Hemlock (Conium maculatum L.): A Comprehensive Reference
1. Identity: Botanical Classification, Nomenclature, and Physical Description
Conium maculatum L., commonly known as hemlock (British English) or poison hemlock (North American English), is a highly poisonous flowering plant and a nitrophile weed species in the carrot family Apiaceae. It is one of the highly poisonous perennial herbaceous flowering plants of the family Apiaceae, native to temperate regions of Europe, West Asia, as well as North Africa, but has been introduced and naturalized in many other areas, including Asia, North America, Australia, and New Zealand.
Conium maculatum is a herbaceous flowering plant that typically grows as a biennial, but can grow as a perennial on occasion. The second-year stems topped with flowers grow to between 0.5 and 3 m (1.6 and 9.8 ft) in height; they are coarse and branch frequently. It has a white carrot-like taproot. The plant's hollow stem is hairless and has characteristic reddish or purple spots. If bruised, the plant has an unpleasant musty odor. The delicate leaves are fern-like and bright green. Tiny white flowers grow in small clusters in late spring.
The genus name reflects the plant's toxic effects. Linnaeus, in 1737, restored the classical Greek name and called the hemlock Conium maculatum, the generic name being derived from the Greek word Konas, meaning "to whirl about," because the plant, when eaten, causes vertigo and death. The specific epithet maculatum is the Latin word meaning "spotted," and refers to the stem markings.
In chemistry, coniine holds two historical records: it is the first alkaloid the chemical structure of which was established (in 1881), and that was chemically synthesized (in 1886).
Common Names and Potential for Confusion
Conium maculatum has many common names that refer to the fact that the plant is highly poisonous. It is known as poison hemlock, deadly hemlock, or poison parsley. Other common names are spotted or European hemlock. Poison hemlock is sometimes confused with spotted water hemlock (Cicuta maculata). Water hemlock is also extremely poisonous but is a different plant that is native to North America. Poison hemlock can easily be misidentified as edible species such as celery, parsnip (for their leaves), or carrots (for their roots).
Preparations and Forms
All vegetative organs, flowers, and fruits contain alkaloids. Hemlock fruits have essentially the same active constituents, but yield a greater portion of coniine than the leaves. Historically, the plant has been prepared in several forms. The dried leaf and juice of the plant were listed in pharmacopoeias of London and Edinburgh from 1864 to 1898, and the last official medicinal recognition appeared in the British Pharmaceutical Codex of 1934 in Great Britain. The dried ripe fruit is official in the British Pharmacopoeia and the Pharmacopoeia of India, but in the Pharmacopoeia of the United States, the full-grown fruit, gathered before it turns from green to yellow and carefully dried, is directed to be used.
Conium maculatum has had several medicinal preparations, such as teas, tinctures, and topical applications, which have been historically used for their purported therapeutic properties. In more modern times, Conium maculatum is nowadays only prepared as a homeopathic remedy. When used as homeopathic medicine, Conium is very diluted; it contains only extremely small amounts of the active but toxic compounds.
2. Traditional and Historical Use
Ancient Greece and Rome
The poison hemlock was one of the better-known poisonous plants, both in Greco-Roman antiquity and in Byzantium. Its healing properties were also appreciated, treating it as a medicinal herb and an ingredient in many pharmacological preparations. Prescriptions containing Conium maculatum were prescribed by the most famous ancient physicians, apothecaries, and botanists, such as Hippocrates of Kos, the precursor of modern pharmacology Pedanius Dioscorides, and Claudius Galen, but also Aulus Cornelius Celsus and Aretaeus of Cappadocia. Their findings were later confirmed by early Byzantine physicians such as Paul of Aegina and Oribasius. Ancient poets, philosophers, and historians such as Plato, Aristophanes, Pliny the Elder, and Nicander of Colophon also mentioned this plant in their works.
The plant's most famous historical use was as an instrument of capital punishment. Poison hemlock has a notorious and deadly history, most famously linked to the execution of the philosopher Socrates in ancient Greece. It was used as a state-sanctioned method of execution, with Socrates forced to drink a lethal dose of hemlock juice after being sentenced to death. The toxicity of hemlock has been known in ancient Greece; the symptoms of the lethal hemlock poisoning of Socrates were described by his pupil Plato.
