Scientific Name(s): Aconitum carmichaelii Debeaux, Aconitum kusnezoffii Rchb., Aconitum napellus L.
Common Name(s): Aconite, Aconiti tuber, Blue rocket, Bushi, Caowu, Chuanwu, Devil's helmet, Friar's cap, Futzu, Helmet flower, Leopard's bane, Monkshood, Shenfu, Soldier's cap, Wolfsbane, Wutou
Medically reviewed by Drugs.com. Last updated on Mar 22, 2023.
Aconite extracts have been used traditionally for analgesic, anti-inflammatory, and antirheumatic purposes; however, use is not recommended for any indication because aconite is highly toxic.
Extreme caution is required. Fresh aconite is extremely toxic, and safe dosing is dependent on processing. Many species are used medicinally in China only after processing. Processing may reduce alkaloid content and/or alter alkaloid composition, thus reducing potency; however, poisoning may still occur after consumption of processed aconite root.
Contraindications have not been identified. However, aconite is considered unsafe for human use.
Avoid use. Adverse effects have been documented. Oral administration, as well as external application, is reported to cause toxic symptoms.
None well documented.
No data. Aconite is considered unsafe for human use, with all effects considered toxic.
Aconitine, the major alkaloid derived from various species of Aconitum, is highly toxic. As little as 2 mg of pure aconite or 1 g of the plant may cause death from paralysis of the respiratory center or cardiac muscle. Clinically important toxicity may develop following percutaneous absorption; even slight contact with the flowers can cause fingers to become numb.
- Ranunculaceae (buttercup)
At least 350 Aconitum species exist throughout the world; about 170 species exist in China,(Fatovich 1992) and more than 100 species are found throughout the temperate zones of the United States and Canada. The plants are also found throughout many parts of Asia, Africa, and Europe.(Lampe 1985) A. napellus is the most common species in Europe and has been naturalized in the eastern United States; A. carmichaelii and A. kusnezoffii are the most common species used in traditional Chinese medicine. Aconitum species are erect perennial plants that grow 0.6 to 1.5 m in height and resemble delphiniums; their characteristic helmet-shaped blue or purple flowers grow in a raceme at the top of the stalk in summer or fall. Occasionally, the flowers may be white, pink, peach, or yellow. The seed pods contain numerous tiny seeds.(Lampe 1985)
Various species of Aconitum have been used for centuries, both medicinally and for their poisonous properties. Some are still used in traditional medicine in India, China, and Japan.(Pullela 2008) The root is the most toxic, although all parts of the plant are considered toxic. The toxicity of the extracts follows the same order as that of the alkaloid content: roots, flowers, leaves, and stems.(Fatovich 1992)
Extracts of Aconitum species have been used orally in traditional medicine to reduce fever associated with colds, pneumonia, laryngitis, croup, and asthma; and for analgesic, anti-inflammatory, hypotensive, diuretic, diaphoretic, cardiac depressant, and sedative effects.(Murayama 1991, Spoerke 1980) In traditional Asian medicine, aconite root extracts are typically mixed with other ingredients, such as licorice or ginger.(Colombo 2009) Shenfu decoction (containing Asian ginseng and aconite root stalk extracts) is a traditional medicine used historically for heart failure.(Wei 2015)
Based on accounts in Chinese and Western sources, a principal ingredient in arrow poisons (used for at least 2,500 years in various parts of China [eg, by the Han people]) was often an extract derived from the tubers of Aconitum species, especially A. carmichaelii Debx.(Bisset 1979)
Historically, aconite was most commonly used in Western cultures as a tincture. It was applied topically as a counter irritant liniment for neuralgia, rheumatism, and sciatica.(Fatovich 1992)
Aconitum is included in the US Food and Drug Administration's poisonous plant database.(Brown 2018)
In homeopathy, aconite has been used to treat fear, anxiety, and restlessness; acute sudden fever; symptoms from exposure to dry, cold weather or very hot weather; tingling, coldness, and numbness; influenza or colds with congestion; and heavy, pulsating headaches.(Boericke 1999)
Alkaloids account for up to 1.5% of the dry weight of Aconitum plant species. A wide variety of alkaloids have been isolated from the various species of aconite, including the major active alkaloid aconitine, as well as mesaconitine, hypaconitine, jesaconitine, napelline, sinomontanitines, lappaconitine, ranaconitine, and others.(Fu 1997, Fu 2006, Murayama 1991, Tai 1992a, Wang 2001) Other alkaloids may be produced by processing (eg, pyro-type aconitine alkaloids by heat(Murayama 1991) or benzylaconines or aconines by hydrolysis). Aconitine and its congeners are considerably more toxic than aconine and related alkaloids.(Lin 2004)
Uses and Pharmacology
Because aconite is highly toxic, use is not recommended for any indication. Raw aconite products are extremely toxic; their alkaloids have a narrow therapeutic index, and the alkaloid type and amount vary by species, place of harvest, and adequacy of processing. Processing may reduce alkaloid content and/or alter alkaloid composition, thus reducing potency(Liu 2017); however, poisoning may still occur after consumption of processed aconite root.(Brown 2018, Lin 2004)
The following pharmacological effects of Aconitum alkaloids have been described: analgesic, anti-inflammatory, and antirheumatic activities(Feng 2003, Hikino 1980); positive inotropic effects(Honerjäger 1983); and regulation of neurological disorders.(Feng 2003, Herzog 1964) However, only limited studies are available, most of which were performed in China and Japan.
