Search Results (485)

Background/Objectives: Patients receiving maintenance hemodialysis (HD) commonly exhibit chronic low-grade inflammation, nutritional disturbances, altered body composition, and metabolic imbalance. Gut dysbiosis may contribute to these abnormalities through the gut–kidney axis; however, the relationship between the gut microbiota composition and host phenotype in HD patients remains incompletely characterized. This study aimed to characterize the gut microbiota composition in maintenance HD patients and assess its cross-sectional associations with demographic, inflammatory, nutritional, dialysis-related, and bioimpedance-derived body composition parameters. Methods: This single-center cross-sectional study included 96 patients with end-stage kidney disease undergoing maintenance HD. The primary objective was to characterize the gut microbiota composition in maintenance HD patients. Secondary objectives were to assess cross-sectional associations with demographic factors (sex, age) and bioimpedance-derived body composition (specifically VAT). Clinical and laboratory data, inflammatory markers, nutritional indicators, malnutrition–inflammation score (MIS), dialysis-related variables, and bioimpedance-derived body composition parameters were collected. Stool samples were analyzed using full-length 16S rRNA sequencing. The gut microbiota composition was assessed using taxonomic profiling, alpha-diversity and beta-diversity analyses, subgroup comparisons, and exploratory distance-based analyses. Associations were interpreted within a descriptive and hypothesis-generating framework. Results: The gut microbiota composition showed marked inter-individual heterogeneity at the genus level, with dominant taxa including Blautia, Faecalibacterium, Streptococcus, Gemmiger, Ruminococcus, Escherichia-Shigella, and Enterococcus. Chao1 richness was higher in men than in women. Shannon entropy and Chao1 richness were positively associated with age and visceral adipose tissue (VAT), while Faith’s phylogenetic diversity increased with age. In contrast, the Gini index was negatively associated with age and VAT, indicating a more even microbial community structure in older individuals and in those with higher visceral adiposity. Beta-diversity analyses suggested modest differences in microbial community structure according to sex and selected body composition-related categories, particularly in sex-stratified analyses. Exploratory distance-based analysis showed a modest association between overall microbiota dissimilarity and host phenotype dissimilarity, although this finding was limited by reduced sample overlap. Conclusions: The gut microbiota composition in maintenance HD patients was highly heterogeneous and showed cross-sectional associations, mainly with sex, age, visceral adiposity, and broader host phenotype. These findings suggest that microbiota variation in HD reflects multidimensional demographic, inflammatory, nutritional, metabolic, and body composition-related factors rather than a single clinical determinant. Larger longitudinal studies integrating standardized dietary, medication, metabolic, and clinical outcome data are needed to determine the prognostic relevance of these microbiota patterns. Full article

Background/Objectives: Sport participation and nutrition are increasingly recognized as key determinants of cognitive function and academic achievement in student populations. However, the biological mechanisms underpinning these associations remain only partially understood. This scoping review aimed to map and synthesize the current evidence on neuroendocrine and autonomic mechanisms linking physical activity, sport participation, and nutrition to cognitive and academic outcomes in students. Methods: A systematic search of electronic databases was performed following PRISMA-ScR guidelines. Studies involving student populations that examined physical activity, sport participation, or dietary patterns in relation to cognitive function and/or academic performance were included. Particular attention was given to studies reporting biological or physiological indicators of underlying mechanisms, including neuroendocrine, autonomic, and brain-based measures. Data were extracted and synthesized qualitatively, with studies categorized according to the type of mechanistic evidence. Results: A total of 76 studies met the inclusion criteria. The available evidence was more extensive for physical activity, sport participation, and fitness-related exposures than for nutrition-related variables or integrated lifestyle models. Cognitive outcomes, particularly executive function, attention, working memory, and memory performance, were assessed more frequently and showed more consistent associations with lifestyle behaviors than academic outcomes, which were less commonly and more heterogeneously evaluated. Mechanistic evidence was unevenly distributed: only a limited subset of studies included direct biological or psychophysiological measures, mainly neuroimaging, brain-derived neurotrophic factors, cortisol-related indices, or heart rate variability. In contrast, inflammatory, metabolic, and gut microbiota-related mechanisms were mostly discussed at a conceptual or indirect level. Overall, the findings indicate a broad associative literature but a relatively small body of studies directly testing biological pathways linking physical activity, nutrition, cognition, and academic performance. Conclusions: Current evidence indicates potential associations between sport participation, nutrition, cognitive outcomes, and multiple biological pathways. However, the scoping nature of the review, the predominance of observational designs, and the limited use of direct mechanistic assessments prevent firm causal conclusions. Future research should prioritize longitudinal and intervention studies integrating behavioral, nutritional, cognitive, academic, and biological measures within the same design. Full article