Anglo-Saxon and Medieval Europe
Hemlock was used in Anglo-Saxon medicine, and is mentioned as early as the tenth century. The common hemlock is a very poisonous plant, but also a marvelous medicine when properly used. Baron Stoerck is said to have been the first that brought it into repute, on account of its extraordinary efficacy in curing scirrhus and other forms of cancers, as well as other diseases supposed to be incurable. It has been successfully used in chronic rheumatism, glandular swellings, and various periodical pains. It has been found of singular use in whooping-cough; applied externally it allays the pains of open and ulcerated cancers.
The 18th Century: Anton von Störck and Systematic Experimentation
A pivotal moment in the documented medicinal history of hemlock came in the 18th century. Anton von Störck was convinced that plants regarded as poisonous still had medicinal applications if employed in carefully controlled quantities. He was particularly interested in the medical possibilities of plants such as hemlock, henbane, jimsonweed, and autumn crocus. His experiments with these plants involved a three-step process: initially used on animals, followed by a personal trial, and finally given to his patients, all the while maintaining a "sliding-scale" approach to determine the optimum dosage. Von Störck described the process and outcomes of his study of hemlock in An Essay on the Medical Nature of Hemlock, published in 1760. Inspired by accounts of successful treatments recorded by early writers like Pliny, von Störck experimented with hemlock extracts and powders. He detailed the outcome of 20 cases he treated, and remained convinced that with proper preparation, hemlock could be a medicinal asset to humankind.
Störck's numerous Latin medical tracts, detailing his experiments into the therapeutic effects of poisonous plants, excited great interest and were translated into German, French, English, Dutch, and Portuguese, rapidly becoming influential medical texts throughout Europe. In 1760, Anton von Störck (1731–1803), an Austrian physician, conducted pioneering experiments in pharmacology by testing a drug for breast cancer (a hemlock extract) on a dog.
Traditional Ethnopharmacological Uses
Conium maculatum Linn. has been traditionally used in the treatment of spasmodic disorders, and to relieve nervous excitation, rheumatic pains in the old and feeble, pain in stomach, pain of gastric ulcer, nervousness, and restlessness. It has been traditionally used externally to treat herpes, erysipelas, and breast tumours, and as an antispasmodic, a sedative, or an analgesic. Historically, poison hemlock was used as medicine to treat muscle spasms and cause sedation, as well as being applied to tumors.
Ethanolic extract of Conium maculatum has long been used in traditional and alternative systems of medicine including homeopathy for the treatment of glandular enlargements, cancerous tumours or hard lumps of testicles, prostate, ovaries, breasts, and/or uterus, particularly in the breast.
As a medicine, Conium is sedative and antispasmodic, and in sufficient doses acts as a paralyser to the centres of motion. In its action it is, therefore, directly antagonistic to that of strychnine, and hence it has been recommended as an antidote to strychnine poisoning, and in other poisons of the same class, and in tetanus.
3. Key Constituents and Active Compounds
Piperidine Alkaloids
One of the most poisonous species amongst higher plants is Conium maculatum. It is a very common nitrophile weed species, belonging to the Apiaceae (formerly Umbelliferae) family. It contains piperidine alkaloids (coniine, N-methyl-coniine, conhydrine, pseudoconhydrine, γ-coniceine), which are formed by the cyclisation of an eight-carbon chain derived from four acetate units. γ-Coniceine is the precursor of the other hemlock alkaloids.
The major alkaloids are: coniine (2-propylpiperidine), N-methyl-coniine (1-methyl-2-propylpiperidine), conhydrine (2-(1-hydroxypropyl)-piperidine), pseudoconhydrine ((5-hydroxypropyl)-piperidine) — the saturated piperidine alkaloids — and γ-coniceine (2n-propyl-1Δ-piperidine), a partially unsaturated one. Conhydrinone and N-methyl-pseudoconhydrine were later isolated.
The biologic activity (and odor) of the plant originates from 10 simple piperidinic alkaloids found within poison hemlock. The two piperidinic alkaloids that are thought to have the principal toxic effect are γ-coniceine and coniine. γ-Coniceine is the more toxic of the two and is the first formed biosynthetically.
The concentrations (both absolute and relative) of the different alkaloids depend on plant varieties, on ecological conditions, and on the age of the plant. The concentration and proportion of the two principal alkaloids also depends on the season, nutrients available, amount of rainfall, and maturation of the plant. All parts of the plant are poisonous, and its toxicity is related to the age of the plant, season, and precipitation. During dry sunny seasons, the concentration of toxic alkaloids is the highest.
