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A systematic review of microbiome changes and impact of probiotic supplementation in children and adolescents with neuropsychiatric disorders.
OBJECTIVES: In recent decades, the diagnostic and therapeutic implications of the microbiome changes and the impact of probiotic supplementation have increased rapidly. However, the potential for clinical translation of microbiome research for children and adolescents with psychiatric disorders is unclear. This review examined available evidence related to gut microbiota as well as the impact of probiotic supplementation on psychiatric disorders in the pediatric population reported to date. METHODS: We performed a literature search for the gut microbiota in child and adolescent population (0-18 years old) with mental health disorders from July 1999 through July 2019 in several databases: ClinicalTrials.gov, Ovid EBM Reviews, Ovid Embase, Ovid Medline, Ovid PsycINFO, Scopus, and Web of Science. RESULTS: A total of 7 studies met inclusion criteria consisting of randomized controlled trials and cohort studies that examined various associations between psychiatric disorders and gut microbiota in youth. Six studies examined the effects of various treatment interventions such as probiotic supplementation on microbiota composition and behaviors. One study showed an increase in prosocial behavior in children with Autism Spectrum Disorder (ASD) and an increase in the Lachnospiraceae family following prebiotic supplementation. Another study suggested that prebiotic supplementation increased bifidobacterial populations for ASD and healthy controls. A study evaluating infant supplementation of prebiotics showed both a decreased likelihood of developing Attention Deficit Hyperactivity Disorder (ADHD) or ASD and decreased gut Bifidobacterium. One study did not find significant differences in microbiome composition after micronutrient treatment. CONCLUSION: The main goal of this systematic review was to comprehensively examine and summarize the current evidence focused on the potential effect of the relationship between microbiota gut composition as well as the effects of probiotic supplementation on psychiatric disorders in children and adolescents. This is a relatively new area of research and the number of included studies is limited. More studies are needed to determine whether gut dysbiosis leads to the development and/or contributes to the severity of mental disorders or whether gut dysbiosis is a result of other processes that accompany mental disorders. CLINICAL SIGNIFICANCE: A better understanding of the specific bacteria contributions, gut-brain pathways, and role in pathophysiological mechanisms in neuropsychiatric disorders in the child and adolescent populations can possibly provide alternative tools for a clinical psychiatrist. Moreover, it may ultimately aid the clinician with intervention strategies, or detect populations at risk for developing neuropsychiatric disorders.
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Delivery of Metabolically Neuroactive Probiotics to the Human Gut.
The human microbiome is a rich factory for metabolite production and emerging data has led to the concept that orally administered microbial strains can synthesize metabolites with neuroactive potential. Recent research from ex vivo and murine models suggests translational potential for microbes to regulate anxiety and depression through the gut-brain axis. However, so far, less emphasis has been placed on the selection of specific microbial strains known to produce the required key metabolites and the formulation in which microbial compositions are delivered to the gut. Here, we describe a double-capsule technology to deliver high numbers of metabolically active cells derived from the 24-strain probiotic product SH-DS01 to the gastrointestinal tract, including the small intestine, where immune responses and adsorption of metabolites into the bloodstream occur. Based on its genome sequence, Limosilactobacillus reuteri SD-LRE2-IT was predicted to have the genetic capacity to de novo produce a specific metabolite of interest to brain health, vitamin B12, which could be confirmed in vitro. Taken together, our data conceptualizes the importance of rationally defined microbial strain characterization based on genomics and metabolomics data, combined with carefully designed capsule technology for delivery of live cells and concomitant functionality in and beyond the gut ecosystem.
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Interactions between gut microbiota, plasma metabolome and brain function in the setting of a HIV cure trial.
