Endometriosis risk and dietary fat consumption

Risks factors for developing “endometriosis” are discussed since 30 years while this is a frequent topic at meetings and factors as heredity, age, menstrual flow etc seem to be common knowledge if judged from the literature and from endometriosis websites. We even suggested 30 years ago that typical endometriosis might not be the cause but the consequence of the Luteinised Unruptured Follicle(LUF) syndrome, and thus not a cause but a consequence of infertility.
The debate however is flawed by the fact that specific end-points are rarely/given. Indeed that risks for developing subtle, typical, cystic and deep lesions might be different. The 4 types of lesions anyway are very different in prevalences varying from 80 to 1% respectively, while pain ranges from no pain to very severe pain in most women.
To the best of our knowledge only heredity is a clearly defined risk factor, which seems to be bigger for severe lesions, thus for cystic ovarian endometriosis, and possibly also deep endometriosis. Also the discussion on the association between endometriosis and cancer is an example of this bias in the literature as is the recent article in human reproductio on dietary fat consumption and the risk for endometriosis (Missmer SA et al A prospective study of dietary fat consumption and endometriosis risk. Hum Reprod 2010;00:1–8.).
For this reason we wrote a letter to the editor in order to address this problem. Click for the full text . In brief we were concerned that the abstract may induce readers conclude that fish oil consumption might be beneficial in preventing endometriosis. Indeed we only know that fish oil consumption can decrease primary dysmenorrhea without any data on endometriosis associated pain, while the implantation data in an animal model are weak and can easily be explained by a reduced inflammatory reaction instead of regression. Also the conclusion that fish oil consumption decreases the risk of endometriosis is at least premature as is their suggestion to remove trans fat from hydrogenated oils from the food supply’. We on the contrary based upon the same data would conclude that women with a high fat intake are less likely to undergo a laparoscopy since a high fatty acid intake can reduce menstrual pain. We in addition asked whether more severe forms such as cystic and deep endometriosis would be affected by diet. In the absence of a response we may assume that these data do not exist.
In conclusion, notwithstanding our appreciation for the meticulous analysis and the nice data, we do not consider that these data today permit the conclusion that diet affects the risk of developing endometriosis, certainly not of severe endometriosis.

Prof P.R. Koninckx and Professor I.A. Brosens