Biosynthesis
The alkaloids derive biosynthetically from acetate units via the polyketide pathway, in contrast to other piperidine alkaloids which derive from lysine. The major alkaloid found in flower buds is γ-coniceine. This molecule is transformed into coniine during the later stages of fruit development. When the concentration of coniine is high, the concentration of γ-coniceine is low, implying that coniine is a revival form of γ-coniceine. An oxidation-reduction system is available between coniine and γ-coniceine in Conium plants by a NADPH-dependent γ-coniceine reductase.
Other Phytochemicals
Conium maculatum has several bioactive constituents, such as alkaloids, flavonoids, and essential oils, which have been studied for their potential medicinal applications. Flavonoids present in the plant exhibit antioxidant and anti-inflammatory properties, contributing to its potential therapeutic value. Phytochemically, C. maculatum has been reported to contain piperidine alkaloids as well as fatty constituents, including palmitic, stearic, oleic, petroselinic, linolenic, and arachidic acids, and unsaponifiable matter containing β-sitosterol.
Upon drying, the toxicity of the plant material is greatly reduced, although not entirely eliminated, implying that the toxic principle might be volatile or unstable.
4. Mechanisms of Action
Nicotinic Receptor Activity
Coniine and γ-coniceine are structurally similar to nicotine, a pyrrolidine alkaloid, and stereospecifically bind to cholinergic ligand-gated sodium channels at nicotinic sites. Similar to nicotine, coniine and related alkaloids have an initial excitatory effect, followed by a depressant effect on the central nervous system.
Toxicity comes from piperidine alkaloids, which mimic nicotine's effect on the autonomous nervous system, giving a clinical picture of nicotinic syndrome with an initial excitatory phase and a secondary inhibitory one. The acute toxic activity of coniine, γ-coniceine, and N-methylconiine consists in the blockage of spinal reflexes through action on the medulla: they produce an initial stimulus followed by the depression of the autonomic ganglia. High doses produce a stimulation of the skeletal muscles and a subsequent neuromuscular blockage through action on nicotinic receptors.
Coniine has a number of pharmacological activities resembling nicotine. It is capable of producing stimulation followed by depression of autonomic ganglia. Animal studies demonstrate that coniine activity on isolated ileum and duodenum is blocked with atropine pretreatment. This implies that coniine stimulates parasympathetic ganglia and explains the observed nicotinic effects following exposure to this plant, which include salivation, mydriasis, and tachycardia, followed by bradycardia. These alkaloids also act as nondepolarizing antagonists at the neuromuscular junction, similar in action to tubocurare.
Neuromuscular Blockade and Respiratory Failure
Coniine, a polyketide-derived alkaloid, is poisonous to humans and animals. It is a nicotinic acetylcholine receptor antagonist, which leads to inhibition of the nervous system, eventually causing death by suffocation in mammals. The compounds are neurotoxins, and the acute effect is death by respiratory failure. If depolarization persists, the cell becomes inactivated, leading to paralysis in the case of muscle tissue. The difference between the action of acetylcholine and that of coniine is that acetylcholine is rapidly degraded, allowing repolarization and thus enabling an on-off cycle required for voluntary muscle contraction — something that becomes impossible after exposure to these depolarizing agents.
Stereoselectivity
The relative potencies of coniine enantiomers on TE-671 cells expressing human fetal nicotinic neuromuscular receptors had the rank order of (−)-coniine > (±)-coniine > (+)-coniine. LD50 values of the coniine enantiomers were 7.0, 7.7, and 12.1 mg/kg for the (−)-, (±)-, and (+)-forms of coniine, respectively, in a mouse bioassay. The results demonstrate a stereoselective difference in the in vitro potencies of the enantiomers of coniine that directly correlates with the relative toxicities of the enantiomers in vivo.
5. Scientific Evidence by Area of Use
5a. Analgesic and Antinociceptive Activity
Preclinical (animal) evidence — no human clinical trials identified
There was an ethnopharmacological tradition of using hemlock as an analgesic, but at the time of early investigation there was no scientific record of the antinociceptive effect of coniine, the major alkaloid compound of hemlock.