BACKGROUND: The intestinal microbiota composition has been linked to neurocognitive impairment in people with HIV (PWH). However, the potential interplay of microbial species and related metabolites, particularly in the context of an HIV cure strategy remains underexplored. The BCN02 trial evaluated the impact of romidepsin (RMD), used as a HIV-1 latency reversing agent and with reported beneficial neurological effects, combined with the MVA.HIVconsv vaccine on virus control during 32-weeks of monitored antiretroviral treatment interruption (MAP) in early-treated HIV-infected individuals. Here, we analyzed longitudinal gut microbiome, plasma metabolome and brain functioning data to identify potential associations and novel putative biomarkers of HIV-associated neurocognitive disorders (HAND). METHODS: Data from fecal shotgun metagenomics, plasma metabolome, cognitive (standardized neuropsychological test score covering 6 cognitive domains, NPZ-6), functional (neuropsychiatric symptoms) and neuroimaging assessments were obtained and evaluated in 18 participants before and after RMD administration, and at the study end (post-MAP follow-up) in the BCN02 trial. RESULTS: Participants with neurocognitive impairment (Lower vs. Higher NPZ-6 score group) were enriched in bacterial species, including Desulfovibrio desulfuricans, Sutterella wadsworthensis and Streptococcus thermophilus, and showed higher 1,2-propanediol degradation microbial pathway levels, before RMD administration. A multi-omics profiling showed significant and positive correlations between these microbial features and lipid-related metabolic pathways, previously linked to neurological disorders (i.e., sphingolipid, ether lipid, and glycerophospholipid metabolism), in participants with neurocognitive impairment, before RMD administration. Three indices (microbial-, metabolite-based and combined) obtained from the discriminant features were assessed longitudinally, showing progressive similarities between NPZ-6 score groups over time. Furthermore, the three indices and related discriminant features correlated negatively with functional outcomes, such as quality of life and daily functioning, and positively with depression, stress and CNS-related symptoms before RMD administration, while these associations became less discernible at the subsequent timepoints. CONCLUSIONS: While the direct effect of the intervention on the observed shifts cannot be conclusively determined in this study settings, these findings strengthen the link between gut bacteria, related metabolites, and neurocognitive function in PWH, and provide an analytical framework for future validation studies aimed at discovering predictive biomarkers for neurocognitive impairment in PWH.
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Gut bacteriome and mood disorders in women with PCOS.
STUDY QUESTION: How does the gut bacteriome differ based on mood disorders (MDs) in women with polycystic ovary syndrome (PCOS), and how can the gut bacteriome contribute to the associations between these two conditions? SUMMARY ANSWER: Women with PCOS who also have MDs exhibited a distinct gut bacteriome with reduced alpha diversity and a significantly lower abundance of Butyricicoccus compared to women with PCOS but without MDs. WHAT IS KNOWN ALREADY: Women with PCOS have a 4- to 5-fold higher risk of having MDs compared to women without PCOS. The gut bacteriome has been suggested to influence the pathophysiology of both PCOS and MDs. STUDY DESIGN, SIZE, DURATION: This population-based cohort study was derived from the Northern Finland Birth Cohort 1966 (NFBC1966), which includes all women born in Northern Finland in 1966. Women with PCOS who donated a stool sample at age 46 years (n = 102) and two BMI-matched controls for each case (n = 205), who also responded properly to the MD criteria scales, were included. PARTICIPANTS/MATERIALS, SETTING, METHODS: A total of 102 women with PCOS and 205 age- and BMI-matched women without PCOS were included. Based on the validated MD criteria, the subjects were categorized into MD or no-MD groups, resulting in the following subgroups: PCOS no-MD (n = 84), PCOS MD (n = 18), control no-MD (n = 180), and control MD (n = 25). Clinical characteristics were assessed at age 31 years and age 46 years, and stool samples were collected from the women at age 46 years, followed by the gut bacteriome