Articles on this page are available in 1 other language: Spanish (7) (learn more)

Overview

Brief Summary

Amanita muscaria is a mycorrhizal basidiomycete fungus. Amanita muscaria is the classic European fairytale mushroom, bearing white gills and white warts on a typically bright red cap. It is known to contains several toxic, psychoactive compounds. This species was originally described from Europe and recent genetic and mophological evidence suggests that there are a number of distinct species worldwide that have been lumped under this name.

Creative Commons Attribution Non Commercial 3.0 (CC BY-NC 3.0)

Supplier: Nathan Wilson

Trusted

Article rating from 2 people

Average rating: 2.5 of 5

Description

The fly agaric is an attractive, vibrantly coloured toadstool, which is familiar and instantly recognisable (3). It has a bright red cap, which fades to an orange or orange-yellowish colour with age. The fluffy white spots on the cap often take on a yellowish tinge as they grow old, and may occasionally be washed away by rain (4). The stem has a bulbous base, and tapers towards the cap (3). This fungus is dangerously poisonous and should NEVER be tasted (2). The name fly agaric derives from the fact that since medieval times it was commonly used as a fly killer, broken up in milk or sprinkled with sugar (3). WARNING: Many species of fungus are poisonous or contain chemicals that can cause sickness. Never pick and eat any species of fungus that you cannot positively recognise or are unsure about. Some species are deadly poisonous and can cause death within a few hours if swallowed.
Creative Commons Attribution Non Commercial Share Alike 3.0 (CC BY-NC-SA 3.0)

© Wildscreen

Source: ARKive

Trusted

Article rating from 1 person

Average rating: 1.0 of 5

Distribution

Range

This widespread toadstool occurs in Europe and North America. It was introduced to Australia, South Africa and New Zealand with pine trees imported from Europe (3).
Creative Commons Attribution Non Commercial Share Alike 3.0 (CC BY-NC-SA 3.0)

© Wildscreen

Source: ARKive

Trusted

Article rating from 0 people

Average rating: 2.5 of 5

Ecology

Habitat

Grows under birch and spruce trees on acidic soils (4).
Creative Commons Attribution Non Commercial Share Alike 3.0 (CC BY-NC-SA 3.0)

© Wildscreen

Source: ARKive

Trusted

Article rating from 0 people

Average rating: 2.5 of 5

Associations

Fungus / associate
basidiome of Chalciporus piperatus is associated with mycelium of Amanita muscaria
Other: major host/prey

Trusted

Article rating from 0 people

Average rating: 2.5 of 5

Conservation

Conservation Status

Status

A common, widespread species (3).
Creative Commons Attribution Non Commercial Share Alike 3.0 (CC BY-NC-SA 3.0)

© Wildscreen

Source: ARKive

Trusted

Article rating from 0 people

Average rating: 2.5 of 5

Threats

This fungus is not threatened.
Creative Commons Attribution Non Commercial Share Alike 3.0 (CC BY-NC-SA 3.0)

© Wildscreen

Source: ARKive

Trusted

Article rating from 0 people

Average rating: 2.5 of 5

Management

Conservation

Conservation action has not been targeted at this species.
Creative Commons Attribution Non Commercial Share Alike 3.0 (CC BY-NC-SA 3.0)

© Wildscreen

Source: ARKive

Trusted

Article rating from 0 people

Average rating: 2.5 of 5

Relevance to Humans and Ecosystems

Risks

Mushroom Poisoning

Mushroom poisoning is caused by the consumption of raw or cooked fruiting bodies (mushrooms, toadstools) of a number of species of higher fungi. The term toadstool (from the German Todesstuhl, death's stool) is commonly given to poisonous mushrooms, but for individuals who are not experts in mushroom identification there are generally no easily recognizable differences between poisonous and nonpoisonous species. Old wives' tales notwithstanding, there is no general rule of thumb for distinguishing edible mushrooms and poisonous toadstools. The toxins involved in mushroom poisoning are produced naturally by the fungi themselves, and each individual specimen of a toxic species should be considered equally poisonous. Most mushrooms that cause human poisoning cannot be made nontoxic by cooking, canning, freezing, or any other means of processing. Thus, the only way to avoid poisoning is to avoid consumption of the toxic species. Poisonings in the United States occur most commonly when hunters of wild mushrooms (especially novices) misidentify and consume a toxic species, when recent immigrants collect and consume a poisonous American species that closely resembles an edible wild mushroom from their native land, or when mushrooms that contain psychoactive compounds are intentionally consumed by persons who desire these effects.

Nature of Disease

Mushroom poisonings are generally acute and are manifested by a variety of symptoms and prognoses, depending on the amount and species consumed. Because the chemistry of many of the mushroom toxins (especially the less deadly ones) is still unknown and positive identification of the mushrooms is often difficult or impossible, mushroom poisonings are generally categorized by their physiological effects. There are four categories of mushroom toxins: protoplasmic poisons (poisons that result in generalized destruction of cells, followed by organ failure); neurotoxins (compounds that cause neurological symptoms such as profuse sweating, coma, convulsions, hallucinations, excitement, depression, spastic colon); gastrointestinal irritants (compounds that produce rapid, transient nausea, vomiting, abdominal cramping, and diarrhea); and disulfiram-like toxins. Mushrooms in this last category are generally nontoxic and produce no symptoms unless alcohol is consumed within 72 hours after eating them, in which case a short-lived acute toxic syndrome is produced.

Diagnosis of Human Illness

A clinical testing procedure is currently available only for the most serious types of mushroom toxins, the amanitins. The commercially available method uses a 3H-radioimmunoassay (RIA) test kit and can detect sub-nanogram levels of toxin in urine and plasma. Unfortunately, it requires a 2-hour incubation period, and this is an excruciating delay in a type of poisoning which the clinician generally does not see until a day or two has passed. A 125I-based kit which overcomes this problem has recently been reported, but has not yet reached the clinic. A sensitive and rapid HPLC technique has been reported in the literature even more recently, but it has not yet seen clinical application. Since most clinical laboratories in this country do not use even the older RIA technique, diagnosis is based entirely on symptomology and recent dietary history. Despite the fact that cases of mushroom poisoning may be broken down into a relatively small number of categories based on symptomatology, positive botanical identification of the mushroom species consumed remains the only means of unequivocally determining the particular type of intoxication involved, and it is still vitally important to obtain such accurate identification as quickly as possible. Cases involving ingestion of more than one toxic species in which one set of symptoms masks or mimics another set are among many reasons for needing this information. Unfortunately, a number of factors (not discussed here) often make identification of the causative mushroom impossible. In such cases, diagnosis must be based on symptoms alone. In order to rule out other types of food poisoning and to conclude that the mushrooms eaten were the cause of the poisoning, it must be established that everyone who ate the suspect mushrooms became ill and that no one who did not eat the mushrooms became ill. Wild mushrooms eaten raw, cooked, or processed should always be regarded as prime suspects. After ruling out other sources of food poisoning and positively implicating mushrooms as the cause of the illness, diagnosis may proceed in two steps. The first step, outlined in Table 1, provides an early indication of the seriousness of the disease and its prognosis.

As described above, the protoplasmic poisons are the most likely to be fatal or to cause irreversible organ damage. In the case of poisoning by the deadly Amanitas, important laboratory indicators of liver (elevated LDH, SGOT, and bilirubin levels) and kidney (elevated uric acid, creatinine, and BUN levels) damage will be present. Unfortunately, in the absence of dietary history, these signs could be mistaken for symptoms of liver or kidney impairment as the result of other causes (e.g., viral hepatitis). It is important that this distinction be made as quickly as possible, because the delayed onset of symptoms will generally mean that the organ has already been damaged. The importance of rapid diagnosis is obvious: victims who are hospitalized and given aggressive support therapy almost immediately after ingestion have a mortality rate of only 10%, whereas those admitted 60 or more hours after ingestion have a 50-90% mortality rate. Table 2 provides more accurate diagnoses and appropriate therapeutic measures. A recent report indicates that amanitins are observable in urine well before the onset of any symptoms, but that laboratory tests for liver dysfunction do not appear until well after the organ has been damaged.

Associated Foods

Mushroom poisonings are almost always caused by ingestion of wild mushrooms that have been collected by nonspecialists (although specialists have also been poisoned). Most cases occur when toxic species are confused with edible species, and a useful question to ask of the victims or their mushroom-picking benefactors is the identity of the mushroom they thought they were picking. In the absence of a well- preserved specimen, the answer to this question could narrow the possible suspects considerably. Intoxication has also occurred when reliance was placed on some folk method of distinguishing poisonous and safe species. Outbreaks have occurred after ingestion of fresh, raw mushrooms, stir-fried mushrooms, home-canned mushrooms, mushrooms cooked in tomato sauce (which rendered the sauce itself toxic, even when no mushrooms were consumed), and mushrooms that were blanched and frozen at home. Cases of poisoning by home-canned and frozen mushrooms are especially insidious because a single outbreak may easily become a multiple outbreak when the preserved toadstools are carried to another location and consumed at another time.

