Glyphosate and Inflammatory Bowel Disease: The Questions New Zealand Isn’t Asking

Canterbury has one of the highest rates of Crohn’s disease ever recorded anywhere on earth.

Not one of the highest in the South Pacific. Not one of the highest in the Southern Hemisphere. One of the highest anywhere on earth.

In 2004, a population-based study by Professor Richard Gearry and colleagues at the University of Otago, Christchurch, put Canterbury’s Crohn’s incidence rate at 16.5 per 100,000 — at the time among the highest in the world. A decade later, that rate had grown 1.6-fold. By January 2024, a new Canterbury prevalence study found that one in every 150 people in the region was living with inflammatory bowel disease. IBD cases in Canterbury have nearly tripled since 2006, from around 1,400 people to more than 4,000. Nationally, approximately 20,000 New Zealanders are now living with IBD, and modelling projects that number will exceed 40,000 by 2045.

Something is driving this. Genetics don’t shift across a single generation. Improved diagnosis accounts for some of the increase — but the researchers themselves are careful to note that diagnostic improvement does not explain the full rise. Gastroenterologists like Professor Gearry describe being “surprised” by the trajectory. The scientific literature has a term for what Canterbury may be experiencing: the “compounding prevalence stage” of the IBD epidemiological model — the phase where incidence has already escalated and cases are accumulating faster than they resolve.

Somewhere in the background of this story is a herbicide that New Zealand uses more of than almost any other developed country — applied to our pasture, our crops, our orchards, our roadsides, and our suburban lawns. Glyphosate. And the question this article asks is not whether glyphosate causes inflammatory bowel disease. The evidence does not support that claim. The question is a different one, and in some ways a more uncomfortable one: is anyone in New Zealand even investigating whether glyphosate might be part of what is happening?

The answer, as best as this investigation can determine, is no.

Crohn’s Disease and Ulcerative Colitis: Why IBD Rates Are Rising and Who Is at Risk

Inflammatory bowel disease is an umbrella term for two closely related but distinct conditions: Crohn’s disease and ulcerative colitis. Both involve chronic, relapsing inflammation of the gastrointestinal tract. Crohn’s can affect any part of the digestive system from mouth to anus; ulcerative colitis is confined to the colon and rectum. Together they produce symptoms that range from debilitating abdominal pain, diarrhoea, and rectal bleeding to fatigue, malnutrition, anaemia, and — in the case of Crohn’s — fistulae and bowel obstruction requiring surgery.

IBD is not IBS. It is not gluten sensitivity. It is not a functional condition that improves with dietary tweaks. It is a structural, immune-mediated disease of the gut lining, and it carries elevated all-cause mortality. A 2025 study using New Zealand’s Integrated Data Infrastructure found that New Zealanders with IBD between 2012 and 2022 had a standardised mortality ratio of 1.69 — meaning they were dying at a rate 69% higher than the general population, from all causes combined.

The conventional scientific consensus holds that IBD arises from a perfect storm: genetic susceptibility, an immune system that misreads gut bacteria as threats, and environmental triggers that nobody has yet fully characterised. Genetics explain why some people get IBD; they cannot explain why IBD rates are rising in every Westernised country, and specifically why New Zealand sits at the high end of a global trend that has been building since the 1970s.

The environmental trigger question is where glyphosate enters.

Glyphosate and Intestinal Permeability: Can a Herbicide Damage the Gut Wall?

To understand the glyphosate-IBD hypothesis, it helps to understand what has gone wrong in the gut of someone with IBD — and what researchers increasingly believe is going wrong before diagnosis.

The intestinal epithelium is a single-cell-thick layer separating the contents of the gut — bacteria, food particles, metabolic products — from the sterile interior of the body. That barrier is not passive. It is actively maintained by proteins called tight junctions, which act like molecular zippers between adjacent epithelial cells, controlling what passes through and what does not. When tight junctions are disrupted, the barrier becomes permeable. Bacterial fragments, lipopolysaccharides, and incompletely digested proteins can enter systemic circulation — activating the immune system, generating inflammation, and, in genetically susceptible individuals, triggering or perpetuating the chronic immune dysregulation that defines IBD.

