New Zealand has 14,000 people living with Parkinson’s disease — a number projected to reach 20,000 by 2040.
Europe is beginning to ask hard questions about the link between pesticide exposure and this epidemic. New Zealand is not.
Parkinson’s disease doesn’t announce itself dramatically. It begins quietly — a slight tremor, a stiffness in the fingers, a subtle change in the way someone walks. By the time a diagnosis is made, the neurons responsible for producing dopamine in the brain’s substantia nigra have often been dying for years, perhaps decades.
What causes that slow, silent destruction? Genetics plays a role in some cases. But for the majority of people diagnosed with Parkinson’s, no clear genetic cause is found. Which leaves a question that is gaining urgent attention in research institutions and regulatory bodies across Europe, even if it has barely registered here: what if a significant proportion of Parkinson’s cases are not inevitable at all — but are the result of long-term exposure to chemicals that we have been assured are safe?
And specifically: what if one of those chemicals is glyphosate — the world’s most widely used herbicide, and the one most liberally applied across New Zealand’s farms, forests, roadsides, and residential gardens?
Parkinson’s Disease in New Zealand Is Rising Faster Than Ageing Alone Explains
The numbers are stark. The number of people with Parkinson’s in New Zealand has been steadily increasing, from an estimated 7,000 in 2006, to 11,000 in 2018, 13,000 in 2023, to 14,000 in 2025, with projections suggesting the number will reach 20,000 by 2040.
Globally, Parkinson’s disease is the world’s fastest growing neurological disorder, with over 10 million cases worldwide, and the number of people living with it globally is projected to more than triple between 2020 and 2050.
The standard explanation for this rise is demographic — an ageing population means more people entering the highest-risk age groups. That is partially true. But it does not fully account for what researchers are observing. The WHO’s 2023 report on neurological disorders noted that Parkinson’s prevalence has doubled worldwide over the past 25 years — a rate of increase that exceeds what ageing demographics alone can explain. A separate WHO technical brief specifically on Parkinson’s disease recommended that governments ban pesticides linked to the disease and reduce exposure to environmental factors associated with Parkinson’s risk.
So here is the first question worth sitting with: if Parkinson’s is rising faster than ageing alone predicts, and if environmental pesticide exposure is a recognised risk factor, why is there no dedicated research programme in New Zealand investigating whether glyphosate exposure — in a country that uses it as extensively as we do — is contributing to our rising case numbers?
What Does the Science Say About Glyphosate and Parkinson’s Disease?
It is important to be precise here, because the science on glyphosate and Parkinson’s is genuinely nuanced — and that nuance cuts in a more troubling direction than either industry defenders or casual dismissers typically acknowledge.
The overall evidence is inconclusive, but sufficient to suggest that there is a biologically plausible link between glyphosate exposure and nigrostriatal cell death, and hence a risk of Parkinson’s disease. Those are not the words of an activist organisation. They come from a 2023 commentary published in The Lancet Planetary Health, written by leading Parkinson’s neurologists.
What does “biologically plausible” mean in practice? Several distinct mechanisms have been identified through which glyphosate could contribute to the neurodegeneration characteristic of Parkinson’s:
In vitro studies suggest that glyphosate can cause oxidative stress, neuroinflammation, and mitochondrial dysfunction — processes that have all been associated with neurodegeneration in the context of Parkinson’s disease.
Research from Arizona State University and the Translational Genomics Research Institute, published in the Journal of Neuroinflammation, found for the first time that glyphosate crosses from the bloodstream into the brain in a dose-dependent manner, triggering increases in TNF-α — a pro-inflammatory marker associated with a range of neurodegenerative disorders including Parkinson’s disease.
Pesticides can cause neurodegeneration by affecting the gut microbiome, as shown in animal studies where glyphosate exposure produced changes in intestinal bacteria — changes that could act as the first event triggering a cascade of neurodegenerative processes, spreading from intestinal neurons via the vagal nerve to the brain.
