Gut and Vaginal Microbiomes in PCOS: Implications for Women’s Health Original paper

What Was Reviewed?

This review paper examined the interrelationship between gut and vaginal microbiota and polycystic ovary syndrome (PCOS), offering a multidimensional analysis of how microbial dysbiosis contributes to the endocrine, metabolic, reproductive, and immune disturbances seen in PCOS. The authors summarized both experimental and clinical studies, with a particular focus on microbiota diversity, microbial shifts in composition, and their functional consequences. The review discussed the role of microbiota in regulating sex hormones, immune homeostasis, insulin sensitivity, gut permeability, inflammation, and neuroendocrine communication via the gut–brain axis. Additionally, the paper explored therapeutic strategies such as fecal microbiota transplantation (FMT) and probiotic interventions, aiming to identify translational opportunities for clinical application.

Who Was Reviewed?

The review compiled findings from human studies, animal models, and in vitro mechanistic research. In human studies, both gut and vaginal microbial profiles were compared between women with PCOS and healthy controls using sequencing techniques such as 16S rRNA analysis. Animal models, including rodent studies, were also incorporated to explore the causal mechanisms by which microbial interventions impact hormonal regulation, insulin resistance, and reproductive health. The reviewed cohorts varied across reproductive age, BMI, and hormonal phenotypes, with many studies focusing on women with hyperandrogenism and menstrual irregularities, the hallmarks of PCOS.

What Were the Most Important Findings?

The review identified significant microbial dysbiosis in both the gut and vaginal microbiota of PCOS patients. In the gut, PCOS was consistently associated with reduced alpha and beta diversity, and increased abundance of pro-inflammatory and metabolically detrimental taxa such as Bacteroides vulgatus, Prevotella copri, and Escherichia/Shigella. Simultaneously, beneficial microbes such as Akkermansia muciniphila and members of Ruminococcaceae were diminished. The vaginal microbiota in PCOS showed decreased Lactobacillus species and increased colonization by pathogens like Gardnerella vaginalis, Prevotella, and Chlamydia trachomatis. These microbial patterns are linked to infertility, implantation failure, and adverse pregnancy outcomes.

Mechanistically, the review described how microbial alterations exacerbate insulin resistance through increased branched-chain amino acids and inflammatory cytokines. It also outlined how gut-derived short-chain fatty acids (SCFAs), bile acids, and estrogen-metabolizing enzymes modulate host endocrine and metabolic functions. Importantly, the review explored the gut–brain axis, implicating microbial metabolites in the modulation of the hypothalamic–pituitary–gonadal axis, contributing to anxiety and reproductive dysfunction in PCOS. These major microbial associations (MMAs) anchor PCOS within a broader systems biology framework, suggesting that dysbiosis impacts not just metabolic markers, but also immune balance, hormone regulation, and reproductive health.

What Are the Implications of This Review?

The implication of this review is its positioning of microbiota as a core regulatory system in the etiology and progression of PCOS, rather than a secondary contributor. For clinicians, this reframing encourages the integration of microbiota profiling into PCOS diagnostics, especially in patients with atypical presentations. The consistent loss of microbial diversity and protective Lactobacillus species, combined with enrichment of inflammatory and hormone-disrupting taxa, provides a microbiome-based signature of PCOS. Therapeutically, the review highlights emerging interventions, including FMT and targeted probiotics as viable approaches to restore microbial equilibrium. The evidence supports the concept that modulating gut and vaginal microbiota could lead to improvements in insulin sensitivity, hormone balance, and fertility outcomes. However, the authors note that most mechanistic insights stem from animal studies, calling for rigorous human trials to validate these strategies in clinical practice.