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Review links gut microbiota dysbiosis to recurrent spontaneous abortion in reproductive-age couples

Review links gut microbiota dysbiosis to recurrent spontaneous abortion in reproductive-age couples
Photo by Brett Jordan / Unsplash
Key Takeaway
Note inconsistent findings linking gut dysbiosis to recurrent spontaneous abortion in reproductive-age couples.

This review evaluates the relationship between gut microbiota dysbiosis and recurrent spontaneous abortion in reproductive-age couples. The scope includes analysis of microbial composition changes observed in this population. The authors synthesize data showing decreased alpha diversity and reduced levels of Bacteroidetes, Lactobacillus, and Bifidobacterium. Conversely, elevated levels of Proteobacteria and Escherichia-Shigella were also noted in the reviewed literature. No specific effect sizes or absolute numbers were reported for these outcomes. The review does not report adverse events or sample sizes for the primary studies included in the synthesis. The authors acknowledge inconsistent findings across the included studies as a key limitation. Funding sources and conflicts of interest were not reported in the source material. The review suggests microbiota-targeted strategies may be relevant for unexplained recurrent spontaneous abortion. However, the evidence remains observational regarding the bidirectional causal relationship between gut dysbiosis and RSA. Clinicians should interpret these associations with caution given the noted inconsistencies and lack of reported certainty metrics.

Study Details

Study typeSystematic review
EvidenceLevel 1
PublishedMay 2026
View Original Abstract ↓
Recurrent spontaneous abortion (RSA) affects 1%–5% of reproductive-age couples, and nearly 50% of cases remain unexplained. This review summarizes recent evidence to elucidate the association between gut microbiota dysbiosis and RSA. We confirm that RSA patients exhibit decreased alpha diversity, reduced levels of Bacteroidetes, Lactobacillus, and Bifidobacterium, and elevated Proteobacteria and Escherichia-Shigella. Gut dysbiosis contributes to RSA through three core pathways: disrupted T helper 17/regulatory T cell balance leading to maternal–fetal immune intolerance; insufficient short-chain fatty acid production and elevated trimethylamine N-oxide causing metabolic disorders; and disrupted estrogen and progesterone metabolism via microbial hydroxysteroid dehydrogenases triggering endocrine dysfunction. We also clarify the bidirectional causal relationship between gut dysbiosis and RSA, summarize inconsistent findings across studies, and highlight the potential of probiotics and dietary interventions. This review provides mechanistic insights and clinical implications for microbiota-targeted strategies in unexplained RSA.
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