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Cherry Laurel Tea

If you pick some Holly for tea, do not confuse American Holly with toxic Cherry Laurel. As I did. 21 Oct 2016 is the day I learned I drank some cyanide. Woot! Note the different numbers of spiky things on the leaves: American Holly has only a few, but Cherry Laurel has a whole bunch.

Easy to make mistakes and not know important differences when you are just starting learning some field. And easy to not differentiate leaves when you are not used to differentiating colors, shapes, textures, vein patterns, etc. Took years for my mind and brain to get used to leaves, plants, and animal tracks before my brain and mind got used to it and could start retaining it all!

I had the Cherry Laurel in two cups of tea on the 17 Oct 2016, and one cup on the 19 Oct 2016, maybe it was. Then found out on Friday, 21 Oct 2016, what I had had.

That got me into a learning and research frenzy to find out what the heck was going on and what I might be facing!

The Dosage

Looking around, I found on the great Wikipedia that a lethal dose is >1.5 mg cynaide/kg body weight.

OK, but how much might I have ingested???? I was not dead or suffering badly, so I was clearly OK, but what happened and what damage might I have done??? How does cyanide poisoning work? What is the mechanism? Can anything be done about it??

I found in Biology: A Functional Approach. Students’ Manual (2nd ed., pub. 1987 by Thomas Nelson and Sons Ltd. ISBN 0-17-448035-0) by MVB Roberts and TJ King that one cherry laurel leaf weights 2.5 g. It says “Aim to have a bunch of leaves which weights about 10 g. This will be about 4 leaves in the case of cherry laurel.”

And according to Herbal Medicine Past and Present: A reference guide to medicinal plants (Duke University Press, second printing 1997, ISBN-10: ‎0822310198 ISBN-13: 978-0822310198) by John K. Crellin and Jame Philpott, a Cherry Laurel leaf is about 5% cyanide when young, rapidly decreasing to 0.4-1.0% as the leaf grows in size: “The cyanide content (from the glycoside prulaurasin) of the young leaves of this evergreen shrub, common in Europe, is\ reputed to be 5 percent, dropping rapidly to about 0.4-1.0 percent as leaf size increases. This high concentration of cyanide has led to fatalities.”

So if I used lets say 10 leaves, they’d weigh 25 g. Let’s estimate 2.5% cyanide. That’s 25×0.025 = 0.625 g cyanide. Then maybe I had 5% of that in the tea, making 0.625×0.05 = 0.03125 g = 31.25 mg.

Lethal dose is >1.5 mg cynaide/kg body weight. I weigh at least 82 kg, making for 0.381 mg/kg. 

Probably a lot less. So maybe “only” a quarter or so of the lethal dose. Thank goodness.


But, to make matters better, HCN is volatile at ordinary temperatures! They say on Wikipedia:

Hydrogen cyanide (HCN), sometimes called prussic acid, is an organic compound[8] with the chemical formula HCN. It is a colorless, extremely poisonous and flammable liquid that boils slightly above room temperature, at 25.6 °C (78.1 °F).

So I might have taken in more one day when smelling Cherry Laurel leaves than I did in my tea.

Mechanisms and Antidotes

In Cyanide poisoning, they say:

Cyanide poisoning is poisoning that results from exposure to any of a number of forms of cyanide. Early symptoms include headache, dizziness, fast heart rate, shortness of breath, and vomiting. This phase may then be followed by seizures, slow heart rate, low blood pressure, loss of consciousness, and cardiac arrest. Onset of symptoms usually occurs within a few minutes. Some survivors have long-term neurological problems.

Toxic cyanide-containing compounds include hydrogen cyanide gas and a number of cyanide salts. Poisoning is relatively common following breathing in smoke from a house fire. Other potential routes of exposure include workplaces involved in metal polishing, certain insecticides, the medication sodium nitroprusside, and certain seeds such as those of apples and apricots. Liquid forms of cyanide can be absorbed through the skin. Cyanide ions interfere with cellular respiration, resulting in the body’s tissues being unable to use oxygen.

