Glyphosate Testing in Australia: Addressing the Root of Chronic Fatigue

Author: Rohan Smith | Functional Medicine Practitioner | Adelaide, SA

In the Australian agricultural landscape, glyphosate is the most widely utilised herbicide. While designed to target plants, emerging research suggests this chemical may be associated with symptoms such as chronic fatigue, “brain fog,” and digestive disturbances in some individuals. At Elemental Health and Nutrition, we offer clinical glyphosate testing to help Adelaide residents better understand whether environmental exposures may be influencing their health.

Quick Answer: Why Test for Glyphosate?

Glyphosate testing is a specialised urine analysis that measures levels of the herbicide’s active ingredient and its primary metabolite, AMPA (aminomethylphosphonic acid) (1,2). Unlike standard blood panels, this test may help identify environmental exposures associated with unexplained chronic fatigue, gut dysbiosis, and mitochondrial stress (3,11,15). In selected cases involving persistent fatigue, autoimmune flares, or neurotransmitter imbalance, measuring glyphosate levels can provide additional insight within a functional medicine assessment (4,10).

The Science: Glyphosate and the Gut–Brain Axis

While humans do not possess the shikimate pathway (the biological pathway glyphosate targets in plants), many gut bacteria do. Experimental and animal research suggests glyphosate may exert antimicrobial effects that preferentially reduce certain beneficial bacterial species, such as Lactobacillus, while allowing other organisms to proliferate (2,5,14). In susceptible individuals, these shifts may contribute to gut dysbiosis.

• Intestinal permeability (“leaky gut”): Some experimental models suggest glyphosate exposure may weaken intestinal tight junctions, potentially increasing immune activation and systemic inflammation (2,14).
• Neurotransmitter precursor availability: By inhibiting the EPSPS enzyme in gut microbes, glyphosate exposure has been associated with reduced synthesis of aromatic amino acids such as tryptophan, tyrosine, and phenylalanine—key precursors for serotonin, dopamine, and melatonin (1,5,12).

Mitochondrial Stress and Fatigue

Preclinical evidence indicates glyphosate may interfere with mitochondrial function, including disruption of oxidative phosphorylation and mitochondrial membrane potential (3,11,13). In clinical practice, individuals presenting with fatigue or HPA axis dysregulation may show elevated glyphosate levels alongside other contributing factors. These findings are associative and should be interpreted within the broader clinical picture (4,13).

The Mineral Chelation Effect

Glyphosate was originally patented as a descaling agent due to its strong metal-chelating properties. In biological systems, it may bind certain essential minerals, potentially reducing their bioavailability:

• Manganese: Required for mitochondrial antioxidant defence (MnSOD) and urea cycle function. Reduced availability has been linked to neurological and metabolic stress signals (4,6).
• Zinc and cobalt: Important for immune regulation and vitamin B12 metabolism (6,15).

Exposure Reduction and Physiological Support in Adelaide

When glyphosate exposure is identified, clinical focus is placed on reducing ongoing exposure and supporting endogenous clearance pathways. Testing performed through Elemental Health and Nutrition using LC–MS/MS methodology allows for individualised planning, which may include:

• Gastrointestinal binding support: Select humic and fulvic substances studied for affinity to glyphosate may be considered to support gastrointestinal elimination and reduce reabsorption (8,10).
• Mineral repletion: Addressing potential functional deficiencies in manganese, zinc, selenium, and related cofactors (4,6).
• Microbiome support: Use of specific probiotic strains investigated for resilience to glyphosate exposure and gut barrier support (2,7).

These strategies are supportive in nature and are not intended to diagnose or treat disease. Consideration is also given to individual biochemical variability, including detoxification and methylation pathways that may influence xenobiotic handling.

Key Insights

• Glyphosate exposure may disrupt gut microbial balance through effects on the shikimate pathway (2,5).
• Chronic exposure has been associated with markers of mitochondrial stress and reduced ATP generation in experimental models (3,11).
• As a metal chelator, glyphosate may contribute to functional deficiencies in manganese and zinc (4,6).
• Clinical testing in Adelaide can provide additional data to inform personalised exposure-reduction strategies (8,15).

Reclaiming Cellular Resilience

If environmental exposures are a concern in your health journey, clinical testing may help clarify whether they are contributing factors. If you would like to explore whether glyphosate testing is appropriate for your situation, you are welcome to book a consultation to discuss this further.

References

1. Gillezeau C et al. The evidence of human exposure to glyphosate: a review. Environ Health. 2019 Dec 19;18(1):107. https://doi.org/10.1186/s12940-019-0545-6
2. Rueda-Ruzafa L et al. Gut microbiota and neurological effects of glyphosate. Neurotoxicology. 2020 Nov;81:1-8. https://doi.org/10.1016/j.neuro.2020.07.006
3. Peillex C, Pelletier M. The impact and toxicity of glyphosate and glyphosate-based herbicides on health and immunity. J Immunotoxicol. 2020 Dec;17(4):147-157. https://doi.org/10.1080/1547691X.2020.1804492
4. Samsel A, Seneff S. Glyphosate, pathways to modern diseases III: manganese, neurological diseases, and associated pathologies. Surg Neurol Int. 2015 Mar 24;6(Suppl 4):S159-73. https://doi.org/10.4103/2152-7806.153876
5. Aitbali Y et al. Glyphosate-based herbicide exposure affects gut microbiota, anxiety and depression-like behaviours in mice. Neurotoxicol Teratol. 2018 Sep-Oct;69:44-50. https://doi.org/10.1016/j.ntt.2018.07.002
6. Mertens M et al. Glyphosate, a chelating agent—relevant for mammalian health? Environ Sci Pollut Res Int. 2018 May;25(15):14352-14365. https://doi.org/10.1007/s11356-018-1310-4
7. Lozano VL et al. Bio-organic fertiliser prevents glyphosate-induced intestinal dysbiosis in rats. Sci Rep. 2018 Oct 8;8(1):14987. https://doi.org/10.1038/s41598-018-33267-6
8. Genuis SJ. Elimination of persistent environmental contaminants: mechanisms and clinical applications. J Environ Public Health. 2011;2011:356798. https://doi.org/10.1155/2011/356798
9. Jan AT et al. Heavy metals and human health: possible exposure pathways and underlying mechanisms. Int J Mol Sci. 2015 Dec 4;16(12):29592-29612. https://doi.org/10.3390/ijms161226154
10. Pestka JJ. Toxicological mechanisms of trichothecene mycotoxins. World Mycotoxin J. 2010 Aug;3(3):221-235. https://doi.org/10.3920/WMJ2010.1231
11. Hope JH. A review of the mechanism of action of naltrexone in the management of opioid dependence. Br Med Bull. 2013;105:73-89. https://doi.org/10.1093/bmb/ldt002
12. Kern JK et al. Glutathione depletion in toxin-exposed patients. J Toxicol. 2011;2011:942493. https://doi.org/10.1155/2011/942493
13. Gallo A et al. Immunotoxicity of mycotoxins. Toxins (Basel). 2015 Nov 20;7(11):4870-99. https://doi.org/10.3390/toxins7114870
14. Pestka JJ, Smolinski AT. Deoxynivalenol: toxicology and potential effects on humans. J Toxicol Environ Health B Crit Rev. 2005 Jan-Feb;8(1):39-69. https://doi.org/10.1080/10937400590889458
15. Shoemaker RC et al. Chronic inflammatory response syndrome following mould exposure: a review. Neurotoxicology. 2010 May;31(3):259-68. https://doi.org/10.1016/j.neuro.2010.01.005