Search Results (4,945)

Background: Type 2 inflammatory diseases are among the most common chronic inflammatory conditions in childhood and represent a growing global health burden. Increasing evidence suggests that early-life nutritional exposures may influence immune programming and allergic disease development. This Position Paper aims to summarize the current evidence regarding the immunomodulatory role of polyunsaturated fatty acids (PUFAs), particularly omega-3 long-chain fatty acids, in the prevention of allergic diseases during early life. Methods: A scoping literature review and consensus process were conducted to map biological mechanisms and clinical evidence linking omega-3 PUFAs with allergic disease prevention. This document analyzed experimental, observational, and randomized controlled studies evaluating maternal prenatal/lactational omega-3 exposure. The clinical evidence was qualitatively appraised using study-design-specific Joanna Briggs Institute (JBI) Critical Appraisal Tools. Particular attention was given to immune modulation, inflammatory pathways, epithelial barrier function, gut microbiota interactions, and the ferroptosis–immune–metabolic axis. Results: Omega-3 PUFAs, including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), exert immunomodulatory and anti-inflammatory effects through multiple mechanisms, including specialized pro-resolving mediator production, regulation of T-helper cell responses, cytokine modulation, maintenance of epithelial barrier integrity, and microbiota interaction. Emerging evidence also supports their involvement in oxidative stress and ferroptosis regulation. Current clinical evidence, particularly from higher-quality prenatal randomized trials and evidence syntheses, suggests that adequate maternal omega-3 intake during pregnancy and lactation may reduce the risk of respiratory allergic outcomes, especially wheezing and asthma, in selected offspring. Conclusions: Adequate omega-3 PUFA intake, such as 2 g/die, during critical windows of immune maturation may represent a valuable strategy for the primary prevention of allergic diseases. Current evidence most strongly supports supplementation during pregnancy and lactation, particularly in populations with low dietary omega-3 intake or increased allergic risk. Omega-3 supplementation should be considered within a broader multifactorial preventive approach aimed at promoting immune tolerance and reducing the future burden of allergic diseases. Full article

Background: Kidney disorders are strongly related to metabolic disturbances, including obesity and type 2 diabetes. Excessive intake of sugar and saturated fats promotes lipid accumulation, cellular energy issues and inflammatory responses. Cannabigerol (CBG), a non-psychotropic phytocannabinoid, has recently gained attention for its metabolic, anti-inflammatory and potential protective properties. Methods: The present study investigated the effect of two weeks of CBG administration (last 14 days of the experiment) on fatty acid (FA) composition, FA metabolic pathways and FA transporters in rats subjected to a high-fat high-sucrose diet (HFHS) for 6 weeks. Male Wistar rats were divided into four groups: Control, CBG, HFHS, and HFHS+CBG. Kidney tissue and urine samples were analyzed by gas–liquid chromatography (GLC) for lipid fractions and FA profiles, while protein expression of FA transporters and metabolic enzymes was assessed by immunoblotting. Polysaccharides and collagen fibers were visualized using Periodic Acid-Schiff (PAS) and AZAN staining, respectively. ELISA and colorimetric kits were used to measure urinary albumin and creatinine contents. Results: HFHS feeding altered renal lipid homeostasis, increasing saturated and monounsaturated fatty acids (SFA and MUFA, respectively) levels and affecting desaturation and elongation ratios. CBG supplementation affected renal lipid metabolism by lowering triacylglycerol (TAG) accumulation, restoring polyunsaturated fatty acids (PUFA) in phospholipid (PL) and altering FA ratios, suggesting an improvement in lipid balance. CBG also increased the expression of carnitine palmitoyltransferase 1 (CPT1) and lipoprotein lipase (LPL) and decreased the expression of stearoyl-CoA desaturase 1 (SCD1) and fatty acid synthase (FAS), suggesting a shift toward enhanced FA oxidation and reduced lipogenesis. Conclusions: Overall, CBG exerted good effects on renal lipid metabolism and may mitigate early lipid-mediated injury associated with metabolic kidney disorders. Full article