Specific cases of mistaken mushroom identity appears frequently. The Early False Morel Gyromitra esculenta is easily confused with the true Morel Morchella esculenta, and poisonings have occurred after consumption of fresh or cooked Gyromitra. Gyromitra poisonings have also occurred after ingestion of commercially available "morels" contaminated with G. esculenta. The commercial sources for these fungi (which have not yet been successfully cultivated on a large scale) are field collection of wild morels by semiprofessionals. Cultivated commercial mushrooms of whatever species are almost never implicated in poisoning outbreaks unless there are associated problems such as improper canning (which lead to bacterial food poisoning). A short list of the mushrooms responsible for serious poisonings and the edible mushrooms with which they are confused is presented in Table 3. Producers of mild gastroenteritis are too numerous to list here, but include members of many of the most abundant genera, including Agaricus, Boletus, Lactarius, Russula, Tricholoma, Coprinus, Pluteus, and others. The Inky Cap Mushroom (Coprinus atrimentarius) is considered both edible and delicious, and only the unwary who consume alcohol after eating this mushroom need be concerned. Some other members of the genus Coprinus (Shaggy Mane, C. comatus; Glistening Inky Cap, C. micaceus, and others) and some of the larger members of the Lepiota family such as the Parasol Mushroom (Leucocoprinus procera) do not contain coprine and do not cause this effect. The potentially deadly Sorrel Webcap Mushroom (Cortinarius orellanus) is not easily distinguished from nonpoisonous webcaps belonging to the same distinctive genus, and all should be avoided.

Most of the psychotropic mushrooms (Inocybe spp., Conocybe spp., Paneolus spp., Pluteus spp.) are in general appearance small, brown, and leathery (the so-called "Little Brown Mushrooms" or LBMs) and relatively unattractive from a culinary standpoint. The Sweat Mushroom (Clitocybe dealbata) and the Smoothcap Mushroom (Psilocybe cubensis) are small, white, and leathery. These small, unattractive mushrooms are distinctive, fairly unappetizing, and not easily confused with the fleshier fungi normally considered edible. Intoxications associated with them are less likely to be accidental, although both C. dealbata and Paneolus foenisicii have been found growing in the same fairy ring area as the edible (and choice) Fairy Ring Mushroom (Marasmius oreades) and the Honey Mushroom (Armillariella mellea), and have been consumed when the picker has not carefully examined every mushroom picked from the ring. Psychotropic mushrooms, which are larger and therefore more easily confused with edible mushrooms, include the Showy Flamecap or Big Laughing Mushroom (Gymnopilus spectabilis), which has been mistaken for Chanterelles (Cantharellus spp.) and for Gymnopilus ventricosus found growing on wood of conifers in western North America. The Fly Agaric (Amanita muscaria) and Panthercap (Amanita pantherina) mushrooms are large, fleshy, and colorful. Yellowish cap colors on some varieties of the Fly Agaric and the Panthercap are similar to the edible Caesar's Mushroom (Amanita caesarea), which is considered a delicacy in Italy. Another edible yellow capped mushroom occasionally confused with yellow A. muscaria and A. pantherina varieties are the Yellow Blusher (Amanita flavorubens). Orange to yellow-orange A. muscaria and A. pantherina may also be confused with the Blusher (Amanita rubescens) and the Honey Mushroom (Armillariella mellea). White to pale forms of A. muscaria may be confused with edible field mushrooms (Agaricus spp.). Young (button stage) specimens of A. muscaria have also been confused with puffballs.

Relative Frequency of Disease

Accurate figures on the relative frequency of mushroom poisonings are difficult to obtain. For the 5-year period between 1976 and 1981, 16 outbreaks involving 44 cases were reported to the Centers for Disease Control in Atlanta (Rattanvilay et al. MMWR 31(21): 287-288, 1982). The number of unreported cases is, of course, unknown. Cases are sporadic and large outbreaks are rare. Poisonings tend to be grouped in the spring and fall when most mushroom species are at the height of their fruiting stage. While the actual incidence appears to be very low, the potential exists for grave problems. Poisonous mushrooms are not limited in distribution as are other poisonous organisms (such as dinoflagellates). Intoxications may occur at any time and place, with dangerous species occurring in habitats ranging from urban lawns to deep woods. As Americans become more adventurous in their mushroom collection and consumption, poisonings are likely to increase.

Course of Disease and Complications

The normal course of the disease varies with the dose and the mushroom species eaten. Each poisonous species contains one or more toxic compounds which are unique to few other species. Therefore, cases of mushroom poisonings generally do not resembles each other unless they are caused by the same or very closely related mushroom species. Almost all mushroom poisonings may be grouped in one of the categories outlined above.

PROTOPLASMIC POISON

Amatoxins

Several mushroom species, including the Death Cap or Destroying Angel (Amanita phalloides, A. virosa), the Fool's Mushroom (A. verna) and several of their relatives, along with the Autumn Skullcap (Galerina autumnalis) and some of its relatives, produce a family of cyclic octapeptides called amanitins. Poisoning by the amanitins is characterized by a long latent period (range 6-48 hours, average 6-15 hours) during which the patient shows no symptoms. Symptoms appear at the end of the latent period in the form of sudden, severe seizures of abdominal pain, persistent vomiting and watery diarrhea, extreme thirst, and lack of urine production. If this early phase is survived, the patient may appear to recover for a short time, but this period will generally be followed by a rapid and severe loss of strength, prostration, and pain-caused restlessness. Death in 50-90% of the cases from progressive and irreversible liver, kidney, cardiac, and skeletal muscle damage may follow within 48 hours (large dose), but the disease more typically lasts 6 to 8 days in adults and 4 to 6 days in children. Two or three days after the onset of the later phase, jaundice, cyanosis, and coldness of the skin occur. Death usually follows a period of coma and occasionally convulsions. If recovery occurs, it generally requires at least a month and is accompanied by enlargement of the liver. Autopsy will usually reveal fatty degeneration and necrosis of the liver and kidney.

Target Populations

All humans are susceptible to mushroom toxins. The poisonous species are ubiquitous, and geographical restrictions on types of poisoning that may occur in one location do not exist (except for some of the hallucinogenic LBMs, which occur primarily in the American southwest and southeast). Individual specimens of poisonous mushrooms are also characterized by individual variations in toxin content based on genetics, geographic location, and growing conditions. Intoxications may thus be more or less serious, depending not on the number of mushrooms consumed, but on the dose of toxin delivered. In addition, although most cases of poisoning by higher plants occur in children, toxic mushrooms are consumed most often by adults. Occasional accidental mushroom poisonings of children and pets have been reported, but adults are more likely to actively search for and consume wild mushrooms for culinary purposes. Children are more seriously affected by the normally nonlethal toxins than are adults and are more likely to suffer very serious consequences from ingestion of relatively smaller doses. Adults who consume mushrooms are also more likely to recall what was eaten and when, and are able to describe their symptoms more accurately than are children. Very old, very young, and debilitated persons of both sexes are more likely to become seriously ill from all types of mushroom poisoning, even those types which are generally considered to be mild.

Many idiosyncratic adverse reactions to mushrooms have been reported. Some mushrooms cause certain people to become violently ill, while not affecting others who consumed part of the same mushroom cap. Factors such as age, sex, and general health of the consumer do not seem to be reliable predictors of these reactions, and they have been attributed to allergic or hypersensitivity reactions and to inherited inability of the unfortunate victim to metabolize certain unusual fungal constituents (such as the uncommon sugar, trehalose). These reactions are probably not true poisonings as the general population does not seem to be affected.

Food Analysis

The mushroom toxins can with difficulty be recovered from poisonous fungi, cooking water, stomach contents, serum, and urine. Procedures for extraction and quantitation are generally elaborate and time-consuming, and the patient will in most cases have recovered by the time an analysis is made on the basis of toxin chemistry. The exact chemical natures of most of the toxins that produce milder symptoms are unknown. Chromatographic techniques (TLC, GLC, HPLC) exist for the amanitins, orellanine, muscimol/ibotenic acid, psilocybin, muscarine, and the gyromitrins. The amanitins may also be determined by commercially available 3H-RIA kits. The most reliable means of diagnosing a mushroom poisoning remains botanical identification of the fungus that was eaten. An accurate pre-ingestion determination of species will also prevent accidental poisoning in 100% of cases. Accurate post-ingestion analyses for specific toxins when no botanical identification is possible may be essential only in cases of suspected poisoning by the deadly Amanitas, since prompt and aggressive therapy (including lavage, activated charcoal, and plasmapheresis) can greatly reduce the mortality rate.

Selected Outbreaks

Isolated cases of mushroom poisoning have occurred throughout the continental United States.

The popular interest in gathering and eating uncultivated mushrooms has been associated with an increase in incidents of serious mushroom-related poisonings. From December 28, 1996, through January 6, 1997, nine persons in northern California required hospitalization after eating Amanita phalloides (i.e., "death cap") mushrooms; two of these persons died. Risks associated with eating these mushrooms result from a potent hepatotoxin. This report describes four cases of A. phalloides poisoning in patients admitted to a regional referral hospital in northern California during January 1997 and underscores that wild mushrooms should not be eaten unless identified as nonpoisonous by a mushroom expert.

Another one occurred in Oregon in October,1988, and involved the intoxication of five people who consumed stir-fried Amanita phalloides. The poisonings were severe, and at this writing three of the five people had undergone liver transplants for treatment of amanitin-induced liver failure.

Other cases have included the July, 1986, poisoning of a family in Philadelphia, by Chlorophyllum molybdites; the September, 1987, intoxication of seven men in Bucks County, PA, by spaghetti sauce which contained Jack O'Lantern mushroom (Omphalotus illudens); and of 14 teenage campers in Maryland by the same species (July, 1987). A report of a North Carolina outbreak of poisoning by False Morel (Gyromitra spp.) appeared in 1986. A 1985 report details a case of Chlorophyllum molybdites which occurred in Arkansas; a fatal poisoning case caused by an amanitin containing Lepiota was described in 1986.

In 1981, two Berks County, PA, people were poisoned (one fatally) after ingesting Amanita phalloides, while in the same year, seven Laotian refugees living in California were poisoned by Russula spp.

In separate 1981 incidents, several people from New York State were poisoned by Omphalotus illudens, Amanita muscaria, Entoloma lividum, and Amanita virosa.