analysis using 16 s rRNA sequencing. Alpha diversity was assessed using observed features and Shannon's index, with a focus on genera, and beta diversity was characterized using principal components analysis (PCA) with Bray-Curtis Dissimilarity at the genus level. Associations between the gut bacteriome and PCOS-related clinical features were explored by Spearman's correlation coefficient. A P-value for multiple testing was adjusted with the Benjamini-Hochberg false discovery rate (FDR) method. MAIN RESULTS AND THE ROLE OF CHANCE: We observed changes in the gut bacteriome associated with MDs, irrespective of whether the women also had PCOS. Similarly, PCOS MD cases showed a lower alpha diversity (Observed feature, PCOS no-MD, median 272; PCOS MD, median 208, FDR = 0.01; Shannon, PCOS no-MD, median 5.95; PCOS MD, median 5.57, FDR = 0.01) but also a lower abundance of Butyricicoccus (log-fold changeAnalysis of Compositions of Microbiomes with Bias Correction (ANCOM-BC)=-0.90, FDRANCOM-BC=0.04) compared to PCOS no-MD cases. In contrast, in the controls, the gut bacteriome did not differ based on MDs. Furthermore, in the PCOS group, Sutterella showed positive correlations with PCOS-related clinical parameters linked to obesity (BMI, r2=0.31, FDR = 0.01; waist circumference, r2=0.29, FDR = 0.02), glucose metabolism (fasting glucose, r2=0.46, FDR < 0.001; fasting insulin, r2=0.24, FDR = 0.05), and gut barrier integrity (zonulin, r2=0.25, FDR = 0.03). LIMITATIONS, REASONS FOR CAUTION: Although this was the first study to assess the link between the gut bacteriome and MDs in PCOS and included the largest PCOS dataset for the gut microbiome analysis, the number of subjects stratified by the presence of MDs was limited when contrasted with previous studies that focused on MDs in a non-selected population. WIDER IMPLICATIONS OF THE FINDINGS: The main finding is that gut bacteriome is associated with MDs irrespective of the PCOS status, but PCOS may also modulate further the connection between the gut bacteriome and MDs. STUDY FUNDING/COMPETING INTEREST(S): This research was funded by the European Union's Horizon 2020 Research and Innovation Programme under the Marie Sklodowska-Curie Grant Agreement (MATER, No. 813707), the Academy of Finland (project grants 315921, 321763, 336449), the Sigrid Jusélius Foundation, Novo Nordisk Foundation (NNF21OC0070372), grant numbers PID2021-12728OB-100 (Endo-Map) and CNS2022-135999 (ROSY) funded by MCIN/AEI/10.13039/501100011033 and ERFD A Way of Making Europe. The study was also supported by EU QLG1-CT-2000-01643 (EUROBLCS) (E51560), NorFA (731, 20056, 30167), USA/NIH 2000 G DF682 (50945), the Estonian Research Council (PRG1076, PRG1414), EMBO Installation (3573), and Horizon 2020 Innovation Grant (ERIN, No. EU952516). The funders did not participate in any process of the study. We have no conflicts of interest to declare. TRIAL REGISTRATION NUMBER: N/A.
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Therapeutic Implications of the Microbial Hypothesis of Mental Illness.
There is increasingly compelling evidence that microorganisms may play an etiological role in the emergence of mental illness in a subset of the population. Historically, most work has focused on the neurotrophic herpesviruses, herpes simplex virus type 1 (HSV-1), cytomegalovirus (CMV), and Epstein-Barr virus (EBV) as well as the protozoan, Toxoplasma gondii. In this chapter, we provide an umbrella review of this literature and additionally highlight prospective studies that allow more mechanistic conclusions to be drawn. Next, we focus on clinical trials of anti-microbial medications for the treatment of psychiatric disorders. We critically evaluate six trials that tested the impact of anti-herpes medications on inflammatory outcomes in the context of a medical disorder, nine clinical trials utilizing anti-herpetic medications for the treatment of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) or schizophrenia, and four clinical trials utilizing anti-parasitic medications for the treatment of schizophrenia. We then turn our attention to evidence for a gut dysbiosis and altered microbiome in psychiatric disorders, and the potential therapeutic effects of probiotics, including an analysis of more than 10 randomized controlled trials of probiotics in the context of schizophrenia, bipolar disorder (BD), and major depressive disorder (MDD).