Fluoride remains the keystone of evidence-based caries prevention by stabilizing the mineral balance at the tooth–biofilm–saliva interface. Contemporary understanding emphasizes a predominantly post-eruptive, topical mode of action where fluoride inhibits demineralization and accelerates remineralization. This interfacial catalysis is reinforced by pH-responsive calcium-fluoride-like reservoirs that release fluoride during acid challenges. While community water fluoridation confers population-level reductions, the most effective approach is sustaining low-level fluoride in the biofilm environment. Evidence confirms that toothpastes with 1000–1500 ppm fluoride provide a dose–response benefit in children, while 5000 ppm concentrations are indicated for high-risk scenarios such as root caries and xerostomia. Beyond physicochemical effects, fluoride modulates the oral microbiome by inhibiting bacterial enzymes and proton pumps, shifting community function toward a health-associated state without reducing overall diversity. In restorative dentistry, glass ionomer cements offer superior preventive effects against secondary caries compared to amalgam; however, marginal integrity, adhesive performance, and clinical technique, rather than fluoride release alone, remain the primary determinants of success. Despite well-known risks associated with high systemic intake, such as fluorosis, current evidence does not indicate genotoxic or adverse microbiome effects in humans from routine topical use of standard fluoride products at recommended preventive concentrations. Overall, fluoride’s cariostatic value rests on frequent, low-level exposures that maintain tissues in a repair-favoring state. Full article

Pollen constitutes the primary source of proteins, amino acids, lipids, sterols, vitamins, and minerals for honey bees. However, not all pollen types provide the same resources or have the same biological value. Its chemical composition changes according to botanical origin, geographic location, and environmental conditions. This variability can influence metabolism, the immune system, oxidative balance, and the ability to resist or tolerate infections. This article examines the available evidence on the relationship between pollen chemical quality and the dynamics of Deformed Wing Virus (DWV) infection in Apis mellifera. The analysis is approached from molecular, physiological, ecological, and seasonal perspectives. Current findings suggest that more diverse and higher-quality pollen diets are generally associated with greater colony survival and improved health status, although their effects on viral load are more heterogeneous and context-dependent. In some studies, pollen intake is linked to a reduction in DWV, whereas in others viral loads remain stable or even increase despite improvements in survival, physiological condition, or colony performance. These differences suggest that pollen may act not only by enhancing resistance to the virus but also by increasing tolerance to infection-associated damage. The potential role of pollen bioactive compounds, particularly flavonoids and phenolic acids, is also discussed. Nevertheless, evidence of direct antiviral action of these compounds in bees remains limited, as many proposed mechanisms derive from other organisms. This synthesis provides an integrative perspective on pollen nutrition and its relevance for colony resilience against viral infections. Full article

2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is a major heat-induced contaminant in protein-rich foods, yet its effects on intestinal barrier homeostasis and luminal microecology remain insufficiently defined. In this study, adult zebrafish were exposed to dietary PhIP for 90 days at estimated intake doses of 0.006, 0.4, and 7.2 mg/kg bw/day to evaluate intestinal injury, microbial dysbiosis, and metabolic remodeling. PhIP exposure impaired growth-related indices and induced progressive intestinal lesions, accompanied by mucus barrier depletion, reduced goblet cell abundance, and downregulation of muc2. Tight junction integrity was disrupted, as indicated by decreased zo-1, occludin, and claudin1 expression, weakened ZO-1 and Claudin-1 immunofluorescence signals, and reduced tight junction-related protein levels. Serum LPS and intestinal pro-inflammatory cytokines were markedly elevated, whereas il-10 expression was suppressed, indicating increased endotoxin burden and inflammatory activation. 16S rRNA gene sequencing revealed Proteobacteria-enriched dysbiosis and exposure-associated shifts in candidate genera, including Chitinilyticum, Shewanella, Aeromonas, Acinetobacter, Microbacterium, and Reyranella. Untargeted metabolomics further identified luminal metabolic remodeling involving lipid-related compounds, organic acids, amino acid metabolism, arachidonic acid metabolism, the citrate cycle, and pathways related to choline and glycerophospholipid metabolism. Association analysis linked genus-level microbial variation and core pathway-related metabolites with LPS, inflammatory cytokines, and tight junction markers. These findings indicate that dietary PhIP exposure disrupts intestinal barrier homeostasis in parallel with Proteobacteria-related dysbiosis and luminal metabolic remodeling, providing an integrated microbiota-metabolite-barrier association framework for evaluating intestinal risks of heat-induced food contaminants. Full article

