Some studies suggest that higher body mass index is associated with increased susceptibility to bacterial vaginosis (BV), but results are conflicting.
Female sex workers aged 16 to 45 years and participating in an open, prospective cohort study in Mombasa, Kenya between 2000 and 2014 were included in this analysis. Up to 2 years of follow-up were included per woman. Body mass index (BMI) was categorized as underweight (≤18.5), normal (18.5–24.9), overweight (25–29.9), and obese (≥30). Bacterial vaginosis was assessed using Nugent scores. Generalized estimating equations were used to estimate relative risks of the association between BMI and BV.
At baseline, 32.1% (n = 625) of 1946 women had BV. Half of women were overweight (31.1%, n = 606) or obese (20.1%, n = 391). Participants contributed 14,319 follow-up visits. Adjusting for age, compared to women with normal BMI, overweight (adjusted relative risk, 0.91; 95% confidence interval, 0.81–1.02) and obese (adjusted relative risk, 0.82; 95% confidence interval, 0.71–0.94) women were at lower risk for BV (joint P = 0.03).
Obese women had a nearly 20% lower risk of BV compared with women with normal BMI. Potential mechanisms for this effect, including possible effects of diet, obesity-associated changes in the gut microbiome, and systemic estrogen levels, should be explored.
A prospective cohort study of female sex workers in Mombasa, Kenya found that obese women had a nearly 20% lower risk of incident bacterial vaginosis compared with normal weight women.
From the *Department of Epidemiology,
†Department of Biostatistics,
‡Department of Global Health, University of Washington, Seattle, WA;
§Research and Programs,
¶Reproductive Health, Kenyatta National Hospital;
∥University of Nairobi Institute of Tropical & Infectious Diseases (UNITID),
**Department of Medical Microbiology, University of Nairobi, Nairobi, Kenya; and
††Department of Medicine, University of Washington, Seattle, WA
Acknowledgments: The authors acknowledge the support from the clinic, laboratory, and administrative staff and the partnerships with the Mombasa County and Coast Provincial General Hospital for their dedication. The authors thank the study participants whose commitment made this research possible. The authors are grateful to Dr. Julie Overbaugh (Fred Hutchinson Cancer Research Center; Seattle, WA) for her input on the article and for her long-term support of the Mombasa Cohort through National Institutes of Health grant R37 AI38518.
Correspondence: Erica Lokken, MS, University of Washington Box 359909, 325 9th, Avenue Seattle, WA 98102. E-mail: email@example.com.
Conflict of Interest and Sources of Funding: RSM receives research funding, paid to the University of Washington, from Hologic Corporation. This work was supported by grants from the National Institutes of Health (R37 AI38518, T32 AI07140 to EML, K24 HD88229 to RSM for mentoring). Infrastructure and logistical support for the Mombasa research site was provided by the University of Washington's Center for AIDS Research (CFAR), a National Institutes of Health funded program (P30 AI027757) which is supported by the following research centers: National Institute of Allergy and Infectious Diseases, National Cancer Institute, National Institute of Mental Health, National Institute on Drug Abuse, Eunice Kennedy Shriver National Institute of Child Health and Development, National Heart, Lung and Blood Institute, and National Center for Complementary and Integrative Health. The content of this paper is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
Received for publication May 16, 2018, and accepted August 18, 2018.