Some science behind the scenes
Cytisine is a pyridine-like alkaloid that is toxic at quite low doses. It is a nicotinic acetylcholine receptor agonist.
Plants that contain the alkaloid in various concentrations include those from several genera of the Faboideae subfamily, including Laburnum, Anagyris, Thermopsis, Cytisus, Genista and Sophora. It is also present in Gymnocladus of the Caesalpinioideae subfamily.
Māmane (Sophora chrysophylla) can contain amounts of cytisine that are lethal to most animals. The Cydia species (moths), use māmane as food. It has been suggested that like Lepidoptera caterpillars, they ‘sequester’ the cytisine to give themselves protection from getting eaten.
Cytisine has been used by the pharmaceutical companies to produce ‘smoking cessation drugs’, but at the moment there is some doubt as to whether the trials were properly conducted. “A 2006 literature review concludes that trials performed with cytisine itself are mostly of poor quality…… ” and "The evidence on cytisine is limited at present, and no firm conclusions can yet be drawn about its effectiveness as an aid to quitting."
The alkaloid first causes nausea, vomiting, heart pain, and headache; then ‘tetanic’ convulsions, ‘renal irritation’ and severe diarrhoea; next comes coma, frothing of the mouth, and unequally diluted pupils.
Death then follows from asphyxiation through its depressive action on the diaphragm. Thus in the end, the final way you would get an experience is via a near death if you were lucky and a final death experience if you were not.
Examples of deaths from Cytisine follow:
Fatal cytosine intoxication and analysis of biological samples with LC–MS/MS - F. Musshof and B. Madea; Institute of Forensic Medicine, Stiftsplatz 12, 53111 Bonn, Germany - 2008
We report about a fatal cytisine intoxication in a 20-year-old man who, according to his mother, had drunken tea prepared from plant material of Laburnum anagyroides with the toxic pyridine-like alkaloid as ingredient, which exhibits pharmacological effects similar to nicotine. Using a liquid chromatographic–mass spectrometric (LC–MS) procedure cytisine was quantified in post-mortem specimens. By exclusion of other causes of death an intoxication was determined as the cause of death with respiratory failure as the pathophysiological mechanism.
Nicotinic plant poisoning - Schep LJ, Slaughter RJ, Beasley DM; National Poisons Centre, Department of Preventive and Social Medicine, University of Otago, Dunedin, New Zealand.
A wide range of plants contain nicotinic and nicotinic-like alkaloids. Of this diverse group, those that have been reported to cause human poisoning appear to have similar mechanisms of toxicity and presenting patients therefore have comparable toxidromes. This review describes the taxonomy and principal alkaloids of plants that contain nicotinic and nicotinic-like alkaloids, with particular focus on those that are toxic to humans. The toxicokinetics and mechanisms of toxicity of these alkaloids are reviewed and the clinical features and management of poisoning due to these plants are described.
…. Plants containing nicotine and nicotine-like alkaloids that have been reported to be poisonous to humans include Conium maculatum, Nicotiana glauca and Nicotiana tabacum, Laburnum anagyroides, and Caulophyllum thalictroides. They contain the toxic alkaloids nicotine, anabasine, cytisine, n-methylcytisine, coniine, n-methylconiine, and gamma-coniceine.
MECHANISMS OF TOXICITY:
These alkaloids act agonistically at nicotinic-type acetylcholine (cholinergic) receptors (nAChRs). The nicotinic-type acetylcholine receptor can vary both in its subunit composition and in its distribution within the body (the central and autonomic nervous systems, the neuromuscular junctions, and the adrenal medulla). Agonistic interaction at these variable sites may explain why the alkaloids have diverse effects depending on the administered dose and duration of exposure.
Nicotine and nicotine-like alkaloids are absorbed readily across all routes of exposure and are rapidly and widely distributed, readily traversing the blood-brain barrier and the placenta, and are freely distributed in breast milk. Metabolism occurs predominantly in the liver followed by rapid renal elimination.
Following acute exposure, symptoms typically follow a biphasic pattern. The early phase consists of nicotinic cholinergic stimulation resulting in symptoms such as abdominal pain, hypertension, tachycardia, and tremors. The second inhibitory phase is delayed and often heralded by hypotension, bradycardia, and dyspnea, finally leading to coma and respiratory failure.
Supportive care is the mainstay of management with primary emphasis on cardiovascular and respiratory support to ensure recovery.
Exposure to plants containing nicotine and nicotine-like alkaloids can lead to severe poisoning but, with prompt supportive care, patients should make a full recovery.
1. Meyler’s Side Effects of Drugs – Elsevier publishing
2. A Modern Herbal – Mrs M Grieve
- Medical Toxicology of Natural Substances – Foods, Fungi, Medicinal Herbs, Plants and Venomous Animals pub. Wiley
- Website of the International Union of Basic and Clinical Pharmacology Database