An outbreak of gastroenterititis during a banquet for 482 people in Vancouver, British Columbia, was reported by the Vancouver Health Department in June, 1991. Seventy-seven of the guests reported symptoms consisting of early onset nausea (15-30 min), diarrhea (20 min-13 h), vomiting (20-60 min), cramps and bloated feeling. Other symptoms included feeling warm, clamminess, numbness of the tongue and extreme thirst along with two cases of hive-like rash with onset of 3-7 days. Bacteriological tests were negative. This intoxication merits special attention because it involved consumption of species normally considered not only edible but choice. The fungi involved were the morels Morchella esculenta and M. elata (M. angusticeps), which were prepared in a marinade and consumed raw. The symptoms were severe but not life threatening. Scattered reports of intoxications by these species and M. conica have appeared in anecodotal reports for many years.

Numerous other cases exist; however, the cases that appear in the literature tend to be the serious poisonings such as those causing more severe gastrointestinal symptoms, psychotropic reactions, and severe organ damage (deadly Amanita). Mild intoxications are probably grossly underreported, because of the lack of severity of symptoms and the unlikeliness of a hospital admission.

US Food and Drug Administration

Trusted

Article rating from 0 people

Average rating: 2.5 of 5

Wikipedia

Amanita muscaria

Amanita muscaria
View the Mycomorphbox template that generates the following list
Mycological characteristics
gills on hymenium
cap is flat or convex
hymenium is free
stipe has a ring and volva
spore print is white
ecology is mycorrhizal
edibility: poisonous or psychoactive

Amanita muscaria, commonly known as the fly agaric (pronounced /ˈæɡərɪk/) or fly Amanita (pronounced /ˌæməˈnaɪtə/), is a poisonous and psychoactive basidiomycete fungus, one of many in the genus Amanita. Native throughout the temperate and boreal regions of the Northern Hemisphere, Amanita muscaria has been unintentionally introduced to many countries in the Southern Hemisphere, generally as a symbiont with pine plantations, and is now a true cosmopolitan species. It associates with various deciduous and coniferous trees. The quintessential toadstool, it is a large white-gilled, white-spotted, usually deep red mushroom, one of the most recognizable and widely encountered in popular culture. Several subspecies, with differing cap colour have been recognised to date, including the brown regalis (considered a separate species), the yellow-orange flavivolata, guessowii, and formosa, and the pinkish persicina. Genetic studies published in 2006 and 2008 show several sharply delineated clades which may represent separate species.

Although generally considered poisonous, deaths are extremely rare, and it has been consumed as a food in parts of Europe, Asia, and North America after parboiling in water. However, Amanita muscaria is now primarily famed for its hallucinogenic properties, with its main psychoactive constituent being the compound muscimol. It was used as an intoxicant and entheogen by the peoples of Siberia and has a religious significance in these cultures. There has been much speculation on traditional use of this mushroom as an intoxicant in places other than Siberia; however, such traditions are far less well-documented. The American banker and amateur ethnomycologist R. Gordon Wasson proposed the fly agaric was in fact the Soma talked about in the ancient Rig Veda texts of India; since its introduction in 1968, this theory has gained both detractors and followers in the anthropological literature.[1]

Contents

Taxonomy and naming

The name of the mushroom in many European languages is thought to have been derived from the fact that it was used as an insecticide, when sprinkled in milk. This practice has been recorded from Germanic- and Slavic-speaking parts of Europe, as well as the Vosges region and pockets elsewhere in France, and Romania.[2] Albertus Magnus was the first to record it in his work De vegetabilibus sometime before 1256,[3] commenting:

vocatur fungus muscarum, eo quod in lacte pulverizatus interficit muscas ("It is called the mushroom of flies, because crushed in milk it kills flies")[4]

Buttons

The 16th century Flemish botanist Carolus Clusius traced the practice of sprinkling it into milk to Frankfurt in Germany,[5] while Carl Linnaeus, the "father of taxonomy", reported it from Småland in southern Sweden where he had lived as a child.[6] He officially described it in Volume Two of his Species Plantarum in 1753, giving it the name Agaricus muscarius,[7] the specific epithet deriving from Latin musca meaning "fly".[8] It gained its current name in 1783, when placed in the genus Amanita by Jean-Baptiste Lamarck and sanctioned by Elias Magnus Fries.

The starting date had been formerly set as January 1 1821, the date of the works of the "father of mycology", Swedish naturalist Elias Magnus Fries, and under these conditions, the full name was Amanita muscaria (L.:Fr.) Hook.. However, a recent revision of the International Code of Botanical Nomenclature in 1987 changed the rules regarding the starting date and primary work for names of fungi, and now names can be considered valid as far back as May 1 1753, the date of publication of Linnaeus's seminal work.[9] Hence, Linnaeus and Lamarck became the namers of the Amanita muscaria (L.) Lam.

English mycologist John Ramsbottom reported that Amanita muscaria was used for getting rid of bugs in England and Sweden, and bug agaric was an old alternate name.[4] French mycologist Pierre Bulliard tried to replicate its fly-killing properties without success in his work Histoire des plantes vénéneuses et suspectes de la France, and proposed a new binomial name Agaricus pseudo-aurantiacus because of this.[10] One compound isolated from the fungus is 1,3-diolein, which is in fact an insect attractor.[11]

An alternative derivation proposes that the term fly- refers not to insects as such but rather the delirium resulting from consumption of the fungus. This is based on the medieval belief that flies could enter a person's head and cause mental illness.[12] Several regional names appear to be linked with this connotation, meaning either "mad-" or "fool's" Amanita caesarea. Hence there is oriol foll "mad oriol" in Catalan, mujolo folo from Toulouse, concourlo fouolo from the Aveyron department in Southern France, ovolo matto from the Province of Trento in Italy. A local dialect name in Fribourg in Switzerland is tsapi de diablhou, which translates as "Devil's hat".[13]

The word toadstool in English does not refer to any particular species, yet it has a more definite specific connotation with A. muscaria in continental Europe. Yet another name is crapaudin in many parts of France, and a Basque term from Guipúzcoa and Biscay is amoroto, further there is Old Danish paddhe stool, Danish paddehat, Dutch padde(n)stoel, Middle Low German paddenstol, Scots paddockstool and German Krötenschwamm[14] , all alluding to toads.[15] The toad is thought to be associated with the mushroom because it symbolizes toxicity and chthonic forces in the same way that the serpent does.[16] Wasson proposed this was due to its being a shamanic and also taboo object and hence unable to be named specifically in ancient Celtic culture.[17] He speculates that the power of this taboo may have perpetuated its maligned reputation while other lethal fungi such as the death cap (A. phalloides) have had few cultural connotations throughout European history.[18] In addition, a common name from China is ha-ma chün, meaning "toad mushroom" (), although the toad does not carry a negative connotation in Chinese culture and symbolism.[19] An unusual name is the Japanese beni-tengu-take "scarlet long-nosed-goblin mushroom".[12]

Classification

Amanita muscaria is the type species of the genus Amanita. By extension, it is also the type species of Amanita subgenus Amanita, as well as section Amanita within this subgenus. Amanita subgenus Amanita includes all Amanita with inamyloid spores. Amanita section Amanita includes those species with patchy universal veil remnants, including a volva that is reduced to a series of concentric rings and the veil remnants on the cap being a series of patches or warts. Most species in this group also have a bulbous base.[20][21] Amanita section Amanita consists of A. muscaria and its close relatives, including A. pantherina (the panther cap), A. gemmata, A. farinosa, and A. xanthocephala.[22] Modern fungal taxonomists have classified Amanita muscaria and its allies this way based on gross morphology and spore inamyloidy. Two recent molecular phylogenetic studies have confirmed this classification as natural.[23][24]

Amanita muscaria varies considerably in its morphology and many authorities recognize a number of subspecies or varieties within the species. In The Agaricales in Modern Taxonomy, German mycologist Rolf Singer listed three subspecies, though without description: A. muscaria ssp. muscaria, A. muscaria ssp. americana, and A. muscaria ssp. flavivolvata.[20]

Contemporary authorities recognize up to seven varieties:

  • var. muscaria, the typical red-and-white spotted variety. Some authorities, such as Rodham Tulloss, only use this name for Eurasian and western Alaskan populations.[21][25]
  • var. flavivolvata is red, with yellow to yellowish-white warts, and occurs in the western regions of the North American continent, from southern Alaska down through the Rocky Mountains, through Central America, to at least Andean Colombia. Rodham Tulloss uses this name to describe all "typical" A. muscaria from indigenous New World populations from Alaska southward.[21][26]
  • var. alba, an uncommon fungus, has a white to silvery white cap with white warts but otherwise similar to the usual form.[21][27]
  • var. formosa, has a yellow to orange-yellow cap with yellowish or tan warts and stem. Some authorities use this name for all A. muscaria fitting this description worldwide (cf. Jenkins), others (cf. Tulloss) restrict its use to Eurasian populations.[21][28]
  • var. guessowii is yellow to orange, with center of cap more orange or reddish orange than the outer part. It is found throughout North America, but is most common in northeastern North America, from Newfoundland and Quebec down to Tennessee. Some authorities (cf, Jenkins) treat these populations as part of A. muscaria var. formosa, while others (cf, Tulloss) recognize it as a distinct variety.[21][28]
  • var. persicina is pinkish to orangish "melon" colored with poorly formed or absent remnants of universal veil on the stem and vasal bulb, known from the Southeastern Coastal areas of the U.S.A, described in 1977.[21][29]
  • var. regalis from Scandinavia and Alaska,[30] is liver-brown and has yellow warts. It appears to be uniformly distinctive and some authorities (cf, Tulloss) treat it as a separate species, while others (cf, Jenkins) treat it as a variety of A. muscaria.[21][31]