Diagnosis is often difficult. It may be suspected in a person following a house fire who has a decreased level of consciousness, low blood pressure, or high lactic acid. Blood levels of cyanide can be measured but take time. Levels of 0.5–1 mg/L are mild, 1–2 mg/L are moderate, 2–3 mg/L are severe, and greater than 3 mg/L generally result in death.

If exposure is suspected, the person should be removed from the source of exposure and decontaminated. Treatment involves supportive care and giving the person 100% oxygen. Hydroxocobalamin (vitamin B12a) appears to be useful as an antidote and is generally first-line. Sodium thiosulphate may also be given.

If hydrogen cyanide is inhaled it can cause a coma with seizures, apnea, and cardiac arrest, with death following in a matter of seconds. At lower doses, loss of consciousness may be preceded by general weakness, dizziness, headaches, vertigo, confusion, and perceived difficulty in breathing. At the first stages of unconsciousness, breathing is often sufficient or even rapid, although the state of the person progresses towards a deep coma, sometimes accompanied by pulmonary edema, and finally cardiac arrest. A cherry red skin color that changes to dark may be present as the result of increased venous hemoglobin oxygen saturation. Despite the similar name, cyanide does not directly cause cyanosis.[failed verification] A fatal dose for humans can be as low as 1.5 mg/kg body weight. Other sources claim a lethal dose is 1–3 mg per kg body weight for vertebrates.

Cyanide is a potent cytochrome c oxidase (COX, a.k.a Complex IV) inhibitor. As such, cyanide poisoning is a form of histotoxic hypoxia, because it interferes with oxidative phosphorylation.

Specifically, cyanide binds to the heme a3-CuB binuclear center of COX (and thus is a non-competitive inhibitor of it). This prevents electrons passing through COX from being transferred to O2, which not only blocks the mitochondrial electron transport chain but also interferes with the pumping of a proton out of the mitochondrial matrix which would otherwise occur at this stage. Therefore, cyanide interferes not only with aerobic respiration but also with the ATP synthesis pathway it facilitates, owing to the close relationship between those two processes.

One antidote for cyanide poisoning, nitrite (i.e. via amyl nitrite), works by converting ferrohemoglobin to ferrihemoglobin, which can then compete with COX for free cyanide (as the cyanide will bind to the iron in its heme groups instead). Ferrihemoglobin cannot carry oxygen, but the amount of ferrihemoglobin that can be formed without impairing oxygen transport is much greater than the amount of COX in the body.

Cyanide is a broad-spectrum poison because the reaction it inhibits is essential to aerobic metabolism; COX is found in many forms of life. However, susceptibility to cyanide is far from uniform across affected species; for instance, plants have an alternative electron transfer pathway available that passes electrons directly from ubiquinone to O2, which confers cyanide resistance by bypassing COX.

The International Programme on Chemical Safety issued a survey (IPCS/CEC Evaluation of Antidotes Series) that lists the following antidotal agents and their effects: oxygen, sodium thiosulfate, amyl nitrite, sodium nitrite, 4-dimethylaminophenol, hydroxocobalamin, and dicobalt edetate (‘Kelocyanor’), as well as several others. Other commonly-recommended antidotes are ‘solutions A and B’ (a solution of ferrous sulfate in aqueous citric acid, and aqueous sodium carbonate, respectively) and amyl nitrite.

Evidence from animal experiments suggests that coadministration of glucose protects against cobalt toxicity associated with the antidote agent dicobalt edetate. For this reason, glucose is often administered alongside this agent (e.g. in the formulation ‘Kelocyanor’). It has also been anecdotally suggested that glucose is itself an effective counteragent to cyanide, reacting with it to form less toxic compounds that can be eliminated by the body. One theory on the apparent immunity of Grigori Rasputin to cyanide was that his killers put the poison in sweet pastries and madeira wine, both of which are rich in sugar; thus, Rasputin would have been administered the poison together with massive quantities of antidote. One study found a reduction in cyanide toxicity in mice when the cyanide was first mixed with glucose. However, as yet glucose on its own is not an officially acknowledged antidote to cyanide poisoning.


