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The Microbiota-Gut-Brain Connection: A New Horizon in Neurological and Neuropsychiatric Disorders.
INTRODUCTION: The microbiota-gut-brain axis (MGBA), a complex two-way connection between the gut microbiota and the brain, has become a key regulator of neurological and neuropsychiatric disorders. Neurological disorders and gut microbiota dysbiosis are linked to these diseases. Changes in gut microbiota can lead to neurotransmitter imbalances, oxidative stress, and neuroinflammation. Gut dysbiosis may contribute to the development of diseases such as depression, autism, schizophrenia, bipolar disorder, Parkinson's disease, Alzheimer's disease, dementia, multiple sclerosis, epilepsy, anxiety, and autism spectrum disorders through immunological regulation, neuroinflammation, and neurotransmitter metabolism changes. METHOD: This review systematically sourced articles related to microbiota gut brain axis, neurological disorders, neuropsychiatric disorders and clinical studies from major medical databases, including Scopus, PubMed, and Web of Science. RESULTS: This review explores the molecular processes underlying MGBA interactions, including vagus nerve signaling, systemic immunological responses, and metabolites produced by microorganisms. The discussion explores the potential of microbiome-targeted treatments like fecal microbiota transplantation, probiotics, and prebiotics as effective treatment methods. The comprehension of the MGBA can revolutionize neurology and psychiatry, introducing innovative diagnostic and therapeutic approaches. Multiple elements, including diet, metabolism, age, stress, and medications, shape the human gut microbiota, and intestinal imbalances can lead to CNS diseases. The MGBA interacts with gut bacteria, and gut dysbiosis is associated with neurological disorders. CONCLUSIONS: The review demonstrates the correlation between gut microbiota and neurologically associated diseases, highlighting its importance in neurogenesis, mental development, emotions, and behaviors. MGBA, mediated by microbial metabolites, affects brain function and neuroinflammation. Interventions like fetal microbiota transplantation, probiotics, and prebiotics can improve microbial balance, but more clinical research is needed.
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A Comprehensive Review of Nutritional Influences on the Serotonergic System.
Serotonin (5-hydroxytryptamine) is a critical monoamine neurotransmitter and hormone that orchestrates a vast array of physiological and psychological processes, including mood, sleep, appetite, and gastrointestinal motility. Serotonin synthesis is dependent on the availability of its dietary precursor, the essential amino acid tryptophan, and it affects biochemical pathways that may be modulated by other nutrients. We conducted a literature search to comprehensively examine the nutritional influences on the serotonergic system. Relevant original research, systematic reviews, meta-analyses, and clinical trial reports were retrieved from PubMed, Scopus, and Google Scholar, with additional articles identified from reference lists of published review papers. Key nutritional determinants of serotonergic function include macronutrients that influence the tryptophan-to-large neutral amino acid ratio (a regulator of tryptophan availability in the brain) and micronutrients, such as B-vitamins, vitamin D, iron, and magnesium, that serve as essential cofactors in serotonin synthesis and metabolism. Emerging evidence also highlights the role of the gut microbiota, shaped by dietary components, prebiotics, and probiotics, in modulating serotonergic function across both central and peripheral systems. Nutritional factors that affect serotonin have been increasingly linked to conditions such as depression, anxiety, sleep disturbances, disordered eating, obesity, and irritable bowel syndrome. Altogether, this review emphasizes the profound impact of nutrition on serotonergic regulation and advocates for targeted dietary approaches as promising catalysts for optimizing human health. Key research gaps and future directions are outlined to help advance the translation of current evidence into precise nutritional guidelines and clinical applications, with the complexity of serotonin pathways as an important consideration.
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Psychobiotics: Mechanisms of Action, Evaluation Methods and Effectiveness in Applications with Food Products.
