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The Gut Microbiota as a Mediator in the Relationship Between Dietary Patterns and Depression.
The interplay between diet, gut microbiota, and depressive symptoms is increasingly recognized, but underlying mechanisms remain unclear. We investigated whether adherence to several dietary patterns relates to gut microbial signatures and whether these profiles are associated with depressive symptoms in an elderly Mediterranean cohort. In 644 participants, 16S ribosomal RNA gene sequencing and dietary intake from a food-frequency questionnaire were obtained at baseline and 1-year follow-up. Adherence scores were computed for the Mediterranean diet adherence score (MEDAS), energy-reduced MEDAS (erMEDAS), Dietary Approaches to Stop Hypertension (DASH), Healthy Plant-Based Diet Index (HPDI), Unhealthy Plant-Based Diet Index (UPDI), and Western Diet Score (WESTDIET). Healthy patterns (erMEDAS, MEDAS, DASH, HPDI) were associated with 22, 28, 24, and 16 genera, of which 82%, 75%, 79%, and 88% showed a protective profile (more abundant with lower, or less abundant with higher, depressive symptoms). UPDI and WESTDIET were associated with 20 and 27 genera, but only 25% and 26% were protective. Mediation analyses indicated that gut microbiota mediated the associations of MEDAS (ACME = -0.066, p = 0.006) and erMEDAS (ACME = -0.029, p = 0.011) with depressive symptoms. This study is among the first to test whether diet shapes a microbiota signature that mediates the diet-depression relationship, adding mechanistic insight into diet-mental health research.
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Intestinal Epithelial Serotonin as a Novel Target for Treating Disorders of Gut-Brain Interaction and Mood.
BACKGROUND & AIMS: Mood disorders and disorders of gut-brain interaction (DGBI) are highly prevalent, commonly comorbid, and lack fully effective therapies. Although selective serotonin reuptake inhibitors (SSRIs) are first-line pharmacological treatments for these disorders, they may impart adverse effects, including anxiety, anhedonia, dysmotility, and, in children exposed in utero, an increased risk of cognitive, mood, and gastrointestinal disorders. SSRIs act systemically to block the serotonin reuptake transporter and enhance serotonergic signaling in the brain, intestinal epithelium, and enteric neurons. Yet, the compartments that mediate the therapeutic and adverse effects of SSRIs are unknown, as is whether gestational SSRI exposure directly contributes to human DGBI development. METHODS: We used transgenic, surgical, and pharmacological approaches to study the effects of intestinal epithelial serotonin reuptake transporter or serotonin on mood and gastrointestinal function, as well as relevant communication pathways. We also conducted a prospective birth cohort study to assess effects of gestational SSRI exposure on DGBI development. RESULTS: Serotonin reuptake transporter ablation targeted to the intestinal epithelium promoted anxiolytic and antidepressive-like effects without causing adverse effects on the gastrointestinal tract or brain; conversely, epithelial serotonin synthesis inhibition increased anxiety and depression-like behaviors. Afferent vagal pathways were found to be conduits by which intestinal epithelial serotonin affects behavior. In utero SSRI exposure is a significant and specific risk factor for development of the DGBI, functional constipation, in the first year of life, irrespective of maternal depressive symptoms. CONCLUSION: These findings provide fundamental insights into how the gastrointestinal tract modulates emotional behaviors, reveal a novel gut-targeted therapeutic approach for mood modulation, and suggest a new link in humans between in utero SSRI exposure and DGBI development.
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Stress matters: Randomized controlled trial on the effect of probiotics on neurocognition.
Probiotics are microorganisms that provide health benefits when consumed. In animals, probiotics reverse gut microbiome-related alterations in depression-like symptoms, in cognition, and in hormonal stress response. However, in humans, a causal understanding of the gut-brain link in emotion and cognition is lacking. Additionally, whether the effects of probiotics on neurocognition are visible only in presence of stress, remains unclear. We investigated the effects of a multispecies probiotic (Ecologic®Barrier) on specific neurocognitive measures of emotion reactivity, emotion regulation, and cognitive control using fMRI. Critically, we also tested whether probiotics can buffer against the detrimental effects of acute stress on working memory. In a double blind, randomized, placebo-controlled, between-subjects intervention study, 58 healthy participants were tested once before and once after a 28-day intervention. Without stress induction, probiotics did not affect brain, behavioral, or related self-report measures. However, relative to placebo, the probiotics group did show a significant stress-related increase in working memory performance after supplementation. This change was associated with intervention-related neural changes in frontal cortex during cognitive control exclusively in the probiotics group. Overall, our results show neurocognitive effects of a multispecies probiotic in healthy women only under challenging situations, buffering against the detrimental effects of stress on cognition.