Type 2 diabetes mellitus is a relevant cardio–renal–metabolic disorder in which chronic low-grade inflammation and oxidative stress have a crucial function in linking insulin resistance, endothelial dysfunction, β-cell impairment, and progressive organ injury. In this context, nutrition has emerged as a key modifiable determinant of metabolic homeostasis, capable of influencing inflammatory signalling, redox balance, mitochondrial function, and gut microbiota–host interactions. The objective of this review is to critically summarise the mechanistic connections among inflammation, oxidative stress, and diabetes progression, and to investigate how dietary factors and patterns, as well as nutrition-responsive biomarkers, influence these pathways and their cardiorenal consequences. We discuss the effects of macronutrient quality, dietary fibre, fatty acids, polyphenols, and specific micronutrients, including vitamin C, vitamin E, selenium, zinc, and magnesium, as well as the role of Mediterranean, DASH, and plant-based diets in improving glycaemic control, endothelial function, and cardio-renal risk profiles. We also summarise established and emerging biomarkers of inflammation and oxidative stress that may improve risk stratification and the evaluation of nutrition-based interventions. Overall, current evidence supports a shift from a purely glucose-centred approach toward an integrated model in which dietary modulation of inflammatory and oxidative pathways helps reduce cardiovascular and renal risk. However, heterogeneity of interventions, variability in biomarker assessment, and interindividual differences in dietary response represent major limitations. Future research should focus on biomarker-informed, precision-oriented nutritional approaches integrated within contemporary cardio–renal–metabolic care. Full article

Background/Objectives: Lipidomics has become a key component of systems biology, enabling comprehensive characterisation of lipid species and their roles in health and disease. As regulators of membrane architecture, energy balance, inflammation, and cellular signalling, lipids offer a powerful framework for understanding metabolic dysfunction. In veterinary medicine, however, lipidomics remains comparatively underdeveloped. In cats, lipid metabolism is central to disorders such as hepatic lipidosis, cystitis, obesity, diabetes mellitus, and chronic inflammatory enteropathies, yet available data remain limited. This systematic review synthesised current evidence on lipidomics and lipid-focused profiling in feline disease and identified lipid alterations with potential clinical relevance. Methods: Following PRISMA 2020 guidelines, PubMed, ScienceDirect, and Scopus were searched for original studies (1994–2026) evaluating lipidomics or lipid-focused profiling in cats. Eligible studies assessed lipid species, fatty acids, lipid mediators, or lipoproteins in disease or physiological states. Owing to methodological heterogeneity, findings were synthesised narratively. Results: Seventeen studies met inclusion criteria, covering hepatic, urinary, gastrointestinal, renal, neurological, oncological, metabolic, and pharmacologically modulated conditions. Recurring alterations involved lipoproteins, triglycerides, phospholipids, sphingolipids, fatty acids, and oxylipins. More consistent patterns emerged in hepatic lipidosis, where lipoprotein disturbances may aid diagnosis; in lower urinary tract disease, where PUFA-derived oxylipins differentiated bacterial from idiopathic cystitis; and in obesity, where phospholipid and triglyceride shifts reflected metabolic risk. Fatty acid remodelling in chronic enteropathies aligned with mucosal inflammation, while sphingolipid changes in neurological disease correlated with severity. Heterogeneity in analytical platforms, dietary control, and study design limited comparability. Conclusions: Feline lipidomics reveals biologically meaningful alterations with emerging diagnostic and prognostic value. Although still developing, lipid-focused approaches may enhance disease characterisation and support translational research. Larger, standardised studies and robust reference datasets are needed to validate lipid signatures for clinical implementation. Full article