A 2006 molecular phylogenetic study of different regional populations of A. muscaria by mycologist József Geml and colleagues found three distinct clades within this species representing, roughly, Eurasian, Eurasian "subalpine", and North American populations. Specimens belonging to all three clades have been found in Alaska; this has led to the hypothesis that this was the center of diversification of this species. The study also looked at four named varieties of this species: var. alba, var. flavivolvata, var. formosa (including var. guessowii), and var. regalis from both areas. All four varieties were found within both the Eurasian and North American clades, evidence that these morphological forms are simply polymorphisms found throughout the species rather than distinct subspecies or varieties.[32] Further molecular study by Geml and colleagues published in 2008 show these three genetic groups, plus a fourth associated with oak–hickory–pine forest in the southeastern United States, and two more on Santa Cruz Island in California, are delineated from each other enough genetically to be considered separate species; thus A. muscaria as it stands currently is a species complex.[33] The complex also includes at least three other closely related taxa currently regarded as species:[25] A. breckonii is a buff-capped mushroom associated with conifers from the Pacific Northwest,[34] and the brown-capped A. gioiosa and A. heterochroma from the mediterranean and Sardinia alone respectively. Both these last two are found with Eucalyptus and Cistus trees and it is unclear whether they are native or have been introduced from Australia.[35][36]

Description

a white-fleshed mushroom with a red skin cut in half
cross section of fruiting body, showing pigment under skin and free gills

A large conspicuous mushroom, Amanita muscaria is generally common and numerous where it grows, and is often found in groups with basidiocarps in all stages of development. Fly agaric fruiting bodies emerge from the soil looking like a white egg, covered in the white warty material of the universal veil. Dissecting the mushroom at this stage will reveal a characteristic yellowish layer of skin under the veil which assists in identification. As the fungus grows, the red color appears through the broken veil and the warts become less prominent; they do not change in size but are reduced relative to the expanding skin area. The cap changes from globose to hemispherical, and finally to plate-like and flat in mature specimens.[37] Fully grown, the bright red cap is usually around 8–20 cm (3–8 in) in diameter, although larger specimens have been found. The red color may fade after rain and in older mushrooms. After emerging from the ground, the cap is covered with numerous small white to yellow pyramid-shaped warts. These are remnants of the universal veil, a membrane that encloses the entire mushroom when it is still very young. The free gills are white, as is the spore print. The oval spores measure 9–13 by 6.5–9 μm, and are non-amyloid, that is, they do not turn blue with the application of iodine.[38] The stipe is white, 5–20 cm high (2–8 in) by 1–2 cm (0.4–0.8 in) wide, and has the slightly brittle, fibrous texture typical of many large mushrooms. At the base is a bulb that bears universal veil remnants in the form of two to four distinct rings or ruffs. Between the basal universal veil remnants and gills are remnants of the partial veil (which covers the gills during development) in the form of a white ring. It can be quite wide and flaccid with age. There is generally no associated smell other than a mild earthiness.[39][40]

Although very distinctive in appearance, the fly agaric has been mistaken for other yellow to red species in the Americas, including Armillaria cf. mellea and the edible Amanita basii—a Mexican species similar to A. caesarea of Europe. Poison control centers in the U.S. and Canada are aware that amarill is a common name for A. caesarea-like species in Mexico, not just the Spanish for 'yellow'.[28] Amanita caesarea can be distinguished as it has an entire orange red cap, lacking the numerous white warty spots of the fly agaric. Furthermore the stem, gills and ring are bright yellow, not white.[41] Finally the volva is a distinct white bag, not broken into scales.[42] In Australia, the introduced fly agaric may be confused with the native vermilion grisette (Amanita xanthocephala), which grows in association with eucalypts. The latter species generally lacks the white warts of A. muscaria and bears no ring.[43]

Distribution and habitat

A. muscaria is a cosmopolitan mushroom, native to conifer and deciduous woodlands throughout the temperate and boreal regions of the Northern Hemisphere,[32] including high elevations of warmer latitudes in regions like the Hindu Kush, the Mediterranean and Central America. A recent molecular study proposes an ancestral origin in the SiberianBeringian region in the Tertiary period before radiating outwards across Asia, Europe and North America.[32] Though generally encountered in autumn, the season can vary in different climates: fruiting occurs in summer and autumn across most of North America, but later in autumn and early winter on the Pacific coast. It is often found in similar locations to Boletus edulis, and may appear in fairy rings.[44] Conveyed with pine seedlings, it has been widely transported into the southern hemisphere, including Australia,[45] New Zealand,[46] South Africa[47] and South America.[32]

Ectomycorrhizal, Amanita muscaria forms symbiotic relationships with a wide variety of trees, including pine, spruce, fir, birch, and cedar. Commonly seen under introduced trees,[48] A. muscaria is the fungal equivalent of a weed in New Zealand, Tasmania and Victoria, forming new associations with southern beech (Nothofagus).[49] It is also invading native rainforest in Australia, where it may be displacing native species.[48] Furthermore, it appears to be spreading northwards, with recent reports placing it near Port Macquarie on the New South Wales north coast.[50] Although it has not spread to eucalypts in Australia, it has been recorded associating with them in Portugal.[51]

Toxicity

a tall red mushroom with a few white spots remaining on the cap
Mature. The white spots may wash off with heavy rainfall

Amanita muscaria poisoning typically occurs in either young children or people ingesting it for a hallucinogenic experience.[12][52][53] Occasionally, immature button forms have been mistaken for edible puffballs.[54] Additionally, the white spots may be washed away during heavy rain and it can then appear similar to the edible A. caesarea.[55]

Amanita muscaria contains a number of biologically active agents, at least two of which, muscimol and ibotenic acid, are known to be psychoactive. A toxic dose in adults is approximately 6 mg muscimol or 30 to 60 mg ibotenic acid,[56][57] this is typically about the amount found in one cap of Amanita muscaria.[58] However, the amount and ratio of chemical compounds per mushroom varies widely from region to region and season to season, which further confuses the issue. Spring and summer mushrooms have been reported to contain up to 10 times as much ibotenic acid and muscimol compared to autumn fruitings.[52]

A fatal dose has been calculated at approximately 15 caps.[59] Deaths from A. muscaria have been reported in historical journal articles and newspaper reports;[60][61][62] however, with modern medical treatment a fatal outcome would be extremely rare.[63] Many older books mistakenly list it as deadly, giving the impression that it is far more toxic than it really is.[64] The North American Mycological Association has stated there are no reliably documented fatalities in the past 100 years.[65] The vast majority (90% or more) of mushroom poisoning deaths are from having eaten either the greenish to yellowish death cap (A. phalloides) or one of the several white Amanita species known as destroying angels.[66]

The active constituents of this species are water soluble, and boiling and then discarding the cooking water will at least partly detoxify A. muscaria.[67] However, drying may increase potency as the process facilitates the conversion of ibotenic acid to the more potent muscimol.[68] According to some sources, once detoxified, the mushroom becomes edible.[69]

Pharmacology

Muscimol, a principal psychoactive agent in A. muscaria.
Ibotenic acid, another psychoactive agent in A. muscaria.

Muscarine, discovered in 1869,[70] was long thought to be the active hallucinogenic agent in A. muscaria. Muscarine binds with muscarinic acetylcholine receptors leading to the excitation of neurons bearing these receptors. The levels in Amanita muscaria, however, are minute when compared with other poisonous fungi,[71] such as Inocybe erubescens or small white Clitocybe species C. dealbata and C. rivulosa, and are too insignificant to play a role in the symptoms of poisoning.[72]

The major toxins involved in poisoning are muscimol (3-hydroxy-5-aminomethyl-1-isoxazole, an unsaturated cyclic hydroxamic acid) and ibotenic acid. Muscimol is the product of the decarboxylation (usually by drying) of ibotenic acid. Muscimol and ibotenic acid were discovered in the mid 20th century.[73][74] Researchers in England,[75] Japan,[76] and Switzerland[74] showed that the effects produced were due mainly to ibotenic acid and muscimol, not muscarine.[11][73] They are not distributed uniformly in the mushroom. Most are detected in the cap of the fruit, rather than in the base, with the smallest amount in the stalk.(Lampe, 1978; Tsunoda et al., 1993) A substantial fraction of ingested ibotenic acid is excreted in the urine unmetabolized quite rapidly, between 20 and 90 minutes after ingestion. Virtually no muscimol is excreted when pure ibotenic acid is eaten but muscimol is detectable in the urine after eating A. muscaria, which contains both ibotenic acid and muscimol.[57]

Ibotenic acid and muscimol are structurally related to each other and to two major neurotransmitters of the central nervous system: glutamic acid and GABA respectively. Ibotenic acid and muscimol act like these neurotransmitters, muscimol being a potent GABAA agonist, while ibotenic acid is an agonist of NMDA glutamate receptors and certain metabotropic glutamate receptors[77] which are involved in the control of neuronal activity. It is these interactions which are thought to cause the psychoactive effects found in intoxication. Muscimol is the agent responsible for the majority of the psychoactivity.[12][58]

Muscazone is another compound more recently isolated from European specimens of the fly agaric. It is a product of the breakdown of ibotenic acid by ultra-violet radiation.[78] Muscazone is of minor pharmacological activity compared with the other agents.[12] Amanita muscaria and related species are known as effective bioaccumulators of vanadium; some species concentrate vanadium to levels of up to 400 times those typically found in plants.[79] Vanadium is present in fruit-bodies as an organometallic compound called amavadine.[79] However, the biological importance of the accumulation process is unknown.[80]

