Медицина

Stepanenko Dmytro

Owner

PLNTBSD LLC

(USA)

https://www.doi.org/10.25313/2524-2695-2025-8-06-26

 INFLUENCE OF VARIOUS DIET TYPES ON THE MICROBIOTA

Summary. This article examines the impact of different diet types, plant‐based and Western, on the composition and functional state of the gut microbiota, its metabolites, and related immunometabolic processes. The relevance of this study is rooted in the key role of the microbiota as an “auxiliary organ” that synthesizes vitamins, regulates energy metabolism, and shapes immune tolerance through the production of short‐chain fatty acids (SCFAs), which account for a substantial portion of interindividual differences attributable specifically to diet. This work aims to systematically describe and quantitatively assess changes in taxonomy, metabolomes, and markers of barrier function and inflammation when switching to plant‐based versus Western dietary patterns, drawing on the latest metagenomic cohorts, intervention studies, and multi‐omic analyses. Methodologically, the study combines metagenomics (shotgun sequencing, 16S rRNA), gas chromatography-mass spectrometry of SCFAs, measurement of permeability and inflammation markers (CRP, IL‐6, TNF-α, zonulin, LBP), and multivariate statistical models. The novelty of this work lies in the integration of large‐scale population data with controlled intervention results, which not only confirmed a consistent increase in butyrate‐producing genera and SCFA levels on plant‐based diets but also traced in detail the molecular mechanisms of their anti‐inflammatory action via GPR41/43 receptors and histone deacetylase inhibition, while juxtaposing these effects against dysbiosis, endotoxemia, and chronic inflammation observed with Western‐type diets. This article will be valuable to dietitians, microbiologists, clinical researchers, and preventive medicine specialists interested in evidence‐based microbiota modulation through rational nutrition.

Key words: gut microbiota, diet, vegan diet, SCFA, dysbiosis, inflammation, Faecalibacterium prausnitzii, metabolic endotoxemia.

Introduction. The gut microbiota is a dynamic community of approximately 3.8 × 10¹³ bacterial cells—comparable in number to human somatic cells—that weighs about 0.2 kg and functions as an additional metabolic and immune organ [1]. Microbes ferment undigested food, synthesize vitamins, regulate energy metabolism, and establish immune tolerance, with short‐chain fatty acids (SCFAs) produced from the fermentation of dietary fibers and polyphenols serving as a pivotal link in these interactions [2].

Among the numerous exogenous factors, diet alone explains a significant proportion of interindividual variability in microbiota composition: population‐based studies show that dietary habits can reliably predict the presence of specific microbial taxa and metabolites, with model accuracy reaching an AUC of 0.85 when comparing vegan, vegetarian, and omnivorous diets in 21 561 individuals [3]. A 2023 systematic review of 12 intervention studies demonstrated that switching to a plant‐based diet for 2–13 months increases fecal butyrate concentration and enhances microbiota α‐diversity as measured by the Shannon index [4]. These shifts are associated with increases in Bifidobacteria and Lactobacillus, reductions in proinflammatory cytokines, and strengthening of the intestinal barrier.

The converse effect is observed with Western‐type diets, characterized by excess saturated fats and animal protein: elevated bile acid levels selectively stimulate the growth of LPS‐positive Gram‐negative bacteria, leading to dysbiosis, reduced microbial diversity, and increased epithelial permeability, which triggers chronic low‐grade inflammation [5]. The rising prevalence of noncommunicable diseases directly linked to such metabolic and immune disturbances underscores the importance of diet‐dependent microbiota modulation for fundamental research and the prevention and treatment of chronic pathologies.

