Abstract
ABSTRACT
Background and Aims
Dysbiosis is the substitution of the normal gut flora with a dysfunctional array of organisms that influences the outcome of multiple inflammatory pathways, contributing to systemic inflammation and various disease states. It has historically been understudied, with outcomes that may directly or indirectly cause pathologies. This review aims to emphasize the understanding of the effects of dysbiosis on female fertility and various approaches to addressing it.
Methods
A comprehensive review was conducted using databases such as PubMed, Scopus, Cochrane Library, and Google Scholar, applying search terms like “Dysbiosis”, “Female Infertility”, “Gut–Brain Axis”, “Reproductive Health”, “Estrobolome”, “Polycystic Ovary Syndrome (PCOS)”, and “Endometriosis”. Articles published in the English language from January 2007 to April 2025, encompassing original research, systematic reviews, randomized controlled studies, and meta‐analyses, were included. Studies not pertinent to therapeutic applications, lacking outcome, or restricted to editorials were excluded.
Results
Gut dysbiosis may be associated with female reproductive disorders (PCOS, endometriosis, ovulatory dysfunction), complications during pregnancy, thyroid dysfunction, and infertility. Altered microbial diversity affects estrogen metabolism, which in turn impacts GnRH, LH regulation, and systemic inflammation. An imbalance in
Prevotella
and other organisms is correlated with hormonal and metabolic dysregulation, poor oocyte quality, and thus infertility.
Conclusion
Gut dysbiosis plays a pivotal role in female reproductive health. The current evidence suggests potential benefits of microbiome modulation therapy, including the use of probiotics or dietary modifications. Many of these studies are observational, small‐scale, and use different methodologies, which restrict our scope. So, larger and standardized interventional studies are required to establish the gut microbiome as a viable therapeutic target for female infertility.