Symptoms

Fly agarics are known for the unpredictability of their effects. Depending on habitat and the amount ingested per body weight, effects can range from nausea and twitching to drowsiness, cholinergic crisis-like effects (low blood pressure, sweating and salivation), auditory and visual distortions, mood changes, euphoria, relaxation, ataxia, and loss of equilibrium.[52][53][58][61]

In cases of serious poisoning it causes a delirium, similar in effect to anticholinergic poisoning it is characterized by bouts of marked agitation with confusion, hallucinations, and irritability followed by periods of central nervous system depression. Seizures and coma may also occur in severe poisonings.[53][58] Symptoms typically appear after around 30 to 90 minutes and peak within three hours, but certain effects can last for a number of days.[55][57] In the majority of cases recovery is complete within 12 to 24 hours.[67] The effect is highly variable between individuals with similar doses potentially causing quite different reactions.[52][57][81] Some cases of intoxication have exhibited headaches up to ten hours afterwards.[57] Retrograde amnesia and somnolence frequently result following recovery.[58]

Treatment

Medical attention should be sought in cases of suspected poisoning. Initial treatment consists of gastric decontamination. If the delay between ingestion and treatment is less than four hours, activated charcoal is given. Gastric lavage can be considered if the patient presents within 1 hour of ingestion.[82] Inducing vomiting with syrup of ipecac is no longer recommended in any poisoning situations.[83]

There is no antidote, and supportive care is the mainstay of further treatment for intoxication. Patients can develop symptoms similar to anticholinergic or cholinergic poisoning; however, the use of atropine or physostigmine as an antidote is not recommended as muscimol and ibotenic acid do not produce a true anticholinergic syndrome nor do they have activity at muscarinic receptors.[84] If a patient is delirious or agitated, this can usually be treated by reassurance and, if necessary, physical restraints. Additionally, benzodiazepine such as diazepam or lorazepam can be used to control combativeness, agitation, muscular overactivity, and seizures.[52] However, small doses of benzodiazepines should be used as they may worsen the respiratory depressant effects of muscimol.[85] Recurrent vomiting is rare but if present may lead to fluid and electrolyte imbalances; intravenous rehydration or electrolyte replacement may be required.[58][86] Serious cases may develop loss of consciousness or coma, and may necessitate intubation and artificial ventilation.[53][87] Hemodialysis can remove the toxins, although this intervention is generally considered unnecessary.[67] With modern medical treatment the prognosis is typically good following supportive treatment.[63][67]

Psychoactive use

Unlike the psychedelic mushrooms of the Psilocybe, Amanita muscaria has been rarely consumed recreationally. However, following the outlawing of psilocybin-containing mushrooms in the United Kingdom, an increased quantity of legal A. muscaria mushrooms began to be sold and consumed.[88]

Siberia

A. muscaria was widely used as an entheogen by many of the indigenous peoples of Siberia. Its use was known among almost all of the Uralic-speaking peoples of western Siberia and the Paleosiberian-speaking peoples of the Russian Far East. However, there are only isolated reports of A. muscaria use among the Tungusic and Turkic peoples of central Siberia and it is believed that entheogenic use of A. muscaria was largely not a practice of these peoples.[89] In western Siberia, the use of A. muscaria was restricted to shamans, who used it as an alternate method of achieving a trance state. (Normally, Siberian shamans achieve a trance state by prolonged drumming and dancing.) In eastern Siberia, A. muscaria was used by both shamans and laypeople alike, and was used recreationally as well as religiously.[89] In eastern Siberia, the shaman would consume the mushrooms, and others would drink his urine.[90] This urine, still containing psychoactive elements may actually be more potent than the A. muscaria mushrooms with fewer negative effects, such as sweating and twitching, suggesting that the initial user may act as a screening filter for other components in the mushroom.[91]

The Koryak of eastern Siberia have a story about the fly agaric (wapaq) which enabled Big Raven to carry a whale to its home. In the story, the deity Vahiyinin ("Existence") spat onto earth, and his spittle became the wapaq, and his saliva becomes the warts. After experiencing the power of the wapaq, Raven was so exhilarated that he told it to grow forever on earth so his children, the people, can learn from it.[92] Among the Koryak, one report held the poor would consume the urine of the wealthy, who could afford to buy the mushrooms.[93]

Other reports of entheogenic use

Beyond Siberia, there are only isolated and unconfirmed reports of the entheogenic use of A. muscaria. The Finnish historian T. I. Itkonen mentions that it was once used among the Sami people, sorcerers in Inari would consume fly agarics with seven spots.[94] In 1979, Said Gholam Mochtar and Hartmut Geerken published an article in which they claim to have discovered a tradition of medicinal and recreational use of this mushroom among a Parachi-speaking group in Afghanistan.[95] There are also unconfirmed reports of religious use of A. muscaria among two Subarctic Native American tribes. Ojibwa ethnobotanist Keewaydinoquay Peschel reported its use among her people, where it was known as the miskwedo.[96][97] This information was enthusiastically received by Wasson, although evidence from other sources was lacking.[98] There is also one account of a Euro-American who claims to have been initiated into traditional Tlicho use of Amanita muscaria.[99]

Soma

In 1968, R. Gordon Wasson proposed that A. muscaria was the Soma talked about in the Rig Veda of India,[100] which received widespread publicity and popular support at the time.[101] He noted that descriptions of Soma omitted description of roots, stems or seeds, which suggested a mushroom,[102] and used the adjective hári "dazzling" or "flaming" which the author interprets as red.[103] One line described men urinating Soma; this recalled the practice of recycling urine in Siberia. Soma is mentioned as coming "from the mountains", which Wasson interpreted as being brought with the Aryan invaders from the north.[104] However, Indian scholars Santosh Kumar Dash and Sachinanda Padhy noted that both the eating of mushrooms and drinking of urine were proscribed, using as a source the Manusmṛti.[105] In 1971, Vedic scholar John Brough from Cambridge University rejected Wasson's theory; he noted the language was too vague to determine a description of Soma.[106]. In his 1976 survey, Hallucinogens and Culture, anthropologist Peter T. Furst evaluated the evidence for and against the identification of the Fly Agaric mushroom as Vedic Soma, concluding cautiously in its favor. [107]

Vikings

A single source for the notion that Vikings used A. muscaria to produce their berserker rages was first suggested by the Swedish professor Samuel Ödman in 1784.[108] Ödman based his theories on reports about the use of fly agaric among Siberian shamans. The notion has become widespread since the 19th century, but no contemporary sources mention this use or anything similar in their description of berserkers. Today, it is generally considered an urban legend or at best speculation that cannot be proven. Muscimol is generally a mild relaxant, but could create a range of reactions within a range of people.[109] It is possible that it could make a person incredibly angry, as well as make them "very jolly or sad, jump about, dance, sing or give way to great fright".[109]

Christianity

Mosaic of red mushrooms, found in the Christian Basilica of Aquileia in northern Italy, dating to before 330 AD.

Biblical scholar John Marco Allegro controversially proposed that the Roman Theology was derived from a sex and psychedelic mushroom cult in his 1970 book The Sacred Mushroom and the Cross,[110] although his theory has found little support by scholars outside the field of ethnomycology. The book was roundly discredited by academics and theologians, including Sir Godfrey Driver, Emeritus Professor of Semitic Philology at Oxford University, and Henry Chadwick, the Dean of Christ Church College, Oxford.[111] Christian author John C. King wrote a detailed rebuttal of Allegro's theory in the 1970 book A Christian View of the Mushroom Myth; he notes neither fly agarics nor their host trees are found in the middle east, and highlights the tenuous nature of the links between biblical and Sumerian names coined by Allegro. He concludes that if the theory was true, the use of the mushroom must have been "the best kept secret in the world" as it was so well concealed for all this time.[112][113]

In Magic Mushrooms in Religion and Alchemy (formerly called Strange Fruit) Clark Heinrich interprets A. muscaria usage by Adam and Eve, Moses, Elijah and Elisha, Isaiah, Ezekiel, Jonah, Jesus and his disciples, and John of Patmos.[114] In the book Apples of Apollo the mushroom is identified in a wide range of mythological tales such as those involving Perseus, Prometheus, Heracles, Jason and the Argonauts, Jesus and the Holy Grail.[115]

Culinary use

The toxins in A. muscaria are water soluble. When sliced thinly, or chopped into thin dice and boiled in plentiful water until thoroughly cooked, it seems to be detoxified.[69] Although its consumption as a food has never been widespread, the consumption of detoxified A. muscaria has been practiced in some localities in Europe (notably by Russian settlers in Siberia) since at least the 19th century, and likely earlier. The German physician and naturalist Georg Heinrich von Langsdorff wrote the earliest published account on how to detoxify this mushroom in 1823. In the late 19th Century, the French physician Félix Archimède Pouchet was a popularizer and advocate of A. muscaria consumption, comparing it to manioc, an important food source in tropical South America that nevertheless must be detoxified before consumption.[69]

Use of this mushroom as a food source also seems to have existed in North America as well. A classic description of this use of A. muscaria by an African-American mushroom seller in Washington D.C. in the late nineteenth century is described by American botanist Frederick Vernon Coville. In this case, the mushroom, after parboiling, and soaking in vinegar is made into a mushroom sauce for steak.[116] It is also consumed as a food in parts of Japan. The most well-known current use as an edible mushroom is in Nagano Prefecture, Japan. There, it is primarily salted and pickled.[117]

A 2008 paper by mycologist David Arora and food historian William Rubel gives a history of consumption of A. muscaria as a food and describes detoxification methods. They advocate that Amanita muscaria be described in field guides as an edible mushroom, though accompanied by a description on how to detoxify it. The authors state that the widespread descriptions in field guides of this mushroom as poisonous is a reflection of cultural bias, as several other popular edible species, notably morels, are toxic unless properly cooked.[69]

