Little is known about the etiology of fibroids. Although certain risk factors have been pinpointed, only hypotheses exist as to what actually causes fibroids to develop.
With many of today’s chronic conditions having an inflammatory component,1 could this also be true for fibroids?
The initial theory linking uterine inflammation and fibroids dates back to the early 1930s.2 Decades later in 2001, this assumption was tested and published in the American Journal of Epidemiology.3 By interviewing 318 women with fibroids, Faerstein, Szklo, and Rosenshein found that those who reported having three or more past episodes of pelvic inflammatory disease were almost four times more likely to have fibroids in comparison to women who never had the disease.
What’s more, the authors of the study found that having reproductive tract infections (RTI) such as chlamydia—a common cause of pelvic inflammatory disease, increased a woman’s risk of fibroids by approximately three-fold; although it was found that this estimate may not have been precise. There was no fibroid risk associated with having genital warts or herpes.
Almost 15 years later, have we gotten any closer to finding whether uterine inflammation plays a role in fibroid formation? A 2015 study in the Journal of Women’s Health4 further investigated this premise.
The study examined ultrasound results and self-reported questionnaires of 1,656 African American women ages 23-34 in the Detroit area who were enrolled in the National Institute of Environmental Health Sciences (NIEHS) Study of Environment, Lifestyle, and Fibroids (SELF).
Moore and her colleagues found that women with a history of bacterial vaginosis had a 21 percent increased risk of having fibroids in general (the study pointed out this was statistically insignificant), 47 percent increased risk of having two or more fibroids, and a 41 percent increased risk of having a larger total fibroid volume.
On the other hand, the authors ironically observed that having a history of chlamydia or pelvic inflammatory disease resulted in a reduced risk of having two or more fibroids.
Given the inconsistency of these results the authors wrote, “Overall, the studies of RTIs and fibroids, including ours, reveal no strong associations.”
“In this large study of young African American women, there was little overall support for an association between women’s self-reported histories of RTIs and subsequent fibroid development,” the authors explained. “Even those having a history of three or more different RTIs or multiple diagnoses of the same RTI showed no indication of elevated odds of fibroids.”
Although results were stated inconclusive, how might we explain the link found between bacterial vaginosis and fibroids, not to mention the findings of previous studies?
Viral and bacterial infections are a known cause of human inflammation5, which in the aforementioned studies, is the proposed reasoning behind fibroid formation.
Uterine fibroids are thought to arise from a single abnormal smooth muscle cell located in the uterine wall.6 Infectious agents have been seen to induce abnormal cell growth3 and it’s thought that inflammation and irritation caused by infection could lead to irregular repair of smooth muscle cells that then lead to fibroid tumor growth.4 5 A closer look at fibroid tissue has even shown increased levels of inflammatory molecules, especially Transforming Growth Factor-Beta (TGF-ß).6
Although we have theories and studies that include interviews and self-reported data that could possibly make a connection, it’s not substantial enough. “Self-reported data…may be subject to error,” Moore and colleagues clarified. “Perhaps a more important problem is that the majority of RTIs can often be [without symptoms], so even those who have not had a previous diagnosis may still have had or currently have an RTI.”
They continued to write, “Some women also may have been tested and were positive but never received their results, did not understand them, or just did not report them due to confidentiality concerns or social desirability bias.”
More attention is needed within this area of women’s healthcare, the authors emphasized. “Future studies are needed to take the next step…to better investigate associations between RTIs and fibroids.”
- Tabas, I. & Glass, C. K. (2013). Anti-inflammatory therapy in chronic disease: challenges and opportunities. Science, 339(6116): 166-172. doi:10.1126/science.1230720
- Witherspoon, J. T., & Butler, V. W. (1934). The etiology of uterine fibroids with special reference to the frequency of their occurrence in the Negro: A hypothesis. Surgery, Gynecology, & Obstetrics, 58(4).
- Faerstein, E., Moyses, S., & Rosenshein, N. B. (2001). Risk factors for uterine leiomyoma: a practice-based case-control study. II. Atherogenic risk factors and potential sources of uterine irritation. American Journal of Epidemiology, 153(1): 11-19.
- Moore, K. R., Cole, S. R., Dittmer, D. P., Schoenback, V. J., Smith, J. S., & Baird, D. D. (2015). Self-Reported Reproductive Tract Infections and Ultrasound Diagnosed Uterine Fibroids in African-American Women. Journal of Women’s Health, 24(6): 489-495. doi:10.1089/jwh.2014.5051
- Wegienka, G. (2012). Are uterine leiomyoma a consequence of a chronically inflammatory immune system? Medical Hypothesis, 79(2): 226-231. doi:10.1016/j.mehy.2012.04.046
- Maybin, J. A., Critchley, H. O. D., & Jabbour. H. N. (2011). Inflammatory pathways in endometrial disorders. Molecular and Cellular Endocrinology, 335(1): 42-51. doi:10.1016/j.mce.2010.08.006