancet Gastroenterol. Hepatol. 2020, 5, 17–30. [Google Scholar] [CrossRef]
  4. Rizzello, F.; Spisni, E.; Giovanardi, E.; Imbesi, V.; Salice, M.; Alvisi, P.; Valerii, M.C.; Gionchetti, P. Implications of the Westernized Diet in the Onset and Progression of IBD. Nutrients 2019, 11, 1033. [Google Scholar] [CrossRef] [PubMed]
  5. Narula, N.; Wong, E.C.L.; Dehghan, M.; Mente, A.; Rangarajan, S.; Lanas, F.; Lopez-Jaramillo, P.; Rohatgi, P.; Lakshmi, P.V.M.; Varma, R.P.; et al. Association of ultra-processed food intake with risk of inflammatory bowel disease: Prospective cohort study. BMJ 2021, 374, n1554. [Google Scholar] [CrossRef]
  6. Stampfli, L.; Nersten, B. Emulsifiers in bread making. Food Chem. 1995, 52, 353–360. [Google Scholar] [CrossRef]
  7. García-Montero, C.; Fraile-Martínez, O.; Gómez-Lahoz, A.M.; Pekarek, L.; Castellanos, A.J.; Noguerales-Fraguas, F.; Coca, S.; Guijarro, L.G.; García-Honduvilla, N.; Asúnsolo, A.; et al. Nutritional Components in Western Diet Versus Mediterranean Diet at the Gut Microbiota–Immune System Interplay. Implications for Health and Disease. Nutrients 2021, 13, 699. [Google Scholar] [CrossRef] [PubMed]
  8. Adolph, T.E.; Zhang, J. Diet fuelling inflammatory bowel diseases: Preclinical and clinical concepts. Gut 2022, 71, 2574–2586. [Google Scholar] [CrossRef]
  9. Sandall, A.; Smith, L.; Svensen, E.; Whelan, K. Emulsifiers in ultra-processed foods in the UK food supply. Public Health Nutr. 2023, 26, 2256–2270. [Google Scholar] [CrossRef]
  10. Sandall, A.M.; Cox, S.R.; Lindsay, J.O.; Gewirtz, A.T.; Chassaing, B.; Rossi, M.; Whelan, K. Emulsifiers Impact Colonic Length in Mice and Emulsifier Restriction is Feasible in People with Crohn’s Disease. Nutrients 2020, 12, 2827. [Google Scholar] [CrossRef]
  11. The Central Bureau of Statistics. Household Income and Expenses from the 2021 Household Expenditure Survey. 2023. Available online: www.cbs.gov.il (accessed on 26 May 2024).
  12. Eicher-Miller, H.; Boushey, C. How Often and How Much? Differences in Dietary Intake by Frequency and Energy Contribution Vary among U.S. Adults in NHANES 2007–2012. Nutrients 2017, 9, 86. [Google Scholar] [CrossRef]
  13. Godny, L.; Elial-Fatal, S.; Arrouasse, J.; Fischler, T.S.; Reshef, L.; Kutukov, Y.; Cohen, S.; Pfeffer-Gik, T.; Barkan, R.; Shakhman, S.; et al. Mechanistic Implications of the Mediterranean Diet in Patients with Newly Diagnosed Crohn’s Disease: Multiomic Results From a Prospective Cohort. Gastroenterology 2025, 168, 952–964.e2. [Google Scholar] [CrossRef] [PubMed]
  14. Lo, C.-H.; Khandpur, N.; Rossato, S.L.; Lochhead, P.; Lopes, E.W.; Burke, K.E.; Richter, J.M.; Song, M.; Korat, A.V.A.; Sun, Q.; et al. Ultra-processed Foods and Risk of Crohn’s Disease and Ulcerative Colitis: A Prospective Cohort Study. Clin. Gastroenterol. Hepatol. 2022, 20, e1323–e1337. [Google Scholar] [CrossRef] [PubMed]
  15. Sarbagili-Shabat, C.; Zelber-Sagi, S.; Isakov, N.F.; Hirsch, A.; Ron, Y.; Grinshpan, L.S.; Cohen, N.A.; Leibovitzh, H.; Thurm, T.; Maharshak, N. High ultra-processed food consumption is associated with clinical exacerbation in patients with Crohn’s disease in remission—A prospective cohort study. Dig. Dis. 2025, 1–17. [Google Scholar] [CrossRef]
  16. Monteiro, C.A.; Cannon, G.; Levy, R.; Moubarac, J.C.; Jaime, P.; Martins, A.P.; Canella, D.; Louzada, M.; Parra, D. NOVA. The star shines bright. World Nutr. 2016, 7, 28–38. [Google Scholar]
  17. Monteiro, C.A.; Cannon, G.; Lawrence, M.; Laura Da Costa Louzada, M.; Machado, P.P. Ultra-Processed Foods, Diet Quality, and Health Using the NOVA Classification System. 2019. Available online: http://www.wipo.int/amc/en/mediation/rules (accessed on 4 July 2024).
  18. Food and Agriculture Organization of the United Nations, World Health Organization. General Standard for Food Additives. 1995. Available online: http://www.fao.org/food/food-safety-quality/scientific-advice/jecfa/jecfa-additives/en/ (accessed on 2 July 2024).
  19. Israel Ministry of Health; Public Health Services; Food Control Services. Food Additives Approved for Use in Israel—List and Conditions. 2022. Available online: https://www.gov.il/BlobFolder/reports/fcs_list/he/files_publications_food_food-addictive-libarary_fcs_list.pdf (accessed on 2 July 2024).