Diet is a modifiable factor that influences multiple pathways relevant to hematologic malignancy, including systemic inflammation, immune cell activity, gut microbiota composition, and cancer cell metabolism. Translation of preclinical findings into clinical practice for hematologic malignancies remains nascent, although momentum is building to evaluate dietary interventions as a component of supportive and disease-modifying care. This review examines the mechanistic rationale for dietary interventions across the spectrum of clonal hematologic disorders and synthesizes current clinical evidence. Anti-inflammatory dietary patterns, particularly the Mediterranean diet, have demonstrated reductions in pro-inflammatory cytokines and may attenuate the inflammatory milieu that fuels clonal expansion. Obesity, which elevates the risk of developing hematologic malignancies and worsens clinical outcomes in diseases such as acute lymphoblastic leukemia (ALL) and acute myeloid leukemia, may be addressed through calorie-restricted, low-fat, or plant-based dietary strategies. Gut microbiota dysbiosis induced by chemotherapy represents another target, with high-fiber and plant-based diets showing promise in restoring microbial diversity and potentially enhancing treatment efficacy. Early-phase clinical trials in multiple myeloma, acute lymphoblastic leukemia, and myeloproliferative neoplasms have established feasibility and yielded preliminary signals warranting larger confirmatory studies. Larger, rigorously designed trials are needed to establish dietary interventions as legitimate therapeutic tools in the management of hematologic malignancies. Full article

Oxidative stress is an important component of cancer biology and is characterized by an imbalance between the production of reactive oxygen species (ROS) and antioxidant defense systems. Excess ROS can cause molecular damage and genomic instability; at the same time, ROS signaling remains necessary for normal cellular function. Redox homeostasis is of particular importance in this balance. The aim of this structured narrative review was to summarize and critically discuss current evidence on how dietary antioxidants influence redox-sensitive pathways involved in cancer prevention, with particular attention to metabolic inflammation, mitochondrial quality control, and gut microbiota-related mechanisms. We performed a structured literature search of Scopus, Web of Science, and PubMed, focusing on articles published between 2021 and 2026. The evidence covered major redox-sensitive pathways, including Nrf2-Keap1-ARE signaling, AMPK-mTOR regulation, NF-κB-mediated inflammation, mitochondrial quality control (autophagy and mitophagy), and inflammasome activation. These pathways, which are involved in tumor initiation and progression, link oxidative stress to metabolic and inflammatory processes. Current evidence suggests that dietary antioxidants act primarily by supporting endogenous defense systems. This may help explain the “antioxidant paradox”, in which antioxidant-rich dietary patterns are associated with a lower risk of cancer. In some studies, high-dose supplementation with isolated antioxidants has produced inconsistent or sometimes adverse results. These effects depend on dose, chemical form, metabolic context, and baseline redox state. The gut microbiota is also an important mediator of antioxidant bioactivity; by converting dietary polyphenols into bioactive metabolites, it can influence systemic redox balance and metabolic signaling. This microbiota-dependent modulation may partially explain inter-individual variability in responses to dietary interventions. In conclusion, dietary antioxidants should be considered as modulators of redox-sensitive signaling networks, not merely as simple radical scavengers. Personalized modulation of redox homeostasis is a future strategy for cancer prevention, with a greater emphasis on whole-diet and biomarker-guided approaches. Full article