So on Friday 21 Oct 2016 I took some activated charcoal pills, ate a quarter cup of honey, ate a few coconut macaroons. I had been taking modified citrus pectin for a week or so before my cyanide tea; it might have helped.

The CDC on Cyanide Toxicity

The CDC also has a toxic profile for Cyanide, about 100 pages long. Some excerpts:

An average fatal dose of 1.52 mg/kg cyanide for humans has been calculated from case report studies of intentional or accidental poisonings (EPA 1987a). The lowest fatal oral dose reported in humans was\ estimated as 0.56 mg/kg cyanide (form not specified) (Gettler and Baine 1938). However, these data were obtained from the case history; furthermore, analytical measurements of the time lack the precision of current technology.

Neurologic toxicity following cyanide ingestions differs depending on length of exposure and the rate at which treatment is administered. Neurological effects of cyanide poisoning in humans may correlate with the amount ingested; however, the exact doses consumed by the victims are usually not known. Tremors were reported in a patient who accidentally ingested an unknown amount of fluid containing 2.3% silver cyanide and 6.9% sodium cyanide (Chen and Rose 1952). Children who ingested a large number of apricot pits experienced various neurological effects ranging in severity from headaches to coma (Lasch and El Shawa 1981). The severity of effects corresponded with the amount of ingested pits. Comatose patients were admitted to a hospital after ingesting 15 mg CN–/kg (Liebowitz and Schwartz 1948), 7.6 mg CN–/kg (Goodhart 1994), 114–229 mg CN–/kg (Kasamo et al. 1993), and 5.7 mg CN–/kg (Valenzuela et al. 1992), all as potassium cyanide. A cancer patient who ingested 3,000 mg of amygdalin soon became comatose and had two general tonic-clonic seizures (Bromley et al. 2005). Although the dose is generally nontoxic, hydrolysis would potentially release 180 mg of cyanide. It was suggested that the patient’s high daily intake of ascorbic acid (4,800 mg/day) may have elevated the rate of hydrolysis in the gut, resulting in increased release of cyanide. Histopathological effects in the brain were noted in an individual who died 4 days after being poisoned with potassium cyanide (Riudavets et al. 2005). Effects included autolysis in several regions of the brain (basal ganglia, thalamus, hypothalamus, and cerebellum), acute hypoxic/ischemic changes (neuronal necrosis) in the cerebellum (Purkinje and granule cells), basal ganglia, hypothalamus, and deep cortical layers (manifest as pseudolaminar necrosis), and apoptosis of glial cells in the white matter.

Cyanogenic glycosides

And it’s more common than you might think (or might have remembered). In Glycoside,” they say:

Cyanogenic glycosides

In this case, the aglycone contains a cyanide group. All of these plants have these glycosides stored in the vacuole, but, if the plant is attacked, they are released and become activated by enzymes in the cytoplasm. These remove the sugar part of the molecule and release toxic hydrogen cyanide. Storing them in inactive forms in the vacuole prevents them from damaging the plant under normal conditions.

An example of these is amygdalin from bitter almonds (but not sweet almonds). Cyanogenic glycosides can also be found in the fruit seeds (and wilting leaves) of many members of the rose family (including cherries, apples, plums, bitter almonds, peaches, apricots, raspberries, and crabapples). Bamboo shoots a staple food in South East Asia, must be thoroughly cooked in order to inactivate the present toxin in its raw form. Cassava, an important food plant in Africa and South America, contains cyanogenic glycosides and, therefore, has to be washed and ground under running water prior to consumption. Sorghum (Sorghum bicolor) expresses cyanogenic glycosides in its roots, and thus is resistant to pests such as rootworms (Diabrotica spp.) that plague its cousin maize (Zea mays L.). It was once thought that cyanogenic glycosides might have anti-cancer properties, but this idea was disproven (see Amygdalin).

