Can glyphosate exposure disrupt gut microbes and intestinal barrier function?

Although glyphosate is designed to target biological pathways unique to plants, emerging research demonstrates it can exert significant off-target effects on mammalian gastrointestinal health.

Microbiome disruption and taxonomic shifts

• Shikimate pathway inhibition: Glyphosate directly inhibits the enzyme 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS). While humans lack this pathway, bioinformatics indicate that approximately 54% of common human gut bacterial species possess sensitive EPSPS enzymes.
• Depletion of beneficial taxa: This selective pressure leads to taxonomic shifts, specifically depleting protective genera like Bifidobacterium and Lactobacillus, which in turn decreases beneficial short-chain fatty acid (SCFA) biosynthesis.

Epithelial barrier impairment

• Tight junction downregulation: Preclinical studies using Caco-2 human epithelial monolayers and animal models (such as piglets and chicks) show that glyphosate exposure downregulates the expression and alters the localization of essential tight junction proteins, including ZO-1, claudin-1, and occludin.
• Increased permeability: This molecular disruption significantly decreases transepithelial electrical resistance (TEER) and increases paracellular flux, compromising the structural integrity of the intestinal barrier.

Bottom line

• Bottom line: Substantial preclinical and bioinformatic evidence supports the claim that glyphosate exposure can disrupt gut microbial ecology through targeted shikimate pathway inhibition and impair intestinal barrier function by compromising tight junction integrity.