Research shows that Ragwort is toxic to animals. Many reports in the press in the UK do not, however, derive their information from proper scientific sources. What is overwhelmingly clear from the scientific journals is that actual poisoning is a rare event. Detailed questions on the number of horse deaths are dealt with here Ragwort horse deaths
There is also the claim from the British Horse Society that exaggerates the toxicity ten thousand fold. See Ragwort is not extremely toxic
The rest of this article deals with general toxicity.
Common ragwort contains compounds that are poisonous to most vertebrates. These are pyrrolizidine alkaloids. These substances occur in other plants as well. In fact, they occur in 3% of the world's flora (Fu et al. 2004). Inside the plants, they occur in a non-toxic form, but after the plant has been eaten it is first changed by the intestines and then broken down by the liver. These processes are necessary for toxicity. The breakdown products formed in the liver are toxic (Stewart & Steenkamp 2001; Chojkier 2003). Contrary to what is often thought by the general public, the alkaloids do not accumulate inside the body of an animal. The fact is that they are excreted in about 24 to 48 hours (Chojkier 2003). It is the damage that is caused to liver cells that can, if sufficient ragwort is consumed at each dose, be cumulative to the point of death occurring.
There is a common unsupported claim that only a few kilograms of ragwort can kill a horse. It has been said in Parliament, and there is a document produced by a Scottish academic source which contains many errors, including an implausibly low toxicity figure with no sources given. It will eventually be the subject of its own page on this site. It has been quoted as true by other government sources, despite the fact that, to the informed eye, it is a poor and rather unscientific document. FOr example it also incorrectly states "A single ragwort plant in a bale of silage can be enough to poison stock." which in the honest opinion of the author of this website is egregiously false in view of what the science actually says. This poor document formed the basis of the Welsh Government's earlier official guidance on ragwort, and it is still referred to as a leaflet on the government of Jersey's website. Given its contents, its use for these matters is problematic.
This page will also eventually contain a link to a dedicated article examining a British Horse Society magazine story , "Danger in the Paddock" (Summer 2024). The piece is problematic as it states that small amounts of ragwort consumed over time cause as much liver damage as large amounts eaten quickly. This is presented as settled fact with no supporting information at all. As you will see below it does not tie in with the science , to be fair to the BHS it is a commoon misperception, but then they have played their part in generating that misperception too, The story includes a sidebar account of an owner who identified her horse's sunburnt nose as a symptom of ragwort poisoning, despite the horse showing no other signs and there being no established link between sunburn and ragwort exposure in that account. The article also states that owners can be prosecuted if a horse falls ill after exposure to ragwort. They fail to explain that any such prosecution would require proof of neglect and thar ragwort was the actual cause of the symptoms. It does not explain that the standard diagnostic markers for ragwort poisoning, including megalocytosis, are non-specific findings that a competent defence could very reasonably contest and defeat as reasonable doubt. A full and detailed analysis of the piece will follow as its own article.
There is a book called Effects of Poisonous Plants on Livestock. It contains papers from a U.S.-Australian symposium on the effects of poisonous plants on domestic livestock. This scientific meeting, called a symposium, was held at Utah State University in Logan, Utah, on 19-24 June 1977. The book was published by Academic Press, which is a highly respected publisher of scientific works. The book includes a chapter by P. T. Hooper of Australia's Arid Zone Research Institute, comparing the pathology of pyrrolizidine alkaloid poisoning. This included ragwort, then called Senecio jacobaea but now called Jacobaea vulgaris, across a number of livestock and laboratory species.
