What if today’s food residues could shape tomorrow’s immune problems, metabolic disorders, and even behavioural challenges?
That’s the uncomfortable question raised by a groundbreaking July 2025 study from researchers at the University of British Columbia. And it’s a question New Zealand regulators can no longer afford to ignore.
In this first-of-its-kind mouse study, scientists exposed pregnant females to glyphosate at two doses: one mimicking typical human dietary intake (0.01 mg/kg/day) and the other matching the EPA’s official “safe limit” (1.75 mg/kg/day). The results? Profound disruptions in gut health, immune signaling, glucose metabolism, hormone balance, and brain behaviour — not just in the first generation of offspring, but in their children too.
Let’s be clear: these weren’t high, artificial doses. The lower exposure — known as the “Average American Diet” or AAD level — was based on realistic food consumption levels reported in U.S. and Canadian dietary surveys. And yet it still caused damage.
Across both F1 and F2 generations, the researchers observed patterns of inflammation, insulin resistance, impaired working memory, gut microbiome shifts, and even signs of enteric neurodegeneration.
If that’s not reason enough to revisit our own safety assumptions in Aotearoa, what is?
“But We’re Not Mice…” Why These Studies Still Matter
It’s a common response. And sure, we’re not mice. But studies like this aren’t designed to predict exactly what will happen in humans — they’re designed to flag what could go wrong.
Rodents are used in toxicology because many of their core biological systems mirror our own — especially when it comes to hormones, metabolism, neurodevelopment, and immune function. Their short life cycles allow researchers to observe long-term, even multi-generational effects far faster than we ever could in humans.
Most of the medications we take, food safety limits we rely on, and chemical approvals regulators grant are first based on rodent studies. When those studies start flashing warning signs across multiple biological systems — at real-world exposure levels — that’s not something to dismiss. That’s something to investigate further.
For more on why rodent studies are still deeply relevant to human health, read:
The Rat Study That Might Be More Human Than You Think
Real-World Exposure, Real-World Risks
Most toxicology studies test huge doses of chemicals — often hundreds or thousands of times higher than what humans would typically consume — in order to observe acute effects. But that approach can miss more subtle, long-term risks that emerge at low but chronic exposure levels.
That’s what makes this study different.
Researchers exposed pregnant mice to glyphosate through their drinking water at:
- 0.01 mg/kg/day – A realistic dietary exposure level derived from food residue data (the AAD dose)
- 1.75 mg/kg/day – The U.S. EPA’s Acceptable Daily Intake (ADI)
Exposure began before conception and continued throughout gestation. After birth, researchers followed the offspring for two generations, evaluating immune function, gut health, hormone signaling, glucose tolerance, behaviour, and microbiome composition.
And they didn’t just study healthy mice. They also included animals genetically prone to colitis — to mimic vulnerable populations more likely to suffer from Western-diet-driven diseases like IBD.
Gut Damage Without Visible Disease
Even though the glyphosate-exposed mice didn’t develop full-blown colitis, their colons told a different story.
In healthy offspring, glyphosate exposure led to:
- Goblet cell depletion – reducing the protective mucus barrier
- Lower mucin-2 expression – critical for gut lining protection
- Increased macrophage infiltration – a sign of immune activation
- Pro-inflammatory cytokines – skewed toward Th1 and Th17 dominance
These changes — collectively known as microscopic colitis — emerged at both the AAD and EPA dose levels. They also persisted into the second generation, suggesting a lasting, heritable impact.
In mice already genetically prone to gut inflammation, the effects were harder to detect. But that’s not reassuring — it may just mean that glyphosate’s impact is masked when inflammation is already high.
Impaired Glucose Metabolism & Hormone Disruption
Healthy offspring exposed to glyphosate before birth also developed:
- Impaired glucose tolerance
- Reduced insulin sensitivity
- Lower GLP-1 levels – a hormone critical for regulating blood sugar and appetite
- Elevated leptin and reduced ghrelin – hinting at leptin resistance and appetite dysregulation
- Tight junction disruption and endotoxemia – markers of leaky gut and immune stress
These effects mirror early warning signs for metabolic syndrome, which includes obesity, type 2 diabetes, and cardiovascular risk.
If anything, the study supports what’s already showing up in human research. In 2023, a longitudinal study from the CHAMACOS cohort found that early-life glyphosate exposure was linked to increased risk of metabolic syndrome by age 18. Notably, urinary glyphosate levels later in life didn’t correlate with the same outcomes — suggesting that the most sensitive window may be prenatal.