The gut-brain-microbiota axis consists of a bilateral communication system that enables gut microbes to interact with the brain, and the latter with the gut. Gut bacteria influence behavior, and both depression and anxiety symptoms are directly associated with alterations in the microbiota. Psychobiotics are defined as probiotics that confer mental health benefits to the host when ingested in a particular quantity through interaction with commensal gut bacteria. The action mechanisms by which bacteria exert their psychobiotic potential has not been completely elucidated. However, it has been found that these bacteria provide their benefits mostly through the hypothalamic-pituitary-adrenal (HPA) axis, the immune response and inflammation, and through the production of neurohormones and neurotransmitters. This review aims to explore the different approaches to evaluate the psychobiotic potential of several bacterial strains and fermented products. The reviewed literature suggests that the consumption of psychobiotics could be considered as a viable option to both look after and restore mental health, without undesired secondary effects, and presenting a lower risk of allergies and less dependence compared to psychotropic drugs.
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Association between maternal stress patterns and neonatal meconium microbiota: A prospective cohort study.
BACKGROUND: This study aimed to identify maternal stress patterns and investigate their associations with neonatal meconium microbiota. METHODS: A total of 465 pregnant women reported their stress conditions, including depression, anxiety, pregnancy-related anxiety, perceived stress, sleep, fear of birth, life events, and adverse childhood experiences. Meconium samples were collected from 348 newborns. Latent class analysis was used to identify the patterns of maternal stress. RESULTS: Three group profiles were identified: "high negative emotion," "high ACEs-low negative emotion," and "low stress." the high ACEs-low negative emotion group and low stress group had higher levels of Chao1 diversity than the high negative emotion group (B = 0.25, P < 0.001; B = 0.18, P < 0.001, respectively). The high ACEs-low negative emotion group had higher levels of Chao1 diversity than the low stress group (B = 0.08, P = 0.001). The variations were observed in the abundance of Bacteroidetes, unidentified_Muribaculaceae, unclassified_Lachnospiraceae, unclassified_Clostridiales, unidentified_Bacteroidales, Oscillospira, and Ruminococcus among different maternal stress patterns. LIMITATIONS: We did not analyze maternal microbiome samples and assessed the gut microbiota at only one time point. CONCLUSIONS: These findings emphasized the need for a comprehensive approach to prenatal care that extends beyond traditional medical interventions. Addressing maternal stress through targeted support and interventions may help newborns benefit from a more favorable gut microbiota landscape.
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Can intestinal microbiota and circulating microbial products contribute to pulmonary arterial hypertension?
Pulmonary arterial hypertension (PAH) is a fatal disease with a median survival of only 5-7 yr. PAH is characterized by remodeling of the pulmonary vasculature causing reduced pulmonary arterial compliance (PAC) and increased pulmonary vascular resistance (PVR), ultimately resulting in right ventricular failure and death. Better therapies for PAH will require a paradigm shift in our understanding of the early pathophysiology. PAC decreases before there is an increase in the PVR. Unfortunately, present treatment has little effect on PAC. The loss of compliance correlates with extracellular matrix remodeling and fibrosis in the pulmonary vessels, which have been linked to chronic perivascular inflammation and immune dysregulation. However, what initiates the perivascular inflammation and immune dysregulation in PAH is unclear. Alteration of the gut microbiota composition and function underlies the level of immunopathogenic involvement in several diseases, including atherosclerosis, obesity, diabetes mellitus, and depression, among others. In this review, we discuss evidence that raises the possibility of an etiologic role for changes in the gut and circulating microbiome in the initiation of perivascular inflammation in the early pathogenesis of PAH.
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Red meat consumption in higher healthy eating index diets is associated with brain health critical nutritional adequacy, and fecal microbial diversity.