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The Role of the Gut Microbiota in Individuals with Irritable Bowel Syndrome: A Scoping Review.
Irritable bowel syndrome (IBS) represents the most prevalent disorder of brain-gut interaction, affecting approximately 10% of the global population. The objective of this study was to examine the mechanisms by which the gut microbiota contributes to the development of IBS. To this end, a review of articles that examined the gut microbiota of IBS patients was conducted. A search was conducted using PubMed and J-STAGE for articles published over the past five years that relate to the gut microbiota in patients with IBS. Individuals diagnosed with IBS display a reduction in alpha diversity and a decline in butyrate-producing bacteria, which collectively indicate a state of dysbiosis within their gut microbiota. Butyrate plays a dual role in the body, acting as a source of nutrition for the intestinal epithelium while also regulating the expression of dopamine transporters and D2 receptors in the central nervous system through epigenetic mechanisms. These characteristics may be linked to dysfunction of the central dopamine D2 pathway and play a role in the formation of various symptoms in IBS.
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Gut Microbiota and Ischemic Stroke: From Pre-Stroke Dysbiosis and Acute-Phase Changes to Therapeutic Applications.
PURPOSE: Ischemic stroke poses a major global health burden, and growing evidence points to the microbiota-gut-brain axis as an important contributor to stroke pathophysiology and recovery. The purpose of this review is to summarize current knowledge on bidirectional gut-brain communication in stroke, establishing gut dysbiosis as an upstream risk factor for stroke onset and examining microbiota dynamics across acute and chronic phases. METHOD: A comprehensive review of the current literature was conducted to synthesize existing evidence on the mechanisms of gut-brain communication, the influence of host factors, post-stroke complications, and candidate therapeutic interventions targeting the MGBA in ischemic stroke. FINDING: Gut dysbiosis acts as a risk factor for stroke through TMAO-mediated atherothrombosis, systemic inflammatory priming, and comorbidity-associated dysbiotic pre-conditioning. Following a stroke, dysbiosis is characterized by a depletion of short-chain fatty acid (SCFA)-producing taxa and an expansion of pro-inflammatory bacteria, particularly Proteobacteria and Enterobacteriaceae. Host factors (age, sex, genetics, and comorbidities) shape microbiota signatures and influence outcomes. Furthermore, post-stroke complications-including cognitive impairment, depression, stroke-associated pneumonia, and gastrointestinal dysfunction-are intimately linked to persistent dysbiosis. Mechanistically, the gut microbiota modulates stroke outcomes through immune regulation, metabolite signaling, blood-brain barrier integrity, and vagal pathways. Candidate therapeutic interventions (probiotics/prebiotics, fecal microbiota transplantation, SCFA supplementation, traditional Chinese medicine, and neuromodulation) demonstrate promising neuroprotective and recovery-enhancing effects, predominantly in preclinical models. CONCLUSION: While targeted interventions like probiotics and dietary fiber supplementation have shown modest benefits in small clinical trials, human clinical evidence remains largely preliminary. The translation of FMT, SCFA supplementation, and neuromodulatory approaches to clinical practice requires validation through rigorous, adequately powered randomized controlled trials. Future precision microbiome medicine demands individualized profiling and phenotype-specific interventions to establish microbiota-targeted strategies as viable adjunctive stroke therapies.
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From Gut to Brain: The roles of intestinal microbiota, immune system, and hormones in intestinal physiology and gut-brain-axis.
