When I don’t understand something, the first thing I do is read more about it. Unfortunately, even in scientific journals, there is little consensus about the disease. Here are some articles and snippets that I found interesting this morning.
da Silva, M. C. M., Ferreira, L. P. S., & Della Giustina, A. (2024). It is time to change the definition: Endometriosis is no longer a pelvic disease. Clinics (Sao Paulo, Brazil), 79, 100326. https://doi.org/10.1016/j.clinsp.2024.100326
“The hypothesis of a brain–body–brain cross-talk”, introduced by Tariverdian and colleagues,31 points out that the peripheral alterations provoked by endometriosis, such as peritoneal inflammation and angiogenesis, would have central repercussions since inflammatory mediators might enter the Central Nervous System (CNS) bypassing/crossing the Blood-Brain Barrier (BBB) or via stimulation of vagal nervous afferents.
Samani and colleagues showed that endometriosis-derived cells can migrate and engraft to distant organs outside the pelvic cavity, including the brain,38indicating that endometriosis lesions could develop in the CNS.… patient who developed psychiatric disorders due to endometriosis lesions in the brain.
It is time for the healthcare and scientific communities to recognize endometriosis no longer as a pelvic, but rather a systemic condition.
Ellis K, Munro D and Clarke J (2022) Endometriosis Is Undervalued: A Call to Action. Front. Glob. Womens Health 3:902371. doi: 10.3389/fgwh.2022.902371
Psychological suffering of women with endometriosis can consist of: (a) anxiety and/or depression ; (b) trauma c) chronic stress of multidimensional losses (i.e., due to the difficulties- pregnancy, loss of work, difficulties in fulfilling family/professional obligations, problems in social relations, and problems in daily activities—e.g., in the form of disturbances with sleeping, eating, movement, sexual intercourse, bowel movements, frequent fatigue, and frustration in achieving goals) [49,50]; (d) a reduction in the perceived quality of life in various domains.
Hormonal birth control does not cure or eliminate endometriosis, but it can help manage pain and heavy bleeding for many individuals by reducing or stopping periods. However, opinions and experiences vary widely; some patients find relief through trial and error, while others experience no improvement or unwanted side effects.
Smolarz, B., Szyłło, K., & Romanowicz, H. (2021). Endometriosis: Epidemiology, Classification, Pathogenesis, Treatment and Genetics (Review of Literature). International journal of molecular sciences, 22(19), 10554. https://doi.org/10.3390/ijms221910554
So far, the pathomechanisms of the formation of endometriosis have not been definitively explained. The theory of Samson (“retrograde menstruation”) is more widespread. It says that the foci of endometriosis arise as a result of the displacement of menstrual blood into the peritoneal cavity through the fallopian tubes [5,6,53].
Literature data indicate that in 80% of women with open fallopian tubes there is a retrograde outflow of menstrual blood, while endometriosis occurs only in some. This suggests the presence of other factors determining the survival of endometrial cells in the peritoneal cavity and their implantation
Signorile PG, Baldi F, Bussani R, D’Armiento M, De Falco M, Boccellino M, Quagliuolo L, Baldi A. New evidence of the presence of endometriosis in the human fetus. Reprod Biomed Online. 2010 Jul;21(1):142-7. doi: 10.1016/j.rbmo.2010.04.002. Epub 2010 Apr 4. PMID: 20471320.
Recently, the presence of ectopic endometrium has been demonstrated in a significant number of human female fetuses (four in 32 cases) analysed by autopsy (Signorile et al., 2009b). This observation has been the first direct and systematic demonstration of the theory of developmentally misplaced endometrial tissue as the cause of endometriosis. The new case presented here reinforces that observation and represents the first step towards a detailed and methodical analysis of this phenomenon. These data, indeed, beg the question as to why pathologists have never described this phenotype; this could be explained by the fact that these are very small lesions, located in a very specific anatomical area that is very rarely investigated during autopsy. In particular, this study carefully analysed the molecular phenotype of this ectopic endometrium, showing that it expresses characteristic markers of the epithelium and of the stroma of the genital tract, such as cytokeratin 7, CA125, oestrogen receptor and CD10. The histological and immunohistochemical analysis of the eutopic and ectopic endometrium shows a very similar phenotype. This observation argues against the possibility that this ectopic endometrium could disappear during the final steps of organogenesis. Interestingly, a similar CD10 staining pattern was also found in the cases of fetal endometriosis presented in Signorile et al. (2009b). It should also be noted that epithelial differentiation and distribution in the uterus occur in the human fetus in a similar way as in the adult (Barberini et al., 2007). Interestingly enough, the existence of choristoma composed of Müllerian remains in adults has been codified and named Mülleriosis, even if this phenomenon has been interpreted, but not demonstrated, as different from endometriosis (Batt et al., 2007). It is speculated that this ectopic endometrium would remain quiescent and asymptomatic until puberty, when the hormonal inputs would cause its regrowth and, consequently, the onset of the symptoms of endometriosis. The clinical and therapeutic implications of this observation are straightforward. Endometriosis should not be considered a recurrent disease and complete surgery can be curative; nevertheless, it would not justify post-operative hormonal treatments. Finally, taking into account the enormous problems of infertility caused by this disease, all information on the pathogenesis of endometriosis, could have important clinical implications for the management of associated infertility.
Nevertheless, these data do not confute the theory of reflux menstruation that is accepted by the majority of the workers involved in endometriosis research. It could be possible that, based on the secondary Müllerian system theory (Lauchlan, 1994), the same milieu of molecules operating in utero and indicated as responsible for the peritoneal implantation might facilitate extrauterine dislocation of endometrium during fetal development from the Müllerian ducts. Further studies in in-vitro and animal models are urgently required in order to fully investigate the Mülleriosis hypothesis and to determine its real clinical value.
I have many thoughts surrounding the pathogenesis of endometriosis, but I barely scraped through undergrad, so I’ll leave that to the professionals. What I will say is this- there is no such thing as an endometriosis specialist when we know next to nothing about the disease. And if you tell me to eat low fodmap I will punch you.
endoreality 
Leave a comment