We evaluated whether red meat consumption, within diets of both high and low healthy eating index (HEI) quality, was associated with differences in brain health-critical micronutrient adequacy, mental health, diet quality, or fecal microbiota composition. Using data from 3643 adults in the American gut project, participants were stratified into four groups: high-HEI (≥ 80) with red meat (HH-R), high-HEI without red meat (HH-NR), low-HEI (< 80) with red meat (LH-R), and low-HEI without red meat (LH-NR). HH-R had higher protein intake and lower carbohydrate intake than HH-NR, with saturated fat levels within recommended limits. Brain health-critical micronutrient adequacies (selenium, vitamin B12, zinc, calcium, vitamin D3, choline) were significantly higher in HH-R (p < 0.001) than HH-NR. Higher HEI scores, irrespective of red meat consumption, were associated with reduced odds of depression (logOR = -2.22), PTSD (logOR = -3.80), and bipolar disorder (logOR = -5.90). Fecal microbiota diversity and richness were highest in HH-R, with higher Bacteroides caccae (padj = 0.003) and Clostridium hathewayi (padj < 0.001), while HH-NR showed higher Bifidobacterium adolescentis and Bacteroides eggerthii (padj < 0.001). Therefore, these findings suggest that the inclusion of red meat in a high-HEI diet improves brain health-supporting micronutrient adequacy without adverse effects on mental health or microbial diversity.
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Effects of inulin-derived difructose anhydrides on DSS-induced colitis-associated behavioral alterations and gut microbiota-related responses in mice.
Ulcerative colitis (UC) has shown a significant upward trend in global incidence and is frequently accompanied by psychiatric comorbidities such as anxiety and depression, severely impairing patients' quality of life. This study investigated the effects of inulin-derived difructose anhydride I (DFA-I) and difructose anhydride III (DFA-III) on dextran sulfate sodium (DSS)-induced UC-associated anxiety- and depression-like behavioral alterations in mice. Through oral administration, behavioral assessments, histopathology, cytokine analysis, gut microbiota sequencing, and short-chain fatty acid (SCFA) measurement, we evaluated the potential associations between DFA intervention and gut microbiota-gut-brain axis-related responses. The results suggested that DFAs, particularly 3% DFA-III, alleviated DSS-induced colonic injury and behavioral abnormalities, reduced serum levels of CORT, IL-6, and TNF-α, modulated hippocampal BDNF/p75NTR-related gene expression, and increased butyrate levels together with alterations in gut microbial composition. These findings provide preliminary evidence suggesting that inulin-derived DFAs may serve as potential prebiotic candidates for alleviating DSS-induced colitis-associated inflammatory and behavioral alterations.
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Regulating environmental arsenic-mediated gut-brain toxicity using chitosan-conjugated luteolin gold nanoparticles.
Anxiety and depression are two major contributors to global disease burden. Amongst various causal factors, exposure to even low doses of environmental heavy metals, like arsenic, can induce anxiety and depression-like behaviour in mammals. Ingestion of arsenic, primarily through contaminated drinking water, severely disrupts the gut microbes, thereby inducing structural and functional abnormalities in the brain. Fecal microbiota transplantation (FMT) from arsenic-exposed mice to recipient healthy mice (As-FMT) enriched LPS-secreting Gram-negative bacteria and upregulated the expression of TLR4 in intestinal epithelial cells. Consequently, inflammation, oxidative stress and compromised barrier integrity in the gut facilitated LPS translocation into the bloodstream and promoted systemic inflammation. The secretomes eventually affected the brain by activating microglia, altering neurotransmitter levels and reducing the glucocorticoid receptor (GR) expression, contributing to appearance of pyknotic nuclei in dentate gyrus of hippocampus and emergence of anxiety- and depression-like behaviour. Luteolin, a flavonoid, devoid of any apparent side-effects, yet known for its anti-inflammatory and antioxidant properties, showed potential in alleviating the gut-brain toxic effects. However, its limited solubility and bioavailability pose challenges for its effectiveness, for which chitosan-conjugated luteolin gold nanoparticles (CH-LuAuNPs) were synthesized. Interestingly, where FMT from arsenic-treated mice to healthy mice showed deleterious effects in the transplanted mice, FMT from arsenic-treated mice co-administered with CH-LuAuNP attenuated As-FMT-mediated disruption of the gut-brain axis. This study highlighted the critical contribution of healthy gut microbiota in preserving neurobehavioural physiology, as well as underscored the potential therapeutic benefits of luteolin nanoparticles in ameliorating arsenic-induced gut dysbiosis and consequent mental disorders.