Cultural depictions

Moritz von Schwind's 1851 painting Ruebezahl features fly agarics.[118]

The red-and-white spotted toadstool is a common image in many aspects of popular culture, especially in children's books, film, garden ornaments, greeting cards, and more recently computer games.[38] Garden ornaments, and children's picture books depicting gnomes and fairies, such as the Smurfs, very often show fly agarics used as seats, or homes.[38][119] Fly agarics have been featured in paintings since the Renaissance,[120] albeit in a subtle manner. In the Victorian era they became more visible, even becoming the main topic of some fairy paintings.[121] Two of the most famous uses of the mushroom are in the video game series Super Mario Bros.,[122] and the dancing mushroom sequence in the 1940 Disney film Fantasia.[123]

Literature

The journeys of Philip von Strahlenberg to Siberia and his descriptions of the use of the mukhomor there was published in English in 1736. The drinking of urine of those who had imbibed the mushroom was commented on by Anglo-Irish writer Oliver Goldsmith in his widely read 1762 novel Citizen of the World.[124] The mushroom had been identified as the fly agaric by this time.[125] Other authors recorded the distortions of the size of perceived objects while intoxicated by the fungus, including naturalist Mordecai Cubitt Cooke in his books The Seven Sisters of Sleep and A Plain and Easy Account of British Fungi.[126] This observation is thought to have formed the basis of the effects of eating the mushroom in the 1865 popular story Alice's Adventures in Wonderland.[127] A hallucinogenic "scarlet toadstool" from Lappland is also featured as a plot element in Charles Kingsley's 1866 novel Hereward the Wake based on the medieval figure of the same name;[128] fly agaric shamanism is explored more recently in the 2003 novel Thursbitch by Alan Garner.[129]

Christmas decorations and Santa Claus

Fly agarics appear on Christmas cards and New Year cards from around the world as a symbol of good luck.[130] The ethnobotanist Jonathan Ott has suggested that the idea of Santa Claus and tradition of hanging stockings over the fireplace is based centrally upon the fly agaric mushroom itself.[81] With its generally red and white color scheme, he argues that Santa Claus's suit is related to the mushroom. He also draws parallels with flying reindeer: reindeer had been reported to consume the mushroom and prance around in an intoxicated manner afterwards.[131] American ethnopharmacologist Scott Hajicek-Dobberstein, researching possible links between religious myths and the red mushroom, notes, "If Santa Claus had but one eye [like Odin], or if magic urine had been a part of his legend, his connection to the Amanita muscaria would be much easier to believe."[132]

The connection was reported to a much wider audience with an article in the magazine of The Sunday Times in 1980,[133] and New Scientist in 1986.[134] Historian Ronald Hutton has since disputed the connection;[135] he noted reindeer spirits did not appear in Siberian mythology, shamans did not travel by sleigh, nor did they wear red and white, or climb out of smoke holes in yurt roofs. Finally, American awareness of Siberian shamanism postdated the appearance of much of the folklore around Santa.[136]