A 2009 preclinical study investigated coniine's analgesic properties. Coniine decreased the number of writhes in the writhing test. Both data indicated an antinociceptive effect of coniine. A rotarod test was also conducted to clarify whether this activity was related to a loss of locomotion or an analgesic activity. None of the chemical agents at those doses caused a loss of locomotor activity. The antinociceptive effect of morphine was potentiated by coniine, which was inhibited by the nicotinic receptor blocker mecamylamine (1 mg/kg). Coniine has an antinociceptive effect via the nicotinic receptors. Coniine caused a prolongation in reaction time in the hotplate test at a 20 mg/kg dose. In addition, it was observed that coniine decreased the number of writhes in the writhing test.
A separate study examined the novel alkaloid conmaculatin. 2-Pentylpiperidine, named conmaculatin, a novel volatile alkaloid related to coniine was identified from Conium maculatum L. Its structure was corroborated by synthesis. Conmaculatin's strong peripheral and central antinociceptive activity in mice was observed in a narrow dose range (10–20 mg/kg). It was found to be lethal in doses higher than 20 mg/kg.
A third study examined the alkaloidal fraction from aerial plant parts. The alkaloidal fraction from Conium maculatum aerial parts exhibited analgesic and anti-inflammatory effects in rats, comparable to diclofenac, with significant paw edema inhibition at 200 mg/kg.
Evidence strength: All analgesic evidence is derived exclusively from preclinical animal models (mice and rats). No human clinical trials have been conducted. The therapeutic window between effective and lethal doses in animal models is exceedingly narrow, underscoring the difficulty of translating these findings to safe human use.
5b. Anti-inflammatory Activity
Preclinical evidence only
Hemlock alkaloids have analgesic (pain-relieving) and anti-inflammatory activity in rats at 200 mg/kg (total alkaloids). Of three alkaloid extracts, the one prepared using methanol for extraction had relatively higher anti-inflammatory (55.93% and 59.32%), analgesic (70.08% and 71.50%), and skeletal muscle relaxant activities (76.83% and 78.51%) at both doses (100 mg/kg and 200 mg/kg) respectively compared to chloroform and water fractions. These results were significantly closer to the standard drugs used in the respective studies.
Evidence strength: Preliminary, rodent-only data. No human data are available. The alkaloid doses reported in animals are far above those that would be associated with safety margins in humans.
5c. Anticancer and Cytotoxic Activity
In vitro and preclinical evidence only
Conium maculatum extract is used as a traditional medicine for cervix carcinoma including homeopathy. However, no systematic work had been carried out to test its anti-cancer potential against cervix cancer cells in vitro. One study investigated whether the ethanolic extract of conium is capable of inducing cytotoxicity in different normal and cancer cell lines, including an elaborate study in HeLa cells. The extract's effects on cell cycle, reactive oxygen species (ROS) accumulation, mitochondrial membrane potential (MMP), and apoptosis were analyzed through flow cytometry. Whether the extract could damage DNA and induce morphological changes was also determined microscopically. Expression of different proteins related to cell death and survival was critically studied by western blotting and ELISA methods. Whether the extract could interact directly with DNA was also determined by circular dichroism (CD) spectroscopy.
In this study, 70–840 μg/mL of drug was supplemented to A375, A549, HepG2, WRL-68, and PBMCs and incubated for 48 hours. In HeLa cell cultures, 70–840 μg/mL of drug was supplemented for 24 and 48 hours. MTT assay was performed to assess cell viability. Treatment with Conium was found to reduce colony formation ability of HeLa cells, and the proliferation assay indicated the reduction in proliferative property of HeLa cells upon treatment with Conium at a dose of 450 μg/mL, with the lowest proliferation achieved at 48 hours of treatment.
Adverse side-effects and lack of scientific validation of some chemotherapeutic agents prevent the use of many traditional medicines claimed to have anti-cancer effects. Ethanolic extract of Conium maculatum has long been used in traditional and alternative systems of medicine, including homeopathy, for the treatment of glandular enlargements and cancerous tumors. However, if and how it acts still remains scientifically unknown.
Evidence strength: Strictly preliminary in vitro (cell culture) evidence. No animal tumor model studies or human clinical trials have been conducted to validate these findings. The gap between cytotoxicity in cell culture and proven anticancer efficacy in vivo in humans is substantial.