  20. Cauvain, S. Technology of Breadmaking; Springer International Publishing: Cham, Switzerland, 2015. [Google Scholar] [CrossRef]
  21. Katsoudas, N.; Tavakoli, P.; Wu, N.; Shapiro, A.; Leach, S.T.; Williams, A.-J.; Paramsothy, R.; Ghaly, S.; Connor, S.J.; Samocha-Bonet, D.; et al. Dietary Emulsifier Exposure in People With Inflammatory Bowel Disease Compared with Healthy Controls: Is There a Cause for Concern? Inflamm. Bowel Dis. 2024, 30, 1241–1250. [Google Scholar] [CrossRef]
  22. Chassaing, B.; Van de Wiele, T.; De Bodt, J.; Marzorati, M.; Gewirtz, A.T. Dietary emulsifiers directly alter human microbiota composition and gene expression ex vivo potentiating intestinal inflammation. Gut 2017, 66, 1414–1427. [Google Scholar] [CrossRef]
  23. Naimi, S.; Viennois, E.; Gewirtz, A.T.; Chassaing, B. Direct impact of commonly used dietary emulsifiers on human gut microbiota. Microbiome 2021, 9, 66. [Google Scholar] [CrossRef]
  24. Elmén, L.; Zlamal, J.E.; Scott, D.A.; Lee, R.B.; Chen, D.J.; Colas, A.R.; Rodionov, D.A.; Peterson, S.N. Dietary Emulsifier Sodium Stearoyl Lactylate Alters Gut Microbiota in vitro and Inhibits Bacterial Butyrate Producers. Front. Microbiol. 2020, 11, 892. [Google Scholar] [CrossRef]
  25. Jiang, Z.; Zhao, M.; Zhang, H.; Li, Y.; Liu, M.; Feng, F. Antimicrobial Emulsifier–Glycerol Monolaurate Induces Metabolic Syndrome, Gut Microbiota Dysbiosis, and Systemic Low-Grade Inflammation in Low-Fat Diet Fed Mice. Mol. Nutr. Food Res. 2018, 62, 1700547. [Google Scholar] [CrossRef]
  26. Swidsinski, A.; Ung, V.; Sydora, B.C.; Loening-Baucke, V.; Doerffel, Y.; Verstraelen, H.; Fedorak, R.N. Bacterial Overgrowth and Inflammation of Small Intestine After Carboxymethylcellulose Ingestion in Genetically Susceptible Mice. Inflamm. Bowel Dis. 2009, 15, 359–364. [Google Scholar] [CrossRef] [PubMed]
  27. Viennois, E.; Bretin, A.; Dubé, P.E.; Maue, A.C.; Dauriat, C.J.; Barnich, N.; Gewirtz, A.T.; Chassaing, B. Dietary Emulsifiers Directly Impact Adherent-Invasive E. coli Gene Expression to Drive Chronic Intestinal Inflammation. Cell Rep. 2020, 33, 108229. [Google Scholar] [CrossRef] [PubMed]
  28. Viennois, E.; Merlin, D.; Gewirtz, A.T.; Chassaing, B. Dietary Emulsifier-Induced Low-Grade Inflammation Promotes Colon Carcinogenesis. Cancer Res. 2017, 77, 27–40. [Google Scholar] [CrossRef] [PubMed]
  29. Abd-Elhakim, Y.M.; Hashem, M.M.; Abo-El-Sooud, K.; Ali, H.A.; Anwar, A.; El-Metwally, A.E.; Mahmoud, E.A.; Moustafa, G.G. Involvement of tumor necrosis factor-α, interferon gamma-γ, and interleukins 1β, 6, and 10 in immunosuppression due to long-term exposure to five common food preservatives in rats. Gene 2020, 742, 144590. [Google Scholar] [CrossRef]
  30. Nagpal, R.; Indugu, N.; Singh, P. Distinct Gut Microbiota Signatures in Mice Treated with Commonly Used Food Preservatives. Microorganisms 2021, 9, 2311. [Google Scholar] [CrossRef]
  31. Hrncirova, L.; Hudcovic, T.; Sukova, E.; Machova, V.; Trckova, E.; Krejsek, J.; Hrncir, T. Human gut microbes are susceptible to antimicrobial food additives in vitro. Folia Microbiol. 2019, 64, 497–508. [Google Scholar] [CrossRef]
  32. Xiao, N.; Ruan, S.; Mo, Q.; Zhao, M.; Liu, T.; Feng, F. Effects of potassium sorbate on systemic inflammation and gut microbiota in normal mice: A comparison of continuous intake and washout period. Food Chem. Toxicol. 2024, 184, 114443. [Google Scholar] [CrossRef]
  33. Fabia, R.; Willen, R.; Ar’Rajab, A.; Andersson, R.; Ahren, B.; Bengmark, S. Acetic Acid-Induced Colitis in the Rat: A Reproducible Experimental Model for Acute Ulcerative Colitis. Eur. Surg. Res. 1992, 24, 211–225. [Google Scholar] [CrossRef]
  34. Deleu, S.; Arnauts, K.; Deprez, L.; Machiels, K.; Ferrante, M.; Huys, G.R.B.; Thevelein, J.M.; Raes, J.; Vermeire, S. High Acetate Concentration Protects Intestinal Barrier and Exerts Anti-Inflammatory Effects in Organoid-Derived Epithelial Monolayer Cultures from Patients with Ulcerative Colitis. Int. J. Mol. Sci. 2023, 24, 768. [Google Scholar] [CrossRef]
  35. Abd-Elhakim, Y.M.; Hashem, M.M.; Anwar, A.; El-Metwally, A.E.; Abo-El-Sooud, K.; Moustafa, G.G.; Mouneir, S.M.; Ali, H.A. Effects of the food additives sodium acid pyrophosphate, sodium acetate, and citric acid on hemato-immunological pathological biomarkers in rats: Relation to PPAR-α, PPAR-γ and tnfα signaling pathway. Environ. Toxicol. Pharmacol. 2018, 62, 98–106. [Google Scholar] [CrossRef]
  36. Daniel, N.; Wu, G.D.; Walters, W.; Compher, C.; Ni, J.; Delaroque, C.; Albenberg, L.; Ley, R.E.; Patterson, A.D.; Lewis, J.D.; et al. Human Intestinal Microbiome Determines Individualized Inflammatory Response to Dietary Emulsifier Carboxymethylcellulose Consumption. Cell Mol. Gastroenterol. Hepatol. 2024, 17, 315–318. [Google Scholar] [CrossRef] [PubMed]