And at the epidemiological level: a study from Washington State found that individuals exposed to land-use associated with glyphosate had 33 percent higher odds of premature mortality from Parkinson’s disease than those who were not exposed.
None of these findings, individually, proves causation. But taken together — a plausible biological mechanism, evidence of blood-brain barrier penetration, gut microbiome disruption as a potential neurodegenerative trigger, and a population-level signal of elevated mortality risk — they constitute a body of evidence that demands serious regulatory attention.
The question is: are they getting it?
Europe Recognises Parkinson’s as an Occupational Disease. New Zealand Does Not.
In May 2026, environmental and health organisations in Spain formally urged their government to classify Parkinson’s disease as an occupational illness for farmers exposed to pesticides. France, Italy, and Germany have already done so — recognising that when a farmer develops Parkinson’s after years of pesticide exposure, that is not simply bad luck, but a foreseeable occupational consequence deserving of compensation, medical support, and legal protection.
This is a significant policy development. It reflects a growing European consensus that the link between pesticide exposure and Parkinson’s is sufficiently established to warrant not just further research, but formal legal recognition and worker protection.
New Zealand has no equivalent programme, no equivalent recognition, and — as far as can be determined from publicly available information — no dedicated research initiative investigating the relationship between glyphosate exposure and neurological disease in our farming communities.
This is particularly striking given that New Zealand is a country where glyphosate is applied extensively across agriculture, horticulture, forestry, and public land management — and where the farming community, by definition, faces the highest and most sustained levels of exposure.
What would it take for a New Zealand farmer who develops Parkinson’s disease after decades of spraying glyphosate-based herbicides to have that connection formally investigated, let alone recognised? Currently, the answer appears to be: nothing, because the infrastructure to ask that question does not exist.
Why Current Glyphosate Safety Tests Cannot Detect Parkinson’s Risk
Here is where the story becomes more troubling. The question of whether glyphosate contributes to Parkinson’s risk is not just difficult to answer — there was broad consensus among experts that the currently existing procedures that are part of existing regulatory actions are likely to give inadequate insight into the actual neurotoxic actions of specific pesticides for the substantia nigra, and consequently offer an inadequate assessment of the risk of developing Parkinson’s disease in the case of human exposure.
The Lancet Planetary Health commentary identified four specific shortcomings in current regulatory neurotoxicity testing for glyphosate:
First, the tests used to assess neurotoxicity are simply not sensitive enough to detect the kind of slow, progressive damage to dopaminergic neurons that characterises Parkinson’s disease. The regulatory toolkit was not designed to find this type of harm, which means it cannot reliably exclude it.
Second, glyphosate doses in animal experiments are probably too low and not representative of everyday exposure — particularly given that glyphosate can travel long distances through the air and there are high concentrations of glyphosate and other pesticides in house dust in homes of farmers and residents living nearby farmland.
Third, only isolated pesticides are tested — a failure we have explored in depth in our companion piece on animal model validity. Real human exposure is never to a single substance in isolation. Glyphosate formulations contain surfactants and adjuvants. Farmers applying glyphosate are simultaneously exposed to other agricultural chemicals, dust, and environmental toxicants. The synergistic effects of these combined exposures on neurological health have never been systematically assessed.
Fourth, and perhaps most critically: pesticides can cause neurodegeneration by affecting the gut microbiome — and evaluation of changes in gut microbiome and downstream neurodegenerative processes should become part of improved regulatory actions — but currently, it is not.
This is a regulatory testing framework that was designed to detect acute toxicity and certain cancer risks. It was not designed to detect the slow, decades-long neurodegenerative process that produces Parkinson’s disease. And when the framework cannot detect a harm, regulators declare the substance safe — even though what they have actually demonstrated is only that their tests did not find what they were not designed to look for.
Flawed Animal Studies Make Glyphosate Neurotoxicity Even Harder to Detect
Regular readers of NMGNZ will know that we have recently published a detailed examination of why the animal studies used to establish glyphosate’s safety limits may be systematically unreliable. That piece is directly relevant here.