Neurodevelopment is a dynamic and multifactorial process, critical in the early stages of life, involving the formation of neural networks, the establishment of synapses, and the maturation of cognitive, social and emotional circuits. In this context, the gut microbiome emerges as an essential regulator of neurodevelopment, exerting influences through multiple biochemical and immunological mechanisms that define the “gut-brain axis”. The microbiota modulates neurodevelopment by regulating neurotransmitters (serotonin, dopamine, GABA), the production of microbial metabolites, including short-chain fatty acids, the modulation of inflammatory cytokines, and vagal signaling to the central nervous system. Recent evidence highlights the role of microbiota in modulating microglia, synaptogenesis, dendritic maturation, and neuronal plasticity, emphasizing how these processes are influenced by microbial activity rather than providing a comprehensive treatise on plasticity itself. Gut microbiota disturbances, or dysbiosis, have been associated with various neuropsychiatric and neurodevelopmental disorders, contributing to cognitive, behavioral, and emotional dysfunctions. This article summarizes, in a narrative manner, the main dysbiosis patterns identified in these disorders and the biological mechanisms by which the microbiome influences neuronal development and function, including immune–neuronal interactions, metabolomic modulation, and neuroendocrine signaling. Finally, emerging directions of intervention aimed at adjusting the microbial profile, such as dietary adjustment, the use of probiotics, prebiotics, symbiotics, and fecal microbiota transplantation, are presented with the aim of positively influencing neurodevelopment and preventing or ameliorating associated dysfunctions. This review emphasizes the need for longitudinal, rigorous, and controlled clinical trials to validate the efficacy of microbiota modulation strategies and to substantiate their integration into individualized pediatric management protocols. Full article

Background/Objectives: Evidence-based nutritional recommendations for obesity management require understanding of sex-specific and age-specific body composition patterns and their associations with metabolic biomarkers, habitual dietary intake and chronic low-grade inflammation. This study aimed to characterize body composition phenotypes in a large clinical cohort of adults with obesity, to evaluate associated metabolic and inflammatory biomarker patterns, to contextualise these patterns against habitual nutrient intake assessed in a dietary subcohort, and to derive age- and sex-specific nutritional recommendations based on the identified patterns. Methods: We performed a cross-sectional analysis of 29,544 adults with obesity (BMI ≥ 30; 21,374 women, 8170 men; age 30–69) who underwent multi-frequency bioelectrical impedance analysis (BIA; InBody 770). Biochemical assessments (fasting glucose, lipid profile, uric acid, HbA1c, insulin) were available for 2019 hospitalized patients from the same population. Habitual dietary intake was quantitatively assessed in a dietary subcohort of 423 patients using the validated Russian software-based questionnaire “Scientific Nutrition Analysis Tool”. Inflammatory biomarkers (high-sensitivity CRP, IL-6) and adipokines (leptin, adiponectin) together with serum 25(OH)D were measured in an inflammation/adipokine subcohort of 116 patients. A body composition phenotype with low relative muscle mass and high visceral fat (VFA ≥ 100 cm²) was defined using FNIH criteria (ALM/BMI < 0.789 men, <0.512 women). Benjamini–Hochberg FDR correction (q < 0.05) was applied for multiple comparisons. Results: The body composition phenotype prevalence increased progressively with age: men 24.6% (30–39) to 42.0% (60–69); women 10.3% (30–39) to 31.8% (60–69). Skeletal muscle mass (SMM) was positively associated with uric acid (r = +0.347, p < 0.001, FDR q < 0.05) and inversely associated with HDL-cholesterol (r = −0.321, p < 0.001, FDR q < 0.05)—both associations with direct nutritional implications. BMI was associated with fasting insulin (r = +0.233, p < 0.001, FDR q < 0.05). Women showed significant age-related metabolic differences between the 30–39 and 60–69 age groups: fasting glucose +12.9%, triglycerides +34.8%, uric acid +15.0% (all p < 0.001); in men, significant differences were observed for fasting glucose (+7.0%) and HbA1c (+5.2%) (both p < 0.001), while lipid parameters did not reach significance. In the dietary subcohort, habitual saturated-fat intake exceeded recommended values in 70–72% of patients of both sexes, dietary fibre intake was below recommended levels in 73–85%, and habitual calcium intake decreased significantly with age in women (1022 → 746 mg/day, p = 0.028). Serum CRP was elevated (median 5.59 mg/L, n = 59). In a separate extended laboratory subcohort, serum oestradiol declined markedly with age in women (55.0 → 16.8 pmol/L between 30–39 and 50–59 years, p < 0.001), consistent with the menopausal transition; serum testosterone in men remained stable across age groups; and 25(OH)D insufficiency (<30 ng/mL) was prevalent in 49.7–55.8% of patients. Conclusions: The identified sex-specific and age-specific body composition patterns provide a rationale, supported by observed dietary and inflammatory patterns, for targeted nutritional intervention: increased dietary protein, omega-3 fatty acids supplementation, low-glycemic-index dietary patterns, and purine restriction with hyperuricemia. Routine BIA-based nutritional screening combined with quantitative dietary assessment should begin at age 30, with preventive monitoring at age 40 and intensification of control at age 50, to guide personalized dietary planning in obesity. Full article

