A common therapeutic approach for oestrogen dependent conditions, such as fibroids and endometriosis is to reduce inflammation - but what does inflammation have to do with oestrogen excess you may ask- here are a few of the mechanisms explained.
Inflammatory agents have an effect on aromatase conversion. Aromatase is an enzyme that promotes the conversion of testosterone into oestrogen, so once activated more oestrogen is produce.
There is a link here to the arachadonic acids - the proinflammatory fats (Omega 6s). Prostaglandings (especially PGE2) synthesised from the arachadonic acid pathway are strong stimulator of aromatase in tissue - (found for example with breastcancerous tissue) and interleukin 1B (together with PGE2 are the most potent stimulators of aromatase activity in fibroids).
And here is where it becomes a viscious cycle - Oestrogen in return stimulates COX 2 (which leads to increase in PGE2)- so the higher the oestrogen levels the higher the inflammation and the higher the inflammation the higher the oestrogen levels are going to be.Ref: Sem Repr Med 2004:22(1):51, Makio Shozu et al. )
The type of oestrogen that we have also makes a difference- we also know that some enzymes that usually regulate the conversion from a stronger to a lesser oestrogen are reduced in endometriosis lesions- thus leading to even more inflammation.