Gut microbial biomarkers for major depressive disorder: a cross-sectional study

Alterations in Gut Microbiota and Serum Metabolome Are Associated with Postpartum Depression

Background: Postpartum depression (PPD) is a prevalent and debilitating disorder, with increasing evidence implicating the gut microbiota–brain axis. However, integrated alterations in gut microbiota and circulating metabolites in PPD remain insufficiently characterized. Methods: Fecal and serum samples were collected from patients with PPD and healthy controls (HC). Depressive symptoms were assessed using the 17-item Hamilton Depression Rating Scale (HAMD-17). Gut microbiota was analyzed by 16S rRNA sequencing, and serum metabolites were profiled using untargeted LC–MS-based metabolomics. Spearman correlation and receiver operating characteristic (ROC) analyses were performed. Results: A total of 63 participants (42 PPD, 21 HC) were included. Significant alterations in gut microbial composition were observed in PPD, including decreased Faecalibacterium and Akkermansia and increased Ralstonia and Fusobacterium. Candidate differential serum metabolic features, including LPE-related and energy-metabolism-related features, were identified. Exploratory correlation analyses suggested distinct microbiota–metabolite association patterns, and several microbial taxa and serum metabolic features were associated with HAMD-17 scores. ROC analysis showed that several taxa and metabolic features exhibited preliminary discriminative performance with this cohort, although further validation is required. Conclusions: PPD was associated with alterations in gut microbiota composition and exploratory circulating metabolite profiles, potentially involving lipid dysregulation, neuroinflammation, steroid-related metabolism, and neurotoxicity-related pathways. The identified taxa and putatively annotated metabolites should be regarded as exploratory PPD-associated candidates rather than validated biomarkers or mechanistic mediators. Further validation in larger, independent cohorts is warranted. These findings may also inform future microbiota- and nutrition-oriented strategies for postpartum mental health management.

Efficacy of Gut Microbiota-Targeted Interventions for Major Depressive Disorder: A Systematic Review and Network Meta-Analysis.

Reproducible Gut Microbiome Alterations in Major Depressive Disorder: A Systematic Review of Taxonomic and Functional Findings

Background/Objectives: Major depressive disorder (MDD) has been increasingly associated with alterations of the gut microbiome through the microbiota–gut–brain axis. However, published findings remain highly heterogeneous, limiting identification of reproducible microbial signatures associated with depression. This systematic review aimed to evaluate reproducible taxonomic and functional gut microbiome alterations in patients with MDD compared with healthy controls. Methods: A systematic literature search was conducted in PubMed/MEDLINE, Scopus, Web of Science Core Collection, and the Cochrane Library for studies published between January 2016 and December 2025. Observational human studies evaluating gut microbiome composition in adults with clinically diagnosed MDD and healthy control groups were included. Methodological quality was assessed using the Newcastle-Ottawa Scale. Due to substantial methodological heterogeneity, findings were synthesized using structured qualitative narrative analysis. Results: Sixteen observational studies were included in the qualitative synthesis. Findings related to alpha diversity were inconsistent across studies, whereas beta diversity alterations demonstrated greater reproducibility across independent cohorts. The most recurrent microbiome pattern involved depletion of short-chain fatty acid (SCFA)-producing bacteria, particularly Faecalibacterium and Roseburia, together with recurrent alterations affecting members of the Ruminococcaceae, Lachnospiraceae, and Clostridia groups. Functional microbiome alterations demonstrated greater consistency than higher-level taxonomic findings and included reduced butyrate synthesis pathways, dysregulated amino acid and tryptophan metabolism, increased lipopolysaccharide biosynthesis, and enrichment of pro-inflammatory microbial signatures. Antidepressant-naïve cohorts generally demonstrated more homogeneous dysbiosis patterns than mixed-treated populations. Conclusions: Current evidence suggests that functional gut microbiome dysregulation may represent a more reproducible biological feature of MDD than isolated taxonomic alterations alone. However, substantial heterogeneity in study design, participant characteristics, sequencing methodologies, and analytical approaches continues to limit clinical translation. Large-scale longitudinal multi-omics studies using standardized methodologies are required to clarify the role of the gut microbiome in depressive disorders and to evaluate the potential utility of microbiome-based biomarkers and interventions in mental health and public health practice.

From gut to brain: data-driven evidence suggests causal contribution of gut-microbiota to major depressive disorder in humans

This study provides the first data-driven evidence for a potential causal role of gut microbiota in the pathophysiology of depression in humans, and employs state-of-the-art causal inference tools within Judea Pearl's framework.

Gut Microbiome in Depression with and without REM Sleep Behavior Disorder.

Gut microbiome provides a candidate approach for potential risk stratification in psychiatric populations, and MDD + RBD may represent a biologically distinct depression subtype associated with potential neurodegenerative risk.

Systematic review of gut microbiota structural characteristics in patients with ischemic stroke

Background Emerging evidence implicates the gut microbiota (GM) in the pathogenesis of ischemic stroke (IS). However, systematic evaluations synthesizing evidence on microbial shifts, functional alterations, and clinical correlations are lacking. This study aimed to comprehensively analyze GM characteristics in IS patients versus healthy controls (HC). Methods A systematic search of PubMed, Web of Science, and Embase was conducted from inception to April 2025. Observational studies comparing GM in IS patients and HC were included. Data on alpha/beta diversity, relative microbial abundance (phylum to species), predicted functional pathways, and microbiota–clinical indicator correlations were extracted. A narrative synthesis summarized the direction and consistency of reported findings. Results Twenty-four studies involving 1,957 participants (1,159 IS, 798 HC) were included. The qualitative synthesis revealed no consistent differences in alpha diversity indices between IS and HC, while significant beta diversity separation was frequently reported (18/22 studies). At the phylum level, an increased relative abundance of Proteobacteria and a decreased abundance of Firmicutes were the most consistent findings in IS patients. Key genera frequently enriched in IS included Lactobacillus, Streptococcus, and Parabacteroides, while Faecalibacterium, Agathobacter, and Blautia were commonly depleted. LEfSe analysis confirmed these discriminative taxa. Predicted functional analysis suggested enrichment of pro-inflammatory pathways (e.g., lipopolysaccharide biosynthesis) and depletion of metabolic and neuroprotective pathways in IS. Clinically, Faecalibacterium abundance correlated negatively with NIHSS and mRS scores, while Lactobacillus and Streptococcus showed positive correlations with stroke severity and inflammatory markers. Conclusion Ischemic stroke is associated with distinct gut microbial dysbiosis characterized by a pro-inflammatory, opportunistic pathogen-enriched, and butyrate-producer-depleted profile. These alterations correlate with disease severity and are linked to predicted disruptions in microbial metabolic functions. However, whether this dysbiosis is a cause, consequence, or exacerbating factor of IS remains to be determined. The gut microbiota may serve as a potential biomarker and therapeutic target in ischemic stroke. Systematic Review Registration https://www.crd.york.ac.uk/PROSPERO/view/CRD420251117510, identifier CRD420251117510.