Why Does Endometriosis Come Back After Surgery? The Gut, Estrobolome, and Bioenergetic Mechanism — The Host Capacity Model reading of endometriosis

The Host Capacity Model is a systems-biology framework that approaches chronic illness from the layer of cellular bioenergetics, gut barrier integrity, microbial community function, and regulatory cofactor pools. The framework is described in full at biomelogic.net/host-capacity-model . In endometriosis, the framework points to five specific mechanisms that together determine whether retrograde-deposited cells establish viable disease. Mechanism 1: The estrobolome and beta-glucuronidase The estrobolome is the collection of gut microbial genes encoding enzymes that metabolize estrogens. The dominant relevant enzyme is beta-glucuronidase, produced primarily by members of the Bacteroidetes phylum and certain Clostridium species. Beta-glucuronidase deconjugates glucuronidated estrogen metabolites in the intestinal lumen, removing the chemical tag that marked them for fecal excretion. The deconjugated estrogens are then reabsorbed across the intestinal epithelium and re-enter enterohepatic circulation. This is a normal physiological process at baseline activity. The hepatic conjugation and beta-glucuronidase deconjugation cycles operate as part of the enterohepatic system that regulates circulating estrogen. The problem in endometriosis is that beta-glucuronidase activity is often substantially elevated due to gut dysbiosis. The Clostridium and Bacteroides expansion that accompanies