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Microbial Therapeutics in Neurocognitive and Psychiatric Disorders.
Microbial therapeutics, which include gut biotics and fecal transplantation, are interventions designed to improve the gut microbiome. Gut biotics can be considered as the administration of direct microbial populations. The delivery of this can be done through live microbial flora, certain food like fiber, microbial products (metabolites and elements) obtained through the fermentation of food products, or as genetically engineered substances, that may have therapeutic benefit on different health disorders. Dietary intervention and pharmacological supplements with gut biotics aim at correcting disruption of the gut microbiota by repopulating with beneficial microorganism leading to decrease in gut permeability, inflammation, and alteration in metabolic activities, through a variety of mechanisms of action. Our understanding of the pharmacokinetics of microbial therapeutics has improved with in vitro models, sampling techniques in the gut, and tools for the reliable identification of gut biotics. Evidence from human studies points out that prebiotics, probiotics and synbiotics have the potential for treating and preventing mental health disorders, whereas with paraprobiotics, proteobiotics and postbiotics, the research is limited at this point. Some animal studies point out that gut biotics can be used with conventional treatments for a synergistic effect on mental health disorders. If future research shows that there is a possibility of synergistic effect of psychotropic medications with gut biotics, then a gut biotic or nutritional prescription can be given along with psychotropics. Even though the overall safety of gut biotics seems to be good, caution is needed to watch for any known and unknown side effects as well as the need for risk benefit analysis with certain vulnerable populations. Future research is needed before wide spread use of natural and genetically engineered gut biotics. Regulatory framework for gut biotics needs to be optimized. Holistic understanding of gut dysbiosis, along with life style factors, by health care providers is necessary for the better management of these conditions. In conclusion, microbial therapeutics are a new psychotherapeutic approach which offer some hope in certain conditions like dementia and depression. Future of microbial therapeutics will be driven by well-done randomized controlled trials and longitudinal research, as well as by replication studies in human subjects.
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Genetic Engineering and Encapsulation Strategies for Lacticaseibacillus rhamnosus Enhanced Functionalities and Delivery: Recent Advances and Future Approaches.
This review addresses the recent advances made through various genetic engineering techniques to improve the properties of Lacticaseibacillus rhamnosus, not only for industrial applications, but also for the health-related benefits. However, due to the strict regulations on microorganisms intended for human consumption, concerning the insufficient characterization degree of the newly isolated strains and the lack of data regarding the safety of the genetically modified (GM) variants, the feasibility of bringing such L. rhamnosus strains to the market and their safety prospects were evaluated. Given their multiple in vivo functions in the contexts of synbiotic and symbiotic functionality, L. rhamnosus strains are more than classic probiotics and need furthermore attention. In the functional food context, this review highlights the impact of L. rhamnosus derived bioactives on the human gut-organ axis, pointing out recently demonstrated molecular mechanisms of action with the host's gut microbiome to reduce the negative effects of obesity and its related metabolic disorders, as well as depression and Parkinson's disease, as the major challenges confronting humans today. Beyond that, considering L. rhamnosus delivery and its postbiotics accessibility to consumers via functional foods, notable progress was made to enhance their stability by developing various encapsulation systems, which are also emphasized.
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Alteration of gut microbiota in migraine patients with irritable bowel syndrome in a Chinese Han population.
