Fu Zi

Name: Fu Zi

Other Names: Processed Aconite

Description: Aconitum (A-co-ní-tum), known as aconite, monkshood, or wolfsbane, is a genus of flowering plant belonging to the buttercup family (Ranunculaceae). There are over 250 species of Aconitum.


Overview
These herbaceous perennial plants are chiefly natives of the mountainous parts of the northern hemisphere, growing in moisture retentive but well draining soils on mountain meadows. Their dark green leaves lack stipules. They are palmate or deeply palmately lobed with 5–7 segments. Each segment again is 3-lobed with coarse sharp teeth. The leaves have a spiral or alternate arrangement. The lower leaves have long petioles.

These are handsome plants, the tall, erect stem being crowned by racemes of large and eye-catching blue, purple, white, yellow or pink zygomorphic flowers with numerous stamens. They are distinguishable by having one of the five petaloid sepals (the posterior one), called the galea, in the form of a cylindrical helmet; hence the English name monkshood. There are 2–10 petals, in the form of nectaries. The two upper petals are large. They are placed under the hood of the calyx and are supported on long stalks. They have a hollow spur at their apex, containing the nectar. The other petals are small and scale like or non forming. The 3–5 carpels are partially fused at the base.

The fruit is a follicle.


Uses
The most common plant in this genus, Aconitum napellus (the Common Monkshood) was considered to be of therapeutic and toxicological importance. Its roots have occasionally been mistaken for horseradish. It has a short underground stem, from which dark-colored tapering roots descend. The crown or upper portion of the root gives rise to new plants. When touched to one's lip, the juice of the aconite root produces a feeling of numbness and tingling. This plant is used as a food plant by some Lepidoptera species including Dot Moth, The Engrailed, Mouse Moth, Wormwood Pug, and Yellow-tail.

The roots of Aconitum ferox supply the Indian (Nepal) poison called bikh, bish, or nabee. It contains large quantities of the alkaloid pseudaconitine, which is a deadly poison. Aconitum palmatum yields another of the bikh poisons. The root of Aconitum luridum, of the Himalaya, is said to be as virulent as that of A. ferox or A. napellus.

Several species of Aconitum have been used as arrow poisons. The Minaro in Ladakh use A. napellus on their arrows to hunt ibex, while the Ainus in Japan used a species of Aconitum to hunt bear.[1] The Chinese also used Aconitum poisons both for hunting,[2] and for warfare.[3]

Many species of Aconitum are cultivated in gardens, having either blue or yellow flowers. Aconitum lycoctonum (Alpine wolfsbane), is a yellow-flowered species common in the Alps of Switzerland. As garden plants the aconites are very ornamental, hardy perennial plants. They thrive well in any ordinary garden soil, and will grow beneath the shade of trees. They are easily propagated by divisions of the root or by seeds; care should be taken not to leave pieces of the root where livestock might eat them, owing to their poisonous character.

Aconite has been ascribed with supernatural powers relating to werewolves and other lycanthropes, either to repel them, relating to aconite's use in poisoning wolves and other animals, or in some way induce their lycanthropic condition, as aconite was often an important ingredient in witches' magic ointments. In folklore, Aconite was also said to make a person into a werewolf if it is worn, smelled, or eaten. They are also said to kill werewolves if they wear, smell, or eat aconite.

Canadian film actor Andre Noble died of aconitine poisoning on July 30, 2004, after accidentally ingesting it.

Aconite was reportedly found in toxicology samples from the former Pakistan cricket coach Bob Woolmer, but his death was later confirmed of natural causes[4].

Aconite have also been known under names such as wolfsbane, leopard's bane, women's bane, Devil's helmet or blue rocket.[5]


Pharmacology of Aconite and Aconitine
Aconite has long been used in the traditional medicine of Asia (India, China and Japan). In Ayurveda the herb is used to increase pitta and to enhance penetration in small doses. However more frequently the herb is detoxified according to the samskaras process and studies, cited in the detoxification section below show that it no longer possesses active toxicity. It is used in traditional Chinese medicine as a treatment for Yang deficiency, "coldness", general debilitation. The herb is considered hot and toxic. It is prepared in extremely small doses. More frequently ginger processed aconite, of lower toxicity, "fu zi" is used. Aconite is one ingredient of Tribhuvankirti, an Ayurvedic preparation for treating a "cold in the head" and fever.[6] Aconite was mixed with patrinia and coix, in a famous treatment for appendicitis described in a formula from the Jingui Yaolue (ca. 220 A.D.)[7] Aconite was also described in Greek and Roman medicine by Theophrastus, Dioscorides, and Pliny the Elder, who most likely prescribed the Alpine species Aconitum lycoctonum. The herb was cultivated widely in Europe, probably reaching England before the tenth century, where it was farmed with some difficulty, but came to be widely valued as an anodyne, diuretic, and diaphoretic.[8] In the nineteenth century much aconite was imported from China, Japan, Fiji, and Tonga, with a number of species used to manufacture alkaloids of varying potency but generally similar effect, most often used externally and rarely internally. Effects of different preparations were standardized by testing on guinea pigs.[9]

In Western medicine preparations of aconite were used until just after the middle of the 20th century, but it is no longer employed as it has been replaced by safer and more effective drugs and treatments. The 1911 British Pharmaceutical Codex regarded the medical uses and toxicity of aconite root or leaves to be virtually identical to that of purified aconitine.[10] Aconite first stimulates and later paralyses the nerves of pain, touch, and temperature if applied to the skin or to a mucous membrane; the initial tingling therefore gives place to a long-continued anaesthetic action. Great caution was required, as abraded skin could absorb a dangerous dose of the drug, and merely tasting some of the concentrated preparations available could be fatal. The local anaesthesia of peripheral nerves can be attributed to at least eleven alkaloids with varying potency and stability.[11] External uses of aconite included treatment of ordinary facial or trigeminal neuralgia, rheumatism, and dental periostitis.

