Why Does Endometriosis Come Back After Surgery? The Gut, Estrobolome, and Bioenergetic Mechanism — Why the standard endometriosis model produces variable results

The standard model of endometriosis pathogenesis rests on Sampson's hypothesis of retrograde menstruation: viable endometrial cells are deposited in the peritoneal cavity through retrograde flow through the fallopian tubes during menstruation, and these cells implant and grow ectopically. The treatment implications follow directly. Reduce the menstrual flow that produces the seeding (hormonal suppression). Remove the lesions that have already implanted (surgery). Suppress the hormonal environment that supports lesion growth (estrogen suppression, progestin therapy). The data do not fully support this model. Retrograde menstruation occurs in approximately 90 percent of women but endometriosis develops in approximately 10 percent. The seeding cannot be the sufficient cause. Something about the recipient environment determines whether retrograde-deposited cells establish viable lesions. The standard model has names for this something (immune surveillance failure, hormonal milieu, peritoneal microenvironment), but it does not specify the mechanism in clinically actionable terms. The mechanism the literature is increasingly converging on, particularly in research from 2022 onward, involves the gut microbiome and its influence on estrogen metabolism, immune function, and inflammatory tone. The Host Capacity Model framework names this convergence and integrates it with the broader sys