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Investigating the effect of vitamin C supplementation on bacterial vaginosis: A systematic review and meta-analysis.

Created on 04 Oct 2026

Authors

Parvin Abedi, Mina Iravani, Somayeh Makvandi, Solmaz Mohammadi, Maryam Zahedian, Parvin Esfandiarinezhad

Published in

Journal of education and health promotion. Volume 15. Pages 355. Epub Aug 31, 2026.

Abstract

Bacterial vaginosis (BV), the most common type of vaginitis, results from reduced vaginal lactobacilli and increased anaerobic bacteria. Vitamin C may aid BV treatment by promoting lactic acid production. This study evaluated the effectiveness of vitamin C in treating BV. To this aim, a systematic search of PubMed, Scopus, Web of Science, and Iranian databases identified randomized clinical trials published up to October 29, 2024. The protocol for this systematic review is registered. Risk of bias was assessed using the Verhagen tool. Mean differences and their 95% confidence intervals (CIs) were calculated using the random-effects model. The quality of the evidence was evaluated with GRADEpro Guideline Development Tool, and statistical analyses were conducted using Review Manager (RevMan v5.3). Substantial heterogeneity (I2 >50%) prompted the use of the random-effects model, subgroup analyses, and sensitivity analyses to investigate its origins. The meta-analysis included six randomized controlled trials of varying quality. Vitamin C showed a nonsignificant positive effect on the Whiff test (relative risk [RR] =1.19, 95% CI: 0.97-1.47, P = 0.09) but significantly improved vaginal pH < 4.5 (RR = 1.57, 95% CI: 1.21-2.03, P = 0.0006). While no significant reduction in vaginal discharge was observed (RR = 1.23, 95% CI: 0.94-1.60, P = 0.13), vitamin C significantly reduced the number of clue cells (RR = 1.34, 95% CI: 1.06-1.68, P = 0.01). Based on these findings, vitamin C supplementation may aid in achieving a vaginal pH < 4.5 and reducing clue cells in BV. However, further large-scale studies are warranted to confirm these results and elucidate the underlying mechanisms.

PMID:
42829769
Bibliographic data and abstract were imported from PubMed on 04 Oct 2026.

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