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Guest Post by Laura Cooper
For much of human history, people have sought to find a way to prove or disprove a person’s guilt. Today, we hope evidence and a fair trial will do this, but people have always wanted a quick and definitive way of doing this. This is where the idea of the trial by ordeal came in. Most people are familiar with the practice of dunking suspected witches in bodies of water in parts of 17th century Europe; if they floated they were guilty and if they sunk they were innocent. But in what was then called the Calabar region (now North-East Nigeria) in the 19th century, a particularly poisonous seed was used in these trials by ordeal. This plant, known as the Calabar bean, Physostigma venenosum, became notorious as a poison. However, the principle lethal chemical of the Calabar bean, phystostigmine, was investigated by a number of physicians in Europe as an antidote to poisoning by atropine. Though both compounds can kill, their methods of murder are mirror images of each other, so that one can be used to cancel out the effects of the other; and so a poison can become a cure.
I can only find reports of the use of P. venenosum in ordeals in reports by Europeans visiting Calabar in 1846, who reported that 120 people died annually in the region by the Calabar bean. A person suspected of a misdeed would be made to consume the bean, likely soaked and crushed to release the toxins rather than whole. If they were guilty they would die, if they were innocent they would survive. It has been reported that swallowing the bean probably won’t result in death, but consuming a crushed seed would release toxins, like Abrus precatorius. Consuming enough seeds can lead to increased salivation, seizures, loss of control of urination and defectation and death by asphyxiation. Physostigmine has an oral LD50 (a dose which will kill half of a large group of mice) of 4.5 mg/kg, and the maximum number of beans reported eaten and survived is 35. Depending on a person’s weight and health, it is possible that one person may survive and another die after being given the same number of beans, and this difference can be attributed to their guilt or innocence.
The bean extract was known by medics in Europe, and extracts were used to constrict the pupil by ophthalmologists. Aware of it’s effects, in 1864 the Prague ophthalmologist Niemetschek suggested that a patient with atropine poisioning be given Calabar bean. Thomas Fraser investigated the effects of P. venenosum extract rigorously, and identified the chemical phystostigmine as the active chemical.
Phystostigmine acts as an acetylcholinesterase inhibitor. This means it prevents the neurotransmitter acetylcholine from being broken down, so the parasympathetic nervous system is continually stimulated. This is the exact opposite effects of atropine, an anticholinergic drug derived from Atropa belladonna, which I have written about before. Atropine causes anticholinergic syndrome, making the patient “dry as a bone, blind as a bat, red as a beet, mad as a hatter, hot as a hare”, as medical students remember it.
But many other chemicals and conditions can cause anticholinergic syndrome, and despite many published cases of phystostigmine being used to treat anticholinergic syndrome safely and effectively, it has been reported as being underused. It could be speculated that this underuse could be due to the gruesome reputation of the source of the chemical, the Calabar bean, and therefore a hesitancy to recommend the drug. But whilst the drug is dangerous at a high enough dose, the ordeals themselves show that it is survivable (if you are innocent, that is!). We return again to the common theme of plant poisons; everything has a lethal dose, even water, what is more interesting is what doses lower than this can do to the human body.
With Valentine’s Day just around the corner, today’s post by Fang from the Visitor Team, is all about love! And for more about the objects and collections at Manchester Museum, have a look at the Curators’ blogs. All about love … Valentine’s Day is coming soon. In anticipation of a day all about love, I’ve taken a […]
Guest Post by Laura Cooper
Poison hemlock (Conium maculatum) is one of the most notorious of poisonous plants. It’s best known as the poison that killed the philosopher Socrates, and may even be indirectly responsible for the deaths of quail eaters, but even this species has been used as a medicine.
Conium maculatum is in the family Apiaceae. Many species in this family resemble hemlock as they possess white flowers in umbels, branches of the stem which form a flat surface, and pinnate leaves, resemble parsely (Petroselinum crispum) and wild carrot (Daucus carota). This has lead to foragers accidentally poisoning themselves, but most are put off by the “mousy” or foetid odour and bitter taste. This and red spots that appear on the base of the plant in spring, traditionally gained when the plant grew at the base of Christ’s cross, are key identification features. It is a common “weed” globally, and was introduced as an ornamental to North America.