Guanfu base A, an alkaloid isolated from the root of the related Aconitum coreanum Rapaics, has demonstrated efficacy as an antiarrhythmic agent in preclinical and clinical studies and has undergone phase 3 clinical trials in China.(Sun 2015) It should be noted that according to a 2016 scientific statement by the American Heart Association regarding drugs that may cause or exacerbate heart failure, aconite is recognized as a product that has possibly harmful cardiovascular effects, such as decreased heart rate and ventricular tachycardia, and that may be harmful for patients with heart failure.(Page 2016)
In animal models, aconitine and related compounds have been shown to possess anti-inflammatory and analgesic properties.(Feng 2003, He 2018, Hikino 1980, Murayama 1991) Studies using mechanical and thermal stimuli to cause pain in mice have shown that, at subanalgesic doses, processed Aconitum root administered orally inhibited the development of morphine tolerance both partially and dose dependently in morphine-naive mice and reversed already developed morphine tolerance in morphine-tolerant mice compared with placebo.(Shu 2006a, Shu 2006b, Shu 2007, Shu 2008)
Results of a study using Japanese kampo preparations suggest that Aconiti tuber may increase nitric oxide production in humans, a possible mechanism for Aconiti tuber's purported effect on improving a peripheral feeling of coldness. Eleven and 13 patients, respectively, received kampo formulas including and excluding Aconiti tuber. Nitrite and nitrate levels were increased at 4 weeks in those taking Aconiti tuber formulas.(Yamada 2005)
Extreme caution is required. Fresh aconite is extremely toxic, and safe dosing is dependent on processing. Many species are used medicinally in China only after processing. Aconite has a narrow therapeutic range. Processing may reduce alkaloid content and/or alter alkaloid composition, thus reducing potency(Liu 2017); however, poisoning may still occur after consumption of processed aconite root.(Brown 2018, Lin 2004) As little as 2 mg of pure aconite or 1 g of aconite plant may cause death.(Singh 1986)
Pregnancy / Lactation
Avoid use. Adverse effects have been documented. Oral administration, as well as external application, is reported to cause toxic symptoms.(McGuffin 1997)
None well documented.
Aconite is considered unsafe for human use, with all effects considered toxic. According to a 2016 scientific statement by the American Heart Association regarding drugs that may cause or exacerbate heart failure, aconite is recognized as a product that has possibly harmful cardiovascular effects, such as decreased heart rate and ventricular tachycardia, and that may be harmful for patients with heart failure. The guidance notes that naturoceuticals are not recommended for the management of heart failure symptoms or for secondary prevention of cardiovascular events, and that nutritional supplements are not recommended for the treatment of heart failure.(Page 2016)
Aconite is a fast-acting toxin. The active principles are aconitine and related alkaloids. As little as 2 mg of pure aconite or 1 g of aconite plant may cause death.(Singh 1986)
Toxicity and death have resulted when the aconite plant has been consumed accidentally, possibly mistaken for wild parsley, horseradish, or other herbs growing in the wild.(Pullela 2008, Spoerke 1980) Very few cases of aconite poisoning have been reported in North America.(Pullela 2008) Most reports have been related to the use of traditional Chinese remedies.(Lin 2004) A retrospective search of the Taiwan National Poison Center database between 1990 and 1999 revealed 17 cases of aconitine poisoning. Thirteen patients ingested aconite root for the treatment of rheumatism or wounds. Two patients had volunteered to test the effects of aconite root in a drug study. Only 2 patients had accidentally ingested the root.(Lin 2004) The Toxicology Reference Laboratory in Hong Kong confirmed 10 cases of aconite poisoning between March 2004 and May 2006. In 4 cases, the aconite herb was not listed in written prescriptions.(Poon 2006) A case report in China described a 48-year-old male with a family history of polycystic kidney disease who ingested 30 mL of herbal medicinal wine made with caowu (A. carmichaelii and A. kusnezoffii) for relief of low back pain. Within minutes, he experienced cardiovascular toxicity (ie, paresthesia, chest distress, dyspnea, premature ventricular bigeminy) that was complicated by polycystic renal hemorrhage. Treatment with hemoperfusion and reduced-dose heparin was successful.(Chen 2015)
Most incidents of aconite toxicity result from the wide variability in strength of home preparations in Asian countries.(Chan 2002) However, more lethal poisonings are being reported in Western countries where the use of herbal remedies is increasing.(Fatovich 1992, McGregor 2008) A homicide attempt(Dobbelstein 2000) and a suicide(Guha 1999) with aconite have also been reported.