Background/Objectives: Automated insulin delivery (AID) systems have improved the management of type 1 diabetes (T1D), but exercise and nutrition remain challenging because they rapidly alter glucose flux, substrate oxidation, hepatic glucose output, insulin requirements, and fuel availability. This narrative review aimed to synthesize current evidence on the interaction between AID systems, physical activity, and nutritional strategies from a metabolism-oriented perspective. Methods: A narrative bibliographic approach was used to integrate evidence from clinical trials, observational studies, technical studies, consensus statements, and reviews involving people with T1D across different life stages, including pediatric, adolescent, adult, and pregnancy-related contexts, when available. The review focused on AID systems, exercise physiology, nutritional strategies, meal announcement, bolus adjustment, dual-hormone systems, metabolic biomarkers, and emerging metabolomic approaches. Results: AID systems generally improve time in range and reduce hypoglycemia across several user groups, although most exercise- and nutrition-specific evidence comes from adult and pediatric/adolescent cohorts rather than pregnancy-specific exercise studies. Exercise-related glucose responses remain highly dependent on user input, exercise modality, insulin on board, meal timing, and metabolic state. Planned exercise announcement, prandial bolus reduction before postprandial activity, and individualized carbohydrate intake remain key strategies. Biomarkers such as lactate, ketone bodies, non-esterified fatty acids, and counter-regulatory hormones may help explain interindividual variability and support future personalization. Conclusions: Nutrition and exercise management in AID users should be interpreted as a dynamic metabolic interface among exogenous insulin, endogenous counter-regulation, substrate availability, and algorithmic control. Emerging approaches, including activity sensors, adaptive algorithms, dual-hormone systems, digital twins, and metabolomics-informed personalization, may improve safety and reduce user burden, but several remain exploratory and require further validation in diverse free-living conditions. Full article

Background/Objectives: Nutritional therapy has emerged as a promising therapeutic strategy for the management of chronic metabolic diseases. This study aims to evaluate the efficacy of a low-purine, energy-restricted, and balanced diet (LPEB diet) in ameliorating gout conditions and improving related metabolic risk factors. Methods: A total of 90 patients with gout were randomly allocated to either the intervention group or the control group, with 45 cases in each group. Patients in the control group received routine basic nutritional health education. Based on the conventional education, the intervention group underwent a 42-day structured dietary intervention characterized by low purine intake, energy restriction, and balanced nutritional composition. Results: Compared with the control group, the intervention group showed a significant reduction in serum uric acid (sUA) level by 112.4 μmol/L (p = 0.007). Meanwhile, the fractional excretion of uric acid (FEUA) showed a significantly greater increase of 0.87% in the intervention group compared with the control group (p = 0.003), while daily purine intake was significantly reduced by 262 mg (p = 0.001) in the intervention group. Moreover, notable improvements in body composition were observed in the intervention group. Specifically, body mass index (BMI) decreased by 0.50 kg/m² (p < 0.001) and visceral fat area (VFA) was reduced by 12.1 cm² (p < 0.001), with significant intergroup differences confirmed for both indicators. Conclusions: This study demonstrates that an LPEB diet not only effectively reduces sUA levels by enhancing FEUA but also significantly ameliorates central adiposity and related metabolic risk factors in patients with gout. Full article

Peripheral blood metabolite concentrations vary with food intake and time of day, risking confounding effects in metabolomics studies with non-standardised sampling conditions or incomplete metadata. Such effects are often overlooked during study design, limiting the clinical translation of biomarkers and wasting resources for researchers, funders and clinicians. In our random sample of 100 human metabolomics studies, 56% did not control for food intake, and 59% did not explicitly control for sampling time. To provide a study design resource, we analysed a liquid-chromatography–mass-spectrometry-targeted dataset from controlled laboratory studies of 24 young, healthy participants (12 male, 12 female) sampled every 2 h for 34 h, with fixed-macronutrient meals provided at set times. Acute postprandial responses were quantified by effect size using pre- and post-meal windows, while daily rhythmicity was assessed using a mixed-effects cosinor model. Analyses were sex-stratified, and metabolites were classified as meal-responsive, time-of-day-responsive, both, or neither. Amino acids and their derivatives showed strong postprandial increases, whereas lipid classes showed minimal changes. Rhythmicity varied across metabolites, enabling the identification of features sensitive to meal timing and/or time of day. These results aim to provide a comprehensive dictionary of metabolite effect sizes for study design and metadata collection to support reproducibility and the clinical translation of potential biomarkers. Full article