A vivid account of hemlock poisoning is given in Plato’s Phaedo, where his teacher Socrates is sentenced to death by consuming a “poison” known to be C. maculatum. After being given the poison, Socrates “walked about until […] his legs began to fail, and then he lay on his back […] the man who gave him the poison […] pressed his foot hard, and asked him if he could feel; and he said, No; […] and so upwards and upwards, and showed us that he was cold and stiff. And he […] said: When the poison reaches the heart, that will be the end. […] in a minute or two […] his eyes were set, and Crito closed his eyes and mouth.” The execution is an apt one for a philosopher, as he retained conscience throughout. However, the description may be idealised to preserve the dignity of Plato’s old teacher, as most hemlock poisonings involve vomiting and seizures in addition to the creeping paralysis.
Hemlock kills by a cocktail of similar chemicals, including γ-coniceine and coniine. Coniine affecting the nicotinic receptors on neurons first to stimulate the nervous system, causing seizures, vomiting and tachycardia. Later it may inhibit the central nervous system, causing brachycardia and paralysis.
One of the most sinister ways of being poisoned by a plant is the rare condition coturnism. It is caused by eating quail, Coturnix coturnix, killed in the Mediterranean whilst migrating north from Africa in the spring (but not when returning in the autumn). It is widely reported that this is due to the quail consuming the seeds of C. maculatum, but there is conflicting evidence. According to E. F. Jelliffe, hemlock drops seed in late summer and autumn, meaning quail migrating north in the spring cannot have eaten this seed. Therefore, the cause of coturnism is still a mystery.
But despite it’s notoriety, C. maculatum features in medieval household remedies. It’s powers of sedation are utilized in a recipe for an anesthetic known as dwale. The recipe involves boiling pig bile, three spoonfuls each of of hemlock juice, opium and henbane, bryony, lettuce and vinegar and adding this to half a gallon of wine. Drinking this would apparently allow a person to fall asleep and be “safely cut”, after which vinegar and salt to the face would revive them. Though the mixture seems effective at knocking a person out, it is questionable that the vinegar would be enough to revive them. However, there is no scientific evidence that “root of hemlock, digged i’ th’ dark” that the witches in Macbeth add to their potion contributed to Macbeth’s false imperviousness.
Guest Post by Laura Cooper
Binomials can be a pain to learn, but they often have a hidden poetry. Deadly nightshade’s common name stresses its notoriety as a poison. But it’s binomial, Atropa belladonna, is far more beautiful and apt. The genus name is derived from Atropus, one of the three Fates of Greek Mythology, whose shears could cut the threads of life. The species name belladonna is the Italian for beautiful woman, named so because of the plant’s use in giving pleasingly dilated pupils. A figurative translation of the name could be femme fatale, appropriate for a plant whose main danger to humans is to the forager lured to pick and eat the glossy black berries.
The Herbarium has a large model of these berries displayed on a cabinet in the main room. It caught my eye as I was returning the gloves I wore to find Atropa belladonna Herbarium sheets. Compared to the shriveled fruits I had just seen, this was a regal fruit with the sepals like a ruff and a grandly arching stem. A belladonna indeed.
Atropa belladonna is one of the most common plants involved in poisoning throughout most of Europe and central Asia, but is still no minor threat. For example, the plant topped the list of plants causing severe poisoning in Switzerland between 1966-1994. Of a total of 24,950 cases of contact with poisonous plants, 135 cases (0.6% of total) were serious poisonings with sufficient information. Atropa belladonna was involved in 42 of these cases, but no deaths were reported. This doesn’t mean the plant should be treated lightly though. It has the potential to be quite dangerous.
As with many poisonous plants, it is very difficult to get an accurate measure of the lethal dose. Some report that an adult would be killed by 10-20 berries, whilst others report a case of children who had eaten eaten up to 40 berries and survived after hospitalisation.
A. belladonna‘s deadly potential is principally derived from three toxins, the tropane alkaloids hyoscine, hyoscyamine and atropine. The toxins have an anticholinergic effect, which means they affect neurones by competing with the neurotransmitter acetylcholine for muscarinic receptors. After a delay, this leads to an inhibition of the parasympathetic nervous system. This produces anticholingeric syndrome, whose symptoms are remembered by the mnemonic, “dry as a bone, blind as a bat, red as a beet, mad as a hatter, hot as a hare”. If the dose is high, this can lead to psychosis, convulsions, respiratory failure and death.
A. belladonna and its derivatives were favoured tool for the poisoner. In the late 19th century, the psychopathic American nurse Jane Toppan used atropine in concert with morphine to kill over 31 people. As atropine and morphine produce opposite responses, atropine “speeds up” the system whilst morphine slows down the body, Toppan balanced the doses of both drugs to prolong her victims’ struggle until a fatal dose was given.
