Search Results (1,631)

Cognitive frailty combines physical frailty with cognitive impairment without dementia, identifying older adults vulnerable to adverse outcomes. Candidate microbiome-related pathways in cognitive frailty include dysfunction of the intestinal epithelial and blood–brain barriers, altered microbial metabolites, systemic and vascular inflammation, anabolic resistance, and neuroinflammation. However, direct evidence is scarce, and most findings derive from physical frailty, sarcopenia, mild cognitive impairment, or Alzheimer’s disease, inviting overinterpretation. This review integrates a multi-database evidence map with a domain-based synthesis of phenotypes, mechanisms, biomarkers, confounding, interventions, and clinical translation. Conducted up to 31 July 2026, the search identified one eligible primary human study directly examining the gut microbiome in cognitive frailty. Its small sample, age and educational imbalances, 16S-based resolution, and lack of external validation preclude clinical biomarker claims despite apparent discrimination. Larger metagenomic frailty studies report lower microbial diversity, gene richness, and butyrate-production capacity, with partial cross-population replication. Dietary, prebiotic, and probiotic trials demonstrate microbiome target engagement and report selected physical or cognitive benefits, but these outcomes are inconsistent, rarely assessed together, and not established as microbiome-mediated; fecal microbiota transplantation remains experimental. The microbiome should be considered a potential component of multidomain risk models rather than a stand-alone biomarker. Translation requires standardized phenotyping, longitudinal multi-omics, causal diagrams, external validation, and trials with concurrent physical and cognitive endpoints. Full article

Chronic stress is a critical predisposing factor for neuropsychiatric and metabolic disorders, profoundly affecting both physical health and behavioral performance. Stress induces gut microbiota dysbiosis and disrupts tryptophan metabolism, notably via the kynurenine (KYN) and 5-hydroxytryptamine (5-HT) pathways. Targeted modulation of the gut–brain axis through probiotics and prebiotics has therefore emerged as a promising approach for preventing and alleviating stress-related disorders, yet the efficacy of specific synbiotic combinations remains largely unexplored. This study investigated the effects of feline milk-derived Lactiplantibacillus plantarum MNN, galacto-oligosaccharides (GOS), and their combination on stress-related behavioral abnormalities and tryptophan metabolism in a mouse model of chronic social defeat stress (CSDS). Behavioral outcomes, gut microbial composition, cecal tryptophan metabolites, and molecular markers associated with serotonin (5-HT) synthesis and neuroplasticity were evaluated. Intervention with MNN, GOS, and MNN + GOS attenuated several CSDS-induced behavioral abnormalities and was associated with alterations in gut microbial composition and cecal tryptophan metabolism. In the SIT, the social interaction ratio increased from 0.307 ± 0.089 in CSDS mice to 0.778 ± 0.042 (p = 0.003), 0.826 ± 0.035 (p = 0.001), 1.445 ± 0.114 (p < 0.0001) in the MNN, GOS, and MNN + GOS groups, respectively. Cecal indoxyl sulfate levels decreased from 1.944 ± 0.286 in CSDS mice to 0.206 ± 0.022 (p < 0.0001), 0.231 ± 0.058 (p < 0.0001) and 0.275 ± 0.018 (p < 0.0001) in the MNN, GOS, and MNN + GOS groups, respectively. The interventions also increased intestinal and hippocampal 5-HT signals and partially restored the expression of tryptophan hydroxylases, brain-derived neurotrophic factor (BDNF), and postsynaptic density protein 95 (PSD95). These findings suggest that MNN, GOS, and MNN + GOS interventions may alleviate stress-related abnormalities, potentially through modulation of the microbiota-tryptophan-5-HT axis. However, the causal role of the gut microbiota and the efficacy of these interventions in cats require further investigation. Full article

