Why Does Endometriosis Come Back After Surgery? The Gut, Estrobolome, and Bioenergetic Mechanism — Why hormonal suppression addresses one source but not all

Continuous oral contraceptives, GnRH agonists, progestins, and aromatase inhibitors all reduce the estrogen exposure that endometriotic lesions experience. They reduce ovarian estrogen production directly. They reduce or eliminate menstrual cycling. They produce real symptomatic benefit in many patients. They do not address the estrogen recirculated from the gut estrobolome. They do not address the systemic inflammation driving lesion-permissive immunology. They do not address the mast cell infiltration of pelvic tissues. They do not address the mitochondrial dysfunction in endometriotic tissue. They suppress one part of the system while the other parts continue to operate. This explains the partial response patterns. Patients on hormonal suppression often experience meaningful but incomplete relief. The pain reduces but does not resolve. The disease persists at the tissue level even when symptoms improve. Discontinuation of the medication is followed by rapid recurrence in most cases. The medication was containment, not treatment of the underlying state. The side effect profile of hormonal suppression is also relevant. GnRH agonists produce a chemically induced menopause with significant bone density, mood, and metabolic consequences. Long-term progestin use carries cardiovascular and breast cancer risks. Aromatase inhibitors are similar. The risk-benefit calculation for long-