However, atropine in the right hands can be a very useful chemical, even a lifesaver. It is the standard antidote for nerve gas poisoning, as it blocks the excess acetylcholine the nerve gas produced. It is also used to dilate eyes for examination by an ophthalmologist and is given to patients after cardiac arrest. Ironically, the very “poison” that Jane Toppan used to kill a victim whose death was originally recorded as heart disease is now used to help save patients from dying from a heart attack. There can always be a useful side to the proverbially deadliest of plants.
For the past few months I’ve been working on a really exciting exhibition opening on the 20th of May: Object Lessons #MMObjectLessons Object Lessons celebrates the scientific model and illustration collection of George Loudon. Each of these finely crafted objects was created for the purpose of understanding the natural world through education, demonstration and display. […]
Last December, Stephen Welsh (Curator of Living Cultures) and I went on a research trip to India for the Courtyard Project, focusing on the South Asia Gallery – a partnership gallery with the British Museum. Neither of us had visited India before, although we were familiar with other parts of South Asia. It was an exciting and hectic schedule and in two weeks we visited Mumbai, Kolkata, Delhi and Kochi – so more or less each compass point of what is an amazing country. The focus of our visit was to meet with museum professionals, artists and to get a real feel for both the historic and archaeological wonders, as well as the contemporary culture of a country that is fast becoming an emerging global superpower. We were joined in Kolkata and Kochi (where we attended the Kochi-Muziris Biennale) by Manchester Museum Director Nick Merriman.
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Guest blog by: Sophie Mogg
Cinnamon is a spice that we have all had the opportunity to try, whether in fancy coffees, liqueurs or delicious buns. Whilst the “true” cinnamon species is Cinnamomum verum, the most common source of cinnamon is Cinnamomum cassia. Both species originate in Asia, with C. verum being native to Sri Lanka (formerly known as Ceylon) and C. cassia originating in southern China. In order to distinguish the cinnamon produced by the two species in the spice trade, cinnamon refers to C. verum whilst cassia refers to C. cassia. This is because, C. verum is more expensive of the two due to its sweeter taste and aroma as less than 30% of cinnamon exports come from Sri Lanka.
Cinnamon has been traded for many thousands of years, with the imports into Egypt reported as early as 2000 BCE so it is no surprise that there are countless tales and historical events that surround this spice. From Sieur de Joinville believing cinnamon was fished from the Nile at the end of the world and Herodotus writing about mystical giant birds (such as a phoenix) that used cinnamon sticks to build their nests, the history of cinnamon is rich in legends of its origin as it wasn’t until 1270 that it was mentioned the spice grew in Sri Lanka. However as sweet as this spice may be it also appears to have a bloody history. Aside from the countless wars raged over the right to trade cinnamon, it was also used on the funeral pyre of Poppaea Sabina, the wife of Nero, in 65 AD. It is said that he burned over a years supply as recompense for the part he played in her death.
There are a total of 5 species (C. burmannii, C. cassia, C. citriodorum, C. loureiroi and C. verum) that produce cinnamon however C. verum and C. cassia are where the majority of international commerce is sourced from. Production of cinnamon is fairly straight forward albeit time-consuming. The outer bark of the tree is shaved off exposing the inner bark which is the cinnamon layer. This inner bark is also shaved off and left to dry, naturally curling as it does. By comparison the cinnamon of C. verum has a more delicate flavour than that of C. cassia as well as having thinner bark that is more easy to crush and produces a much more smooth texture.
Cinnamon is prominent in the practice of Ayurveda medicine as well as traditional Chinese medicine, being one of the 50 fundamental herbs. Traditionally it has been used to treat a wide variety of ailments from digestive problems, respiratory problems, arthritis and infections. In traditional Chinese medicine it is believed that cinnamon is able to treat these ailments through it’s ability to balance the Yin and Wei as well being a counterflow for Qi. These terms are aptly explained here for those who are interested. While there is little scientific evidence for the treatment of digestive and respiratory disorders, cinnamon does appear to possess antibacterial, antifungal and antimicrobial properties which may help to fight infections although at this moment in time it is inconclusive in studies trialled on humans. Cinnamon produced from C. cassia coumarin, which thins the blood, can be toxic to the liver in high concentrations so it is advised that only a few grams per day be consumed.
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