Diffuse Idiopathic Skeletal Hyperostosis (DISH) is a systemic, non-inflammatory skeletal disorder characterized by progressive calcification and ossification of spinal ligaments and entheses. Its strong associations with aging, obesity, type 2 diabetes, and metabolic syndrome raise the possibility that metabolic and inflammatory pathways may contribute to disease development. The gut microbiota participates in nutrient metabolism, short-chain fatty acid production, bile-acid transformation, intestinal-barrier maintenance, and immune regulation; these functions provide a plausible framework for examining whether intestinal dysbiosis may influence spinal and musculoskeletal tissues. This narrative review therefore evaluates the potential relationship between gut microbiota, DISH, and related spinal degenerative diseases. It considers the nutritional, metabolic, immunological, and host-interaction functions of the gut microbiota before examining proposed gut–spine, gut–bone, gut–joint, gut–disc, gut–ligament, and gut–muscle pathways. Particular attention is given to the apparent paradox that most microbiome–bone evidence concerns osteoporosis and bone loss, whereas DISH is characterized by excessive ectopic bone formation. Differences in short-chain fatty acid concentration, receptor expression, local versus systemic signaling, and osteoblast–osteoclast microenvironments may produce divergent skeletal effects, but these mechanisms have not been tested directly in DISH. Recent studies support associations between selected microbial taxa and intervertebral disc degeneration or spinal stenosis; however, direct clinical evidence linking gut microbiota to DISH remains limited. Consequently, dietary modification, probiotics, prebiotics, and fecal microbiota transplantation should be regarded as research considerations rather than established treatments for DISH. Well-characterized case–control and longitudinal studies integrating microbiome profiling, metabolomics, inflammatory markers, and serial imaging are required to determine whether reproducible microbial or metabolite signatures precede DISH onset or progression. The pathways discussed in this review are therefore presented as biologically plausible, testable hypotheses and not as established causal relationships. Full article

Fresh and soft cheeses feature high moisture content, elevated water activity, and nutrient richness, creating favorable conditions for foodborne pathogens including Listeria monocytogenes, Salmonella spp., Shiga toxin-producing Escherichia coli, and Staphylococcus aureus, which can contaminate products via post-pasteurization biofilm formation on processing equipment. Because conventional thermal and chemical preservation methods can compromise organoleptic and nutritional quality, biological control strategies have emerged as promising alternatives to enhance microbiological safety. This review critically evaluates three biopreservation modalities along their technological maturity gradient: bacteriophages and endolysins, antimicrobial peptides (AMPs) and bacteriocins, and postbiotics. Bacteriophages present high operational readiness, supported by regulatorily cleared commercial preparations; however, their lytic activity is frequently constrained by low temperatures, acidic pH, and matrix-bound fat. AMPs and bacteriocins—anchored by nisin—are extensively researched, with contemporary innovation focusing on advanced delivery vehicles, including active packaging, nanoencapsulation, and in situ bacteriocinogenic starter cultures, to preserve peptide stability throughout ripening. Postbiotics—here referring specifically to preparations consistent with the International Scientific Association for Probiotics and Prebiotics (ISAPP) consensus definition of inanimate microorganisms and/or their components, as distinct from the cell-free supernatants and fermentates most often tested in cheese—offer good physicochemical stability and dose control, albeit with lower and more variable intrinsic antimicrobial potency. Across all modalities, multi-target hurdle approaches consistently outperform single-agent applications, with surface-targeted delivery representing the dominant engineering strategy. Persistent limitations across all strategies include post-treatment bacterial regrowth, matrix interference, non-standardized activity units, and unresolved regulatory status. Moving forward, standardized, full-shelf-life challenge trials in real cheese matrices under harmonized storage conditions are imperative to benchmark these biointerventions head-to-head against conventional methods and live protective cultures. Full article

Co-encapsulating probiotics with prebiotic substrates (PRO–PRE) is widely proposed as a route to functional dairy products, yet the terminology and the supporting evidence are applied inconsistently. This structured narrative review examines PRO–PRE co-encapsulation in dairy matrices and, as a complementary field, the encapsulation of milk-derived bioactive peptides. Scopus, Web of Science Core Collection, and PubMed were searched for publications from 1 January 2015 to 1 September 2026. Of 663 records retrieved, 420 remained after deduplication and 330 after screening; 117 were prioritized for technological assessment. Protection is consistent but partial: encapsulated Lacticaseibacillus rhamnosus in ice cream declined by 0.61 log CFU/g over 50 days of frozen storage, compared with 0.97 log CFU/g for free cells. Adding a substrate is not invariably beneficial, since sweet-whey–inulin microcapsules in Greek-style yogurt and inulin in ultrafiltered white cheese conferred no advantage over the carrier alone. Outcomes depend on strain, carrier, encapsulation method, and dairy matrix, and no method proved superior on every criterion. Physical co-localization was frequently reported as synbiotic function without evidence of selective substrate utilization. No validated dairy system combining a probiotic, a confirmed prebiotic, and a characterized milk-derived peptide was identified, and clinical validation is still lacking. Full article