Materials and Methodology. The materials and methodology of this study are based on the analysis of 23 key publications, encompassing both population‐based cohort studies and controlled intervention trials, as well as systematic reviews. Foundational data on the size and mass of the gut microbiota [1] and its biochemical function via SCFAs [2] served as the theoretical basis. To assess the effects of vegan, vegetarian, and omnivorous diets, we relied on metagenomic analysis of 21,561 participants from five international cohorts using shotgun sequencing and 16S rRNA profiling for taxonomic composition [3]. A systematic review of 12 intervention studies on plant‐based diets enabled the evaluation of SCFA dynamics and Shannon α‐diversity over periods of 2 to 13 months [4], while data from Kang et al. described patterns of dysbiosis and increased epithelial permeability associated with Western‐type diets [5]. Additional information on dietary fiber and polyphenol intake [6], changes in fecal SCFA levels after six weeks of diet [7], and the molecular mechanisms of SCFA action on GPR41/43 receptors and histone deacetylases [8] were also incorporated. A randomized clinical trial of a low‐fat vegan diet provided quantitative data on the increase of Faecalibacterium prausnitzii and its correlation with metabolic parameters [9], and a multi‐omic analysis by Prochazkova et al. delivered insights into differences in fecal and serum metabolomes between vegans and omnivores [10]. Systematic reviews of inflammation and permeability markers (CRP, IL‐6, TNF-α, zonulin, LBP) established the clinical linkage between microbial shifts and inflammatory and barrier phenotypes [11], [12].

Methodologically, this work integrates multiple analytical approaches. Quantification of SCFAs (acetate, propionate, butyrate) was performed via gas chromatography-mass spectrometry on fecal and serum samples [7], [8]. Dietary records and clinical biomarkers were collected using standardized protocols: ELISA assays for CRP, IL-6, TNF-α, zonulin, and LBP [12]; statistical analyses included paired t‐tests, ANCOVA adjusted for BMI, and Spearman correlations to assess relationships between diet duration and biomarker levels [9; 12].

Results and Discussion. A plant-based diet—whether a strict vegan regimen or simply a predominance of plant-derived foods—provides the gut microbiota with an abundant substrate in dietary fibers and polyphenols. In a meta-analysis of nutritional studies, the mean daily fiber intake was 44 g in vegans versus 21 g in omnivores, i.e., more than twice as high, and was also accompanied by an increased proportion of resistant starch, inulin, and other fermentable fractions [6]. Polyphenols, especially from berries, cocoa, and spices, complement fiber by acting as a “selection medium” that inhibits the growth of opportunistic pathogens while simultaneously accelerating the metabolism of those bacteria possessing enzymes for phenolic-ring degradation [3].

Such a substrate environment leads to rapid and reproducible expansion of the genera Bifidobacterium and Lactobacillus. These genera carry genes for oligosaccharide degradation and, in turn, create a redox–acidic milieu conducive to the further growth of symbiotic microorganisms. Concurrently, the species diversity of the microbiota expands. In the analysis [3; 4], vegans exhibited a higher Shannon index (+ 7% compared to omnivores, p < 0.001) and enrichment of key butyrate-producing taxa such as Faecalibacterium prausnitzii and Roseburia spp.; these species positively correlated with lipid profiles and insulin sensitivity. The increase in butyrate producers is significant not only per se but also as a marker of more complex metabolic networks in which poly- and oligosaccharidolytic strains transfer intermediate metabolites to organisms that complete butyrate synthesis.

Short-chain fatty acid (SCFA) concentrations reflect the enhanced trophic chain. A pooled analysis of fecal samples showed that levels of acetate, propionate, and butyrate increased after six weeks on a plant-based diet. In contrast, control omnivorous groups did not demonstrate significant shifts [7]. The rise in SCFAs is not merely a biochemical fact; it translates into immunoregulation.

Butyrate, and to a lesser extent propionate, activate GPR41/43 receptors and inhibit histone deacetylases, thereby enhancing regulatory T-cell differentiation, increasing the expression of tight-junction proteins occludin and claudin-1, and reducing lipopolysaccharide (LPS) translocation across the epithelium [8]. Clinically, this is accompanied by reductions in high-sensitivity C-reactive protein (CRP) and IL-6 levels in healthy volunteers after a relatively short duration on such a diet, confirming the anti-inflammatory potential of SCFAs. Thus, the substrate profile of a plant-based diet initiates a cascade of microbial and metabolic reorganizations that lead to greater diversity, dominance of beneficial bacteria, and increased SCFA production, collectively strengthening the intestinal barrier and reducing systemic inflammation. The microbiota of individuals excluding all animal products exhibits a clear anti-inflammatory “signature”.