Hooper's chapter gives the cattle figure: 0.14 kg of dried ragwort per kg of bodyweight to produce poisoning. This is equivalent to 14% of bodyweight. He treats horses as approximately equivalent in sensitivity, based on comparative evidence across multiple published studies rather than a direct feeding trial in horses. For a 500 kg animal, that's around 70 kg of dried plant. If we then convert this figure to fresh weight, using a conservative ×4 factor for moisture content, assuming that the plant is 75% water, the figure rises to roughly 280 kg, which is more than half the animal's own bodyweight. Sheep are very different, and Hooper records in his research that they need over 2 kg of dried plant per kg bodyweight to develop chronic disease. This is by far the highest threshold of the species studied, standing at around 200 times the quantity needed to poison a pig, by his own comparative ranking. Translating this similarly to fresh plant, we get 8 times the bodyweight for sheep.
To quote the actual research:
Sheep required more than 2.0 kg of dried plant/kg body weight (BW) to poison them compared with a mean of 1.5 kg/kg BW mice, 0.5 kg/kg BW rats, 0.14 kg/kg BW cattle, and 0.05 kg/kg BW chickens.
Another study is by a scientist called Craig and his colleagues (Craig et al. 1991), published in the Journal of Equine Veterinary Science. It involved Shetland ponies and crosses, and it is important to realise that they are more susceptible, because the threshold below which animals get poisoned by a given dose is lower for smaller animals. The biochemistry behind this is explained further down this article, and there are detoxification routes which have to be overwhelmed before any toxic effect occurs, some of which include natural antidotes and repair systems which are all smaller in capacity in smaller animals.
The dosages below are taken directly from the paper. There is no question that consumption via contaminated hay is a real problem, but to show the effect on grazing animals eating fresh plant, the measured toxic doses have been multiplied as though the dried ragwort used in the trial had instead been fresh ragwort disguised in the feed. This gives a proper sense of how toxic fresh ragwort actually is. A conservative figure of 75% water content has been assumed, as before.
Fresh weight figures assume 75% moisture content (dried weight × 4).
| Pony | Bodyweight | Dried ragwort consumed | % of bodyweight (dried) | Fresh ragwort equivalent | % of bodyweight (fresh) | Day of death |
|---|---|---|---|---|---|---|
| 1 | 159 kg | 17 kg | 10.7% | 68 kg | 42.8% | 173 |
| 2 | 168 kg | 30 kg | 17.9% | 120 kg | 71.4% | 296 |
| 3 | 150 kg | 27 kg | 18.0% | 108 kg | 72.0% | 296 |
| 4 | 164 kg | 12 kg | 7.3% | 48 kg | 29.3% | 119 |
| Pony | Bodyweight | Dried ragwort consumed | % of bodyweight (dried) | Fresh ragwort equivalent | % of bodyweight (fresh) | Day of death |
|---|---|---|---|---|---|---|
| 1 | 146 kg | 9 kg | 6.2% | 36 kg | 24.7% | 49 |
| 2 | 155 kg | 10 kg | 6.5% | 40 kg | 25.8% | 406 |
| 3 | 244 kg | 14 kg | 5.7% | 56 kg | 23.0% | 56 |
| 4 | 257 kg | 17 kg | 6.6% | 68 kg | 26.5% | 322 |
The idea that even the smallest amount of ragwort will damage an animal's liver has no basis in science.
We know from the meaning of the word "cumulative" in toxicity, and from the experimental studies, that neither ragwort itself nor the alkaloids it contains are cumulative in animals. There are thresholds before damage occurs, and the damage only becomes possible once absorbed quantities of the toxins are large enough to overwhelm the animal's own defences against them.
First we need to be precise about the word itself: the Oxford English Dictionary, the definitive dictionary of English usage, defines "cumulative" as something built up through successive additions, increasing in force as each new portion is added. In the science, it is clear that this is not happening, and it's damage that fits this description, not the alkaloids themselves, which don't stay or accumulate in the tissue in any sense at all.
Before any of this can happen, the alkaloids first have to get through the digestive tract. Gut bacteria destroy a portion of what's ingested, and not everything that survives digestion is absorbed into the bloodstream. What does get through isn't yet toxic, as pyrrolizidine alkaloids only become dangerous once converted into reactive breakdown products, and that conversion is far from a certainty. Fu et al. (2004), writing in Drug Metabolism Reviews, describe how the reactive pyrrolic esters formed during this process are highly prone to being neutralised on contact with water and with glutathione, one of the cell's principal detoxifying molecules, before they ever reach anything they could damage.