OBJECTIVE: Migraine is frequently reported in patients with irritable bowel syndrome (IBS), and emerging evidence suggests that gut microbiota plays a role in migraine and IBS. However, alterations in the gut microbiome in migraine patients with IBS remain unknown. This study aimed to explore the compositions of gut microbiota in migraine patients with IBS in a Chinese Han population. METHODS: Sixteen migraine patients with IBS and thirteen age- and gender-matched IBS patients with similar dietary and lifestyle habits were enrolled in this pilot study. Demographic data, clinical data, eating habits, lifestyle habits, comorbidities, and medications were recorded using a unified case registration form. Questionnaires for the Migraine Disability Assessment (MIDAS), Pittsburgh Sleep Quality Index (PSQI), Hamilton Anxiety Scale (HAMA), and Hamilton Depression Scale (HAMD) were completed. Fecal samples were collected, and microbial DNA was extracted. Gut microbiota 16S ribosomal RNA (16S rRNA) gene sequencing targeting the V4 region was performed using the Illumina HiSeq 2500 high-throughput sequencing platform. The relationships between gut microbiota and clinical characteristics of migraine were analyzed. RESULTS: The structure of gut microbiota differed between migraine patients with IBS and patients with IBS, while the richness and diversity of gut microbiota in migraine patients with IBS showed no significant difference from that of patients with IBS. We found a higher relative abundance of the genus Parabacteroides and a lower relative abundance of the genera Paraprevotella, Lachnospiraceae_UCG-010, Lactococcus, Collinsella, and Comamonas in migraine patients with IBS than in patients with IBS. According to random forest predictive models, the phylum Bacteroidota shows the most important role in migraine patients with IBS. Furthermore, no statistical correlation was found between significantly different taxa at the genus level and migraine clinical data. CONCLUSION: This study identified that altered gut microbiota occurred in Chinese Han migraine patients with IBS, but no correlation was found between gut microbiota and the clinical characteristics of migraine. Further study is needed to better understand the role of gut microbiota in the pathogenesis of migraine in IBS.
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Schaftoside, a functional flavonoid from fenugreek (Trigonella foenum-graecum L.), alleviates depression and cognitive deficits via the microbiome-gut-brain axis in stressed mice.
Depression involves dysregulation of central and peripheral networks, with gut microbiota alterations increasingly implicated in pathogenesis. Trigonella foenum-graecum L. (fenugreek), a functional food and medicinal herb, has been used traditionally for neurological disorders, yet its specific neuroprotective constituents remain poorly characterized. This study evaluated the antidepressant potential of schaftoside, the predominant flavonoid of fenugreek seed flavonoids, and explored its mechanisms involving the microbiome-gut-brain axis in a chronic restraint stress (CRS) mouse model. Male Kunming mice were subjected to CRS and orally administered schaftoside (20, 50, and 125 mg kg-1) or fluoxetine (10 mg kg-1) for 28 days. Behavioral assessments (tail suspension, forced swim, novel object recognition, and Y-maze) demonstrated that schaftoside dose-dependently ameliorated depressive-like behaviors and cognitive impairments. It attenuated hippocampal neuronal damage and neuroinflammation, restoring hippocampal 5-HT, NE, and ACh levels. Intestinal barrier integrity was improved, evidenced by enhanced tight junction proteins (ZO-1, occludin) and mucin (MUC2) expression, alongside reduced colonic pro-inflammatory cytokines and elevated IL-10. 16S rRNA profiling revealed that schaftoside reshaped gut microbiota composition, notably suppressing stress-enriched Bacteroides and promoting butyrate-producing Butyricicoccus. Untargeted metabolomics identified restoration of tryptophan and α-linolenic acid metabolism pathways. Spearman correlation analysis revealed significant associations between specific gut genera, fecal metabolites, and host inflammatory/neurochemical markers. Hippocampal transcriptomics indicated enrichment of cAMP signaling, dopaminergic, and serotonergic synapse pathways. Fecal microbiota transplantation (FMT) from schaftoside-treated donors partially recapitulated the behavioral, anti-inflammatory, and intestinal barrier-protective effects in antibiotic-pretreated recipient mice, accompanied by restoration of the gut microbiota and metabolite profiles. These findings demonstrate that schaftoside, the major flavonoid of fenugreek seeds, exhibits promising antidepressant-like potential through modulation of the microbiome-gut-brain axis, supporting the functional food application of fenugreek-derived flavonoids for stress-related mood disorders.
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The schizophrenia and gut microbiota: A bibliometric and visual analysis.