Chronic kidney disease (CKD) appears linked to changes in the gut microbiota, intestinal barrier defects, and microbiota-driven changes in metabolite profiles. Experimental evidence links gut microbiota disturbances to kidney injury through pathways such as microbial metabolism, inflammation, immune signals, and epithelial barrier dysfunction. Still, applying this knowledge in clinical practice for patients with CKD remains difficult. For instance, one study on indoxyl sulfate and p-cresyl sulfate levels in a patient showed that, beyond being synthesized by the intestinal microbiota, the host can also metabolize or alter these metabolites. In addition, they undergo impaired renal clearance and can be secreted by the tubules. Moreover, most human microbiome-related studies are observational, making it difficult to determine the causal role of bacterial dysbiosis. Disease, dietary factors, medication, and other comorbid conditions are major confounders. Microbiota-directed means of altering the composition of the microbiota, such as changing diet, using prebiotics, probiotics, synbiotics, oral adsorbents, and even fecal microbiota transplantation, have, to varying degrees, affected the composition of the gut microbiota, levels of uremic toxins, short-chain fatty acids, and markers of inflammation. They have also been connected to leaky gut syndrome. However, evidence that these actions delay eGFR decline or prevent kidney failure, cardiovascular events, hospitalization, or mortality remains limited. Postbiotics and microbiota-derived metabolites in pure form are distinct experimental therapies and need to be assessed independently. This article reviews the gut kidney axis at different levels of evidence and distinguishes preclinical mechanisms, human associations, surrogate biomarker responses, and clinical outcomes. It points out why impressive mechanistic and biomarker results have not translated into better kidney or cardiovascular outcomes. Future research should use standardized methodologies, provide more detail on microbial functions and host metabolite metabolism, and test microbiome-targeted therapies in sufficiently powered randomized controlled trials with meaningful endpoints. Full article

The gut microbiota is increasingly recognized as an important modulator of cardiovascular health, demonstrating complicated interactions among diet, metabolism, immunology and host physiology. Evidence is accumulating that changes in the composition and function of the gut microbiome may contribute to the pathogenesis of atherosclerosis, hypertension, heart failure, thrombosis and other cardiovascular phenotypes through mechanisms involving microbial metabolites, intestinal barrier dysfunction, inflammation and metabolic dysregulation. In this context, the key question of this narrative review is: how far can modulation of the gut microbiome and its metabolic functions be a clinically meaningful approach in the prevention and treatment of cardiovascular disease, and which of the currently available microbiome-targeted approaches have sufficient mechanistic and clinical evidence to justify translation into cardiovascular practice? To answer this question, we review the evidence linking the gut microbiome to major cardiovascular phenotypes, such as atherosclerosis, hypertension, heart failure, thrombosis and atrial fibrillation, with particular focus on the mechanisms through which microbial metabolites, intestinal barrier dysfunction, inflammation and metabolic dysregulation may affect cardiovascular risk. We then review current and emerging strategies for microbiome modulation, including dietary interventions, prebiotics, probiotics, synbiotics, postbiotics, fecal microbiota transplantation and targeted inhibition of microbial metabolic pathways such as trimethylamine (TMA)/trimethylamine N-oxide (TMAO) production. We also examine bidirectional interactions between cardiovascular drugs and gut microbiome and the role of these interactions in the development of precision methods to cardiovascular prevention and treatment. Finally, we outline the major limitations of the current evidence and highlight goals for future mechanistic, translational and clinical research. Full article