→ Read our summary of glyphosate’s metabolic effects
Disrupting the Gut-Brain Axis
The impacts weren’t limited to the gut or metabolism. Glyphosate-exposed offspring also showed changes in neurodevelopment and behaviour.
In healthy second-generation mice:
- Locomotor activity was reduced
- Working memory declined
- Serum kynurenine dropped – a neuroprotective metabolite tied to mood and cognition
Colitis-susceptible mice didn’t show the same outward behavioural changes, but they did develop enteric neuroinflammation, including:
- Elevated α-synuclein, GFAP, and SNAP-25 expression in gut tissue
- Reduced serotonin levels – a neurotransmitter central to gut-brain signaling
These findings raise the disturbing possibility that prenatal glyphosate exposure might contribute to subclinical neurodevelopmental or neurodegenerative risks through gut-mediated pathways.
Microbiome Shifts: Not Just “Friendly Fire”
The gut microbiome — our inner ecosystem of bacteria — plays a central role in regulating immunity, metabolism, and mental health. Disrupt it, and the body suffers.
This study found that prenatal glyphosate exposure triggered:
- ↓ Akkermansia muciniphila – protective, anti-inflammatory, GLP-1-supporting
- ↑ Parabacteroides distasonis – linked to colitis and depression in animal models
- ↑ Christensenellaceae – associated with Parkinson’s and neuroinflammation
- ↑ Bifidobacterium spp. – commonly thought of as “good,” but overgrowth seen in IBD flares
- ↑ Cyanobacteria (Gastranaerophilales) – not normally abundant in the gut, but thrive on phosphorus… like what glyphosate delivers
These shifts weren’t always visible at the level of total microbial diversity — but at the taxonomic and metabolite levels, the differences were real and biologically significant.
And worryingly, they persisted across generations.
Microbe–Metabolite Interactions Matter
Digging deeper, the researchers looked at how microbial changes correlated with key metabolites:
- Akkermansia abundance positively correlated with GLP-1
- Parabacteroides distasonis negatively correlated with both GLP-1 and tryptophan
- Generational shifts in these associations were observed, suggesting lasting reprogramming of host–microbe dynamics
If our microbes are mini-chemical factories, then glyphosate seems to be rearranging the production lines.
This supports growing evidence that glyphosate isn’t just a weedkiller — it’s an unintended microbiome modulator with downstream consequences for immune balance, hormone regulation, and brain signaling.
A Pattern of Subtle, Lasting Harm
One of the most important takeaways from the study is the non-monotonic dose-response pattern:
Some effects were actually stronger at lower doses (AAD) than at the higher EPA dose.
This is consistent with what’s seen with endocrine disruptors — chemicals that interfere with hormones and biological signaling at tiny doses, but whose effects may plateau or even reverse at higher exposures.
It’s one of the reasons the old toxicology maxim “the dose makes the poison” no longer holds up for many modern chemicals.
Why This Matters for New Zealand
We’re often told not to worry because glyphosate levels in our food fall below regulatory “safe” thresholds. But this study directly challenges that assumption.
Even the lowest dose — calculated from real food samples and matching a typical Western diet — caused:
- Gut inflammation
- Hormonal shifts
- Memory deficits
- Behavioural changes
- Multigenerational persistence
And yet, the Ministry for Primary Industries (MPI) is still considering increasing allowable glyphosate residues on wheat, oats, barley, and legumes — some by up to 9,900%.
→ See our article: Why Raising MRLs Threatens Public Health
If glyphosate’s impacts are this profound before a baby has even taken its first breath, how can we possibly justify exposing New Zealand families to more?
Where This Leaves Us
This isn’t just about mice. The gut-brain axis, the microbiome, immune development, metabolic regulation — they’re all part of the same system in humans, too. And early-life disruption of that system has lifelong consequences.
We don’t need more proof that glyphosate is dangerous in high doses. What we need is to acknowledge that low, real-world doses over time — especially in pregnancy and early life — can be just as harmful.
If regulators won’t act, communities must.
What You Can Do
✅ Share this article to raise awareness about prenatal glyphosate risks
✅ Support our independent food testing campaign to find out what’s really in our bread, cereal, and honey
✅ Ask your school, council, or sports club to stop using glyphosate near children
✅ Demand that your MP oppose the proposed MRL increases
✅ Join our mailing list for updates, test results, and action alerts
→ Sign Up for the Newsletter | Make a Donation
One More Thing: This Was Only About Glyphosate
It’s worth remembering: this study didn’t test Roundup® or any other commercial herbicide formulation.