  37. Barnes, E.L.; Nestor, M.; Onyewadume, L.; de Silva, P.S.; Korzenik, J.R.; Aguilar, H.; Bailen, L.; Berman, A.; Bhaskar, S.K.; Brown, M.; et al. High Dietary Intake of Specific Fatty Acids Increases Risk of Flares in Patients with Ulcerative Colitis in Remission During Treatment with Aminosalicylates. Clin. Gastroenterol. Hepatol. 2017, 15, 1390–1396.e1. [Google Scholar] [CrossRef]
  38. Tomassen, M.M.M.; Govers, C.; Vos, A.P.; de Wit, N.J.W. Dietary fat induced chylomicron-mediated LPS translocation in a bicameral Caco-2cell model. Lipids Health Dis. 2023, 22, 4. [Google Scholar] [CrossRef]
  39. Yang, F.; Zhang, S.; Tian, M.; Chen, J.; Chen, F.; Guan, W. Different Sources of High Fat Diet Induces Marked Changes in Gut Microbiota of Nursery Pigs. Front. Microbiol. 2020, 11, 859. [Google Scholar] [CrossRef] [PubMed]
  40. Gori, M.; Altomare, A.; Cocca, S.; Solida, E.; Ribolsi, M.; Carotti, S.; Rainer, A.; Francesconi, M.; Morini, S.; Cicala, M.; et al. Palmitic Acid Affects Intestinal Epithelial Barrier Integrity and Permeability In Vitro. Antioxidants 2020, 9, 417. [Google Scholar] [CrossRef]
  41. Sylvetsky, A.C.; Clement, R.A.; Stearrett, N.; Issa, N.T.; Dore, F.J.; Mazumder, R.; King, C.H.; Hubal, M.J.; Walter, P.J.; Cai, H.; et al. Consumption of sucralose- and acesulfame-potassium-containing diet soda alters the relative abundance of microbial taxa at the species level: Findings of two pilot studies. Appl. Physiol. Nutr. Metab. 2024, 49, 125–134. [Google Scholar] [CrossRef]
  42. Hanawa, Y.; Higashiyama, M.; Kurihara, C.; Tanemoto, R.; Ito, S.; Mizoguchi, A.; Nishii, S.; Wada, A.; Inaba, K.; Sugihara, N.; et al. Acesulfame potassium induces dysbiosis and intestinal injury with enhanced lymphocyte migration to intestinal mucosa. J. Gastroenterol. Hepatol. 2021, 36, 3140–3148. [Google Scholar] [CrossRef] [PubMed]
  43. Takagi, T.; Naito, Y.; Higashimura, Y.; Ushiroda, C.; Mizushima, K.; Ohashi, Y.; Yasukawa, Z.; Ozeki, M.; Tokunaga, M.; Okubo, T.; et al. Partially hydrolysed guar gum ameliorates murine intestinal inflammation in association with modulating luminal microbiota and SCFA. Br. J. Nutr. 2016, 116, 1199–1205. [Google Scholar] [CrossRef]
  44. Wu, X.; Huang, X.; Ma, W.; Li, M.; Wen, J.; Chen, C.; Liu, L.; Nie, S. Bioactive polysaccharides promote gut immunity via different ways. Food Funct. 2023, 14, 1387–1400. [Google Scholar] [CrossRef]
  45. Dia, V.P.; Gonzalez de Mejia, E. Differential gene expression of RAW 264.7 macrophages in response to the RGD peptide lunasin with and without lipopolysaccharide stimulation. Peptides 2011, 32, 1979–1988. [Google Scholar] [CrossRef]
  46. Karner, M.; Kocjan, A.; Stein, J.; Schreiber, S.; von Boyen, G.; Uebel, P.; Schmidt, C.; Kupcinskas, L.; Dina, I.; Zuelch, F.; et al. First Multicenter Study of Modified Release Phosphatidylcholine “LT-02” in Ulcerative Colitis: A Randomized, Placebo-Controlled Trial in Mesalazine-Refractory Courses. Am. J. Gastroenterol. 2014, 109, 1041–1051. [Google Scholar] [CrossRef] [PubMed]
  47. Cheon, J.H.; Kim, J.S.; Kim, J.M.; Kim, N.; Jung, H.C.; Song, I.S. Plant sterol guggulsterone inhibits nuclear factor-κB signaling in intestinal epithelial cells by blocking IκB kinase and ameliorates acute murine colitis. Inflamm. Bowel Dis. 2006, 12, 1152–1161. [Google Scholar] [CrossRef]
  48. Velde, A.A.T.; Brüll, F.; Heinsbroek, S.E.M.; Meijer, S.L.; Lütjohann, D.; Vreugdenhil, A.; Plat, J. Effects of Dietary Plant Sterols and Stanol Esters with Low- and High-Fat Diets in Chronic and Acute Models for Experimental Colitis. Nutrients 2015, 7, 8518–8531. [Google Scholar] [CrossRef]
  49. Hu, P.; Yuan, M.; Guo, B.; Lin, J.; Yan, S.; Huang, H.; Chen, J.-L.; Wang, S.; Ma, Y. Citric Acid Promotes Immune Function by Modulating the Intestinal Barrier. Int. J. Mol. Sci. 2024, 25, 1239. [Google Scholar] [CrossRef] [PubMed]
  50. Yan, H.; Wang, H.; Zhang, X.; Li, X.; Yu, J. Ascorbic acid ameliorates oxidative stress and inflammation in dextran sulfate sodium-induced ulcerative colitis in mice. Int. J. Clin. Exp. Med. 2015, 8, 20245–20253. [Google Scholar]
  51. Peter, K.; Rehli, M.; Singer, K.; Renner-Sattler, K.; Kreutz, M. Lactic acid delays the inflammatory response of human monocytes. Biochem. Biophys. Res. Commun. 2015, 457, 412–418. [Google Scholar] [CrossRef]
  52. Wang, Y.; Jian, C.; Salonen, A.; Dong, M.; Yang, Z. Designing healthier bread through the lens of the gut microbiota. Trends Food Sci. Technol. 2023, 134, 13–28. [Google Scholar] [CrossRef]
  53. Hou, J.K.; Abraham, B.; El-Serag, H. Dietary intake and risk of developing inflammatory bowel disease: A systematic review of the literature. Am. J. Gastroenterol. 2011, 106, 563–573. [Google Scholar] [CrossRef]
  54. Martinez-Medina, M.; Denizot, J.; Dreux, N.; Robin, F.; Billard, E.; Bonnet, R.; Darfeuille-Michaud, A.; Barnich, N. Western diet induces dysbiosis with increased E coli in CEABAC10 mice, alters host barrier function favouring AIEC colonisation. Gut 2014, 63, 116–124. [Google Scholar] [CrossRef]