Aconitine's toxicity is characterized by a burning or tingling sensation of the lips, tongue, mouth, and throat almost immediately following ingestion. Numbness of the throat, difficulty with speech, salivation, nausea, vomiting, dizziness, and diarrhea may occur, as well as visual blurring or yellow-green color vision distortion, weakness, and incoordination. Paresthesia may spread over the entire body. Toxicity mainly affects CNS, heart, and muscle tissues, primarily resulting in cardiovascular complications.(Fu 2006, Guha 1999, Lin 2004, McGregor 2008, Pullela 2008) Cardiac arrhythmias with unusual electrical characteristics have been observed following aconite poisoning.(Smith 2005, Tai 1992b) Putrescine, a compound used experimentally as a molecular probe, has been shown to attenuate aconitine-induced arrhythmias.(Bazzani 1989) Death from aconitine may follow secondary to cardiac arrhythmia,(Lampe 1985) which can occur unpredictably within minutes or days.(Spoerke 1980) Several case reports describe poisonings with aconite or its constituents, resulting in ventricular tachycardia, other arrhythmias, and death.(Fatovich 1992, Gupta 1999, Imazio 2000, Mak 2000, Ortuño Andériz 1999, Pullela 2008)
A single dose of aconitine 0.6 mg/kg administered intraperitoneally to rabbits caused histopathologic damage to the myelin sheath of the visual pathway, spinal cord, and peripheral nerves.(Kim 1991) Similarly, aconitine has demonstrated arrhythmogenic and cardiotoxic effects on myocardium in anesthetized cats.(Sheikh-Zade 2000) Some experiments have used aconitine to artificially induce arrhythmias in laboratory animals to study the antiarrhythmic effects of other drugs.(Pau 2000, Zhang 1999)
A review has summarized the toxicological mechanisms of Aconitum alkaloids, which include the following: binding to voltage-dependent sodium channels, which induces a hyperpolarized state, resulting in permanent activation of the channel; modulation of neurotransmitter release and receptors, particularly norepinephrine and acetylcholine; promotion of lipid peroxidation of the cardiac system, possibly causing cardiac arrhythmias; and induction of cellular apoptosis in the heart, liver, and other organs. Most of the cardiotoxic and neurotoxic effects of aconite can be explained by these mechanisms, including its effect on calcium imbalance.(Fu 2006) Toxicity due to apoptosis of tubular epidermal cells has been documented in studies of mice.(Xu 2016)
General supportive measures form the basis of aconite toxicity management and include fluids for dehydration, intravenous pressor agents (eg, dobutamine, dopamine) for hypotension, and resuscitative measures when indicated.(Lin 2004, McGregor 2008) Gastric lavage or induction of emesis following an injection of atropine has been recommended, particularly for bradycardia.(Duke 1985, Wood 2020) Control of cardiac dysrhythmias has been attempted with various antiarrhythmic agents (eg, lidocaine, amiodarone, flecainide, procainamide, mexiletine)(Lin 2004); however, no single antiarrhythmic drug has been uniformly effective.(McGregor 2008, Tai 1992a) Amiodarone and flecainide have been reasonable first-line choices.(Lin 2004, Tai 1992a, Yeih 2000) Several cases of successful treatment using percutaneous cardiopulmonary support and bypass in the first 24 hours have been reported.(Fitzpatrick 1994, Niinuma 2002, Ohuchi 2000) Charcoal hemoperfusion has also been used in patients with ventricular arrhythmias unresponsive to antiarrhythmic agents and supportive care, and may have played a critical role in patient survival.(Lin 2002, Lin 2004) Recovery time is dependent on the amount of intoxication; mildly intoxicated patients may take 1 to 2 days to recover, whereas patients with cardiovascular complications may take 7 to 9 days to recover.(Lin 2004)
Evidence suggests that aconite may lose potency after undergoing certain manufacturing procedures; therefore, processed aconite may not have a toxicity profile similar to that of crude plant material.(Thorat 1991)
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