It tested glyphosate — the so-called “active ingredient” that gets most of the regulatory attention.
But glyphosate rarely travels alone.
Most weedkillers on the market contain a cocktail of other chemicals — known as formulants or co-formulants — designed to make the glyphosate more effective. These additives help the chemical penetrate plant (and potentially animal) tissues more efficiently by breaking down cell barriers, altering absorption, or increasing chemical stability.
And unlike glyphosate, these extra ingredients are often shielded as proprietary trade secrets, meaning we have little to no public data about their safety — and they’re rarely tested in long-term studies.
So if even pure glyphosate — without all the chemical boosters — is capable of disrupting development across generations…
What happens when you add the rest of the mix?
That’s a question New Zealand regulators have so far avoided. But for the sake of future generations, it can’t be avoided much longer.
Resources & References
When evidence begins to stack across species, disciplines, and decades, we can’t afford to look the other way. The following research highlights the growing case against glyphosate’s “safe” reputation — from cellular toxicity to transgenerational effects, metabolic dysfunction, and gut-brain disruption. It’s time regulators stop pretending these studies don’t exist.
Full study: Prenatal exposure to dietary levels of glyphosate disrupts metabolic, immune, and behavioral markers across generations in mice
ScienceDirect, (2025)
This is the central mouse study we’ve been discussing: prenatal exposure to glyphosate at dietary and regulatory doses caused lasting disruptions in immune, metabolic, microbiome, and behavioural systems across two generations. It serves as a strong real‑world warning about low‑level exposure.
Findings from the CHAMACOS Study
Association of Lifetime Exposure to Glyphosate and Aminomethylphosphonic Acid (AMPA) with Liver Inflammation and Metabolic Syndrome at Young Adulthood
Eskenazi et al. (2023)
In a human epidemiological study, researchers followed children into young adulthood and found that higher glyphosate / AMPA exposure in childhood was associated with increased risk of liver inflammation and metabolic syndrome.
Is the Use of Glyphosate in Modern Agriculture Resulting in Increased Neuropsychiatric Conditions Through Modulation of the Gut‑Brain‑Microbiome Axis?
Barnett JA, Bandy ML & Gibson DL (2022)
This perspective article explores how chronic glyphosate exposure might influence neurodevelopment and behaviour by disrupting the gut microbiome and the gut‑brain axis. The authors discuss mechanisms such as loss of beneficial gut bacteria (e.g. Lactobacillus, Ruminococcaceae), reduced microbial metabolites (SCFAs, indoles), increased inflammation, HPA axis activation, and transgenerational effects.
Gut microbiota and neurological effects of glyphosate
Rueda‑Ruzafa L et al. (2019)
This review summarizes evidence linking glyphosate‑induced dysbiosis (microbial imbalance) in the gut to neurological outcomes, including emotional, cognitive, and neurodegenerative changes. It highlights how glyphosate may disproportionately kill beneficial microbes, enabling overgrowth of harmful bacteria that produce neurotoxic metabolites.
Ethoxylated adjuvants of glyphosate-based herbicides are active principles of human cell toxicity
Mesnage R, Bernay B, Séralini GE.
Toxicology, 2013.
This study found that the so-called “inert” ingredients in glyphosate-based herbicides — particularly ethoxylated surfactants like POEA — were often more toxic to human cells than glyphosate itself. The researchers concluded that full formulations, not just glyphosate, must be evaluated for real-world health impacts.
Co-formulants in glyphosate-based herbicides disrupt aromatase activity in human cells
Defarge N, Takács E, Lozano VL, et al.
Toxicology Reports, 2016.
This study revealed that common co-formulants in glyphosate products can interfere with aromatase, an enzyme critical to human hormone balance. The findings suggest that even at low levels, these additives may contribute to endocrine disruption — a risk not accounted for when only testing glyphosate alone.
Differential effects of glyphosate and Roundup on human placental cells
Richard S et al.
Environmental Health Perspectives, 2005.
In this early but influential study, researchers showed that Roundup was more toxic than glyphosate alone, especially to human placental cells. The herbicide formulation caused cell death and disrupted hormonal function, raising concerns about reproductive health risks from real-world exposures.
If this level of independent research is out there, why isn’t it being reflected in our food policies? Why are New Zealand authorities still basing safety decisions on outdated science and industry reassurances?
At what point do we stop dismissing the warning signs — and start listening?
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