This is not a fringe hypothesis. Intestinal barrier dysfunction — what is often called “leaky gut,” though that term is contested — is now well established in the scientific literature on IBD pathogenesis. A 2025 review in Inflammatory Bowel Diseases describes intestinal barrier dysfunction as one of the defining features of IBD, involving increased intestinal permeability that enables bacterial toxins, antigens, and other harmful substances to cross the epithelial barrier. Research has also found elevated levels of zonulin — a protein that regulates the opening of tight junctions — in IBD patients, with levels correlating with disease activity.

The question relevant to this investigation is whether glyphosate can damage tight junctions and increase intestinal permeability at concentrations relevant to human dietary exposure.

In vitro research — cell culture studies — suggests it can. Work published in clinical nutrition literature has demonstrated that glyphosate can decrease transepithelial electrical resistance in intestinal epithelial cell lines, a standard measure of barrier integrity. While in vitro findings cannot be directly extrapolated to the human gut, they establish biological plausibility: glyphosate has the capacity to act on the cell machinery that maintains the intestinal barrier.

What is more recent, and more striking, is animal research that moves beyond cell studies.

Glyphosate at Regulatory Safe Levels Worsens Colitis: What a 2026 Study Found

In April 2026, the Journal of Agricultural and Food Chemistry published a study that deserves close attention. Researchers in China fed mice glyphosate at the regulatory “safe” level — the Acceptable Daily Intake set by food safety authorities — and then induced colitis. The outcome was unambiguous: compared to controls, the glyphosate-exposed mice experienced significantly worsened colitis.

The mechanism the researchers identified is specific enough to be worth describing. Glyphosate exposure increased the abundance of a gut bacterium called Bacteroides thetaiotaomicron. That bacterium produces palmitic acid, which in elevated concentrations activates a signalling cascade called the JAK-STAT pathway. The JAK-STAT pathway is a well-established driver of intestinal inflammation — it is, in fact, the target of a class of IBD drugs called JAK inhibitors, which are now used in the treatment of both Crohn’s disease and ulcerative colitis.

“Glyphosate, at the regulatory limit food safety authorities consider safe for daily human exposure, shifted the gut microbiome in a way that turned up a biological dial already implicated in IBD — and turned it up hard enough to worsen induced colitis in an animal model.”

This is animal research. It cannot be directly applied to humans. It does not prove that eating food containing glyphosate residues causes or worsens IBD in people. What it does is something that should interest regulators and clinicians: it identifies a specific, biologically coherent mechanism by which glyphosate exposure could plausibly contribute to intestinal inflammation in individuals already carrying IBD risk.

And it raises an uncomfortable question. The Acceptable Daily Intake for glyphosate was not set with JAK-STAT pathway activation or gut microbiome disruption in mind. It was set using older toxicological frameworks — frameworks that, as this series has documented in earlier articles, were designed to detect acute organ damage in laboratory animals, not subtle perturbations of microbial communities in a living gut.

Glyphosate and the Gut Microbiome: Why 54% of Your Core Gut Bacteria May Be at Risk

Running beneath this specific study is a broader body of research that has been accumulating since approximately 2015.

Glyphosate’s mechanism of action — the one that makes it an effective herbicide — is the inhibition of an enzyme called EPSPS, which sits within the shikimate pathway used by plants and microorganisms to synthesise aromatic amino acids. Because humans do not have the shikimate pathway, this has long been cited as the primary basis for glyphosate’s safety: it targets a pathway we don’t have.

The difficulty with that reassurance is that our gut bacteria do have the shikimate pathway. And as bioinformatics analysis by Leino, Helander, Puigbò and colleagues at the University of Turku found, approximately 54% of core human gut bacterial species are potentially sensitive to glyphosate based on their EPSPS enzyme structure.

Why the “it only targets plant pathways” argument doesn’t hold

Glyphosate has long been considered safe for humans because we don’t have the shikimate pathway it targets. What we do have is a gut microbiome — and our gut bacteria do have the shikimate pathway. University of Turku researchers found that 54% of core human gut bacterial species are potentially sensitive to glyphosate. The regulatory safety case was built on a human biology argument that stops at the gut wall.

A 2023 review in Gut Microbes from APC Microbiome Ireland at University College Cork — the Walsh, Hill, and Ross paper cited in earlier NMGNZ articles on celiac disease and microbiome disruption — laid out the emerging evidence systematically. That review noted that glyphosate’s potential to inhibit the growth of beneficial microbes in the gut, or alter their functionality, is a serious topic warranting further investigation. It also noted honestly that controlled human studies remain scarce, and that the evidence base for specific human health effects is not yet settled.