5d. Neurotoxicity and Documented Human Poisoning Cases
Case reports and case series — robust clinical documentation of harmful effects
The most extensively documented human evidence for Conium maculatum's pharmacological activity in humans comes from poisoning case reports. A published review highlighted the symptomatology in three Conium maculatum intoxication incidents, one of which was fatal. A number of studies were reviewed to update and summarize the relevant literature on the incidence, sociodemographic variables, method of poisoning, pathophysiology, diagnosis, variables associated with survival and fatality, management, and treatment. Results show that hemlock poisoning is relatively rare, although incidence varies in different regions, despite its worldwide distribution. Hemlock poisoning is more common in European and especially Mediterranean countries. The majority of the patients are adult males over 38 years of age. The clinical course of hemlock poisoning includes neurotoxicosis, tremor, vomiting, muscle paralysis, respiratory paralysis/failure, rhabdomyolysis, and acute renal failure.
Poison hemlock is a plant that is poisonous to humans and animals. Accidental ingestion of the plant may result in central nervous system depression, respiratory failure, acute rhabdomyolysis, acute renal failure, and even death. The main treatment of hemlock poisoning is supportive care. One documented case involves a 6-year-old girl admitted to the emergency department with complaints of burning sensation in the mouth, hypersalivation, tremor in hands, and ataxia after ingestion of poison hemlock. The hemlock was mistaken for parsley and consumed.
6. Body Systems and Health Areas Associated with Hemlock
Nervous System
Signs and symptoms following exposure tend to follow a biphasic pattern. Initially, the stimulatory effect of nicotinic stimulation includes nausea and vomiting, excess salivation, diarrhea, and abdominal pain. In the cardiovascular system, hypertension and tachycardia reflect increased autonomic tone, and pallor from vasoconstriction in the peripheral blood vessels is also common. Early neurologic effects include ataxia, tremor, restlessness, headache, visual and hearing disturbances, dizziness, confusion, muscle fasciculation, miosis, seizures, diaphoresis, and tachypnea.
The initial stimulatory effect is classically followed by a more pronounced inhibitory phase caused by the "paradoxical" inhibition of the nicotinic cholinergic receptors. Hypotension, bradycardia, cardiac brady-arrhythmias, and ventricular fibrillation can ensue. Central effects are characterized by stupor and coma. Increasing neuromuscular blockage can lead to ptosis, muscular weakness, and paralysis, while bradypnea, apnea, and respiratory failure, alongside with cardiovascular collapse, is the cause of death.
Musculoskeletal System
The presence of rhabdomyolysis and acute tubular necrosis has been demonstrated in patients who died from hemlock poisoning. Some of these patients had acute kidney injury. Rhabdomyolysis has been reported, and acute kidney injury and renal failure are specific symptoms that are only reported in human poisoning.
Renal System
Coniine has significant toxic effects on the kidneys. Muscle weakness or paralysis, bradycardia, and central nervous system depression may develop in some patients due to increased cholinergic stimuli. Rhabdomyolysis and acute renal failure have also been reported in some cases as a consequence of Conium maculatum poisoning.
Cardiovascular System
Coniine-induced respiratory paralysis with damage to the respiratory center in the medulla can cause death. Tachycardia is followed by bradycardia induced by Conium alkaloids that behave like biphasic nicotine.
Integumentary System (Dermal)
Contact of the leaves with bare skin can result in rash and persistent blisters through phototoxicity, the sensitisation of the skin to sunlight.
Reproductive and Developmental System
Besides its acute effects, C. maculatum has been found to induce a chronic teratogenic activity on livestock and humans. Chronic non-lethal ingestion by pregnant livestock leads to foetal malformations. Teratogenic effects have been reported, including skeletal malformations, cleft palate, etc., which vary depending on the stage of gestation during which the pregnant animals consumed the plant. C. maculatum alkaloids can be transferred to milk and to fowl muscle tissue, through which the former can reach the human food chain.
7. Reported Dosages in Studies
Given the extreme toxicity of Conium maculatum, the concept of a therapeutic dosage is almost entirely confined to historical and preclinical contexts. The following dosages are reported strictly as stated in the cited sources and not as recommendations.
- The toxic dose in humans is thought to be 60 mg of coniine, and the fatal dose is 150–300 mg.
