The observation, stated once
People with endometriosis report allergic-type and multi-system reactivity symptoms more often than expected.
Through the mechanism
Endometriotic lesions are densely populated with mast cells, sitting against small nerve fibers that have grown into the lesion. Mediator release there is not a coincidental allergy — it is part of how the lesion produces pain.
Estrogen upregulates mast-cell activity. A monthly hormonal rise therefore raises pelvic mediator release and systemic reactivity at the same time, which is why flares synchronize.
Mediators sensitize the same nerve fibers they were recruited to protect, feeding the pain-processing mechanism directly.
Read this way, cyclical hives, cyclical gut reactivity and cyclical pelvic pain are one signal in three places rather than three unrelated problems.
What it changes in practice
- Log reactivity against cycle phase before concluding a food is the trigger.
- A mediator-blocking trial is reasonable when reactivity is multi-system, with a defined endpoint.
- Treating pelvic disease and mediator load together tends to outperform either alone.
Hold this loosely
Mast cells in lesions are well documented; that MCAS as a syndrome is more prevalent in endometriosis is plausible but not firmly established.