That caveat is important and must be held. The research architecture — mostly animal studies, in vitro work, and epidemiological correlations — does not yet constitute proof of causation in humans. What it constitutes is a credible biological mechanism that has not been disproven, combined with a rising disease burden that has not been explained.

The IBD literature itself has a clear position on the role of the gut microbiome: it is central. IBD is characterised by dysbiosis — disruption of the normal microbial community — and the inflammatory response that drives both Crohn’s disease and ulcerative colitis depends heavily on how the immune system reads microbial signals from the gut. If glyphosate is selectively suppressing the beneficial bacteria that help maintain immune tolerance in the gut, the downstream consequences would, on current scientific understanding, look something like IBD in those with the relevant genetic predisposition.

Is that what is happening? Unknown. Is it biologically coherent? Yes.

Could Glyphosate Exposure Affect IBD Risk Across Generations? What Animal Research Suggests

One finding in this literature is too striking to pass over without comment, even though it sits at the more speculative end of the evidence base.

A 2024 preprint study from a Canadian IBD research group — Barnett and colleagues — examined the effects of prenatal glyphosate exposure in mice at dietary levels. The findings extended across generations. F1 and F2 offspring — the children and grandchildren, in animal terms, of glyphosate-exposed mothers — showed increased microscopic colon damage and elevated pro-inflammatory cytokines compared to unexposed controls. In colitis-susceptible mice, glyphosate-exposed lineages also showed increased expression of RELM-β, a goblet cell mediator implicated in colitis development.

The researchers described this as the first study to highlight the transgenerational effects of glyphosate at previously-deemed-safe exposure levels on colitis-related pathology.

What this raises — carefully, as a hypothesis — is whether the IBD burden we are seeing emerge in younger New Zealanders might reflect not just their own glyphosate exposure but the cumulative biological consequences of a generation of agricultural and dietary exposure in their parents. The epigenetic mechanisms by which environmental exposures in one generation alter disease risk in the next are an active and contested area of science. This finding is in mice, at a preprint stage, and should be read with appropriate scepticism. But it should also be noted, because the same scepticism that demands we not overstate the evidence should equally demand we not ignore it.

Glyphosate Exposure in New Zealand: Agriculture, Roadsides, and What MPI’s Rules Don’t Cover

New Zealand is not a light glyphosate user. The herbicide is applied across agricultural land, horticulture, forestry, roadsides, and residential gardens. The October 2025 MPI ruling — restricting glyphosate application on wheat, barley, and oats grown for human consumption to pre-emergence use only — acknowledged the exposure concern for domestic grain, though it stopped well short of a blanket restriction.

But that ruling has limits. Imported grain and grain products — bread, breakfast cereals, pasta, processed foods — continue to enter New Zealand assessed against MRL limits that were not designed with gut microbiome effects in mind. The testing regime looks for residue levels that are acutely toxic. It does not look for residue levels sufficient to selectively alter microbial populations in the human gut over years of dietary exposure.

There is also the question of non-dietary exposure. Glyphosate is applied by councils to roadsides and reserves, by farmers to paddocks, and by homeowners to driveways and gardens. Dermal and inhalation exposure routes are real, even if the scientific literature has not yet established whether glyphosate absorbed through skin or inhaled as spray drift reaches gut microbiome bacteria at concentrations sufficient to disrupt microbial populations — a caveat that must be acknowledged.

Neither MPI nor EPA New Zealand conducts independent research into these exposure pathways. Both defer to overseas regulatory bodies — the US EPA and EFSA in Europe — whose own assessments have been the subject of substantial scientific controversy, as documented in earlier articles in this series examining the Monsanto Papers and the current US Supreme Court proceedings in Monsanto v. Durnell.

What New Zealand Gastroenterologists Know — and What No One Has Asked Them

There is no evidence that New Zealand gastroenterologists are investigating glyphosate as a potential environmental contributor to IBD in this country. This is not a criticism of those clinicians. The literature connecting glyphosate specifically to IBD is recent, largely preclinical, and not yet at a stage that would typically prompt clinical investigation.

But the broader question — what environmental factors are driving IBD’s rise in New Zealand — is one that gastroenterologists are openly asking. Professor Gearry’s description of being “surprised” by Canterbury’s trajectory, and his acknowledgement that IBD incidence is now rising among the Māori population, points to a disease pattern that cannot be attributed solely to genetic inheritance or urbanisation.

