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Cotgreave IA, Moldeus P

Oral pathogens, especially P.g , can upregulate hepatic flavin-containing monooxygenase 3 (FMO3) through their derived products and promote the conversion of TMA to TMAO, while simultaneously disrupting the intestinal barrier and disturbing the gut microbiota structure, forming an oralgutliver pathogenic pathway (Wang et al., 2024

Furthermore, any intact glutathione that does manage to cross the intestinal wall is immediately routed to the liver via the portal vein, where it is subjected to heavy "first-pass metabolism." Because of this rigorous digestive and hepatic breakdown, early pharmacokinetic studies demonstrated that standard oral glutathione often fails to significantly boost serum or intracellular levels, rendering many traditional, over-the-counter supplements highly ineffective for chronic illness management

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