After oral ingestion, CDG releases D-glucaric acid which is metabolized to D-glucaro-1,4-lactone (GL). GL is the biologically active inhibitor of beta-glucuronidase enzyme.
Beta-glucuronidase is produced primarily by gut bacteria (E. coli, Clostridium, Bacteroides) and to a lesser extent by host tissues. Elevated beta-glucuronidase activity is common in dysbiosis, constipation, high-meat diets, and certain disease states.
When the liver detoxifies estrogens and other compounds, it conjugates them with glucuronic acid (Phase II glucuronidation), making them water-soluble for biliary excretion. These conjugates pass into the gut for elimination. If beta-glucuronidase activity is high, the glucuronide bond is cleaved in the gut, releasing free (unconjugated) estrogen/toxin which can be reabsorbed across the intestinal wall back into circulation - the 'enterohepatic recirculation' pathway.
By inhibiting beta-glucuronidase, CDG/GL keeps conjugated estrogens and toxins LOCKED in their glucuronide form, ensuring they pass through the gut and are eliminated in stool rather than reabsorbed. This effectively increases the elimination of estrogens, xenobiotics, and bile acids.
CDG also induces hepatic Phase II UGT (UDP-glucuronosyltransferase) enzymes, increasing the rate at which the liver conjugates compounds for excretion - working synergistically with the beta-glucuronidase inhibition.
Cancer chemoprevention: animal models of mammary, colon, and skin carcinogenesis show CDG reduces tumor formation, attributed to enhanced clearance of carcinogens and pro-carcinogens before they damage DNA.