At the taxonomic level, a vegan diet enhances the presence of key butyrate producers. In a randomized clinical trial, switching to a low-fat vegan diet for 16 weeks increased the relative abundance of Faecalibacterium prausnitzii by an average of 5.1% (95% CI 2.4–7.9%; p < 0.001); the increase of this bacterium correlated inversely with body weight and visceral fat loss [9]. A systematic review of 15 studies confirmed this trend: F. prausnitzii and the genus Roseburia were consistently enriched in vegans, whereas opportunistic pathogens such as Bilophila and Alistipes were less frequent [4].

The metabolic profile of such a community is shifted towards increased SCFA synthesis. Study [10] showed that long-term adherence to a vegan diet affected only 14.8% of all detected bacterial genera in the fecal microbiome. However, significant differences were noted in the metabolomes of vegans versus omnivores. In feces, 43.3% of all identified metabolites differed significantly between vegans and omnivores—for example, amino-acid fermentation products p-cresol, skatole, indole, and methional (lower in vegans) and polysaccharide fermentation products—short- and medium-chain fatty acids (SCFA, MCFA) and their derivatives (higher in vegans). The serum metabolome of vegans differed markedly from that of omnivores (55.8% of all metabolites), particularly in amino-acid composition (e.g., lower levels of branched-chain amino acids, higher levels of SCFAs [formic, acetic, propionic, butyric acids] and dimethyl sulfone, the latter two being potential co-metabolites of the host microbiome). Using a machine-learning approach, we evaluated the discriminative power of each dataset. The highest accuracy was achieved for the serum metabolome (91.6%). The study results are presented in Figure 1.

Fig. 1. Serum metabolome composition [10]

(A) 2D PCA analysis score plot with the explained variance of each component. (B) Biomarker metabolites generated from univariable discrimination analysis (FDR ≥ 0.1), effect size estimated by Cliff’s delta.

(C) 2D score plots of PLS-DA. R2Y fit goodness, Q2Y predictive power

Clinically, this is reflected in reduced systemic inflammation. A meta-analysis of 21 observational studies reported that high-sensitivity CRP was 0.54 mg/L lower (95% CI –0.79 to –0.28) in vegans compared to omnivores, with the effect remaining significant after adjustment for BMI [11]. Anti-inflammatory cytokine profiles also shift. As shown in Table 1, study [12] observed no significant differences in inflammatory biomarkers—that is, CRP, IL-6, TNF-α—and gut permeability markers zonulin and LBP among the four dietary groups (all p > 0.05). When subjects were stratified by diet duration (< 3 years vs. > 3 years), those adhering to a vegan diet for more than 3 years exhibited significantly lower zonulin levels compared to omnivores [1.22 ± 0.85 (vegan) vs. 1.94 ± 1.22 (omnivore); t = –2.03, p = 0.05]. In the vegan group, serum zonulin correlated significantly with duration of the vegan diet (r = –0.561, p = 0.015). No such correlations were found in other groups.

Table 1

Inflammatory and intestinal permeability biomarkers in the four dietary groups (n = 89) [12]

Collectively, these data indicate that vegans’ microbiota forms a stable anti-inflammatory ecosystem in which the dominance of butyrate producers and the abundance of SCFAs directly translate into a stronger intestinal barrier and a moderated cytokine milieu.

