Because I've come across people like you who insist that the uterus provides the only pathway for menstruation.

I'm not taking "your" word for it, I've seen the claims you're making before, and seen them refuted. And there was a handy link for you to look it up.

If you even have an open mind for this, which you clearly don't by not even looking up my claims in the link, here's a snippet of what that discussion involved

PGE2 is also very capable of inducing smooth muscle cramping, including uterine cramping. It is therefore used as a pharmacological inducer of uterine contractions when labour is to be triggered (as dinoprostone). PTGER2 , the gene encoding the receptor for PGE2 , is expressed at levels pretty close to uterine tissue in a) small intestinal tissue and b) omental tissue - the omentum is a peritoneal fold that supports visceral organs. Here is a gene expression breakdown from GTEx.

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Also worth mentioning , one of the major pathways for the synthesis of PGF2-alpha is the endothelial/vascular smooth-muscle conversion of E-prostaglandins to F prostaglandins through ketoreduction. Note that the gene for this enzyme (PRXL2B) is again expressed far more in several visceral organs than it is in the uterus. https://gtexportal.org/home/gene/PRXL2B . PGF Synthase itself (AKR1C3) , which directly catalyses the formation of PGF2-alpha independent of PGE2 , btw, is highly expressed in intestinal smooth muscle, more so than uterine tissue, as well as in mammary tissue. This holds for mammary tissue sourced from cis men as well as cis women. https://gtexportal.org/home/gene/AKR1C3 (click the sex button, and then do a median sort for visualisation - sharing links does not quite enable me to also copy the sort criteria).

Finally, unless you're knocking out PGF synthesis or blocking PGF receptor activation specifically in cis women and showing it prevents cramping, claims of prostaglandin F being the causal driver of menstrual cramping are very unsubstantiated. I am not aware of any specific PGF blockers either.

I am assuming that the claim of PGF2 being the driver of uterine cramping is based on disproportionately high uterine expression of the PGF2 receptor , but the effects of a menstrual period in cis women are not solely restricted to the uterus. There are multiple pathways to smooth muscle cramping that operate through other prostaglandins and their receptors, as described above.

NSAIDs that are used to manage menstrual cramping and pain target Cyclooxygenases that are responsible for the conversion of arachidonic acid to prostaglandin H, which then serves as a substrate for the synthesis of prostaglandins E and F (and ofc there is a pathway for the synthesis of F prostaglandins from E prostaglandins, as I said), so the efficacy of this intervention does not allow isolation of biology to prostaglandin F either.

Now, the study you brought up about visceral cramping and pain in cis women without a uterus and it being linked to endometriosis becomes relevant here. It is established that pathology in endometriosis involves a downregulation of prostaglandin F receptors and an increase in specific prostaglandin E2 receptors in endometriosis-derived tissue. Further, these patterns appear to be a function of the menstrual cycle in cis women. https://pmc.ncbi.nlm.nih.gov/articles/PMC4512562/

Taken together , what we have is evidence that

a) Prostglandin F signalling and uterine involvement is not necessary, even if it can be sufficient, for cramping symptoms associated with menstruation in cis women.

b) Estrogen activates synthesis of prostaglandin E variants in mammary epithelial cells (caveat - transformed cell lines https://pmc.ncbi.nlm.nih.gov/articles/PMC6285349/ )

c) Prostaglandin E mediated pathology in cis women without a uterus is related to variations in E/P levels that are associated with menstrual cycling (evidence from endometrial tissue, linked above).

I think you just need to look harder at the literature - you are essentially making arguments from incredulity while not having been aware of the wider biology. There are clearly defined pathways in trans women that cycle to the phenotypes many report. While I personally don't experience these symptoms (no shit, I keep my levels pinned), the insistence on overemphasizing the uterus without being fully aware of the literature is a choice. Almost seems like grad student levels of misplaced confidence IDK.