The international IBD research community has documented a range of environmental suspects: antibiotic use, dietary changes (ultra-processed foods, reduced fibre), reduced microbial diversity in early childhood, and altered sanitation. These are not mutually exclusive with glyphosate exposure — they may be operating simultaneously, and the scientific literature is increasingly focused on the cumulative effect of multiple environmental stressors on the gut microbiome rather than any single cause.

What is absent from that conversation in New Zealand is any serious investigation of agricultural chemical exposure as a factor. In France, Parkinson’s disease linked to pesticide exposure is formally recognised as an occupational disease. No equivalent research programme or regulatory framework exists here, for Parkinson’s or for IBD.

The Question MPI’s MRL Framework Has Never Asked About Glyphosate and IBD

The October 2025 MPI ruling on pre-harvest glyphosate application was a significant regulatory step. It recognised that residue levels in conventionally harvested grain for human consumption warranted restriction. It is worth acknowledging.

It is also worth asking what question that ruling did not address.

MPI’s MRL framework is a residue framework. It asks: at what concentration does glyphosate in food cause measurable harm according to established toxicological endpoints? The endpoints used in that framework are, broadly, acute organ toxicity, carcinogenicity (contested), and reproductive toxicity in conventional laboratory animal models.

What the MRL framework does not ask is: at what dietary exposure level does glyphosate alter the composition of the human gut microbiome in ways that increase intestinal permeability, activate inflammatory pathways, or — in genetically susceptible individuals — contribute to the onset or progression of immune-mediated gastrointestinal disease?

That question has not been asked, because the regulatory framework was designed before the gut microbiome’s role in immune regulation was understood at anything like its current level. The scientific understanding has moved. The regulatory framework has not kept pace.

“The scientific understanding has moved. The regulatory framework has not kept pace.”

Canterbury has one of the highest IBD rates ever recorded in the world. New Zealand has no dedicated research programme investigating whether the herbicide its farmers spray on their crops, its councils spray on its roadsides, and its homeowners spray on their gardens might be contributing to that fact.

Those two things should not be able to coexist without discomfort.

What New Zealand Needs to Do: Research, Regulation, and the Unanswered IBD Question

This series does not call for the immediate ban of glyphosate. The evidence does not justify that, and making claims beyond what the evidence supports would undermine the legitimate scientific concern at the heart of this investigation.

What the evidence does justify — clearly, and urgently — is this:

• A dedicated New Zealand research programme should investigate whether dietary and environmental glyphosate exposure correlates with IBD incidence. The data infrastructure exists: New Zealand’s Integrated Data Infrastructure contains IBD diagnostic records, and glyphosate exposure could be estimated through dietary surveys, occupational exposure data, and residential proximity to agricultural spray.
• The MRL framework should be reviewed with gut microbiome endpoints explicitly included. If the regulatory acceptable daily intake for glyphosate was derived without any consideration of effects on the shikimate pathway in gut bacteria — and it was — that omission is no longer defensible.
• Someone should ask Professor Gearry, publicly, whether Canterbury’s gastroenterology research programme has ever received a grant to investigate agricultural chemical exposure as an environmental trigger for IBD. If the answer is no, the next question writes itself.

No More Glyphosate NZ is an independent advocacy organisation. This article draws on peer-reviewed epidemiology, preclinical toxicology, and published gut microbiome research. We encourage readers to consult the primary sources and form their own conclusions.

Further Reading

On IBD rates in New Zealand

• Forbes, A.J. et al. (2025). Incidence, prevalence and mortality of inflammatory bowel disease in New Zealand 2006–2022 using hospital information in the Integrated Data Infrastructure. Internal Medicine Journal. onlinelibrary.wiley.com/doi/10.1111/imj.70291 — The first national-level IBD epidemiological study in New Zealand, finding nearly 20,000 people living with IBD and a standardised mortality ratio 69% above the general population.
• Forbes, A.J. et al. (2025). Compounding prevalence of inflammatory bowel disease in a 2024 population-based study from Canterbury, New Zealand. Journal of Gastroenterology and Hepatology. pmc.ncbi.nlm.nih.gov/articles/PMC12125484 — Canterbury 2024 prevalence study finding one in 150 people living with IBD, a rate 2.8 times higher than the same region in 2005.
• Su, H.Y., Gupta, V., Day, A.S. & Gearry, R.B. (2016). Rising incidence of inflammatory bowel disease in Canterbury, New Zealand. Inflammatory Bowel Diseases, 22(9), 2238–2244. pubmed.ncbi.nlm.nih.gov/27482976 — The 2014 Canterbury incidence study showing a 1.6-fold increase over the preceding decade and one of the highest Crohn’s disease rates in the world.
• University of Otago (2024). Global study charts growing health burden of IBD. otago.ac.nz/news/newsroom/global-study-charts-growing-health-burden-of-ibd — Professor Richard Gearry on Canterbury IBD cases nearly tripling since 2006 and the projection of 40,000 New Zealanders living with IBD by 2045.

