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Prenatal exposure to the world’s most common weedkiller can reshape the gut, brain, and behavior, raising questions about current safety limits.
Even extremely small amounts of the herbicide glyphosate can harm gut health, disrupt metabolism, and change behavior in mice, scientists say. The effects aren’t limited to the exposed animals—they pass on to their children and grandchildren.
The new research, to be published Nov. 1 in Science of the Total Environment, suggests that prenatal exposure to glyphosate disrupts gut bacteria, hormones, and brain signaling in mice. Even at doses far below current safety guidelines, the herbicide is linked to inflammation, metabolic problems involving appetite and blood sugar, and signs of neurological risk.
“Our findings demonstrate that prenatal glyphosate exposure, at doses consistent with real-world dietary intake, can disrupt multiple physiological systems across generations,” the researchers say.
Glyphosate, best known as the active ingredient in Roundup®, is the most widely used herbicide in the world, with more than 160 million kilograms applied annually in North America. Once thought safe because it targets a plant-specific pathway absent in humans, glyphosate may still indirectly harm people by disrupting gut microbes, immune responses, and hormone systems — especially during pregnancy and early life, according to emerging evidence.
Exposure to glyphosate has been linked to cancer, liver and kidney disease, endocrine disruption, fertility issues, neurotoxicity, and other health concerns, despite industry pushback. Earlier this year, research showed glyphosate significantly harmed the health of babies in rural U.S. communities over the past two decades, especially those already at risk of poor birth outcomes.
Other long-term studies, such as the CHAMACOS cohort, link early-life glyphosate exposure to higher risks of liver and cardiometabolic disorders by age 18.
This study, conducted by researchers at the University of British Columbia and the University of Alberta in Canada, shows mice exposed to glyphosate before birth were less active overall, moved shorter distances and at slower speeds, and showed weaker working memory (the ability to store and process information). The mice also explored less, suggesting reduced curiosity or mild movement difficulties.
Prenatal exposure caused microscopic inflammation, similar to that observed in early-stage colon inflammation (colitis). Gut damage, loss of protective mucus, and chronic inflammation persisted in the grandchildren (F2 generation).
Other key findings include:
Metabolic problems: Offspring had difficulty processing sugar, exhibited insulin resistance, and produced lower levels of GLP-1, a hormone that regulates blood sugar.
Microbiome disruption: Prenatal exposure to glyphosate altered gut bacteria and their function. Bacteria linked to depression, Parkinson’s disease, and metabolic disease increased, along with chemical changes, including excess acetate, which, at high levels, can disturb metabolism and drive nervous system overstimulation.
Hormonal shifts: Appetite hormones were thrown off balance. Ghrelin (which triggers hunger) was lower, while leptin (which signals fullness) was higher, a pattern seen in obesity and weakened gut barriers. In healthy mice, glyphosate exposure altered the production of key metabolic hormones, potentially linking it to endotoxemia—a potentially hazardous condition where toxins from gut bacteria leak into the bloodstream.
Gut–brain signals: The herbicide disrupted the normal links between bacteria and key chemicals, such as GLP-1 and tryptophan metabolites, both of which are vital for blood sugar control, mood, and immunity. Strongest effects were seen in the grandchildren. Overall, higher glyphosate exposure was associated with lower GLP-1 levels suggesting lasting impacts on metabolism and gut-brain signaling across generations.
Colon barrier weakness: In healthy mice glyphosate reduced mucus-producing cells, thinning the gut barrier and making it easier for bacteria to cross into tissue and activate the immune system. These effects weren’t seen in colitis-prone mice, whose existing inflammation may have masked them.