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Maternal milk fat globule membrane enriched gut L. murinus and circulating SCFAs to improve placental efficiency and fetal development in intrauterine growth restricted mice model.
Intrauterine growth restriction (IUGR) caused by placental dysfunctions leads to fetal growth defects. Maternal microbiome and its metabolites have been reported to promote placental development. Milk fat globule membrane (MFGM) is known for its diverse bioactive functions, while the effects of gestational MFGM supplementation on the maternal gut microbiota, placental efficiency, and fetal development remained unclear. In this study, low protein diet-induced IUGR decreased the litter birth weight, fetal birth weight, and the fetal/placental ratio in pregnant mice, while gestational MFGM supplementation restored these impairments. Meanwhile, MFGM supplementation during gestation enriched intestinal Lactobacillus murinus (L. murinus) and increased luminal and circulating short chain fatty acids (SCFAs) in IUGR pregnant mice, which improved placental efficiency and fetal development due to an enhanced antioxidant capacity and a decreased inflammation. In addition, fecal microbiota transplantation (FMT) with MFGM-derived microbiota reprinted the promoted phenotypes of maternal litter characteristics, gut L. murinus enrichment, placental efficiency, and fetal gut development in MFGM-fed pregnant mice, which were also recapitulated by exogenous administration with L. murinus or SCFAs cocktail. Mechanically, MFGM, MFGM-derived microbiota, L. murinus, or SCFAs cocktail activated IUGR-induced depressive phosphorylation of PI3K-Akt signaling in the placenta. Moreover, in vitro placental cells cultivation under amino acid shortage model (AAS) or oxygen-glucose shortage model (OGS) was used to validate that MFGM-derived key microbial and circulating SCFAs cocktails can alleviate placental oxidative stress and inflammation via activating PI3K/Akt signaling. Taken together, gestational MFGM supplementation enriched intestinal L. murinus and circulating SCFAs of IUGR pregnant mice, thereby improving placental efficiency, fetal growth, and intestinal functions of IUGR fetus. Our findings will provide theoretical support for the application of MFGM in the maternal-placental-fetal nutrition to address pregnancy malnutrition-induced IUGR.
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ILSI Europe perspective review: site-specific microbiota changes during pregnancy associated with biological consequences and clinical outcomes: opportunities for probiotic interventions.
Pregnancy induces notable alterations in the gut, vaginal, and oral microbiota driven by hormonal, immune, metabolic, dietary, and environmental factors. During pregnancy, the gut microbiota is characterized by increased proportions of the genus Bifidobacterium and the phyla Pseudomonadota (formerly Proteobacteria) and Actinomycetota (formerly Actinobacteria). These changes occur alongside reduced alpha diversity and greater beta diversity, changes that influence maternal metabolism and fetal development. Shifts in gut and oral microbiota have been associated with complications such as preterm birth (PTB), pre-eclampsia, and gestational diabetes (GDM), though patterns are sometimes inconsistent. The vaginal microbiota remains Lactobacillus-dominant during pregnancy, with reduced diversity leading to reduced risk of pathogenic infection and increased diversity has been linked with a higher risk of PTB. Hormonal changes also affect the oral microbiota, potentially increasing pathogenic species and contributing to adverse outcomes like PTB. Probiotic supplementation during pregnancy has significant potential to reduce adverse pregnancy outcomes; however, clinical studies are still limited. Probiotics may be effective in alleviating maternal constipation and lead to lower PTB risk, particularly by modulating the vaginal microbiota, but they have limited impact on GDM. In the context of maternal mental health, some studies suggest benefits of probiotics in reducing anxiety, but effects on depression are inconclusive. This perspective examines how pregnancy-related microbial shifts, both natural and probiotic-induced, affect maternal and fetal health and highlights potential opportunities for the innovative use of probiotics during the gestation period.