The brain has a higher energy demand per unit weight than any other organ in the body; however, links between metabolism, diet and neurological function have historically been underexplored. This partly stems from early assumptions that brain metabolism is primarily dependent on glucose and ketone bodies, whereas more recent evidence indicates broader metabolic flexibility and complex cell-type specialisation. In the past few decades, brain metabolism has become increasingly recognised as relevant to neurological and mental health, and many neurodegenerative disorders are accompanied by changes in brain energy utilisation. In parallel, epidemiological studies associate hypercaloric dietary patterns and metabolic disorders—particularly type-2 diabetes mellitus—with increased risk of later cognitive decline and sporadic Alzheimer’s disease, although causal pathways remain difficult to establish in humans. In this narrative review, we summarise selected findings linking “unhealthy” diets to synaptic function, focusing on synaptic plasticity, neuroinflammation and adult hippocampal neurogenesis, and we distinguish between evidence from human observational studies and mechanistic insights from animal and cellular models. We also discuss candidate mechanisms—including insulin resistance-linked signalling changes, lipid-driven inflammatory amplification, oxidative stress, and altered lipid handling—that may contribute to synaptic vulnerability. Finally, we outline translational considerations and key knowledge gaps (including physiological exposure levels and heterogeneity of experimental paradigms) that currently limit inference from preclinical models to clinical intervention. Full article

Background/Objectives: Psoriasis and Hashimoto’s thyroiditis are chronic immune-mediated disorders affecting distinct target organs but sharing overlapping pathogenic mechanisms, including gut dysbiosis, impaired intestinal barrier function, and systemic immune dysregulation. Growing evidence highlights the gut–skin and gut–thyroid axes as important interfaces linking microbial alterations to immune-mediated inflammation. This review aims to synthesize current knowledge on gut microbiota alterations in psoriasis and Hashimoto’s thyroiditis, with particular emphasis on intestinal permeability, immune pathways, and microbiome-derived metabolites. Methods: A narrative review of experimental and human observational studies was conducted to evaluate evidence on gut microbiota composition, intestinal barrier integrity, immune regulation, bile acid metabolism, and dietary influences in psoriasis and Hashimoto’s thyroiditis. The relevant literature examining mechanistic pathways and clinical associations was included. Results: Both conditions are associated with altered gut microbial composition, including reduced abundance of short-chain fatty acid–producing taxa, which may impair epithelial barrier integrity and promote systemic immune activation. Increased intestinal permeability and enhanced Th17-driven inflammatory responses are reported in both diseases. Recent studies suggest that dysregulated bile acid metabolism may influence intestinal permeability and immune balance along the gut–skin–thyroid axis, although direct clinical data remain limited. Dietary patterns, particularly anti-inflammatory and Mediterranean diets, are consistently associated with increased microbial diversity, improved metabolic profiles, and reduced systemic inflammation. However, most human evidence is observational. Conclusions: The gut microbiome represents a potential mechanistic link connecting diet, intestinal barrier function, immune regulation, and organ-specific autoimmunity in psoriasis and Hashimoto’s thyroiditis. While microbiome-targeted interventions show biological plausibility, well-designed, mechanistically informed randomized controlled trials are required to establish causality and clinical relevance. Full article