  55. Bancil, A.S.; Sandall, A.M.; Rossi, M.; Chassaing, B.; Lindsay, J.O.; Whelan, K. Food Additive Emulsifiers and Their Impact on Gut Microbiome, Permeability, and Inflammation: Mechanistic Insights in Inflammatory Bowel Disease. J. Crohns Colitis. 2021, 15, 1068–1079. [Google Scholar] [CrossRef]
  56. Narula, N.; Chang, N.H.; Mohammad, D.; Wong, E.C.; Ananthakrishnan, A.N.; Chan, S.S.; Carbonnel, F.; Meyer, A. Food Processing and Risk of Inflammatory Bowel Disease: A Systematic Review and Meta-Analysis. Clin. Gastroenterol. Hepatol. 2023, 21, 2483–2495.e1. [Google Scholar] [CrossRef]
  57. Lerner, A.; Matthias, T. Changes in intestinal tight junction permeability associated with industrial food additives explain the rising incidence of autoimmune disease. Autoimmun. Rev. 2015, 14, 479–489. [Google Scholar] [CrossRef]
  58. Clemente-Suárez, V.J.; Beltrán-Velasco, A.I.; Redondo-Flórez, L.; Martín-Rodríguez, A.; Tornero-Aguilera, J.F. Global Impacts of Western Diet and Its Effects on Metabolism and Health: A Narrative Review. Nutrients 2023, 15, 2749. [Google Scholar] [CrossRef] [PubMed]
  59. Garzón, R.; Hernando, I.; Llorca, E.; Rosell, C.M. Understanding the effect of emulsifiers on bread aeration during breadmaking. J. Sci. Food Agric. 2018, 98, 5494–5502. [Google Scholar] [CrossRef]
  60. Tirosh, A.; Calay, E.S.; Tuncman, G.; Claiborn, K.C.; Inouye, K.E.; Eguchi, K.; Alcala, M.; Rathaus, M.; Hollander, K.S.; Ron, I.; et al. The short-chain fatty acid propionate increases glucagon and FABP4 production, impairing insulin action in mice and humans. Sci. Transl. Med. 2019, 11, eaav0120. [Google Scholar] [CrossRef] [PubMed]
  61. Adler, G.K.; Hornik, E.S.; Murray, G.; Bhandari, S.; Yadav, Y.; Heydarpour, M.; Basu, R.; Garg, R.; Tirosh, A. Acute effects of the food preservative propionic acid on glucose metabolism in humans. BMJ Open Diabetes Res. Care 2021, 9, e002336. [Google Scholar] [CrossRef]
  62. Deol, P.; Ruegger, P.; Logan, G.D.; Shawki, A.; Li, J.; Mitchell, J.D.; Yu, J.; Piamthai, V.; Radi, S.H.; Hasnain, S.; et al. Diet high in linoleic acid dysregulates the intestinal endocannabinoid system and increases susceptibility to colitis in Mice. Gut Microbes. 2023, 15, 2229945. [Google Scholar] [CrossRef]
  63. Whelan, K.; Bancil, A.S.; Lindsay, J.O.; Chassaing, B. Ultra-processed foods and food additives in gut health and disease. Nat. Rev. Gastroenterol. Hepatol. 2024, 21, 406–427. [Google Scholar] [CrossRef]
  64. Martini, G.R.; Tikhonova, E.; Rosati, E.; DeCelie, M.B.; Sievers, L.K.; Tran, F.; Lessing, M.; Bergfeld, A.; Hinz, S.; Nikolaus, S.; et al. Selection of cross-reactive T cells by commensal and food-derived yeasts drives cytotoxic TH1 cell responses in Crohn’s disease. Nat. Med. 2023, 29, 2602–2614. [Google Scholar] [CrossRef]
  65. Wine, E. Could Gut and Food-Derived Yeast Be Responsible for Activating T Cells in Crohn’s Disease? Gastroenterology 2024, 166, 351–352. [Google Scholar] [CrossRef]
  66. Zimmermann, J.; De Fazio, L.; Kaden-Volynets, V.; Hitzmann, B.; Bischoff, S.C. Consumption of Yeast-Fermented Wheat and Rye Breads Increases Colitis and Mortality in a Mouse Model of Colitis. Dig. Dis. Sci. 2022, 67, 4422–4433. [Google Scholar] [CrossRef]
  67. Da Ros, A.; Polo, A.; Rizzello, C.G.; Acin-Albiac, M.; Montemurro, M.; Di Cagno, R.; Gobbetti, M.; Howell, K.S. Feeding with Sustainably Sourdough Bread Has the Potential to Promote the Healthy Microbiota Metabolism at the Colon Level. Microbiol. Spectr. 2021, 9, e00494-21. [Google Scholar] [CrossRef] [PubMed]
  68. Levine, A.; Wine, E.; Assa, A.; Boneh, R.S.; Shaoul, R.; Kori, M.; Cohen, S.; Peleg, S.; Shamaly, H.; On, A.; et al. Crohn’s Disease Exclusion Diet Plus Partial Enteral Nutrition Induces Sustained Remission in a Randomized Controlled Trial. Gastroenterology 2019, 157, 440–450.e8. [Google Scholar] [CrossRef]
  69. Svolos, V.; Hansen, R.; Nichols, B.; Quince, C.; Ijaz, U.Z.; Papadopoulou, R.T.; Edwards, C.A.; Watson, D.; Alghamdi, A.; Brejnrod, A.; et al. Treatment of Active Crohn’s Disease With an Ordinary Food-based Diet That Replicates Exclusive Enteral Nutrition. Gastroenterology 2019, 156, 1354–1367.e6. [Google Scholar] [CrossRef] [PubMed]
  70. Suskind, D.L.; Wahbeh, G.; Gregory, N.; Vendettuoli, H.; Christie, D. Nutritional Therapy in Pediatric Crohn Disease: The Specific Carbohydrate Diet. J. Pediatr. Gastroenterol. Nutr. 2014, 58, 87–91. [Google Scholar] [CrossRef]
  71. Halmos, E.P.; Godny, L.; Vanderstappen, J.; Sarbagili-Shabat, C.; Svolos, V. Role of diet in prevention versus treatment of Crohn’s disease and ulcerative colitis. Frontline Gastroenterol. 2024, 15, 247–257. [Google Scholar] [CrossRef] [PubMed]
