Can glyphosate and triclosan disrupt the gut microbiome?

Environmental exposure to glyphosate and triclosan can directly alter the structural and functional landscape of the gut microbiome through distinct, compound-specific enzymatic pathways.

Mechanistic pathways of disruption

• Glyphosate EPSPS inhibition: Glyphosate competitively inhibits the 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS) enzyme in the bacterial shikimate pathway. This acts as a selective antimicrobial pressure, suppressing beneficial commensals with sensitive Class I EPSPS (such as Lactobacillus and Bifidobacterium), while allowing opportunistic pathogens with resistant Class II EPSPS (such as Clostridium and Salmonella) to survive. This inhibition causes an accumulation of upstream intermediates (shikimate and 3-dehydroshikimate) and depletes downstream aromatic amino acids.
• Triclosan fatty-acid synthesis inhibition: Triclosan targets bacterial enoyl-acyl carrier protein reductase (ENR, such as FabI or FabK), halting essential bacterial fatty-acid synthesis. This selective pressure shifts metabolic pathways toward acetyl-CoA fermentation and alters the metabolism of vitamins, essential fatty acids, and bile acids.

Dysbiosis and reduced microbial resilience

• Loss of short-chain fatty acids (SCFAs): Both toxicants significantly suppress the microbial production of vital SCFAs, including acetate, propionate, and butyrate.
• Compromised colonization resistance: The resulting reduction in taxonomic alpha diversity and alteration of beta diversity drive gut dysbiosis. The depletion of key commensal taxa and SCFA metabolites impairs the gut's colonization resistance, reducing overall microbial resilience and increasing susceptibility to opportunistic pathogen expansion, inflammatory signaling, and metabolic dysregulation.

Bottom line

• Preclinical models show that glyphosate and triclosan disrupt the gut microbiome by inhibiting the EPSPS and ENR pathways, respectively. These enzymatic disruptions deplete essential short-chain fatty acids, drive taxonomic dysbiosis, and compromise the microbial community's resilience against pathogens.