Introduction: Many studies suggest that dietary factors may significantly influence the development and severity of acne lesions. Objective: The aim of this study was to evaluate the effect of an anti-inflammatory diet on acne severity in patients with acne vulgaris. Methods: This study included 92 participants who followed an individualized dietary intervention tailored to their energy requirements. Acne severity was assessed at baseline and after four weeks of dietary intervention using the Investigator’s Static Global Assessment scale. Results: After four weeks, a reduction in acne severity was observed in 68 of 92 participants (73.91%). The mean acne severity score decreased from 3.3 ± 0.6 to 2.4 ± 0.7 points. The dietary intervention also resulted in statistically significant reductions in body weight (p < 0.0001), body mass index (p < 0.0001), fat mass (p < 0.0001), visceral fat (p = 0.0386), and metabolic age (p = 0.0004). Conclusions: The balanced diet characterized by a low glycemic index and anti-inflammatory properties, combined with reduced intake of saturated fatty acids, sugar, and salt, as well as the elimination of dairy products and highly processed and high glycemic index foods, presumably through the synergistic effect of all the components of the diet, was found to be effective in the reduction of acne severity in the study group. This study supports the feasibility of the applied dietary pattern and suggests possible benefit for patients with acne. Considering the promising results obtained in this study, further research conducted in larger patient populations would be valuable. Full article

Micronutrient status is strongly influenced by dietary patterns; however, the extent to which plant-forward dietary patterns versus omnivorous diets shape micronutrient profiles and their associations with blood pressure, body composition, and cardiovascular health remains unclear. This cross-sectional study aimed to comprehensively assess associations between blood micronutrient profiles, blood pressure, and body composition in adults, with analyses stratified by dietary patterns to compare omnivorous and plant-forward dieters. Secondary cross-sectional analyses were conducted using data from an exploratory study of 488 Austrian adults (median age: 38 y [IQR 21]; 48% female, 52% male). Participants were classified as omnivores (n = 260) or plant-forward dieters (including 194 flexitarians, 25 vegetarians, and 9 vegans; n = 228). Blood pressure and anthropometric measurements were obtained alongside fasting venous blood sample analysis to quantify a comprehensive panel of micronutrient, hematological, lipid, and inflammatory biomarkers. Micronutrient concentrations were standardized (scaled −1 to +1, truncated ±3) and evaluated for deficiency or excess according to sex-specific reference ranges. Linear regression was used to analyze the association of micronutrients with BMI, including age and sex as covariates. Vitamin D showed the highest micronutrient deficiency, observed in 96% of omnivores and 93% of plant-forward dieters. Across both dietary subgroups, multiple micronutrients, together with age and sex, were significant correlates of body weight, body mass index, and blood pressure (p < 0.05). Significant differences between omnivores and plant-forward dieters were observed for blood pressure, lipid, hematological, and inflammatory markers, with participants adhering to plant-forward dietary habits exhibiting lower blood pressure and more favorable lipid profiles (p < 0.05). The findings highlight the potential of diet-type-specific strategies for personalized cardiometabolic risk management. Full article