Anorexia nervosa (AN) is characterized by severe dietary restriction with effects that extend beyond body weight to gastrointestinal function, dietary tolerance and the gut microbiome. Weight restoration remains central to treatment, but studies suggest that microbial composition, microbial metabolites and gastrointestinal symptoms may not recover at the same pace as body mass. This narrative review examines gut microbiome alterations in AN through the clinical context of refeeding and dietetic care. Human and translational studies describe changes in microbial diversity, including shifts in carbohydrate fermenting taxa and their downstream metabolic products such as short-chain fatty acids (including butyrate), mucin-degrading taxa, neuroactive fecal metabolites, immune markers and microbial functional pathways. During refeeding, the substrates available to the gut microbiome are shaped by planned increases in energy intake, the extent to which planned meals are consumed, gastrointestinal tolerance, oral supplement use, constipation, laxative exposure or other medication, dietary variety and the gradual return of fermentable substrates. Current intervention evidence does not support routine use of probiotics, prebiotics or synbiotics for weight restoration, eating-disorder psychopathology or targeted microbiome modulation. Fiber-containing foods, fermented foods and dietary diversity may be relevant to dietary substrate exposure and gastrointestinal tolerance, but their use during AN rehabilitation should be framed as pragmatic dietetic care rather than as established microbiome-specific treatment. Their introduction should remain secondary to adequate energy provision, tolerance, normalization of eating patterns and avoidance of reinforcing restrictive behaviors. Dietitians can translate microbiome-related knowledge into cautious nutritional decision-making while ensuring that patient care remains centered on rehabilitation, safety and dietary adequacy. Full article

The growing demand for dairy-free functional foods has created a need for fruit-based products that simultaneously provide probiotics, prebiotics, and bioactive compounds. This study evaluated seven high-fruit synbiotic-designed sorbets prepared with raspberries, strawberries, haskap berries, apples, or plums, and two variants with blackcurrants, containing 45–55% fruit, 3% inulin, and Lactiplantibacillus plantarum 299v added at two inoculum levels. Sucrose was added to the mixture, and in one variant of the blackcurrant, it was replaced with erythritol, which can affect, among other things, the sweetness, hardness, melting point, mouthfeel, and freezing point of frozen desserts. Erythritol was used to evaluate the effect on these characteristics in one variant. The addition of one and two probiotic capsules to each sorbet was also compared. The viability of the probiotics (as LAB) before and after freezing, physicochemical composition, color, hardness, melting, aeration, antioxidant properties, consumer acceptance, and purchase intention were assessed using univariate and multivariate statistical analyses. After freezing, the number of viable cells remained at approximately 7.05–7.18 log CFU/g in the single-capsule variants and 7.45–7.51 log CFU/g in the two-capsule variants, confirming the high immediate viability of the probiotic cells. The fruit type and its content in the matrix significantly differentiated acidity, sugars, color, hardness, degree of growth, melting properties, phenolic compounds, anthocyanins, antioxidant activity, and sensory quality. The dark berry sorbets showed a particularly high content of bioactive compounds. Consumer responses varied significantly between formulations, with taste, texture, and consistency demonstrating the strongest associations with overall acceptance. The results demonstrate that fruit sorbets can serve as practical, dairy-free carriers for Lactiplantibacillus plantarum 299v and inulin, while retaining fruit-specific functional and sensory properties. Full article

Musk, a precious traditional Chinese medicine, is secreted by the male forest musk deer (Moschus berezovskii). The gut microbiota plays an essential role in host metabolism, yet its relationship with musk traits remains poorly understood. Here, 16S rRNA sequencing of 89 fecal samples was integrated with musk quality (color and moisture) and yield data to investigate how fecal bacterial communities influence these traits. Distinct microbial consortia were associated with musk traits. Aromatic and sulfur-metabolizing taxa (norank_f_Actinomycetaceae, Nocardioides, Rhodococcus, and Mailhella) were associated with degradation of aromatic compounds and sulfur-containing amino acids, potentially contributing to muscone and other bioactive aroma components. Short-chain fatty acid (SCFA) producing taxa (Blautia, Phascolarctobacterium, Oscillospiraceae UCG-005, unclassified_f_Lachnospiraceae, Anaerovorax, Parabacteroides, Prevotellaceae_UCG-003, Christensenellaceae R-7 group, and Bacteroides) were capable of fiber decomposition and may supply energy for steroid synthesis via SCFAs, favoring high-quality musk formation. Ketogulonicigenium vulgare was linked to anti-inflammatory polypeptides and steroids. These potential indicators may facilitate early selection of high-yielding deer, inform probiotic/prebiotic interventions, and support dietary strategies to improve gut health and musk productivity, thereby reducing poaching and promoting the sustainable conservation of this endangered species. Full article