BACKGROUND: Many studies have explored the link between the gut microbiota and schizophrenia. To date, there have been no bibliometric analyses to summarize the association between the gut microbiota and schizophrenia. We aimed to conduct a bibliometric study of this association to determine the current status and areas for advancement in this field. MATERIALS AND METHODS: Publications related to the gut microbiota and schizophrenia were retrieved from the Web of Science Core Collection (WoSCC). The WoSCC literature analysis wire and VOSviewer 1.6.16 were used to conduct the analysis. RESULTS: In total, 162 publications were included in our study. The publications generally showed an upward trend from 2014. A total of 873 authors from 355 organizations and 40 countries/regions contributed to this field. The leading authors were Timothy Dinan, John F Cryan, and Emily Severance. The leading institutions were Johns Hopkins University, the University College Cork, and the University of Toronto. The most productive countries were the United States (US), China, and Canada. In total, 95 journals contributed to this field. Among them, the top three productive journals were Schizophrenia Research, Progress in Neuro Psychopharmacology Biological Psychiatry, and Frontiers in Psychiatry. The important keywords in the clusters were gut microbiome, bipolar disorder, schizophrenia, antipsychotics, weight gain, metabolic syndrome, gut-brain axis, autism, depression, inflammation, and brain. CONCLUSION: The main research hotspots involving the connection between schizophrenia and the gut microbiota were the characteristics of the microbiota composition in schizophrenia patients, the gut-brain axis, and microbial-based interventions for schizophrenia. The studies about the association between gut microbiota and schizophrenia are limited, and more studies are needed to provide new insights into the gut microbiota in the pathogenesis and treatment of schizophrenia.
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Influence of Environmental Factors in the Development and Outcomes of Inflammatory Bowel Disease.
Inflammatory bowel disease (IBD), which mainly comprises Crohn's disease (CD) and ulcerative colitis (UC), is a term for chronic inflammatory diseases of the gut arising due to a dysregulated immune response to a dysbiotic gut microbiome on a background of genetic predisposition. However, genetics explains a small fraction of risk, and the external environment plays a large and important role in disease pathogenesis and natural history. Cigarette smoking, one of the earliest- and most-studied risk factors, increases the risk of CD onset and is associated with severe disease. In contrast, although smoking cessation increases the risk of UC onset and relapse, current smoking appears to be protective. Appendectomy is inversely associated with the risk of UC. Various dietary factors may influence risk of IBD, including an inverse association with dietary fiber. Exclusion diets have anecdotal reports of efficacy but lack evidence from rigorous clinical trials. Psychosocial factors such as depression, stress, and sleep disturbance play a role in onset as well as in determining natural history. There is an important need for rigorous studies robustly informing the association and mechanism(s) of influence of the external environment on IBD risk and for clinical trials examining the efficacy of alteration of the environment in ameliorating the course of IBD.
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Role of Tryptophan in Microbiota-Induced Depressive-Like Behavior: Evidence From Tryptophan Depletion Study.
During the past decade, there has been a substantial rise in the knowledge about the effects of gut microbiota on host physiology and behavior, including depressive behavior. Initial studies determined that gut microbiota can regulate host tryptophan levels, which is a main serotonin precursor. A dysfunctional serotonergic system is considered to be one of the main factors contributing to the development of depression. Therefore, we hypothesized that regulation of brain tryptophan and serotonin can explain, at least partly, the effects of microbiota on depressive behavior. To test this hypothesis, we examined depressive-like behavior and brain levels of serotonin and tryptophan, of germ free (GF) and specific-pathogen free (SPF) mice under basal conditions, or after acute tryptophan depletion (ATD) procedure, which is a method to decrease tryptophan and serotonin levels in the brain. In basal conditions, GF mice exhibited less depressive-like behavior in sucrose preference, tail-suspension and forced swim tests, compared to SPF mice. In addition, in mice that were not subjected to ATD, GF mice displayed higher levels of tryptophan, serotonin and 5-hydroxyindoleacetic acid (the main degradation product of serotonin) in medial prefrontal cortex (mPFC) and hippocampus (HIPPO), compared to SPF mice. Interestingly, ATD increased depressive-like behavior of GF, but not of SPF mice. These behavioral changes were accompanied by a stronger reduction of tryptophan, serotonin and 5-hydroxyindoleacetic acid in mPFC and HIPPO in GF mice after ATD, when compared to SPF mice. Therefore, the serotonergic system of GF mice is more vulnerable to the acute challenge of tryptophan reduction, and GF mice after tryptophan reduction behave more similarly to SPF mice. These data provide functional evidence that microbiota affects depression-like behavior through influencing brain tryptophan accessibility and the serotonergic system.