  72. Lammers, K.M.; Lu, R.; Brownley, J.; Lu, B.; Gerard, C.; Thomas, K.; Rallabhandi, P.; Shea-Donohue, T.; Tamiz, A.; Alkan, S.; et al. Gliadin Induces an Increase in Intestinal Permeability and Zonulin Release by Binding to the Chemokine Receptor CXCR3. Gastroenterology 2008, 135, 194–204.e3. [Google Scholar] [CrossRef]
  73. Mohan, M.; Chow, C.-E.T.; Ryan, C.N.; Chan, L.S.; Dufour, J.; Aye, P.P.; Blanchard, J.; Moehs, C.P.; Sestak, K. Dietary Gluten-Induced Gut Dysbiosis Is Accompanied by Selective Upregulation of microRNAs with Intestinal Tight Junction and Bacteria-Binding Motifs in Rhesus Macaque Model of Celiac Disease. Nutrients 2016, 8, 684. [Google Scholar] [CrossRef]
  74. Bascuñán, K.A.; Araya, M.; Roncoroni, L.; Doneda, L.; Elli, L. Dietary Gluten as a Conditioning Factor of the Gut Microbiota in Celiac Disease. Adv. Nutr. 2020, 11, 160–174. [Google Scholar] [CrossRef]
  75. Armstrong, H.; Mander, I.; Zhang, Z.; Armstrong, D.; Wine, E. Not All Fibers Are Born Equal; Variable Response to Dietary Fiber Subtypes in IBD. Front. Pediatr. 2021, 8, 620189. [Google Scholar] [CrossRef]
  76. Armstrong, H.K.; Bording-Jorgensen, M.; Santer, D.M.; Zhang, Z.; Valcheva, R.; Rieger, A.M.; Kim, J.S.-H.; Dijk, S.I.; Mahmood, R.; Ogungbola, O.; et al. Unfermented β-fructan Fibers Fuel Inflammation in Select Inflammatory Bowel Disease Patients. Gastroenterology 2023, 164, 228–240. [Google Scholar] [CrossRef] [PubMed]
  77. Fitzpatrick, J.A.; Gibson, P.R.; Taylor, K.M.; Halmos, E.P. Development of Novel High and Low Emulsifier Diets Based upon Emulsifier Distribution in the Australian Food Supply for Intervention Studies in Crohn’s Disease. Nutrients 2024, 16, 1922. [Google Scholar] [CrossRef]
  78. Willett, W.C.; Sacks, F.; Trichopoulou, A.; Drescher, G.; Ferro-Luzzi, A.; Helsing, E.; Trichopoulos, D. Mediterranean diet pyramid: A cultural model for healthy eating. Am. J. Clin. Nutr. 1995, 61, 1402S–1406S. [Google Scholar] [CrossRef]
  79. Bach-Faig, A.; Berry, E.M.; Lairon, D.; Reguant, J.; Trichopoulou, A.; Dernini, S.; Medina, F.X.; Battino, M.; Belahsen, R.; Miranda, G.; et al. Mediterranean diet pyramid today. Science and cultural updates. Public Health Nutr. 2011, 14, 2274–2284. [Google Scholar] [CrossRef] [PubMed]
  80. Barber, T.M.; Kabisch, S.; Pfeiffer, A.F.H.; Weickert, M.O. The Effects of the Mediterranean Diet on Health and Gut Microbiota. Nutrients 2023, 15, 2150. [Google Scholar] [CrossRef]
  81. Sofi, F.; Cesari, F.; Abbate, R.; Gensini, G.F.; Casini, A. Adherence to Mediterranean diet and health status: Meta-analysis. BMJ 2008, 337, a1344. [Google Scholar] [CrossRef]
  82. Godny, L.; Reshef, L.; Pfeffer-Gik, T.; Goren, I.; Yanai, H.; Tulchinsky, H.; Gophna, U.; Dotan, I. Adherence to the Mediterranean diet is associated with decreased fecal calprotectin in patients with ulcerative colitis after pouch surgery. Eur. J. Nutr. 2020, 59, 3183–3190. [Google Scholar] [CrossRef] [PubMed]
  83. Godny, L.; Dotan, I. Is the Mediterranean Diet in Inflammatory Bowel Diseases Ready for Prime Time? J. Can. Assoc. Gastroenterol. 2024, 7, 97–103. [Google Scholar] [CrossRef]
  84. Hashash, J.G.; Elkins, J.; Lewis, J.D.; Binion, D.G. AGA Clinical Practice Update on Diet and Nutritional Therapies in Patients With Inflammatory Bowel Disease: Expert Review. Gastroenterology 2024, 166, 521–532. [Google Scholar] [CrossRef]
  85. Chicco, F.; Magrì, S.; Cingolani, A.; Paduano, D.; Pesenti, M.; Zara, F.; Tumbarello, F.; Urru, E.; Melis, A.; Casula, L.; et al. Multidimensional Impact of Mediterranean Diet on IBD Patients. Inflamm. Bowel Dis. 2021, 27, 1–9. [Google Scholar] [CrossRef]
  86. Yanai, H.; Fischler, T.S.; Goren, I.; Eran-Banai, H.; Ollech, E.J.; Snir, Y.; Broitman, Y.; Barkan, R.; Pfeffer-Gik, T.; Godny, L.; et al. A Real-World Prospective Cohort Study of Patients with Newly Diagnosed Crohn’s Disease Treated by a Multidisciplinary Team: 1-Year Outcomes. Crohns Colitis 2023, 360, otad064. [Google Scholar] [CrossRef] [PubMed]
  87. Haskey, N.; Estaki, M.; Ye, J.; Shim, R.K.; Singh, S.; Dieleman, A.L.; Jacobson, K.; Gibson, D.L. A Mediterranean Diet Pattern Improves Intestinal Inflammation Concomitant with Reshaping of the Bacteriome in Ulcerative Colitis: A Randomised Controlled Trial. J. Crohns Colitis. 2023, 17, 1569–1578. [Google Scholar] [CrossRef] [PubMed]
  88. Lewis, J.D.; Sandler, R.S.; Brotherton, C.; Brensinger, C.; Li, H.; Kappelman, M.D.; Daniel, S.G.; Bittinger, K.; Albenberg, L.; Valentine, J.F.; et al. A Randomized Trial Comparing the Specific Carbohydrate Diet to a Mediterranean Diet in Adults With Crohn’s Disease. Gastroenterology 2021, 161, 837–852.e9. [Google Scholar] [CrossRef] [PubMed]
  89. Strisciuglio, C.; Cenni, S.; Serra, M.R.; Dolce, P.; Martinelli, M.; Staiano, A.; Miele, E. Effectiveness of Mediterranean Diet’s Adherence in Children with Inflammatory Bowel Diseases. Nutrients 2020, 12, 3206. [Google Scholar] [CrossRef]