Background: The gut microbiota–brain axis is a highly integrated bidirectional communication network operating through neural, neuroendocrine, immune, and metabolic pathways that maintain central nervous system homeostasis and has emerged as a promising complementary therapeutic target for neurological and neuropsychiatric disorders. Objective: The objective of this study is to systematically evaluate the effects of prebiotics, probiotics, and psychobiotics on gut–brain communication and neurological and behavioral outcomes, including neuroinflammatory markers, HPA-axis parameters, and microbial metabolites. Methods: A systematic review was conducted in accordance with the PRISMA 2020 guidelines. Literature searches of PubMed, Scopus, and Google Scholar from 2020 up to March 2026 identified 81 eligible studies (48 preclinical studies, 27 randomized controlled trials, and 6 quasi-experimental clinical studies) from 7358 records. Primary outcomes were systematically categorized into four domains: (1) cognitive performance and social/adaptive behavior; (2) neuroinflammatory markers (TNF-α, IL-6, IL-1β) and barrier integrity; (3) HPA-axis parameters (cortisol/corticosterone); and (4) neuroactive microbial metabolites (short-chain fatty acids and tryptophan derivatives). Methodological quality and risk of bias were assessed independently by two reviewers using the SYRCLE tool for preclinical studies and the Joanna Briggs Institute (JBI) tools for randomized and quasi-experimental clinical trials, with summary visualizations generated using the robvis web application (version 0.3.0). Results: Neurodegenerative diseases (n = 31; 38.3%) and mood disorders (n = 29; 35.8%) were the most frequently investigated conditions. Probiotics predominated (n = 61), followed by prebiotics (n = 12) and synbiotics (n = 8). Descriptively, 92% of included studies reported improvements in at least one evaluated outcome. However, this unweighted observation reflects effect direction rather than clinical magnitude, encompassing primary and secondary endpoints across highly heterogeneous sample sizes, study designs, and risk-of-bias profiles. Conclusions: Microbiota-targeted interventions show promise as complementary strategies for neurological disorders; however, substantial methodological heterogeneity, unstandardized dosing, and the absence of quantitative meta-analysis preclude definitive clinical recommendations. Successful translation will require harmonized protocols, strain-specific functional characterization, and precision microbiota-based trials. Full article

Osteoporosis is a major skeletal disorder. Increasing evidence suggests that gut microbiota-derived mechanisms may contribute to bone remodeling. The biological rationale for a gut–bone axis is well supported, but the clinical relevance of microbiome-targeted interventions remains uncertain. In this narrative review, we focus on prebiotics, probiotics, synbiotics, and postbiotics. We searched in the literature the progress from mechanistic observations to measurable skeletal outcomes in humans. We searched PubMed, Scopus, and Web of Science for literature published mainly between 2021 and 2026. We also included earlier studies when they were important for the mechanistic framework. The evidence was evaluated according to intervention type and outcome. We focused on bone turnover markers, bone mineral density, and the duration of exposure required for these outcomes to become clinically meaningful. Recent randomized trials and meta-analyses were also compared in a semi-quantitative synthesis to show where findings are consistent and where they remain conflicting. Full article