See also

References

  1. ^ Furst, Peter T. (1976). Hallucinogens and Culture. Chandler & Sharp. pp. 96–108. ISBN 0-88316-517-1. 
  2. ^ Wasson, Soma:Divine Mushroom of Immortality, p 198.
  3. ^ Magnus A. (1256). "Book II, Chapter 6; p 87 and Book VI, Chapter 7; p 345". De vegetabilibus. 
  4. ^ a b Ramsbottom, p 44.
  5. ^ Clusius C. (1601). "Genus XII of the pernicious mushrooms". Rariorum plantarum historia. 
  6. ^ (Latin) Linnaeus C. (1745). Flora svecica [suecica] exhibens plantas per regnum Sueciae crescentes systematice cum differentiis specierum, synonymis autorum, nominibus incolarum, solo locorum, usu pharmacopæorum. Holmiae. (Laurentii Salvii).. 
  7. ^ (Latin) Linnaeus C (1753). "Tomus II". Species Plantarum. Holmiae (Laurentii Salvii). p. 1172. 
  8. ^ Simpson DP. (1979). Cassell's Latin dictionary (5 ed.). London: Cassell Ltd. p. 883. ISBN 0-304-52257-0. 
  9. ^ Esser K; Lemke PA. (1994). The Mycota: a comprehensive treatise on fungi as experimental systems for basic and applied research. Springer. p. 181. ISBN 3540664939. 
  10. ^ Wasson, Soma:Divine Mushroom of Immortality, p 200.
  11. ^ a b Benjamin, Mushrooms: poisons and panaceas, p 306–07.
  12. ^ a b c d e Michelot D; Melendez-Howell LM. (2003). "Amanita muscaria: chemistry, biology, toxicology, and ethnomycology". Mycological Research 107 (Pt 2): 131–46. doi:10.1017/S0953756203007305. PMID 12747324. http://www.erowid.org/references/refs_view.php?A=ShowDocPartFrame&C=ref&ID=6472&DocPartID=6005. 
  13. ^ Wasson, Soma:Divine Mushroom of Immortality, p 194.
  14. ^ Niels Åge Nielsen, Dansk etymologisk Ordbog
  15. ^ Wasson, Soma:Divine Mushroom of Immortality, p 187.
  16. ^ Wasson, Soma:Divine Mushroom of Immortality, p 190.
  17. ^ Wasson, Soma:Divine Mushroom of Immortality, p 190–91.
  18. ^ Wasson, Soma:Divine Mushroom of Immortality, p 192.
  19. ^ Wasson, Soma:Divine Mushroom of Immortality, p 189.
  20. ^ a b Singer R. (1986). The Agaricales in modern taxonomy (4th ed.). Koenigstein, West Germany: Koeltz Scientific Books. ISBN 3874292541. 
  21. ^ a b c d e f g h Jenkins DT. (1986). Amanita of North America. Mad River Press. ISBN 0-916422-55-0. 
  22. ^ Tulloss RE; Yang Z-L (2009). "Amanita sect. Amanita". Studies in the Genus Amanita Pers. (Agaricales, Fungi). http://pluto.njcc.com/~ret/amanita/sectaman.html. Retrieved 2009-02-14. 
  23. ^ Moncalvo JM; Drehmel D; Vilgalys R. (July 2000). "Variation in modes and rates of evolution in nuclear and mitochondrial ribosomal DNA in the mushroom genus Amanita (Agaricales, Basidiomycota): phylogenetic implications". Molecular Phylogenetics and Evolution 16 (1): 48–63. doi:10.1006/mpev.2000.0782. PMID 10877939. http://www.biology.duke.edu/fungi/mycolab/publications/moncalvo2000mpe.pdf. Retrieved 2009-02-16. 
  24. ^ Drehmel D; Moncalvo JM; Vilgalys R. (1999). (abstract) "Molecular phylogeny of Amanita based on large subunit ribosomal DNA sequences: implications for taxonomy and character evolution". Mycologia 91 (4): 610–18. doi:10.2307/3761246. http://www.biology.duke.edu/fungi/mycolab/publications/amanitaMYCOLOGIA.html (abstract). Retrieved 2009-02-16. 
  25. ^ a b Tulloss, R. E. (2008). "Amanita muscaria (L. : Fr.) Lam. var. muscaria". Studies in the Genus Amanita Pers. (Agaricales, Fungi) - Tulloss RE, Yang Z-L.. http://pluto.njcc.com/~ret/amanita/species/muscmusc.html. Retrieved 2009-02-14. 
  26. ^ Tulloss RE; Yang Z-L. (2008). "Amanita muscaria subsp. flavivolvata Singer". Studies in the Genus Amanita Pers. (Agaricales, Fungi). http://pluto.njcc.com/~ret/amanita/species/muscflav.html. Retrieved 2009-02-14. 
  27. ^ Phillips R. (1991). Mushrooms of North America. Boston: Little, Brown & Co. ISBN 0-316-70612-4 (hardcover) ISBN 0-316-70613-2 (paperback). 
  28. ^ a b c Tulloss RE; Yang Z-L. (2006). "Amanita muscaria var. guessowii Veselý". Studies in the Genus Amanita Pers. (Agaricales, Fungi). http://pluto.njcc.com/~ret/amanita/species/muscgues.html. Retrieved 2009-02-14. 
  29. ^ Tulloss RE; Yang Z-L. (2008). "Amanita muscaria var. persicina Dav. T. Jenkins". Studies in the Genus Amanita Pers. (Agaricales, Fungi). http://pluto.njcc.com/~ret/amanita/species/muscpers.html. Retrieved 2009-02-14. 
  30. ^ Miller OK. (1982). "Higher fungi in Alaskan subarctic tundra and taiga plant communities". in Laursen GA; Ammirati JF. Arctic and alpine mycology. Seattle: University of Washington Press. pp. 123–49. ISBN 0295958561. 
  31. ^ Tulloss RE; Yang Z–L. (2007). "Amanita regalis (Fr.) Michael"". Studies in the Genus Amanita Pers. (Agaricales, Fungi). http://pluto.njcc.com/~ret/amanita/species/regaliss.html. Retrieved 2009-02-14. 
  32. ^ a b c d Geml J; Laursen GA; O'Neill K; Nusbaum HC; Taylor DL. (January 2006). "Beringian origins and cryptic speciation events in the fly agaric (Amanita muscaria)" ([dead link]). Molecular Ecology 15 (1): 225–39. doi:10.1111/j.1365-294X.2005.02799.x. PMID 16367842. http://users.iab.uaf.edu/~jozsef_geml/AmanitaME.pdf. 
  33. ^ Geml J; Tulloss RE; Laursen GA, et al. (2008). "Evidence for strong inter- and intracontinental phylogeographic structure in Amanita muscaria, a wind-dispersed ectomycorrhizal basidiomycete". Molecular Phylogenetics and Evolution 48 (2): 694–701. doi:10.1016/j.ympev.2008.04.029. PMID 18547823. http://mercury.bio.uaf.edu/~lee_taylor/pdfs/Geml_Mol-Phylo-Evol_2008.pdf. Retrieved 2009-20-28. 
  34. ^ Tulloss, R. E. (2007). "Amanita breckonii Ammirati & Thiers". Studies in the Genus Amanita Pers. (Agaricales, Fungi) - Tulloss RE, Yang Z-L.. http://pluto.njcc.com/~ret/amanita/species/breckoni.html. Retrieved 2009-03-09. 
  35. ^ Tulloss, R. E. (2007). "Amanita gioiosa S. Curreli ex S. Curreli". Studies in the Genus Amanita Pers. (Agaricales, Fungi) - Tulloss RE, Yang Z-L.. http://pluto.njcc.com/~ret/amanita/species/gioiosas.html. Retrieved 2009-03-09. 
  36. ^ Tulloss, R. E. (2007). "Amanita heterochroma S. Curreli". Studies in the Genus Amanita Pers. (Agaricales, Fungi) - Tulloss RE, Yang Z-L.. http://pluto.njcc.com/~ret/amanita/species/heteroch.html. Retrieved 2009-03-09. 
  37. ^ Zeitlmayr L. (1976). Wild mushrooms: an illustrated handbook. Hertfordshire, UK: Garden City Press. ISBN 0-584-10324-7. 
  38. ^ a b c Arora, D. (1986). Mushrooms demystified: a comprehensive guide to the fleshy fungi (2nd ed.). Berkeley: Ten Speed Press. pp. 282–83. ISBN 0-89815-169-4. 
  39. ^ Jordan P; Wheeler S. (2001). The ultimate mushroom book. Hermes House. ISBN 0831730803. 
  40. ^ Phillips R. (2006). Mushrooms. Pan MacMillan. p. 140. ISBN 0-330-44237-6. 
  41. ^ Haas H. (1969). The young specialist Looks at fungi. Burke. p. 94. ISBN 0222794143. 
  42. ^ Krieger LCC (1967). The mushroom handbook. Dover. ISBN 0486218619. 
  43. ^ Grey P. (2005). Fungi Down Under: the Fungimap guide to Australian fungi. Melbourne: Royal Botanic Gardens. p. 21. ISBN 0-646-44674-6. 
  44. ^ Benjamin, Mushrooms: poisons and panaceas, p 305.
  45. ^ Reid DA. (1980). "A monograph of the Australian species of Amanita Persoon ex Hooker (Fungi)". Australian Journal of Botany Supplementary Series 8: 1–96. 
  46. ^ Segedin BP; Pennycook SR. (2001). "A nomenclatural checklist of agarics, boletes, and related secotioid and gasteromycetous fungi recorded from New Zealand". New Zealand Journal of Botany 39 (2): 285–348. http://www.royalsociety.org.nz/includes/download.aspx?ID=88806. 
  47. ^ Reid DA; Eicker A. (1991). "South African fungi: the genus Amanita". Mycological Research 95: 80–95. doi:10.1016/S0953-7562(09)81364-6. 
  48. ^ a b Fuhrer BA. (2005). A field guide to Australian fungi. Melbourne: Bloomings Books. pp. 24. ISBN 1-876473-51-7. 
  49. ^ Hall IR; Stephenson SE; Buchanan PK; Yn W; Cole AL (2003). Edible and poisonous mushrooms of the world. New Zealand Institute for Crop & Food Research Limited. pp. 130–1. ISBN 0-4781-0835-4. 
  50. ^ May T. (2006). "News from the Fungimap president". Fungimap Newsletter (Melbourne) 29: 1. http://www.rbg.vic.gov.au/?f=16290. 
  51. ^ Keane PJ; Kile GA.; Podger FD (2000). Diseases and pathogens of eucalypts. Canberra: CSIRO Publishing. pp. 85. ISBN 0643065237. 
  52. ^ a b c d e Benjamin DR. (1992). "Mushroom poisoning in infants and children: the Amanita pantherina/muscaria group". Journal of Toxicology: Clinical Toxicology 30 (1): 13–22. doi:10.3109/15563659208994442. PMID 1347320. 
  53. ^ a b c d Hoegberg LC; Larsen L; Sonne L; Bang J; Skanning PG; (2008). "Three cases of Amanita muscaria ingestion in children: two severe courses [abstract]". Clinical Toxicology 46 (5): 407–8. doi:10.1080/15563650802071703. 
  54. ^ Benjamin, Mushrooms: poisons and panaceas, p 303–04.
  55. ^ a b Brvar, M.; Mozina, M.; Bunc, M. (May 2006). "Prolonged psychosis after Amanita muscaria ingestion". Wien. Klin. Wochenschr. 118 (9–10): 294–7. doi:10.1007/s00508-006-0581-6. PMID 16810488. 
  56. ^ Theobald W; Büch O; Kunz HA; Krupp P; Stenger EG; Heimann H. (March 1968). "[Pharmacological and experimental psychological studies with 2 components of fly agaric (Amanita muscaria)]" (in German). Arzneimittelforschung 18 (3): 311–5. PMID 5696006. 
  57. ^ a b c d e Chilton WS (1975). "The course of an intentional poisoning". MacIlvanea 2: 17. 
  58. ^ a b c d e f Satora, L.; Pach, D.; Butryn, B.; Hydzik, P.; Balicka-Slusarczyk, B.; (June 2005). "Fly agaric (Amanita muscaria) poisoning, case report and review". Toxicon 45 (7): 941–3. doi:10.1016/j.toxicon.2005.01.005. PMID 15904689. 
  59. ^ Benjamin, Mushrooms: poisons and panaceas, p 309.
  60. ^ Cagliari GE. (1897). "Mushroom poisoning". Medical Record 52: 298. 
  61. ^ a b Buck, R. W. (August 1963). "Toxicity of Amanita muscaria". JAMA 185: 663–4. PMID 14016551. 
  62. ^ "Vecchi's death said to be due to a deliberate experiment with poisonous mushrooms". New York Times. 19 December 1897. http://query.nytimes.com/mem/archive-free/pdf?_r=1&res=9E0CEFD71630E132A2575AC1A9649D94669ED7CF. Retrieved 2009-02-02. 