  90. Godny, L.; Reshef, L.; Fischler, T.S.; Elial-Fatal, S.; Pfeffer-Gik, T.; Raykhel, B.; Rabinowitz, K.; Levi-Barda, A.; Perets, T.; Barkan, R.; et al. Increasing adherence to the Mediterranean diet and lifestyle is associated with reduced fecal calprotectin and intra-individual changes in microbial composition of healthy subjects. Gut Microbes. 2022, 14, 2120749. [Google Scholar] [CrossRef]
  91. Martinez-Steele, E.; Khandpur, N.; Batis, C.; Bes-Rastrollo, M.; Bonaccio, M.; Cediel, G.; Huybrechts, I.; Juul, F.; Levy, R.B.; Louzada, M.L.d.C.; et al. Best practices for applying the Nova food classification system. Nat. Food. 2023, 4, 445–448. [Google Scholar] [CrossRef]
  92. Dangarembizi, R.; Erlwanger, K.; Rummel, C.; Roth, J.; Madziva, M.; Harden, L. Brewer’s yeast is a potent inducer of fever, sickness behavior and inflammation within the brain. Brain Behav. Immun. 2018, 68, 211–223. [Google Scholar] [CrossRef]
  93. Lindberg, E.; Magnusson, K.E.; Tysk, C.; Jarnerot, G. Antibody (IgG, IgA, and IgM) to baker’s yeast (Saccharomyces cerevisiae), yeast mannan, gliadin, ovalbumin and betalactoglobulin in monozygotic twins with inflammatory bowel disease. Gut 1992, 33, 909–913. [Google Scholar] [CrossRef]
  94. Wang, W.; Xie, R.; Cao, Q.; Ye, H.; Zhang, C.; Dong, Z.; Feng, D.; Zuo, J. Effects of glucose oxidase on growth performance, clinical symptoms, serum parameters, and intestinal health in piglets challenged by enterotoxigenic Escherichia coli. Front. Microbiol. 2022, 13, 994151. [Google Scholar] [CrossRef]
  95. Paradis, M.-E.; Couture, P.; Gigleux, I.; Marin, J.; Vohl, M.-C.; Lamarche, B. Impact of systemic enzyme supplementation on low-grade inflammation in humans. PharmaNutrition 2015, 3, 83–88. [Google Scholar] [CrossRef]
  96. Bjorck, S.; Bosaeus, I.; Ek, E.; Jennische, E.; Lönnroth, I.; Johansson, E.; Lange, S. Food induced stimulation of the antisecretory factor can improve symptoms in human inflammatory bowel disease: A study of a concept. Gut 2000, 46, 824–829. [Google Scholar] [CrossRef] [PubMed]
  97. Gibbs, D.C.; Fedirko, V.; Baron, J.A.; Barry, E.L.; Flanders, W.D.; McCullough, M.L.; Yacoub, R.; Raavi, T.; Rutherford, R.E.; Seabrook, M.E.; et al. Inflammation Modulation by Vitamin D and Calcium in the Morphologically Normal Colorectal Mucosa of Patients with Colorectal Adenoma in a Clinical Trial. Cancer Prev. Res. 2020, 14, 65–76. [Google Scholar] [CrossRef] [PubMed]
  98. Peuranen, S.; Tiihonen, K.; Apajalahti, J.; Kettunen, A.; Saarinen, M.; Rautonen, N. Combination of polydextrose and lactitol affects microbial ecosystem and immune responses in rat gastrointestinal tract. Br. J. Nutr. 2004, 91, 905–914. [Google Scholar] [CrossRef]
  99. Gerasimidis, K.; Nichols, B.; McGowan, M.; Svolos, V.; Papadopoulou, R.; Kokkorou, M.; Rebull, M.; Gonzalez, T.B.; Hansen, R.; Russell, R.K.; et al. The Effects of Commonly Consumed Dietary Fibres on the Gut Microbiome and Its Fibre Fermentative Capacity in Adults with Inflammatory Bowel Disease in Remission. Nutrients 2022, 14, 1053. [Google Scholar] [CrossRef]
  100. Chen, X.; Hou, Y.; Liao, A.; Pan, L.; Yang, S.; Liu, Y.; Wang, J.; Xue, Y.; Zhang, M.; Zhu, Z.; et al. Integrated Analysis of Gut Microbiome and Adipose Transcriptome Reveals Beneficial Effects of Resistant Dextrin from Wheat Starch on Insulin Resistance in Kunming Mice. Biomolecules 2024, 14, 186. [Google Scholar] [CrossRef]
  101. Zhang, S.; Sun, Y.; Nie, Q.; Hu, J.; Li, Y.; Shi, Z.; Ji, H.; Zhang, H.; Zhao, M.; Chen, C.; et al. Effects of four food hydrocolloids on colitis and their regulatory effect on gut microbiota. Carbohydr. Polym. 2023, 323, 121368. [Google Scholar] [CrossRef]
  102. Kim, C.; Kovacs-Nolan, J.; Yang, C.; Archbold, T.; Fan, M.; Mine, Y. L-cysteine supplementation attenuates local inflammation and restores gut homeostasis in a porcine model of colitis. Biochim. Biophys. Acta (BBA)—Gen. Subj. 2009, 1790, 1161–1169. [Google Scholar] [CrossRef]
  103. Richie, T.G.; Heeren, L.; Kamke, A.; Monk, K.; Pogranichniy, S.; Summers, T.; Wiechman, H.; Ran, Q.; Sarkar, S.; Plattner, B.L.; et al. Limitation of amino acid availability by bacterial populations during enhanced colitis in IBD mouse model. mSystems 2023, 8, e0070323. [Google Scholar] [CrossRef]
  104. Nickerson, K.P.; Homer, C.R.; Kessler, S.P.; Dixon, L.J.; Kabi, A.; Gordon, I.O.; Johnson, E.E.; de la Motte, C.A.; McDonald, C.; Kufer, T.A. The Dietary Polysaccharide Maltodextrin Promotes Salmonella Survival and Mucosal Colonization in Mice. PLoS ONE 2014, 9, e101789. [Google Scholar] [CrossRef]