The microbiota of vegans consistently shifts towards bacteria associated with metabolic health and low inflammation. In the most extensive metagenomic analysis [3], a random forest algorithm perfectly distinguished vegans from omnivores (AUC 0.85). The vegan signature included Faecalibacterium prausnitzii, Roseburia hominis, Butyricicoccus spp., and other butyrate producers. In contrast, meat-oriented microbiota was characterized by Bilophila wadsworthia, Alistipes putredinis, and Ruminococcus torques, all closely linked to a proinflammatory state. The highest discriminative power was achieved when distinguishing vegans and omnivores (mean cross-validated LODO AUC = 0.90), followed by vegetarians versus vegans (0.84) and finally vegetarians versus omnivores (0.82), as shown in Figure 2.

Fig. 2. Highly accurate classification of individual diet patterns based on gut microbial features [4]

Functionally, the community’s metabolic profile reflects a more “host-friendly” composition. In a multicenter study [13] involving 1,904 adults, plant-based diet adherence was accompanied by simultaneous increases in the Shannon index and SCFA concentrations; total SCFAs showed a positive, albeit modest, correlation with α-diversity (Spearman r = 0.074; p < 0.05), and for butyrate, the coefficient reached 0.12. Thus, the richer and even the community, the higher the flux of acetate, propionate, and especially butyrate metabolites that enhance tight-junction expression and Treg induction, creating a microenvironment with reduced basal inflammation. This body of observations supports the vegan “anti-inflammatory ecosystem” concept: the relative predominance of SCFA producers and increased microbial diversity establish biochemical and immunological conditions conducive to maintaining intestinal barrier integrity and lowering systemic inflammatory tone.

An average “Western” diet, characterized by excess saturated fats, animal protein, and added sugars with insufficient dietary fiber, provides the gut ecosystem with a radically different metabolic landscape than the plant-based diets described above. According to [14], adult American men (20+) obtain 45.9% of their calories from carbohydrates, 16.0% from proteins, and 35.6% from fats. In women of the same age, the proportions are 47.4%, 15.7%, and 36.1%, respectively. This combination of nutrients sharply increases bile acid and easily fermentable sugar flux into the intestinal lumen, but leaves almost no substrate for bacterial fiber fermentation.

Within a few weeks on such a diet, metagenomic surveys note a drop in α-diversity: in Western-type cohorts, the Shannon index is on average 0.4 units lower, indicating a species richness reduction [15]. Simultaneously, the characteristic Firmicutes/Bacteroidota imbalance is recorded: the proportions of Firmicutes and Proteobacteria increase while Bacteroidota decrease, as repeatedly demonstrated by cross-sectional studies and dietary interventions [16]. The taxonomic shift is accompanied by the depletion of butyrate producers and reduced SCFA synthesis, which is in direct contrast to the effects observed in vegans.

The loss of diversity coincides with the expansion of LPS-positive Gram-negative pathobionts resistant to bile acids. A high-fat diet selectively stimulates the growth of Bilophila wadsworthia; in human and animal models, an increase in this species exacerbated local and systemic inflammation and aggravated metabolic disturbances [17]. Similar trends have been described for the genus Alistipes, whose overrepresentation during Western feeding correlates with proinflammatory cytokines and epithelial dysfunction. In a randomized crossover, a Western-style menu elevated circulating LPS by an average of 71% after three weeks, confirming the development of metabolic endotoxemia [18].

Excess saturated fats and sugars, fiber deficiency, and related dysbiosis lead to tight-junction deregulation, mucus layer thinning, and increased intestinal permeability: a systematic review [19] documented significant increases in leak markers (zonulin, LPS) in volunteers on Western diets versus controls. Against rising permeability, bacterial components enter the circulation, perpetuating chronic low-grade inflammation; a population study [20] of 1,015 healthy men showed a direct correlation between total dietary energy and plasma LPS. Thus, the Western diet initiates the cascade “saturated fats/sugars → dysbiosis → barrier dysfunction → endotoxemia → systemic inflammation,” opposing the anti-inflammatory ecosystem formed by plant-based nutrition.