Internal uses were also pursued, to slow the pulse, as a sedative in pericarditis and heart palpitations, and well diluted as a mild diaphoretic, or to reduce feverishness in treatment of colds, pneumonia, quinsy, laryngitis, croup, and asthma due to exposure. Taken internally, aconite acts very notably on the circulation, the respiration, and the nervous system. The pulse is slowed, the number of beats per minute being actually reduced, under considerable doses, to forty, or even thirty, per minute. The blood-pressure synchronously falls, and the heart is arrested in diastole. Immediately before arrest, the heart may beat much faster than normally, though with extreme irregularity, and in the lower animals the auricles may be observed occasionally to miss a beat, as in poisoning by veratrine and colchicum. The action of aconitine on the circulation is due to an initial stimulation of the cardio-inhibitory centre in the medulla oblongata (at the root of the vagus nerves), and later to a directly toxic influence on the nerve-ganglia and muscular fibres of the heart itself. The fall in blood-pressure is not due to any direct influence on the vessels. The respiration becomes slower owing to a paralytic action on the respiratory centre and, in warm-blooded animals, death is due to this action, the respiration being arrested before the action of the heart. Aconite further depresses the activity of all nerve-terminals, the sensory being affected before the motor. In small doses, it therefore tends to relieve pain, if this is present. The activity of the spinal cord is similarly depressed. The pupil is at first contracted, and afterwards dilated. The cerebrum is totally unaffected by aconite, consciousness and the intelligence remaining normal to the last. The antipyretic action which considerable doses of aconite display is not specific but is the result of its influence on the circulation and respiration and of its slight diaphoretic action.


Homeopathic Use
Aconite is used in homeopathy. [12] for complaints that begin after a fright or sudden shocking events. [13][verification needed].


Toxicology
In a few minutes after the introduction of a poisonous dose of aconite, marked symptoms supervene. The initial signs of poisoning are referable to the alimentary canal. There is a sensation of burning, tingling, and numbness in the mouth, and of burning in the abdomen. Death usually supervenes before a numbing effect on the intestine can be observed. After about an hour, there is severe vomiting. Much motor weakness and cutaneous sensations similar to those above described soon follow. The pulse and respiration steadily fail, death occurring from asphyxia. As in strychnine poisoning, the patient is conscious and clear-minded to the last. The only post-mortem signs are those of asphyxia. The treatment is to empty the stomach by tube or by a non-depressant emetic. The physiological antidotes are atropine and digitalis or strophanthin, which should be injected subcutaneously in maximal doses. Alcohol, strychnine, and warmth must also be employed. It must be noted that these "antidotes" are historical ones, as few toxicological centers today would recommend warmth, digitalis, or strychnine for any poisonings.

The above description of poisoning is characteristic of an oral administration. It should however be noted that aconitine may be easily absorbed through the skin, and poisoning may occur through this route simply by picking the leaves without the use of gloves; the toxin in the sap is absorbed through the skin. From practical experience, the sap oozing from eleven picked leaves will cause cardiac symptoms for a couple of hours. In this event, there will be no gastrointestinal effects. Tingling will however start at the point of absorption, and extend up the arm to the shoulder, after which the heart will start to be affected. The tingling will be followed by numbness—it is fairly unpleasant. As remarked above, atropine is an antidote. Atropine is a constituent of Belladonna.

Aconitine is a potent neurotoxin that blocks tetrodotoxin-sensitive sodium channels. Pretreatment with barakol—10 mg/kg IV the compound is isolated from the leaves of Cassia siamea Lam—reduces the incidence of aconitine-induced ventricular fibrillation and ventricular tachycardia, as well as mortality. 5 μg/kg IV of tetrodotoxin also had the same effect. The protective effects of barakol are probably due to the prevention of intracellular sodium ion accumulation.

Canadian actor, Andre Noble died in July 2004 from poisoning following the accidental consumption of aconite from Monkshood during a camping trip.

Aconite was reported by the Sunday Mirror to have been used as poison in the murder of Pakistan cricket coach, Bob Woolmer during the 2007 Cricket World Cup. However there is now evidence that Bob Woolmer was not actually murdered.[14]


Detoxification
There are methods of processing aconite to reduce toxicity in both Chinese medicine and Ayurveda. In Chinese medicine, the traditional pao zhi or preparation of aconite is to steam with ginger in a fairly elaborate procedure. Due to the variable levels of toxicity in any given sample of the dried herb, there are still issues with using it. Most but not all cases of aconite toxicity in Taiwan were due to the consumption of unprocessed aconite.[15][16]

According to an article by the Indian scientists Thorat and Dahanukar, "Crude aconite is an extremely lethal substance. However, the science of Ayurveda looks upon aconite as a therapeutic entity. Crude aconite is always processed i.e. it undergoes 'samskaras' before being utilized in the Ayurvedic formulations. This study was undertaken in mice, to ascertain whether 'processed' aconite is less toxic as compared to the crude or unprocessed one. It was seen that crude aconite was significantly toxic to mice (100% mortality at a dose of 2.6 mg/mouse) whereas the fully processed aconite was absolutely non-toxic (no mortality at a dose even 8 times as high as that of crude aconite). Further, all the steps in the processing were essential for complete detoxification" [17]