  105. Laudisi, F.; Di Fusco, D.; Dinallo, V.; Stolfi, C.; Di Grazia, A.; Marafini, I.; Colantoni, A.; Ortenzi, A.; Alteri, C.; Guerrieri, F.; et al. The Food Additive Maltodextrin Promotes Endoplasmic Reticulum Stress–Driven Mucus Depletion and Exacerbates Intestinal Inflammation. Cell. Mol. Gastroenterol. Hepatol. 2019, 7, 457–473. [Google Scholar] [CrossRef]
  106. Nickerson, K.P.; McDonald, C.; Mizoguchi, E. Crohn’s Disease-Associated Adherent-Invasive Escherichia coli Adhesion Is Enhanced by Exposure to the Ubiquitous Dietary Polysaccharide Maltodextrin. PLoS ONE 2012, 7, e52132. [Google Scholar] [CrossRef] [PubMed]
  107. Wang, S.; Zhang, S.; Huang, S.; Wu, Z.; Pang, J.; Wu, Y.; Wang, J.; Han, D.; Mostarica-Stojković, M. Resistant Maltodextrin Alleviates Dextran Sulfate Sodium-Induced Intestinal Inflammatory Injury by Increasing Butyric Acid to Inhibit Proinflammatory Cytokine Levels. BioMed Res. Int. 2020, 2020, 7694734. [Google Scholar] [CrossRef]
  108. Ray, S.C.; Baban, B.; Tucker, M.A.; Seaton, A.J.; Chang, K.C.; Mannon, E.C.; Sun, J.; Patel, B.; Wilson, K.; Musall, J.B.; et al. Oral NaHCO3 Activates a Splenic Anti-Inflammatory Pathway: Evidence That Cholinergic Signals Are Transmitted via Mesothelial Cells. J. Immunol. 2018, 200, 3568–3586. [Google Scholar] [CrossRef] [PubMed]
Nutrients 17 02120 g001
Figure 1. Food processing levels of industrial breads. (A) Levels of food processing. All screened breads were assigned into one of three categories: low processed (green), medium processed (orange), or highly processed (red). (B) Number of FAs in each category beyond the basic bread recipe, compared across processing levels using the Kruskal–Wallis test followed by Dunn’s post hoc analysis. (C) Bread prices per 100 g compared across processing levels using the Kruskal–Wallis test. *** p < 0.001.
Figure 1. Food processing levels of industrial breads. (A) Levels of food processing. All screened breads were assigned into one of three categories: low processed (green), medium processed (orange), or highly processed (red). (B) Number of FAs in each category beyond the basic bread recipe, compared across processing levels using the Kruskal–Wallis test followed by Dunn’s post hoc analysis. (C) Bread prices per 100 g compared across processing levels using the Kruskal–Wallis test. *** p < 0.001.
Nutrients 17 02120 g001
Nutrients 17 02120 g002
Figure 2. Prevalence of FAs and technological ingredients in industrial breads. (A) Commonly used FAs and technological ingredients. Prevalence rates of FAs and technological ingredients in industrial breads (n = 233). The colors represent the classification of each FA to a different processing level, medium processed (orange) or highly processed (red). FAs, food additives. (B) Prevalence of emulsifiers and preservatives in breads. The two groups of the most common additives were furthermore analyzed. A star or a circle signifies if it was linked to microbiome alterations or IBD or gut inflammation, respectively, in the literature review. E-481, Sodium stearoyl lactylate; E-471, Mono- and diglycerides of fatty acids; E-472e, DATEM; E-466, Sodium carboxy methyl cellulose (CMC); E-282, Calcium propionate; E-202, Potassium sorbate; E-260, Acetic acid; E-203, Calcium sorbate; E-262(ii), Sodium diacetate. (C) The prevalence of leavening agents. Yeast (n = 119), Yeast + Sourdough (n = 80), Sourdough (n = 30), None (n = 4).
Figure 2. Prevalence of FAs and technological ingredients in industrial breads. (A) Commonly used FAs and technological ingredients. Prevalence rates of FAs and technological ingredients in industrial breads (n = 233). The colors represent the classification of each FA to a different processing level, medium processed (orange) or highly processed (red). FAs, food additives. (B) Prevalence of emulsifiers and preservatives in breads. The two groups of the most common additives were furthermore analyzed. A star or a circle signifies if it was linked to microbiome alterations or IBD or gut inflammation, respectively, in the literature review. E-481, Sodium stearoyl lactylate; E-471, Mono- and diglycerides of fatty acids; E-472e, DATEM; E-466, Sodium carboxy methyl cellulose (CMC); E-282, Calcium propionate; E-202, Potassium sorbate; E-260, Acetic acid; E-203, Calcium sorbate; E-262(ii), Sodium diacetate. (C) The prevalence of leavening agents. Yeast (n = 119), Yeast + Sourdough (n = 80), Sourdough (n = 30), None (n = 4).
Nutrients 17 02120 g002
Table 1. The three different categories of FAs and ingredients used in bread products. The green category considered as ‘low processed’ includes ingredients typically found in homemade breads, the orange category—‘medium processed’—includes ingredients that extend beyond the basic bread recipe, and the red category includes both officially defined FAs and technological ingredients that contribute to the overall processing level. * Yeast is commonly used in homemade bread; therefore, it was categorized as “green”.