The neurotoxicity gap in glyphosate testing is not only a question of which tests are conducted — it is also a question of whether the animals used in those tests are capable of detecting the neurological harm in question. As we documented, standard laboratory rodents are bred and housed under conditions that produce chronic stress, suppressed melatonin, and disrupted gut microbiomes as baseline features of their biology. These are not incidental details. Chronic stress, melatonin disruption, and gut dysbiosis are all factors that directly influence neuroinflammation and dopaminergic neuron vulnerability — the very mechanisms relevant to Parkinson’s disease.
In other words: even the animal studies that are conducted to assess glyphosate’s neurological safety are using animals whose neurological baseline is already significantly compromised. If those animals fail to develop Parkinson’s-like pathology after glyphosate exposure, what does that actually tell us about what will happen to a New Zealand farmer who has spent thirty years spraying Roundup?
Probably less than we have been led to believe.
Glyphosate, the Gut Microbiome, and the Path to Parkinson’s Disease
One of the more compelling emerging areas of research concerns the relationship between glyphosate, the gut microbiome, and Parkinson’s disease — and it deserves particular attention because it may help explain why the link has been so difficult to establish through conventional toxicological testing.
The gut-brain axis — the bidirectional communication pathway between the intestinal nervous system and the brain — is now understood to play a significant role in the development of Parkinson’s disease. Research published in recent years has shown that Parkinson’s pathology may actually begin in the gut, with abnormal protein aggregates forming in intestinal neurons years or decades before they appear in the brain.
Glyphosate is a well-documented disruptor of the gut microbiome. It acts as an antibiotic, selectively killing certain bacterial species while allowing others to proliferate — shifting the microbial community away from the diverse, balanced ecosystems associated with health and toward the inflammatory, dysbiotic communities associated with disease. If this disruption creates the conditions in the intestinal nervous system that initiate the earliest stages of Parkinson’s pathology, then we would expect glyphosate exposure to increase Parkinson’s risk through a mechanism that conventional neurotoxicity testing — which looks at brain tissue directly — would entirely miss.
This is not a settled science. But it is a biologically coherent hypothesis supported by a growing body of evidence. And it suggests that our failure to find a definitive regulatory answer to the glyphosate-Parkinson’s question may say more about the limitations of our testing methods than about the absence of risk.
What New Zealand Should Be Asking MPI and EPA About Glyphosate and Parkinson’s
The European trajectory is instructive. France, Italy, and Germany did not wait for absolute proof before recognising pesticide-associated Parkinson’s as an occupational disease. They applied a precautionary logic: the evidence is sufficient, the disease is serious and irreversible, and the cost of being wrong — in human suffering and in the moral debt owed to workers whose health was sacrificed for agricultural productivity — is too high to justify continued inaction.
New Zealand is not Europe. But we are a country that applies glyphosate at scale, that has a farming population with sustained high-level exposure, and that has a rapidly growing Parkinson’s burden with no clear plan to investigate environmental contributions to that burden.
So what should we be asking?
We should be asking MPI and the EPA whether current neurotoxicity testing requirements for glyphosate are adequate to detect the slow, progressive dopaminergic damage that produces Parkinson’s disease — and if not, why approval has been granted and maintained in the absence of adequate testing.
We should be asking whether any research programme exists — or is planned — to investigate Parkinson’s incidence among New Zealand’s farming communities and its potential relationship to pesticide exposure.
We should be asking what obligation New Zealand has to farmers who may have developed Parkinson’s disease as a consequence of occupational glyphosate exposure — and whether the absence of formal recognition of this possibility is a scientific position, or simply a convenient one.
And we should be asking whether a country that prides itself on caring for the people who grow its food is comfortable continuing to let those people bear an unacknowledged and uninvestigated neurological risk — simply because the regulatory framework used to assess that risk was never designed to find it.
Parkinson’s Disease Is Irreversible. That Is Why the Glyphosate Question Cannot Wait.