History, Rasputin, Chemistry, and Biology

In Grigori Rasputin, they say:

Grigori Yefimovich Rasputin (/ræˈspjuːtɪn/; Russian: Григорий Ефимович Распутин [ɡrʲɪˈɡorʲɪj jɪˈfʲiməvʲɪtɕ rɐˈsputʲɪn]; 21 January [O.S. 9 January] 1869 – 30 December [O.S. 17 December] 1916) was a Russian mystic and self-proclaimed holy man who befriended the family of Nicholas II, the last Emperor of Russia, and gained considerable influence in late Imperial Russia.

Rasputin was born to a peasant family in the Siberian village of Pokrovskoye in the Tyumensky Uyezd of Tobolsk Governorate (now Yarkovsky District of Tyumen Oblast). He had a religious conversion experience after taking a pilgrimage to a monastery in 1897. He has been described as a monk or as a “strannik” (wanderer or pilgrim), though he held no official position in the Russian Orthodox Church. He traveled to Saint Petersburg in 1903 or the winter of 1904–1905, where he captivated some church and social leaders. He became a society figure and met Emperor Nicholas and Empress Alexandra in November 1905.

In late 1906, Rasputin began acting as a healer for the imperial couple’s only son, Alexei, who suffered from hemophilia. He was a divisive figure at court, seen by some Russians as a mystic, visionary, and prophet, and by others as a religious charlatan. The high point of Rasputin’s power was in 1915 when Nicholas II left St. Petersburg to oversee Russian armies fighting World War I, increasing both Alexandra and Rasputin’s influence. Russian defeats mounted during the war, however, and both Rasputin and Alexandra became increasingly unpopular. In the early morning of 30 December [O.S. 17 December] 1916, Rasputin was assassinated by a group of conservative noblemen who opposed his influence over Alexandra and Nicholas.

Yusupov said he invited Rasputin to his home shortly after midnight and ushered him into the basement. Yusupov offered Rasputin tea and cakes which had been laced with cyanide. Rasputin initially refused the cakes but then began to eat them and, to Yusupov’s surprise, appeared unaffected by the poison. Rasputin then asked for some Madeira wine (which had also been poisoned) and drank three glasses, but still showed no sign of distress. At around 2:30 am, Yusupov excused himself to go upstairs, where his fellow conspirators were waiting.

In “Anecdotes for Chemistry Teachers: The murder of Rasputin,” The Royal Society of Chemistry writes:

It seems possible that the potassium cyanide used by Yussupov could have been stored in damp conditions. Atmospheric carbon dioxide reacts with moisture to form the weak acid carbonic acid: CO2(g) + H2O(l) → H2CO3(aq)

This is a weak acid (pKa 6.3) but it is strong enough to react with potassium cyanide to form hydrocyanic acid (pKa 9.3) and potassium hydrogencarbonate. H2CO3(aq) + KCN(s) → KHCO3(s) + HCN(g)

Hydrocyanic acid (hydrogen cyanide) is covalently bonded and the molecule is a gas at room temperature. The gaseous hydrocyanic acid would have escaped into the air leaving behind the harmless potassium hydrogencarbonate. This is a white powder and would be visually indistinguishable from the potassium cyanide.

And in Cyanide poisoning, they say:

It has also been anecdotally suggested that glucose is itself an effective counteragent to cyanide, reacting with it to form less toxic compounds that can be eliminated by the body. One theory on the apparent immunity of Grigory Rasputin to cyanide was that his killers put the poison in sweet pastries and madeira wine, both of which are rich in sugar; thus, Rasputin would have been administered the poison together with massive quantities of antidote. One study found a reduction in cyanide toxicity in mice when the cyanide was first mixed with glucose.[24] However, as yet glucose on its own is not an officially acknowledged antidote to cyanide poisoning.

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