Polycystic Ovarian Syndrome May Be Caused By An Imbalance In Gut Bacteria
Polycystic ovarian syndrome (PCOS) is one of the most common hormone imbalances in young women. It affects approximately 1 in 10 women of reproductive age and is the most common cause of menstrual disturbances and impaired ovulation.
Now researchers have discovered a link between abnormally high levels of harmful microbes in the intestines and the condition.
The majority of women with PCOS are overweight or obese, and it is well known that insulin resistance (syndrome X) is a major contributor to the condition. Even slim women with PCOS tend to be insulin resistant. New research has discovered a link between bad bugs in the intestines and insulin resistance. According to the researchers:
“This novel paradigm in PCOS aetiology suggests that disturbances in bowel bacterial flora ("Dysbiosis of Gut Microbiota") brought about by a poor diet creates an increase in gut mucosal permeability, with a resultant increase in the passage of lipopolysaccharide (LPS) from Gram negative colonic bacteria into the systemic circulation. The resultant activation of the immune system interferes with insulin receptor function, driving up serum insulin levels, which in turn increases the ovaries production of androgens and interferes with normal follicle development. Thus, the Dysbiosis of Gut Microbiota (DOGMA) theory of PCOS can account for all three components of the syndrome-anovulation/menstrual irregularity, hyper-androgenism (acne, hirsutism) and the development of multiple small ovarian cysts.”
We are increasingly discovering the critical role that gut microbes play in our health. An imbalance in gut bugs can create or aggravate almost any disease or symptom. If you want to optimize your gut health and improve polycystic ovarian syndrome, the 15 Day Cleanse and information in this article may help.
Dysbiosis of Gut Microbiota (DOGMA)--a novel theory for the development of Polycystic Ovarian Syndrome. Kelton Tremellen, Karma Pearce
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Medical Hypotheses (Impact Factor: 1.05). 04/2012; 79(1):104-12. DOI:10.1016/j.mehy.2012.04.016