- Coniine caused a prolongation in reaction time in the hotplate test at 20 mg/kg dose in mice.
- Conmaculatin's strong peripheral and central antinociceptive activity in mice was observed in a narrow dose range (10–20 mg/kg). It was found to be lethal in doses higher than 20 mg/kg.
- LD50 values of the coniine enantiomers were 7.0, 7.7, and 12.1 mg/kg for the (−)-, (±)-, and (+)-forms of coniine, respectively, in mice.
- Hemlock alkaloids have analgesic and anti-inflammatory activity in rats at 200 mg/kg (total alkaloids).
- In in vitro HeLa cell studies, a reduction in proliferative property was observed upon treatment with Conium extract at a dose of 450 μg/mL over 48 hours.
- Unripe C. maculatum seeds were historically dried and stored to be used as an antispasmodic, a sedative, or an analgesic, but the medicinal importance of hemlock is very limited because of the closeness between therapeutic and poisonous levels.
8. Safety, Toxicology, and Notable Interactions
General Toxicity
Poison hemlock (C. maculatum), from the Apiaceae family, is regarded as one of the most poisonous plants in Europe. Its toxicity is related to nicotinic alkaloids, the most potent being coniine. All parts of the plant are toxic, particularly the seeds and roots, and especially when ingested.
Misidentification Risk
Poison hemlock can easily be misidentified as edible species such as celery or parsnip (for their leaves), or carrots (for their roots). In documented cases, hemlock has been mistaken for parsley and consumed. Accidental ingestion of some plants that closely resemble edible vegetables may produce serious signs of poisoning and even lead to death.
Secondary Poisoning via Animal Products
As described in an 11-case report in Italy, people are usually poisoned indirectly by eating small birds or rabbits that have consumed hemlock buds. Intoxication can happen even after the animals were frozen for storage.
Seasonal and Environmental Variability of Toxin Content
All parts of the plant are poisonous, and its toxicity is related to the age of the plant, season, and precipitation. During dry sunny seasons, the concentration of toxic alkaloids is the highest. The levels of γ-coniceine in relation to coniine vary widely according to environmental conditions and to provenance of the plants.
Absence of Antidote
No antidote is currently available for hemlock poisoning. Gastrointestinal lavage and activated charcoal can be used within one hour of ingestion, although without strong evidence that this reduces absorption. The mainstay of treatment of severe intoxication is hemodynamic optimization and mechanical ventilation, likely early in the clinical course. Rhabdomyolysis should be managed with aggressive volume replacement and high urine output; hemoperfusion or hemodialysis has been used without clinical or experimental support.
Teratogenicity
The plant Conium maculatum produced congenital defects in calves born to cows gavaged with the fresh green plant during days 50–75 of gestation. Both arthrogryposis and spinal curvature were produced and were similar to the defects produced by the piperidine alkaloid coniine. The arthrogrypotic manifestations of the condition markedly increased in severity as the animals aged. The losses produced by C. maculatum chronic toxicity may be largely underestimated, at least in some regions, because of the difficulty in associating malformations in offspring with the much earlier maternal poisoning.
Phototoxicity
Contact of the leaves with bare skin can result in rash and persistent blisters through phototoxicity, the sensitisation of the skin to sunlight.
Interaction with Nicotinic and Cholinergic Pharmacological Agents
The antinociceptive effect of morphine was potentiated by coniine in animal studies, and this was inhibited by the nicotinic receptor blocker mecamylamine (1 mg/kg). Based on its mechanism as a nicotinic receptor agonist/antagonist, C. maculatum alkaloids would be expected to interact pharmacodynamically with agents affecting cholinergic transmission, including nicotinic and muscarinic receptor modulators; however, this has not been systematically studied in humans.
Pharmacopoeia and Regulatory Status
From 1864 to 1898 hemlock was officially listed as a medicine in the London and Edinburgh pharmacopoeias. The last listing of it was in the British Pharmaceutical Codex in 1934. No current major pharmacopoeia or regulatory body — including the NIH Office of Dietary Supplements, the European Medicines Agency (EMA), or the German Commission E — carries an approved monograph endorsing the therapeutic use of Conium maculatum as a dietary supplement or herbal medicine. Its use in the Western regulatory context is confined to highly diluted homeopathic preparations, which contain negligible concentrations of the parent alkaloids.
References
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