The intestine plays numerous roles in the normal physiology of our body. Gut-brain axis (GBA) is a complex communication network linking the gastrointestinal (GI) tract and central nervous system (CNS). This bidirectional system integrates endocrine, neural, and immune signals, impacting host metabolism and cognition. The gut microbiota, a critical component of the GBA, significantly impacts gut hormones, neurotransmission, neural development, and other components of gut-brain-axis. The microbiota-gut-brain axis facilitates communication via metabolites such as short chain fatty acids (SCFAs), and neurotransmitters such as dopamine, γ-amino butyric acid (GABA) and serotonin. The microbiota influences gut peptide production, including ghrelin, glucagon like pepetide-1 (GLP-1), serotonin, and cholecystokinin (CCK), thereby modulating nutrient absorption and immune responses. Gut hormones such as ghrelin, CCK, GLP-1, gastric inhibitory peptide (GIP), serotonin (5-HT), neurotensin, peptide YY (PYY) and melatonin play key roles in the GBA. These hormones play several roles including modulation of appetite and satiety, metabolism of nutrients such as lipid and glucose, insulin and glucagon secretion, and influence on gut inflammation, mood, learning and cognition. The interaction between gut microbiota and these hormones underscores their role in maintaining gut-brain homeostasis. Dysbiosis, or microbial imbalance, is linked to altered stress responses, anxiety, and depressive behaviors, highlighting the therapeutic potential of microbiota modulation. Despite the significant roles of gut hormones and microbiota in the GBA, literature on their cellular and molecular mechanisms is limited, and often based on animal models. This review synthesizes current understanding of hormones secreted by the intestine, their physiological effects and the cellular and molecular mechanisms of action underlying these effects, with a focus on their roles in the GBA. By elucidating these complex relationships, the review aims to advance research and clinical applications, offering insights into gastrointestinal and systemic health.
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Risk factors for developing irritable bowel syndrome: systematic umbrella review of reviews.
BACKGROUND: Irritable bowel syndrome (IBS) is a debilitating disorder affecting 4-9% of the global population. It is a multifaceted disorder with complex and varied causes. This review aims to consolidate the evidence regarding IBS risk factors by examining existing systematic reviews and meta-analyses, covering potential genetic, immunological, psychological, and dietary causes. METHODS: Systematic literature searches were conducted in MEDLINE, Embase and Cochrane library databases. Study selection and data extraction were conducted independently by four authors, with discrepancies resolved by consensus with a senior author. Systematic reviews examining risk factors of IBS development were eligible for review. Results were narratively synthesized. Quality of reviews were analysed using AMSTAR 2, and evidence were appraised using GRADE methodology. RESULTS: A total of 69 systematic reviews were included in this study. Most reviews were of "critically low" quality, while the remaining were "low" quality. Common shortcomings included the absence of a list of excluded studies with justifications for their exclusion and inadequate consideration of the risk of bias in individual studies. Eight major categories of risk factors for IBS identified were as follows: dietary, genetic, environmental, psychological, gut microbiome, socio-economic, physiological, and pathological, albeit overlaps exist. The most frequently reported risk factors for IBS development were female gender and anxiety disorders, with overall GRADE evaluation of "low"; depression and gastroenteritis, with overall GRADE evaluation of "moderate". CONCLUSIONS: Clinical practice should prioritize recognition of these risk factors. Future reviews should improve their reporting of results based on the PRISMA guidelines, to enhance the quality of research in this field. PROTOCOL REGISTRATION: PROSPERO CRD42023493739.
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Electro-microbial interplay in the gut-brain axis: An emerging paradigm for gut microbiota modulation via vagus nerve stimulation.
The treatment of central nervous system disorders remains a clinical challenge, highlighting an urgent need for innovative therapeutic strategies. The gut-brain axis represents a complex bidirectional communication network between the gastrointestinal tract and the brain, with the vagus nerve serving as a critical pathway for signal transmission. Vagus nerve stimulation (VNS), an established therapy for drug-resistant epilepsy and depression, has been shown to modulate the composition and functional output of gut microbiota, which in turn influences disease progression. Concurrently, gut microbiota and their metabolites such as short-chain fatty acids can regulate vagal activity through feedback mechanisms. This bidirectional interaction operates through neural, immune and metabolic pathways. This review provides a systematic review of the mechanisms through which VNS influences gut microbiota, and how microbial products feedback to regulate vagus nerve activity and the integrated pathways underlying this cross-talk, for the sake of providing insights into novel therapeutic approaches targeting the gut-brain interface.