The Gut Microbiota: a Novel Player in the Pathogenesis of Uterine Fibroids

Abstract

Uterine fibroid is a common gynecological disorder that affects women of reproductive age and has emerged as a major public health concern. The symptoms have a negative influence on both their physical health and quality of life. The cost of treatment has a significant impact on the disease's burden. Even though its origin is uncertain, estrogen is thought to be a key player in fibroid pathophysiology. Many theories, including those based on genetic and environmental factors, explain what causes hyper-estrogenic condition in fibroid patients. One such possibility that is currently being explored is the hypothesis that an altered gut microbiome can contribute to the development of diseases characterized by estrogen dominance. Gut dysbiosis is often a "hot area" in the health sciences. According to a recent study, uterine fibroid patients have altered gut microbiome. A variety of risk factors influence both fibroid development and gut homeostasis. Diet, lifestyle, physical activity, and environmental contaminants have an impact on estrogen and the gut flora. A better understanding of uterine fibroids' pathophysiology is required to develop effective preventative and treatment options. A few ways by which the gut microbiota contributes to UF include estrogen, impaired immune function, inflammation, and altered gut metabolites. Therefore, in the future, while treating fibroid patients, various strategies to deal with changes in the gut flora may be advantageous. For developing suggestions for clinical diagnosis and therapy, we reviewed the literature on the relationship between uterine fibroids and the gut microbiota.

Keywords: Estrogen; Gut microbiota; Lifestyle; Lipopolysaccharides; Short chain fatty acids; Uterine fibroid.

Fig. 1

Possible mechanisms that could link gut dysbiosis and the development of uterine fibroids [, , , , –63]. A dysbiotic gut results in an altered microbiome which triggers the following pathways i) interferes with the estrobolome functioning and results in hyperestrogenic state leading to uterine fibroids, ii) altered levels of gut metabolites such as short chain fatty acids (SCFA) which triggers immune dysregulation and induce inflammation and also leads to hyperestrogenic state, iii) interferes the gut permeability leading to a leaky gut and endotoxemia which could dysregulate the immune function