Vaccine responses differ substantially among individuals and across populations. Although factors such as age, genetics, and vaccine type are recognized contributors, they do not fully explain this heterogeneity. Emerging evidence suggests that the human microbiota, particularly the gut microbiota, may modulate immune responses to vaccination and represents a potentially modifiable component of immunity. This review integrates data from human studies, microbiota-targeted clinical trials, and experiments using germ-free and humanized models to clarify the mechanisms underlying microbiota–immune system interactions during vaccination. Identified mechanisms include pattern-recognition receptor signaling, modulation of innate immune activation, regulation of germinal-center responses, maintenance of mucosal barrier integrity, and the influence of microbial metabolites on T and B lymphocytes. The relevance of these pathways varies by age, developmental stage, and vaccine platform, including live-attenuated, inactivated, subunit, viral-vector, and mRNA vaccines. Additional factors such as diet, antibiotic exposure, infections, medications, and environmental or social determinants also affect both the microbiota and vaccine outcomes. Current research explores approaches to improve vaccine potency through microbiota modulation using probiotics, prebiotics, synbiotics, postbiotics, and engineered microbes, though clinical results remain inconsistent. A greater understanding of microbiota–vaccine interactions may enable personalized immunization strategies; however, further research is required to establish causality and identify actionable microbial targets. Longitudinal studies using multi-omics, advanced cellular analyses, robust clinical trials, and in silico modeling are essential to determine whether microbiome-based interventions can improve vaccine efficacy and durability. Full article

Acute kidney injury (AKI) is a common critical syndrome with high morbidity and mortality, and a subset of patients may progress to chronic kidney disease. Recent studies have revealed that gut microbiota and their metabolites play pivotal roles in the pathogenesis of AKI. Under AKI conditions, the gut microbiota composition undergoes significant alterations, characterized by decreased beneficial bacteria and expansion of opportunistic pathogens, accompanied by impaired intestinal barrier and disordered microbial metabolism. Gut microbiota metabolites can be classified into protective metabolites (short-chain fatty acids, secondary bile acids, tryptophan metabolites, D-amino acids, and polyamines) and toxic metabolites (indoxyl sulfate, p-cresyl sulfate, trimethylamine N-oxide, and endotoxin). The former exert renoprotective effects through anti-inflammatory, antioxidant, and barrier-maintaining mechanisms, while the latter aggravate kidney injury via oxidative stress, inflammation activation, and hemodynamic disturbance. Based on the gut–kidney axis theory, interventions targeting gut microbiota (probiotics, prebiotics, fecal microbiota transplantation) and those targeting metabolites (supplementation of protective metabolites, removal of toxic metabolites) have shown promising prospects. This narrative review summarizes the characteristics of gut microbiota changes, classification and function of key metabolites, core mechanisms driving AKI, and microbiota-based intervention strategies, aiming to provide novel insights for early recognition and precision prevention of AKI. Full article

Introduction: Selective serotonin reuptake inhibitors (SSRIs) remain the first-line pharmacological treatment for depressive disorders. However, long-term treatment is often accompanied by weight gain, which negatively impacts medication adherence and cardiometabolic health. Emerging evidence suggests that, in addition to their effects on the central nervous system (CNS), SSRIs may alter the composition and metabolic activity of the gut microbiome, potentially contributing to metabolic disorders. However, the mechanisms linking SSRI-induced microbial changes to weight regulation remain poorly understood. Methods: This narrative review summarizes the current evidence regarding the interactions between SSRIs, the gut microbiome, host metabolism, and weight regulation. Experimental, translational, and clinical studies were critically assessed, with particular emphasis on recent systematic reviews, meta-analyses, randomized controlled trials, and mechanistic studies. A conceptual mechanistic framework was developed based on the available evidence. Results: Experimental and clinical studies indicate that SSRIs can modify both the taxonomic composition and functional activity of the gut microbiota. These changes may influence the production of microbiota-derived metabolites, including short-chain fatty acids, bile acids, and tryptophan metabolites, thereby influencing gut barrier integrity, low-grade inflammation, gut hormone secretion, appetite regulation, and energy homeostasis. Current evidence also suggests that dietary interventions—including increased dietary fiber intake, adherence to a Mediterranean diet, and microbiota-targeted strategies using prebiotics, probiotics, synbiotics, and postbiotics—can beneficially modulate these pathways. However, no randomized, controlled trials have specifically assessed whether such interventions prevent SSRI-associated weight gain. Conclusions: Taken together, the available evidence raises the possibility that gut microbiota alterations may contribute to SSRI-associated weight gain, although this hypothesis has not yet been directly tested in studies evaluating the complete mechanistic pathway. Full article