Gut Microbiota in Schizophrenia: Taxonomic Shifts, Beta- Diversity Alterations, and Biomarker Potential: A Systematic Review

Emerging evidence implicates the gut–brain axis in the pathophysiology of schizophrenia, yet literature regarding specific microbiome alterations remains inconsistent. This study aims to synthesize evidence on gut microbiota diversity and taxonomic composition in individuals with schizophrenia compared to healthy controls. Unlike prior meta-analyses, this study integrates quantitative alpha diversity synthesis with cross-taxonomic qualitative analysis and contextualizes findings within functional frameworks of the gut–brain axis, highlighting the methodological heterogeneity that limits biological interpretation. A systematic review and meta-analysis were conducted following PRISMA 2020 guidelines. Electronic databases (Web of Science, PubMed, MDPI) were searched for observational studies published between 2017 and 2025. Forty-eight studies met inclusion criteria for qualitative synthesis, with 14 providing sufficient data for random-effects meta-analyses of alpha diversity. Meta-analyses revealed no statistically significant differences in alpha diversity indices (Shannon, Simpson, Chao1, ACE, Observed) between patients and controls, despite high heterogeneity. Conversely, beta diversity analyses generally demonstrated significant differences in microbial community composition. Taxonomic synthesis identified recurrent but heterogeneous dysbiotic patterns characterized by the depletion of short-chain fatty acid-producing taxa (e.g., Faecalibacterium, Roseburia, Lachnospiraceae) and enrichment of pro-inflammatory taxa (e.g., Proteobacteria, Fusobacterium). Schizophrenia is associated with evidence of compositional alterations and functional shifts rather than a global loss of microbial richness. These findings highlight candidate taxa that may warrant further investigation in biomarker-focused studies and microbiome-based therapeutics. However, these findings should be interpreted cautiously due to substantial heterogeneity and limited control for key confounders such as antipsychotic medication, diet, and life-style factors.