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Effects of dietary FODMAP content on the faecal microbiome and gastrointestinal physiology in healthy adults: a randomised, controlled cross-over feeding study.
The effect of dietary FODMAP (fermentable oligo-, di- and mono-saccharides and polyols) in healthy adults is poorly documented. This study compared the specific effects of low and moderate FODMAP intake (relative to typical intake) on the faecal microbiome, participant-reported outcomes and gastrointestinal physiology. In a single-blind cross-over study, twenty-five healthy participants were randomised to one of two provided diets, 'low' (LFD) <4 g/d or 'moderate' (MFD) 14-18 g/d, for 3 weeks each, with ≥ 2-week washout between. Endpoints were assessed in the last week of each diet. The faecal bacterial/archaeal and fungal communities were characterised by eighteen participants from whom high-quality DNA was extracted by 16S rRNA and internal transcribed spacer 2 (ITS2) profiling and metagenomic sequencing. There were no differences in gastrointestinal or behavioural symptoms (fatigue, depression, anxiety) or faecal characteristics and biochemistry (including SCFA). Mean colonic transit time (telemetry) was 23 (95 % CI: 15, 30) h with the MFD compared with 34 (24, 44) h with LFD (n 12; P = 0·009). Fungal diversity (richness) increased in response to MFD, but the bacterial richness was reduced, coincident with the expansion of the relative abundances of Bifidobacterium, Anaerostipes and Eubacterium. Metagenomic analysis showed expansion of polyol-utilising Bifidobacteria and Anaerostipes with MFD. In conclusion, short-term alterations of FODMAP intake are not associated with symptomatic, stool or behavioural manifestations in healthy adults, but remarkable shifts within the bacterial and mycobiome populations were observed. These findings emphasise the need to quantitatively assess all microbial domains and their interrelationships to improve understanding of the consequences of diet on gut function.
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The role of the indoles in microbiota-gut-brain axis and potential therapeutic targets: A focus on human neurological and neuropsychiatric diseases.
At present, a large number of relevant studies have suggested that the changes in gut microbiota are related to the course of nervous system diseases, and the microbiota-gut-brain axis is necessary for the proper functioning of the nervous system. Indole and its derivatives, as the products of the gut microbiota metabolism of tryptophan, can be used as ligands to regulate inflammation and autoimmune response in vivo. In recent years, some studies have found that the levels of indole and its derivatives differ significantly between patients with central nervous system diseases and healthy individuals, suggesting that they may be important mediators for the involvement of the microbiota-gut-brain axis in the disease course. Tryptophan metabolites produced by gut microbiota are involved in multiple physiological reactions, take indole for example, it participates in the process of inflammation and anti-inflammatory effects through various cellular physiological activities mediated by aromatic hydrocarbon receptors (AHR), which can influence a variety of neurological and neuropsychiatric diseases. This review mainly explores and summarizes the relationship between indoles and human neurological and neuropsychiatric disorders, including ischemic stroke, Alzheimer's disease, Parkinson's disease, multiple sclerosis, cognitive impairment, depression and anxiety, and puts forward that the level of indoles can be regulated through various direct or indirect ways to improve the prognosis of central nervous system diseases and reverse the dysfunction of the microbiota-gut-brain axis. This article is part of the Special Issue on "Microbiome & the Brain: Mechanisms & Maladies".
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Could psychobiotics and fermented foods improve mood in middle-aged and older women?
Menopause is a natural physiological phase during which women experience dramatic hormonal fluctuations. These lead to many symptoms, such as depression and anxiety, which, in turn, can negatively affect quality of life. Proper nutrition has an influential role in alleviating depression as well as anxiety. It is well known that gut microbiota dysbiosis contributes to the development of mood disorder. There is mounting evidence that modulating the gut-brain axis may aid in improving mood swings. In this context, this narrative review summarizes recent findings on how aging changes the composition of the gut microbiota and on the association between gut microbiota and mood disorders. In addition, it evaluates the effectiveness of psychobiotics and fermented foods in treating mood swings in middle-aged and older women. A search was done using PubMed, Scopus, and Google Scholar, and thirteen recent articles are included in this review. It is evident that psychobiotic supplementation and fermented foods can improve mood swings via several routes. However, these conclusions are based on only a few studies in middle-aged and older women. Therefore, long-term, well-designed randomized controlled trials are required to fully evaluate whether psychobiotics and fermented foods can be used to treat mood swings in this population.
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Long-Term Exposure to Ceftriaxone Sodium Induces Alteration of Gut Microbiota Accompanied by Abnormal Behaviors in Mice.
Background: Growing evidence points out that a disturbance of gut microbiota may also disturb the gut-brain communication. However, it is not clear to what extent the alteration of microbiota composition can modulate brain function, affecting host behaviors. Here, we investigated the effects of gut microbiota depletion on emotional behaviors. Methods: Mice in the experimental group were orally administered ceftriaxone sodium solution (250 mg/ml, 0.2 ml/d) for 11 weeks. The open-field test and tail-suspension test were employed for the neurobehavioral assessment of the mice. Fecal samples were collected for 16s rDNA sequencing. The serum levels of cytokines and corticosterone were quantified using enzyme-linked immunosorbent assays. The immunohistochemistry method was used for the detection of brain-derived neurotrophic factor (BDNF) and c-Fos protein. Results: The gut microbiota for antibiotic-treated mice showed lower richness and diversity compared with normal controls. This effect was accompanied by increased anxiety-like, depression-like, and aggressive behaviors. We found these changes to be possibly associated with a dysregulation of the immune system, abnormal activity of the hypothalamic-pituitary-adrenal axis, and an alteration of neurochemistry. Conclusions: The findings demonstrate the indispensable role of microbiota in the gut-brain communication and suggest that the absence of conventional gut microbiota could affect the nervous system, influencing brain function.
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Microbial regulation of a lincRNA-miRNA-mRNA network in the mouse hippocampus.
Aim: To comprehensively understand microbiota-regulated lincRNA-miRNA-mRNA networks in psychiatric disorders. Materials & methods: Integrated analyses of lincRNAs, mRNAs and miRNAs, obtained by microarray analysis of hippocampus from specific pathogen-free, germ-free and colonized germ-free mice, were performed. Results: Expression of 139 mRNAs, seven miRNAs and one lincRNA was restored following colonization. The restored transcripts were mainly involved in CREB and Ras/MAPK signaling pathways. RNA transcription and post-transcriptional regulation were the primary perturbed functions. Finally, 12 lincRNAs, six miRNAs and 47 mRNAs were included in a lincRNA-miRNA-mRNA network, and lincRNA0926-miR-190a-5p-Celf4 interactions may play a pivotal role in this regulatory network. Conclusion: This study provides clues for understanding the molecular basis of gut microbiota-brain interactions in depressive- and anxiety-like behaviors.
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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.