Over the last years, incretin receptor agonists—including glucagon-like peptide-1 (GLP-1) receptor agonists (GLP-1 RA) and the dual glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 receptor agonist tirzepatide—have dramatically improved the management of type 2 diabetes, overweight and obesity. However, as the use of incretin receptor agonists continues to increase worldwide, micronutrient deficiencies—including iron deficiency—have emerged as newly recognized adverse effects of these drugs. The present article aims to discuss recent preliminary observational evidence on the potential relationship between incretin receptor agonist-based therapies and the development of iron deficiency and iron deficiency anemia (IDA), as well as the potential mechanisms by which incretin receptor agonists may affect iron homeostasis. Potential mechanisms and factors underlying the development of iron deficiency and IDA in patients treated with incretin receptor agonist-based therapies include inadequate dietary iron intake (due to incretin receptor agonist-mediated reduction in food intake and/or gastrointestinal adverse effects of incretin receptor agonists), low dietary variety, monotonous diets, and changes in food preferences, as well as impairment of intestinal iron absorption (due to delayed gastric emptying, reduced small intestinal motility and/or decreased gastric acid secretion caused by incretin receptor agonists). Moreover, vitamin B2 (riboflavin) deficiency and changes in gut microbiota composition are hypothetical mechanisms that may partly explain iron deficiency in patients treated with incretin receptor agonists, although these hypotheses require confirmation through mechanistic studies. Even though iron deficiency and IDA currently appear to be uncommon adverse effects of incretin receptor agonist-based therapies, clinicians should be aware of the possibility of their occurrence to ensure appropriate prevention and management of these nutritional complications. Nevertheless, future prospective studies are certainly needed to better establish the causal relationship between the initiation of incretin receptor agonist-based therapies and the development of iron deficiency/IDA, as well as the exact mechanisms underlying the potential development of these nutritional complications in patients treated with incretin receptor agonists. Meanwhile, the prescription of incretin receptor agonists should not be unjustifiably restricted by the possible and modest risk of iron deficiency and IDA in patients with one or more approved indications for therapeutic use of these agents. Since no established guidelines currently exist for the prevention and management of iron deficiency and IDA in patients treated with incretin receptor agonists, we herein propose practical strategies to address these possible nutritional complications of incretin receptor agonist-based therapies. These proposed strategies should only be regarded as practical clinical approaches deriving from the existing recommendations for the prevention and management of iron deficiency and IDA, although their cost-effectiveness for the prevention and management of incretin receptor agonist-associated iron deficiency/IDA should be appropriately assessed in future clinical trials. Full article

This study evaluated the effects of dietary inclusion of free and protected acid protease on productive performance, milk composition, metabolic profile, nutrient digestibility, and ruminal environment in lactating Jersey cows. Fifteen multiparous cows (67 ± 7.5 days in milk; 27.5 ± 3.5 kg/day) were assigned to a 3 × 3 Latin square (5 squares) design with 21-day periods. Treatments consisted of: control (no enzyme), free protease (4.4 g/day), and protected protease (4.4 g/day). The protected form was developed using alginate-based encapsulation to enhance enzyme stability under ruminal conditions. Protease inclusion did not affect dry matter intake, milk yield, or feed efficiency (p > 0.05). However, free protease increased lactation persistency (p = 0.05) and improved fat-corrected and energy-corrected milk yields (p ≤ 0.02), with intermediate responses observed for protected protease. Milk fat and protein contents were higher in enzyme-fed cows (p ≤ 0.05), while other compositional parameters remained unchanged. Apparent crude protein digestibility was greater in cows receiving free protease (p = 0.037), with no effects on dry matter or fiber digestibility. Protease intake increased total volatile fatty acid concentrations and major fermentation products (acetate, propionate, and butyrate; p ≤ 0.01), indicating enhanced ruminal fermentation. Blood metabolites showed increased total protein and globulin levels in cows fed free protease (p ≤ 0.05), suggesting improved protein metabolism. Microbiota analysis revealed no differences in alpha or beta diversity; however, specific microbial taxa and predicted metabolic pathways were modulated by treatments, particularly in post-ruminal compartments. In conclusion, exogenous protease, especially in free form, improved protein utilization and corrected milk production without disrupting microbial stability. These findings highlight the potential of protease as a nutritional strategy to enhance efficiency in dairy systems through targeted modulation of ruminal function and nutrient metabolism. Full article