Background/Objectives: Diet and mental health constitute two significant modifiable factors affecting Inflammatory Bowel Disease (IBD). The present exploratory study explores potential interrelationships between mental health and eating patterns in IBD patients in Greece. Methods: A mixed-methods approach was followed. Two hundred and eighty-three individuals living with IBD in Greece (n = 110 UC, n = 173 CD) participated in an online questionnaire survey examining demographic characteristics, anxiety, depression, and dietary attitudes. Fourteen semi-structured interviews explored the lived experiences of diet, mental health, and disease among IBD patients. Results: Quantitative study revealed that 45.77% of patients scored above the clinical cutoff for anxiety (GAD-7 ≥ 10) and 48.37% for depression (PHQ-9 ≥ 10). Patients with UC exhibited a significantly higher prevalence of moderate to severe anxiety (54.5% vs. 37.0%, p = 0.004) and depression (54.5% vs. 42.2%, p = 0.042) compared to CD. Disordered eating attitudes were present in 27.22% of the total sample, with no significant differences between diagnostic groups (p = 0.985). Thematic analysis revealed three overarching themes, namely (a) ‘life in two phases: IBD impact on health’, (b) ‘mental health and diet interplay—their perceived impact on IBD’ and (c) ‘coping strategies for managing IBD’. Conclusions: Our findings highlight the dynamic interplay among diet, mental health, and IBD experience. The study underscores the importance of developing holistic biopsychosocial interventions integrating medical, dietary, and psychological components for IBD management. Full article

Systemic inflammation is influenced by regular physical activity and diet. While moderate exercise can transiently alter inflammatory markers, high-intensity activity may increase muscle turnover without substantially elevating systemic inflammation. The combined effects of physical activity and dietary inflammatory potential in healthy young men remain poorly defined. In this cross-sectional observational study, 233 healthy men aged 18–30 years were categorized according to physical activity level: low (NA, n = 52), moderate (A, n = 93), and high (S, n = 88). Anthropometry and body composition were assessed using bioelectrical impedance. Dietary intake was recorded over 4 days and used to calculate the Dietary Inflammatory Index (DII). Blood samples were collected and analyzed for complete blood counts, high-sensitivity C-reactive protein (hs-CRP), serum amyloid A (SAA), and creatine kinase (CK). Differences between groups were evaluated using the Kruskal–Wallis test with Dunn’s post hoc correction, and principal component analysis (PCA) was performed to explore multivariate inflammatory patterns. The highest BMI, fat percentage, and DII were observed in low-activity men, whereas fat-free mass and CK activity were greatest in highly active men. Slightly higher systemic inflammatory markers (hs-CRP and SAA) were observed in moderately active men compared to other groups. PCA revealed two principal axes: PC1 representing systemic inflammation and PC2 representing leukocyte distribution. Weak associations were found between DII and these components, indicating a limited link between dietary inflammatory potential and circulating inflammatory biomarkers. Body composition is strongly influenced by physical activity, with high activity promoting lean mass and moderate activity associated with modest elevations in inflammatory markers. Dietary inflammatory potential was only weakly associated with systemic inflammation, suggesting that exercise-induced physiological stress may play a more prominent role in shaping inflammatory profiles in healthy young men. Full article

Background/Objectives: Diet is a primary and modifiable determinant of gut microbiota composition, diversity, and metabolic activity, thereby shaping microbial-derived metabolites, immune and inflammatory signalling, neuroendocrine regulation, and neural communication with the central nervous system. Western dietary patterns, characterised by high intake of ultra-processed foods, saturated fats, and low dietary fibre, are consistently associated with gut dysbiosis, impaired intestinal barrier function, chronic low-grade inflammation, and increased risk of depression, anxiety, cognitive impairment, and neurodegenerative disorders. Methods: This narrative review synthesises evidence from human observational studies, randomised controlled trials, animal models, and mechanistic investigations examining interactions among diet, gut microbiota, and mental health or neurobiological outcomes. Literature searches were conducted in PubMed, Scopus, and Web of Science for articles published up to December 2025. Results: The study highlights the therapeutic potential and limitations of dietary interventions, prebiotics, probiotics, and psychobiotics, and critically evaluates them. Also facilitates an improved understanding of diet–microbiome–brain interactions, which may help the development of personalised, nutrition-based strategies integrated into mental health prevention and clinical care. Conclusions: These findings support diet-based, microbiome-informed strategies as scalable adjuncts in mental health prevention and care. Full article