A new study shows that glyphosate triggers Alzheimer’s-like neuroinflammation in mice, which is still visible after 6 months. The mice are not only affected as test animals and model organisms for humans, but also directly. This is because in the field (and not only) they eat the highly contaminated grains after siccation, which are not analysed for residues.

The fact that the long-term risks of glyphosate for mammals are clear in many areas of application was also established by the EFSA when glyphosate was re-authorised. (Link).

Die Frage, ob nur Glyphosatformulierungen, nicht aber Glyphosat selbst ein neurotoxisches Potenzial haben, musste offen bleiben, auch wenn dieser Unterschied für die Maus im Feld nicht relevant ist.

The question of whether only glyphosate formulations, but not glyphosate itself, have a neurotoxic potential had to remain open, even if this difference is not relevant for the mouse in the field.

However, a recent study now shows for the first time that neuroinflammation caused by glyphosate, similar to Alzheimer’s disease, is still detectable in the brains of mice even after 6 months. In addition to the inflammation itself, altered proteins, pathological changes and AMPA (glyphosate degradation product)  were also found in the brains of animals with the typical anxiety behaviour. (Link) / (Link).

The mouse is not only the model mammal here, which (in this case almost literally) takes the biscuit for all other animals and also for us humans in the laboratory. Mice also live in the very fields where large quantities of food contaminated with glyphosate can be found: in fields where desiccation has been used or cover crops have been destroyed.

During the siccation of cereals and pulses, which has only recently been banned in the EU but is still widely used internationally, the still very green grains in particular absorb a lot of glyphosate. They then dry out and are sieved back onto the field by the combine harvester as grains that are too small. The large, ripe grains with lower contamination are harvested and analysed, but not what the animals eat in the field with significantly higher contamination. Therefore, high doses in trials can be quite realistic.

With the best will in the world, it is therefore not enough to simply look at residues in food or to realise that humans do not eat cover crops. In addition to mice, there are enough vegetarians among the animals (including insects, whose intestinal flora is massively disrupted by glyphosate) that eat exactly what is left in the field without a maximum quantity limit. The regulations on waiting times and re-entry bans are also only read by humans.

The times when chemicals could be assessed and withdrawn from the market based on simple toxicological mechanisms are largely over, at least in the EU. Many substances that are obviously toxic have been withdrawn from the market or at least their release and exposure has been severely restricted. The complexity of research into causes is increasing, but the effects remain.

But we still have insect mortality, biodiversity loss, rising cancer rates and a growing number of neurodegenerative diseases that cannot be easily (or even yet) explained. Just because the effects are more complex, we must not downplay the ‘evidence’. The precautionary principle also tells us that we must act early and appropriately in suspected cases of possible major or irreversible damage. This is the only way to ensure that the future remains grandchild-friendly.

Banning everything may be disruptive, but it is hardly innovative in the long term. We need high-yield and stable agriculture with affordable labour and socially acceptable prices – but sustainably.

That is why we need to work together to recognise risks and damage and then take appropriate action. Taking action means finding better solutions. crop.zone makes its contribution to this with electrophysical plant control in the field, e.g. in siccation to reduce the use of glyphosate.