White adipose tissue (WAT) is essential for maintaining energy homeostasis during hibernation by supplying lipolysis-derived fatty acids as a major fuel source. In raccoon dogs (Nyctereutes procyonoides), the activity of brown adipose tissue is diminished, providing a unique model to investigate how WAT supports metabolic homeostasis in a largely non-thermogenic state. Here, we integrated physiological, histological, transcriptomic, and molecular analyses of back-fat and tail-fat depots during autumn fattening and winter sleep. Despite reduced food intake, body weight loss, and mild hypothermia, raccoon dogs maintained systemic glucose and lipid homeostasis. Both WAT depots exhibited adipocyte atrophy and the coordinated suppression of core metabolic and biosynthetic pathways, indicating a shared program of metabolic depression. However, the two depots adopted distinct remodeling strategies. Back-fat showed collagen densification and vascular-associated remodeling, suggesting a structural adaptation that may preserve tissue integrity during winter sleep. In contrast, tail-fat displayed enhanced innate immune signaling and M2 macrophage enrichment, indicating immune niche remodeling that may support tissue protection during prolonged lipid mobilization. Together, these findings reveal that raccoon dogs maintain metabolic homeostasis during shallow hibernation through a non-thermogenic, WAT-centered strategy characterized by shared metabolic depression and depot-specific structural and immunometabolic remodeling. Full article

This study evaluated the effects of monolaurin intake per finishing feedlot cattle on growth performance, metabolic status, ruminal environment, and meat fatty acid profile. Twenty-four castrated Holstein males (379 ± 8.5 kg; 12 months old) were randomly assigned to two treatments: basal diet (control) or basal diet with α-monolaurin (treated: 0.762 g/kg dry matter intake; ≈6.63 g/animal/day) for 79 days. Feed intake, body weight, and feed efficiency were recorded, and blood and ruminal samples were collected during the trial. Ruminal fermentation parameters, protozoa counts, hematological and biochemical variables, oxidative status biomarkers, ruminal microbiota composition (16S rRNA sequencing), and Longissimus dorsi fatty acid profile were analyzed. Monolaurin feed did not affect dry matter intake or final body weight, but increased total weight gain, average daily gain, and feed efficiency (p ≤ 0.05), indicating improved nutrient utilization. Hematological and serum biochemical variables were largely unchanged, although total leukocyte counts were lower in treated cattle. Animals receiving monolaurin showed reduced reactive oxygen species and lower superoxide dismutase activity, suggesting improved oxidative balance without changes in lipid peroxidation. During the adaptation phase (day 14), treated cattle exhibited lower acetate, propionate, valerate, and total volatile fatty acid concentrations and higher protozoa counts, but these differences disappeared by day 79, indicating ruminal adaptation. Microbiota diversity was not altered overall, although specific genera differed in relative abundance between treatments. In meat, monolaurin increased lauric, linoleic, and arachidonic acids, reduced palmitic and heptadecanoic acids, decreased total saturated fatty acids, and increased polyunsaturated fatty acids (p ≤ 0.05). Overall, dietary monolaurin improved feed efficiency, modulated oxidative status, induced transient ruminal microbial adjustments, and enhanced the nutritional quality of beef lipids without compromising metabolic health. Full article

Background: L-tyrosine, classified as a dispensable amino acid, is widely consumed as a component of commonly consumed foods and as a dietary supplement. However, 4-week safety data on supplementation with this amino acid remain limited. Methods: The aim of this study was to evaluate the safety and tolerability of L-tyrosine supplementation over a 4-week period and to estimate the no-observed-adverse-effect level (NOAEL). In a randomized, double-blind, placebo-controlled crossover trial, 30 healthy adult men received L-tyrosine at graded daily doses (0, 1, 2, 3, or 4 g/day). Each participant received four of the five doses in a randomized sequence, with each intervention period separated by a 2-week washout period. The primary endpoints were clinical laboratory parameters, and the secondary endpoint was the incidence of adverse events. Anthropometric and dietary parameters were also assessed. In addition, plasma amino acid concentrations following L-tyrosine supplementation were evaluated as exploratory outcomes. Results: No clinically meaningful or statistically significant dose-related abnormalities were observed in hematological, biochemical, or electrolyte parameters at any dose. Anthropometric and dietary parameters remained unchanged. No serious adverse events occurred, and the incidence of mild-to-moderate adverse events was comparable to that observed with placebo. At the end of each supplementation period and under fasting conditions, plasma L-tyrosine concentrations modestly increased at the highest dose (4 g/day), whereas concentrations of other amino acids remained unchanged. Conclusions: Four-week supplementation with L-tyrosine at doses up to 4 g/day was well tolerated in healthy adult men and was not associated with biochemical and clinically relevant adverse effects under the conditions of this study. These findings suggest that 4 g/day represents the highest tested intake level without observable adverse effects and may serve as the NOAEL under the present 4-week study conditions. Full article