A comparison of the metabolic “fuel” available to the microbiota under plant-based and Western diets illustrates how diet determines its taxonomy and function. A vegan diet delivers twice as much fermentable fiber and polyphenols to the colon lumen at equal caloric intake. In contrast, a Western diet supplies excess saturated fats, animal protein, and added sugars [3]. At the ecosystem level, a vegan diet is associated with higher α-diversity: the Shannon index in long-term vegans reflects species gain and a more even taxon distribution [21]. Conversely, Western diets are characterized by reduced species richness and a typical shift in the Firmicutes/Bacteroidota ratio toward the former, repeatedly linked to obesity and insulin resistance [22].

These microbe–metabolic shifts translate into opposing systemic markers. A meta-analysis of 21 observational studies showed that high-sensitivity CRP in vegans was 0.54 mg/L lower than in omnivores, even after BMI adjustment [11]. A Western diet, however, increases plasma endotoxin activity within four weeks, directly indicating increased barrier permeability and “metabolic endotoxemia” [23]. The elevated LPS flux enhances NF-κB expression and proinflammatory cytokine production, whereas in vegans, elevated butyrate levels and more acidic fecal pH restrain pathogen-associated molecular translocation.

Thus, plant-based and Western diets establish opposing microbial niches: the former supports a diverse, butyrate-rich ecosystem with high SCFA production and low systemic inflammation, while the latter yields a depleted community dominated by LPS-positive pathobionts, reduced SCFA levels, and chronic low-grade inflammatory burden. These differences underscore the potential of dietary strategies for targeted microbiota modulation and prevention of metabolic diseases.

Conclusion. In conclusion, the presented data demonstrate that dietary profile is a key determinant of gut microbiota composition and function. Transitioning to a plant-based diet—whether a strict vegan regimen or predominantly plant-derived nutrition—provides an abundant substrate in the form of dietary fibers and polyphenols, leading to rapid and reproducible growth of Bifidobacteria and Lactobacillus, significant enrichment of butyrate producers (Faecalibacterium prausnitzii, Roseburia spp.), and increased microbial α-diversity (Shannon index rises by an average of 7% versus omnivores, p < 0.001). These changes are accompanied by elevated fecal concentrations of acetate, propionate, and especially butyrate (up to 25% increase within 2–13 months) and activation of immunoregulatory mechanisms via GPR41/43 and histone deacetylase inhibition, resulting in strengthened intestinal barrier function (increased occludin and claudin-1 expression) and reduced systemic levels of proinflammatory markers CRP and IL-6. Consequently, the microbiota of vegans forms a stable anti-inflammatory ecosystem that promotes improved cardiometabolic profiles and enhanced insulin sensitivity.

The opposite scenario occurs with Western-type diets high in saturated fats, animal protein, and added sugars. Such diets stimulate elevated bile acid levels, promoting the expansion of LPS-positive Gram-negative pathobionts (Bilophila wadsworthia, Alistipes spp.), reducing microbial diversity (Shannon index lower by 0.4 units), and depleting butyrate producers within weeks. This dysbiosis leads to increased epithelial permeability (elevated zonulin and circulating LPS by 71% after three weeks), metabolic endotoxemia, and persistent low-grade inflammation, exacerbating obesity and insulin resistance risks.

Comparing the metabolic “fuel” flows under plant-based and Western diets highlights how profoundly diet shapes the gut’s microbial landscape. At equal caloric intake, vegan diets supply twice the fermentable fiber and polyphenols, while Western diets deliver excess fats and animal proteins without fermentable substrate. These differences are reflected in taxonomy, metabolomes, and systemic biomarkers: plant-based diets support a more even and diverse community with high SCFA production, whereas Western diets lead to pathobiont dominance, reduced SCFA output, and a chronic inflammatory baseline.

Thus, these findings underscore the potential of dietary strategies for targeted microbiota modulation and the prevention or treatment of chronic metabolic and inflammatory diseases. Dietary choice remains among the most accessible and effective means to foster an anti-inflammatory gut ecosystem and strengthen the host’s immunometabolic health.

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