Parkinson’s disease is irreversible. There is no cure. The neurons that are lost do not regenerate. By the time a diagnosis is made, years of damage have already occurred.
That irreversibility is precisely why the precautionary principle matters here more than in almost any other context. If glyphosate exposure is contributing to Parkinson’s disease — even as one factor among several, even at a population level rather than in every exposed individual — then every year of inaction is a year in which preventable neurological damage is accumulating in people who are not being warned, not being protected, and not being given the information they would need to make their own choices about their exposure.
The science does not yet allow us to say definitively that glyphosate causes Parkinson’s disease. But the science is saying something else with increasing clarity: we have not tested this question adequately, the biological pathways through which such harm could occur are real and identified, and the regulatory frameworks that have been used to declare glyphosate safe were not designed to detect this type of harm.
In the face of an irreversible disease that is rising faster than demography alone explains, that should be more than enough to demand a serious answer.
This article draws on peer-reviewed research and publicly available regulatory documents. We encourage readers to consult the primary sources and form their own conclusions.
Further Reading
On glyphosate, neurotoxicity, and Parkinson’s disease
- Bloem, B.R. & Boonstra, T.A. (2023). The inadequacy of current pesticide regulations for protecting brain health: the case of glyphosate and Parkinson’s disease. The Lancet Planetary Health, 7, e948–e949. thelancet.com — The key peer-reviewed commentary identifying four structural failures in how regulatory neurotoxicity testing fails to assess Parkinson’s risk.
- Bloem, B.R. et al. (2023). Glyphosate and neurotoxicity — a call for scientific renewal. Nature Reviews Neurology. nature.com — Calls for new approaches to assessing the neurotoxicity of glyphosate following the EU’s ten-year renewal of its approval.
- Caballero, M. et al. (2018). Estimated Residential Exposure to Agricultural Chemicals and Premature Mortality by Parkinson’s Disease in Washington State. International Journal of Environmental Research and Public Health. gmoevidence.com summary — The Washington State study finding 33% higher odds of premature Parkinson’s mortality in glyphosate-exposed populations.
- Winstone, J.K. et al. (2022). Glyphosate infiltrates the brain and increases pro-inflammatory cytokine TNFα: implications for neurodegenerative disorders. Journal of Neuroinflammation, 19(193). ncbi.nlm.nih.gov — The first study to confirm glyphosate crosses the blood-brain barrier in vivo, with associated neuroinflammatory markers. Arizona State University / Translational Genomics Research Institute.
On Parkinson’s disease prevalence in New Zealand
- New Zealand Brain Research Institute. Prevalence and Incidence of Parkinson’s in New Zealand (2025). nzbri.org — The primary NZ data source on Parkinson’s case numbers, trends, and ethnic variation.
On the European policy response
- PAN Europe / Ecologistas en Acción / WWF Spain (2026). Call on Spain to recognise Parkinson’s as an occupational disease. pan-europe.info — The May 2026 formal request to the Spanish government, noting France, Italy, and Germany have already granted recognition.
On glyphosate, the gut microbiome, and neurodegeneration
- Kulcsarova, K. et al. (2023). Pesticides and the microbiome-gut-brain axis: Convergent pathways in the pathogenesis of Parkinson’s Disease. Journal of Parkinson’s Disease. pubmed.ncbi.nlm.nih.gov — Detailed review of how pesticide-driven gut microbiome disruption may initiate the neurodegenerative cascade in Parkinson’s.
- Walsh, L., Hill, C. & Ross, R.P. (2023). Impact of glyphosate on the composition and functionality of the gut microbiome. Gut Microbes. ncbi.nlm.nih.gov — Comprehensive review of glyphosate’s documented effects on gut microbial communities.
Related NMGNZ investigation
- No More Glyphosate NZ. Is Glyphosate Really Safe? Why the Animal Studies Say Less Than You Think. nomoreglyphosate.nz — Our companion piece examining why the preclinical animal models used to establish glyphosate’s safety limits may systematically underestimate harm.
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