Is the vaginal microbiota to blame for painful periods?

When it comes to painful periods, we’re not all in the same boat. There is significant variability between women when it comes to the intensity of menstrual pain, the number of painful areas or associated gastrointestinal symptoms. The biological causes of this variability remain poorly understood but researchers are now focusing their attention on the vaginal microbiota. Indeed, the symptoms/pain intensity of dysmenorrhea (sidenote: Dysmenorrhea  Medical term for menstrual pain or cramps. )  may be exacerbated by inflammation that results from changes to this microbiota. Although the vaginal microbiota has already been studied in relation to several gynecological conditions (vaginosis, miscarriage and endometriosis), this study is the first to focus on the link between the composition of the vaginal microbiota during menstruation and the intensity of period pain.

Heterogeneous vaginal microbiota

In a pilot study, 20 women filled out questionnaires and were classified into three groups according to the pain they experienced during their period: “mild localized pain”, “severe localized pain”, or “severe multiple pain and gastrointestinal symptoms”. The vaginal microbiota was analyzed both during menstruation and outside of menstruation. The results showed that the vaginal microbiota composition significantly varied between women as well as over the course of the menstrual cycle, but the composition during menstruation varied even more depending on intensity of pain. In particular, during menstruation, women with more severe dysmenorrhea had a lower abundance of lactobacilli and a higher abundance of potentially pro-inflammatory bacteria.

Hope for women in pain

Although limited in terms of size, age groups studied and ethnic diversity, this pilot study is a first step towards larger studies on associations between the intensity of pain during menstruation and the composition of the vaginal microbiota. The researchers hypothesize that during menstruation endometrial tissue is broken down, releasing compounds (prostaglandins) that may cause uterine muscle contractions and increased sensitivity, thus contributing to menstrual pain. Certain bacteria in the vaginal microbiota may promote the release of these compounds and of pro-inflammatory cytokines that exacerbate the symptoms of dysmenorrhea. If these hypotheses are confirmed, the pilot study would underline the importance of taking into account inter-individual differences and the dynamics of the vaginal microbiota during the menstrual cycle. These findings may contribute to the development of personalized dysmenorrhea treatments and/or biomarkers, ultimately improving women’s quality of life.