Glutathione is the same substance that allows paracetamol to be taken safely in normal doses. It is only once the body's supply is exhausted that paracetamol becomes dangerous. The same buffering capacity is what happens with ragwort's alkaloids.
Duringer et al. (2004), in the American Journal of Veterinary Research, set out three separate metabolic routes the liver can take with these compounds, and only one of the three produces anything toxic. Oxidation by cytochrome P450 enzymes, the liver's standard molecular machinery for breaking down foreign compounds, can generate a reactive metabolite known as DHP, capable of binding to DNA. But the same class of enzymes, working alongside other enzymes called flavin-containing monooxygenases, can instead convert the alkaloids into N-oxides: stable, highly water-soluble compounds that are simply excreted in the urine, in a completely harmless manner. A third route, via carboxylesterase enzymes, breaks the alkaloids down into non-toxic components entirely. To of the three available pathways lead nowhere near toxicity.
Even where the toxic metabolite does form and reach DNA, the damage isn't automatically harmful, as cells have their own repair systems for exactly this kind of damage. It is only when repair is outpaced by repeated, high-level exposure that any lasting harm results. What accumulates, at every stage of this process, is damage to cells that have already been repeatedly overwhelmed, and it is never the alkaloids themselves. This layering of biochemical resistance is part, at least, of the explanation of why species vary so much in their tolerance. Animals that encounter pyrrolizidine-alkaloid plants regularly in their natural range seem to have evolved a correspondingly higher tolerance for them and this is borne out in the experimental data that we have. We see that poisoning in livestock tends to occur where that natural balance is disrupted, in the case of contaminated hay, or animals with nothing else left to graze.
The clearest experimental confirmation of an actual threshold comes from Molyneux et al. (1991). These scientists carried out experiments working with a related pyrrolizidine-alkaloid-containing plant, Senecio riddellii, on calves. Calves that were dosed daily for 20 days at 45 mg of total alkaloid per kg of bodyweight all developed clinical disease and abnormal serum enzymes. Those calves given one-tenth of that dose, just 4.5 mg/kg per day, for the same 20 days showed neither. They showed no signs of harm. A ten times smaller daily dose was the difference between universal clinical disease and no detectable effect whatsoever.
The biochemistry and the experiments agree here. Ragwort poisoning clearly has a threshold. It is not the case that every dose counts and causes problems. We have a research example that backs up what we know from the biochemistry here. There are multiple detoxification routes. There is a repair system for the damage that does occur.
This matter of the toxicity pathway, and the matter of cumulative toxicity, is covered in more detail in a dedicated article: Ragwort is not strictly a cumulative poison.
Ragwort's toxicity is all too customarily overestimated. The figures given in press coverage, in official guidance, and even in some veterinary advice, rarely stand up against the primary experimental literature once that literature is actually checked. Just as this page was being finished, the author received a message from a colleague pointing to a Facebook post from a vet stating that no amount is safe for a horse to eat, one of the very claims debunked above. The Hooper cattle figure, the Craig ponies, give us the same information.. The dose of fresh ragwort needed to poison an animal sits somewhere between around a quarter and over half of its own bodyweight, consumed continuously over weeks, not the few kilograms so often claimed.
We also know, from the biochemistry and from the actual experiments, that small doses have no effect at all. The detoxification pathways set out by Fu and by Duringer explain why this is the case, and Molyneux and his colleagues showed it directly. Calves given one tenth of a toxic dose for the same twenty days showed no clinical signs and no serum enzyme changes whatsoever. Ragwort poisoning has a threshold, below which no damage opccurs, and it is a very long way below where a lot of poor publicity shows it to be.