  63. ^ a b Tupalska-Wilczyńska, K.;; Ignatowicz, R.; Poziemski, A.; Wójcik, H.; Wilczyński, G.; (1996). "[Poisoning with spotted and red mushrooms--pathogenesis, symptoms, treatment]" (in Polish). Wiad. Lek. 49 (1–6): 66–71. PMID 9173659. 
  64. ^ Arora, Mushrooms demystified, p 894.
  65. ^ "Mushroom poisoning syndromes". North American Mycological Association (NAMA) website. NAMA. http://www.namyco.org/toxicology/poison_syndromes.html. Retrieved 2009-03-22. 
  66. ^ Benjamin, Mushrooms: poisons and panaceas, p 200.
  67. ^ a b c d Piqueras, J. (10 January 1990). "Amanita muscaria, Amanita pantherina and others". IPCS INTOX Databank. http://www.intox.org/databank/documents/fungi/aminita/pimg026.htm. Retrieved 2008-12-08. 
  68. ^ Benjamin, Mushrooms: poisons and panaceas, p 310.
  69. ^ a b c d Rubel, W.; Arora, D. (2008). "A Study of Cultural Bias in Field Guide Determinations of Mushroom Edibility Using the Iconic Mushroom, Amanita Muscaria,as an Example". Economic Botany 62 (3): 223–43. 
  70. ^ Schmiedeberg O.; Koppe R. (1869) (in German). Das Muscarin, das giftige Alkaloid des Fliegenpilzes. Leipzig: F.C.W. Vogel. OCLC 6699630. 
  71. ^ Eugster, C. H. (July 1968). "[Active substances from the toadstool]" (in German). Naturwissenschaften 55 (7): 305–13. doi:10.1007/BF00600445. PMID 4878064. 
  72. ^ Benjamin, Mushrooms: poisons and panaceas, p 306.
  73. ^ a b Bowden, K.; Drysdale, A. C.; Mogey, G. A. (June 1965). "Constituents of Amanita muscaria". Nature 206 (991): 1359–60. doi:10.1038/2061359a0. PMID 5891274. 
  74. ^ a b Eugster, C. H.; Müller, G. F.; Good, R. (June 1965). "[The active ingredients from Amanita muscaria: ibotenic acid and muscazone]" (in German). Tetrahedron Lett. 23: 1813–5. doi:10.1016/S0040-4039(00)90133-3. PMID 5891631. 
  75. ^ Bowden, K.; Drysdale, A. C. (March 1965). "A novel constituent of Amanita muscaria". Tetrahedron Lett. 12: 727–8. doi:10.1016/S0040-4039(01)83973-3. PMID 14291871. 
  76. ^ Takemoto, T.; Nakajima, T.; Yokobe, T. (December 1964). "[Structure of ibotenic acid]" (in Japanese). Yakugaku Zasshi 84: 1232–33. PMID 14266560. 
  77. ^ Jørgensen, C. G.; Bräuner-Osborne, H.; Nielsen, B. et al. (May 2007). "Novel 5-substituted 1-pyrazolol analogues of ibotenic acid: synthesis and pharmacology at glutamate receptors". Bioorganic & Medicinal Chemistry 15 (10): 3524–38. doi:10.1016/j.bmc.2007.02.047. PMID 17376693. 
  78. ^ Fritz, H.; Gagneux, A. R.; Zbinden, R.; Eugster, C. H. (1965). "The structure of muscazone.". Tetrahedron Letters 6: 2075–76. doi:10.1016/S0040-4039(00)90133-3. 
  79. ^ a b Garner, C. D.; Armstrong, E. M.; Berry, R. E. et al. (May 2000). "Investigations of Amavadin". Journal of Inorganic Biochemistry 80 (1–2): 17–20. doi:10.1016/S0162-0134(00)00034-9. PMID 10885458. http://linkinghub.elsevier.com/retrieve/pii/S0162-0134(00)00034-9. 
  80. ^ Hubregtse, T.; Neeleman, E.; Maschmeyer, T.; Sheldon, R. A.; Hanefeld, U.; Arends, I. W. (May 2005). "The first enantioselective synthesis of the amavadin ligand and its complexation to vanadium". Journal of Inorganic Biochemistry 99 (5): 1264–7. doi:10.1016/j.jinorgbio.2005.02.004. PMID 15833352. 
  81. ^ a b Ott, J. (1976). Hallucinogenic Plants of North America. Berkeley, CA: Wingbow Press. ISBN 0914728156. 
  82. ^ Vale, J. A.; Kulig, K.; American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists (2004). "Position paper: gastric lavage". Journal of Toxicology - Clinical Toxicology 42 (7): 933–43. doi:10.1081/CLT-200045006. PMID 15641639. 
  83. ^ "Position paper: Ipecac syrup". Journal of Toxicology - Clinical Toxicology 42 (2): 133–43. 2004. PMID 15214617. 
  84. ^ Dart, R. C. (2004). Medical toxicology. Philadelphia, PA: Lippincott Williams & Wilkins. pp. 1719–35. ISBN 0781728452. 
  85. ^ Brent, J.; Wallace, K. L.; Burkhart, K. K.; Phillips, S. D.; Donovan, J. W. (2005). Critical care toxicology: diagnosis and management of the critically poisoned patient. Philadelphia, PA: Elsevier Mosby. pp. 1263–75. ISBN 0815143877. 
  86. ^ Benjamin, Mushrooms: poisons and panaceas, p 313.
  87. ^ Bosman, C. K.; Berman, L.; Isaacson, M.; Wolfowitz, B.; Parkes, J. (October 1965). "Mushroom poisoning caused by Amanita pantherina. Report of 4 cases". South African Medical Journal 39 (39): 983–86. PMID 5892794. 
  88. ^ European Monitoring Centre for Drugs and Drug Addiction, p 17.
  89. ^ a b Nyberg, H. (1992). "Religious use of hallucinogenic fungi: A comparison between Siberian and Mesoamerican Cultures". Karstenia 32 (71–80). 
  90. ^ Wasson, Soma: Divine Mushroom of Immortality, p 161.
  91. ^ Diaz, J. (1996). How Drugs Influence Behavior: A Neurobehavioral Approach. Upper Saddle River, N.J.: Prentice Hall. ISBN 0023287640. 
  92. ^ Ramsbottom, p 45.
  93. ^ Wasson, Soma: Divine Mushroom of Immortality, pp 234–35.
  94. ^ Wasson, Soma: Divine Mushroom of Immortality, p 279.
  95. ^ "Several Shutulis asserted that Amanita-extract would be administered orally as a medicine for treatment of psychotic conditions, as well as externally as a therapy for localized frostbite."Mochtar, S. G.; Geerken, H.; Werner. P. G. (trans) (1979). "The Hallucinogens Muscarine and Ibotenic Acid in the Middle Hindu Kush: A contribution on traditional medicinal mycology in Afghanistan" (in German). Afghanistan Journal. pp. 62–65. http://www.erowid.org/plants/amanitas/references/journal/1979_mochtar_afghanistan1.shtml. Retrieved 2009-02-23. 
  96. ^ Peschel, Keewaydinoquay (1978). Puhpohwee for the people: a narrative account of some uses of fungi among the Ahnishinaubeg. Cambridge, MA: Botanical Museum of Harvard University. ISBN 1879528185. 
  97. ^ (French) Navet, E. (1988). "Les Ojibway et l'Amanite tue-mouche (Amanita muscaria). Pour une éthnomycologie des Indiens d'Amérique du Nord". Journal de la Société des Américanistes 74: 163–80. doi:10.3406/jsa.1988.1334. 
  98. ^ Letcher, p 149.
  99. ^ Larsen, S. (1976). The Shaman's Doorway. New York, NY: Station Hill Press. ISBN 0892816724. 
  100. ^ Wasson, Soma:Divine Mushroom of Immortality, p 10.
  101. ^ Letcher, p 145.
  102. ^ Wasson, Soma:Divine Mushroom of Immortality, p 18.
  103. ^ Wasson, Soma:Divine Mushroom of Immortality, p 36–37.
  104. ^ Wasson, Soma:Divine Mushroom of Immortality, p 22–24.
  105. ^ Letcher, p 146.
  106. ^ Brough, J. (1971). "Soma and Amanita muscaria". Bulletin of the School of Oriental and African Studies (BSOAS) 34: 331–62. 
  107. ^ Furst, Peter T. (1976). Hallucinogens and Culture. Chandler & Sharp. pp. 96–108. ISBN 0-88316-517-1. 
  108. ^ (Swedish) Ödman S. (1784) Försök at utur Naturens Historia förklara de nordiska gamla Kämpars Berserka-gang (An attempt to Explain the Berserk-raging of Ancient Nordic Warriors through Natural History). Kongliga Vetenskaps Academiens nya Handlingar 5: 240–247 (In: Wasson, 1968)
  109. ^ a b Hoffer, A.; Osmond, H. (1967). The Hallucinogens. Academic Press. pp. 443–54. ISBN 0-12-351850-4. 
  110. ^ Allegro, J. (1970). The Sacred Mushroom and the Cross: A Study of the Nature and Origins of Roman Theology within the Fertility Cults of the Ancient Near East. London: Hodder and Stoughton. ISBN 0-340-12875-5. 
  111. ^ Letcher, p 160.
  112. ^ King, J. C. (1970). A Christian View of the Mushroom Myth. London: Hodder and Stoughton. ISBN 0-350-12597-7. 
  113. ^ Letcher, p 161.
  114. ^ Heinrich, C. (2002). Magic Mushrooms in Religion and Alchemy. Park Street Press. pp. 64–134. ISBN 089281997-9. 
  115. ^ Ruck, Carl; Staples, B. D.; Clark, H. (2001). The Apples of Apollo. Carolina Academic Press. ISBN 0-89089-924-X. 
  116. ^ Coville, F. V. 1898. Observations on Recent Cases of Mushroom Poisoning in the District of Columbia. United States Department of Agriculture, Division of Botany. U. S. Government Printing office, Washington, D.C.
  117. ^ Phipps, A. G.; Bennett, B.C.; Downum, K. R. (2000). Japanese use of Beni-tengu-dake (Amanita muscaria) and the efficacy of traditional detoxification methods. Florida International University, Miami, Florida. 
  118. ^ "Art Registry: 1750-1850". Mykoweb. http://www.mykoweb.com/art-registry/1750-1850.html. Retrieved 2009-02-26. 
  119. ^ Benjamin, Mushrooms: poisons and panaceas, p 295.
  120. ^ "The Registry of Mushrooms in Works of Art". Mykoweb. http://www.mykoweb.com/art-registry/index.html. Retrieved 2009-02-16. 
  121. ^ "Mushrooms in Victorian Fairy Paintings, by Elio Schachter". Mushroom, the Journal of Wild Mushrooming. http://www.mushroomthejournal.com/bestof/VicFP.html. Retrieved 2009-02-16. 
  122. ^ Li, C.; Oberlies, N. H. (December 2005). "The most widely recognized mushroom: chemistry of the genus Amanita". Life Sciences 78 (5): 532–38. doi:10.1016/j.lfs.2005.09.003. PMID 16203016. 
  123. ^ Ramsbottom, p 43.
  124. ^ Letcher, p 122.
  125. ^ Letcher, p 123.
  126. ^ Letcher, p 125.
  127. ^ Letcher, p 126.
  128. ^ Letcher, p 127.
  129. ^ Letcher, p 129.
  130. ^ Wasson, Soma:Divine Mushroom of Immortality, p 204.
  131. ^ Wasson, Soma:Divine Mushroom of Immortality, p 238.
  132. ^ Hajicek-Dobberstein, S. (October 1995). "Soma siddhas and alchemical enlightenment: psychedelic mushrooms in Buddhist tradition". Journal of Ethnopharmacology 48 (2): 99–118. doi:10.1016/0378-8741(95)01292-L. PMID 8583800. http://linkinghub.elsevier.com/retrieve/pii/0378-8741(95)01292-L. 
  133. ^ Taylor, R. (21 December 1980). "Who is Santa Claus?". Sunday Times Magazine (London: Times Newspapers Ltd): 13–17. 
  134. ^ Morgan, A. (December 1986). "Who put the toad in toadstool?". New Scientist 25: 44–47. 
  135. ^ Hutton, R. (1996). The Stations of the Sun: A History of the Ritual Year in Britain. Oxford: Oxford University Press. pp. 118–19. 
  136. ^ Letcher, p 139.

Cited texts

Creative Commons Attribution Share Alike 3.0 (CC BY-SA 3.0)

Source: Wikipedia

Unreviewed

Article rating from 0 people

Average rating: 2.5 of 5

Disclaimer

EOL content is automatically assembled from many different content providers. As a result, from time to time you may find pages on EOL that are confusing.

To request an improvement, please leave a comment on the page. Thank you!