Table 1. The three different categories of FAs and ingredients used in bread products. The green category considered as ‘low processed’ includes ingredients typically found in homemade breads, the orange category—‘medium processed’—includes ingredients that extend beyond the basic bread recipe, and the red category includes both officially defined FAs and technological ingredients that contribute to the overall processing level. * Yeast is commonly used in homemade bread; therefore, it was categorized as “green”.
Low ProcessedMedium ProcessedHighly Processed
Baking sodaAdded fiberAcidity regulators
Canola oilEnzymesAdded gluten
Olive oilL-cysteineAnticaking agents
SourdoughMaltBaking improver
SugarSoy flourEmulsifiers
Vitamin C Flavorings
Yeast * Palm oil, soy oil, or unspecified vegetable oil
Preservatives
Stabilizers
Sweeteners: acesulfame K, maltodextrin, dextrose
Wheat starch or corn starch
Table 2. Emulsifiers and preservatives present in industrial breads, their prevalence, and possible effects on microbiome or inflammation. ↓—decrease, ↑—increase.
Table 2. Emulsifiers and preservatives present in industrial breads, their prevalence, and possible effects on microbiome or inflammation. ↓—decrease, ↑—increase.
GroupFood
Additive		E-NumberPrevalence (in Screened Breads) (%)ModelEffect on
Microbiome		Effect on
Inflammation		Ref
EmulsifiersSSLE-48137%In vitro—fecal microbiota↓ Clostridiaceae, Lachnospiraceae, Ruminococcaceae
↓ Butyrate
↑ Bacteroidaceae, Enterobacteriaceae
↑ Propionate
↑ LPS and flagellin 		[24]
EmulsifiersMDGsE-47122%Murine model—miceChanges β-diversity and microbial composition
↓ Akkermansia, Bifidobacterium, Lactobacillus, Lupinus luteus
↑ Bacteroides acidifaciens, E. coli		↑ LPS, IL-1β, IL-6, and TNF-α levels in serum[25]
EmulsifiersDATEME-472e16%Human microbiota—MBRAs↓ Bacterial density
↓ Lactobacillales members, including Streptococcus genus
↓ Faecalibacterium		 [23]
EmulsifiersCMCE-4662%M-SHIME, murine model—mice↑ Bioactive flagellin-related gene expressions
↑ IL-6 expression		↑ Intestinal inflammation[22]
EmulsifiersCMCE-4662%MBRAs↓ Lactobacillales members, Streptococcus genus [23]
EmulsifiersCMCE-4662%Murine model—mice↑ Bacterial adherence
↑ Bacterial overgrowth		 [26]
EmulsifiersCMCE-4662%Murine model—mice↑ E. coli ability to adhere and invade IEC
↑ Expression of virulence factors		 [27]
EmulsifiersCMCE-4662%Murine model—mice↑ Bioactive fecal LPS and flagellin↑ Shortened colons
↑ Splenomegaly		[10,28]
PreservativesCalcium propionateE-28248%Murine model—rats In serum:
↓ IgG and IgM
↑ IL-4 expression
mRNA expression:
↑ TNF-α expression		[29]
PreservativesPotassium sorbate E-20218%Murine model—rats In serum:
↓ IgG and IgM
↑ IL-4 expression
mRNA expression:
↑ TNF-α expression and IFNγ 		[29]
PreservativesPotassium sorbate E-20218%Murine model—mice↓ α-diversity
↑ Parabacteroides and Adlercreutzia 		[30]
PreservativesPotassium sorbate E-20218%In vitro—fecal microbiota ↓ E. Coli [31]
PreservativesPotassium sorbate E-20218%Murine model—mice↓ Lachnospiraceae
↓ Isobutyric acid production		↑ IL-1β levels in serum
↑ Inflammatory cell infiltration in the liver		[32]
Preservatives,
Acidity regulators		Acetic acidE-26014%Murine model—rats ↑ Colitis[33]
Preservatives,
Acidity regulators		Acetic acidE-26014%Organoid-derived colonic epithelial monolayer culture ↑ Improved epithelial resistance
↑ Regulation of HIF1α, MUC2, and MKI67
↓ Expression of: IL8, TNFα, CLDN1		[34]
Preservatives,
Acidity regulators		Sodium hydrogen acetateE-262(ii)0.40%Murine model—rats ↓ IgG and IgM levels
↓ PPAR-α, PPAR-γ expression
↑ TNF-α expression		[35]
SSL, stearoyl-2-lactylate; LPS, lipopolysaccharides; MDGs, mono- and diglycerides of fatty acids; E. coli, Escherichia coli; DATEM, diacetyl tartaric acid esters of mono- and diglycerides of fatty acids; MBRAs, Mini Bio Reactor Arrays; CMC, carboxymethyl cellulose; M-SHIME, Simulator of the Human Intestinal Microbial Ecosystem; IEC, intestinal epithelial cells.
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MDPI and ACS Style

Shakhman, S.; Pfeffer-Gik, T.; Elial-Fatal, S.; Broitman, Y.; Yanai, H.; Gophna, U.; Dotan, I.; Godny, L. Industrial Bread Composition: Potential Implications for Patients with Inflammatory Bowel Disease. Nutrients 2025, 17, 2120. https://doi.org/10.3390/nu17132120

AMA Style

Shakhman S, Pfeffer-Gik T, Elial-Fatal S, Broitman Y, Yanai H, Gophna U, Dotan I, Godny L. Industrial Bread Composition: Potential Implications for Patients with Inflammatory Bowel Disease. Nutrients. 2025; 17(13):2120. https://doi.org/10.3390/nu17132120

Chicago/Turabian Style

Shakhman, Shelly, Tamar Pfeffer-Gik, Sarine Elial-Fatal, Yelena Broitman, Henit Yanai, Uri Gophna, Iris Dotan, and Lihi Godny. 2025. "Industrial Bread Composition: Potential Implications for Patients with Inflammatory Bowel Disease" Nutrients 17, no. 13: 2120. https://doi.org/10.3390/nu17132120

APA Style

Shakhman, S., Pfeffer-Gik, T., Elial-Fatal, S., Broitman, Y., Yanai, H., Gophna, U., Dotan, I., & Godny, L. (2025). Industrial Bread Composition: Potential Implications for Patients with Inflammatory Bowel Disease. Nutrients, 17(13), 2120. https://doi.org/10.3390/nu17132120

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