On glyphosate, colitis, and IBD mechanisms

• Liu, J.B. et al. (2026). Dietary glyphosate at the regulatory “safe” level worsens colitis via a gut microbiota-derived palmitic acid-JAK-STAT pathway. Journal of Agricultural and Food Chemistry, 74(14), 11797–11813. pubs.acs.org/doi/10.1021/acs.jafc.5c17487 — Animal study finding that glyphosate at the regulatory acceptable daily intake worsened induced colitis via increased Bacteroides thetaiotaomicron, palmitic acid accumulation, and JAK-STAT pathway activation.
• Barnett, J.A. et al. (2024). Prenatal exposure to dietary levels of glyphosate disrupts metabolic, immune, and behavioural markers across generations in mice. Preprint, bioRxiv. biorxiv.org/content/10.1101/2024.08.27.609990 — First study to examine transgenerational effects of dietary-level glyphosate exposure on colitis-related pathology; findings should be read as hypothesis-generating pending peer review.
• Ananthakrishnan, A.N. et al. (2018). Environmental triggers in IBD: a review of progress and evidence. Nature Reviews Gastroenterology & Hepatology, 15, 39–49. pubmed.ncbi.nlm.nih.gov/29018271 — Authoritative review of the environmental factors implicated in IBD’s global rise, including dietary changes, antibiotic exposure, and microbial diversity loss.

On glyphosate and the gut microbiome

• Walsh, L., Hill, C. & Ross, R.P. (2023). Impact of glyphosate (Roundup™) on the composition and functionality of the gut microbiome. Gut Microbes. ncbi.nlm.nih.gov/pmc/articles/PMC10561581 — Comprehensive review from APC Microbiome Ireland finding that 54% of core human gut bacterial species are potentially sensitive to glyphosate, while noting the controlled human evidence base remains limited.
• Ignácio, A.D.C. et al. (2024). Effects of glyphosate exposure on intestinal microbiota, metabolism and microstructure: a systematic review. Food & Function, 15, 7757. pubs.rsc.org/en/content/articlelanding/2024/fo/d4fo00660g — 2024 systematic review of glyphosate’s effects on intestinal microbiota and gut microstructure across multiple animal and in vitro studies.
• NMGNZ (2025). Glyphosate and the gut microbiome: what the science says. nomoreglyphosate.nz/glyphosate-microbiome-impact

On intestinal barrier function and IBD

• Selvakumar, B. & Samsudin, R. (2025). Intestinal barrier dysfunction in inflammatory bowel disease: pathophysiology to precision therapeutics. Inflammatory Bowel Diseases, 31(12), 3450–3464. academic.oup.com/ibdjournal/article-abstract/31/12/3450/8313912 — November 2025 review establishing intestinal barrier dysfunction — including tight junction disruption and zonulin upregulation — as a defining feature of IBD pathogenesis.

Related NMGNZ articles in this series

• Glyphosate and celiac disease: could glyphosate be killing the Rothia bacteria that protect you? nomoreglyphosate.nz/glyphosate-celiac-disease-rothia-gut-bacteria
• Glyphosate and Parkinson’s disease: is New Zealand asking the right questions? nomoreglyphosate.nz/glyphosate-parkinsons-disease-new-zealand
• Is glyphosate really safe? Why the animal studies say less than you think. nomoreglyphosate.nz/glyphosate-animal-models-safety-science
• Monsanto v. Durnell: Bayer’s bid to end Roundup cancer lawsuits. https://nomoreglyphosate.nz/monsanto-durnell-lawsuits-bayer-supreme-court/
• MPI: the missing data. nomoreglyphosate.nz/mpi-missing-data

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