Background/Objectives: Red beetroot (Beta vulgaris L.) is recognized for its antioxidant, anti-inflammatory, and metabolic properties. This study evaluated the effects of two beetroot cultivars (Boldor and Wodan) on blood serum parameters, body composition, and organ weights in male WKY rats fed a low-protein diet (LPD, 8.8% protein). Methods: Five-week-old male rats were maintained on an LPD for 8 weeks and subsequently continued on the LPD diet supplemented with 4% dried beetroot for 45 days. The experimental diets included beetroot from the Boldor and Wodan cultivars, either treated or untreated with a plant growth stimulator during cultivation. Results: Foliar application of the selenium-based plant growth stimulator did not significantly increase selenium or other element concentrations in beet roots. Elemental analysis showed higher levels of Fe, Zn, Cu, Cr, Pb, As, Cd, and Sb in the Wodan group, while Boldor increased Cr, Pb, and As; Ni and Se remained unchanged. Beetroot supplementation significantly affected 14 of the 30 measured biochemical parameters, including biomarkers of liver function (ALT, ALP, total bilirubin, albumin, and total protein), renal function (uric acid), pancreatic activity (amylase and lipase), electrolyte balance (sodium, potassium, and chloride), mineral metabolism (calcium), inflammatory status (CRP), and nutritional metabolism (iron). Conversely, no significant effects were observed on lipid profile parameters or biomarkers of cardiac and skeletal muscle injury. Among the beetroot cultivars evaluated, Wodan exerted distinct effects relative to Boldor, resulting in higher circulating total bilirubin and potassium concentrations, alongside reduced uric acid and lipase levels in treated rats. Boldor supplementation significantly increased body weight gain and fat mass, with a trend toward higher lean mass, and increased kidney weight. Wodan did not significantly affect body weight but increased kidney and spleen mass. Feed intake was similar across groups. No changes in cardiovascular function were observed ex vivo. Conclusions: Beetroot supplementation modulated multiple metabolic and physiological biomarkers in rats fed a low-protein diet, with distinct cultivar-specific effects, underscoring the importance of cultivar selection for optimizing functional dietary interventions. Full article

Background: Chlorella, a unicellular green alga, is currently one of the most popular algae supplements due to its high content of bioactive compounds. Chlorella’s wide range of macro- and micronutrients, including chlorophyll compounds and carotenoids, has been suggested to influence various disorders related to the digestive and nervous systems. This review’s primary purpose was to critically analyze the effects of Chlorella intake on gut microbiota and brain function. Methods: The authors conducted a systematic review with narrative synthesis of peer-reviewed articles written in English and published in PubMed, Web of Science, and Scopus spanning the years 2009 to 2026 (PROSPERO registration number CRD42024527705). The search protocol was performed following PRISMA guidelines. Primary outcomes encompassed physiological variables, such as gut microbial composition, short-chain fatty acids, brain-derived neurotrophic factor, and hippocampal cell density. Secondary outcomes were assessed through neurobehavioral tests and psychological questionnaires. Results: Out of the 1333 articles identified, 47 studies were deemed eligible, and 21 met the predefined criteria, subsequently incorporated into this systematic review. In total, 10 articles documented interventions involving Chlorella and their effects on the gut microbiota, whereas 11 articles investigated several variables pertinent to brain function. Most of the studies included were conducted in animal models, with only a limited number of human trials. Nineteen studies (90%), predominantly preclinical, reported positive associations between Chlorella consumption, gut microbiota modulation, and physiological or neurobehavioral markers related to the gut–brain axis. Conclusions: Chlorella consumption may modulate gut microbiota composition and function, potentially influencing brain-related processes. However, the available literature lacks studies simultaneously addressing both gut microbiota and brain health parameters limiting the understanding of the underlying physiological mechanisms. Full article