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Amanita muscaria, commonly known as the fly agaric (IPA: [ˈægərɪk]) or fly Amanita, 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 plentiful 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]

DescriptionEdit

File:Amanita muscaria After Rain.jpg

A large conspicuous mushroom, Amanita muscaria is generally common and numerous where it grows, and is often found in groups with [[asidiocarps 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.[2] 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.

Distribution and habitatEdit

File:Amanita muscaria Marriott Falls 1.jpg

A. muscaria is a cosmopolitan mushroom, native to conifer and deciduous woodlands throughout the temperate and boreal regions of the Northern Hemisphere,[3] including high elevations of warmer latitudes in regions like the Hindu Kush, the Mediterranean and Central America.

ToxicityEdit

Amanita muscaria poisoning typically occurs in either young children or people ingesting it for a hallucinogenic experience.[4][5][6] Occasionally, immature button forms have been mistaken for edible puffballs.[7] Additionally, the white spots may be washed away during heavy rain and it can then appear similar to the edible Amanita caesarea.[8]

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,[9][10] this is typically about the amount found in one cap of Amanita muscaria.[11] 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.[5]

A fatal dose has been calculated at approximately 15 caps.[12] Deaths from A. muscaria have been reported in historical journal articles and newspaper reports;[13][14][15] however, with modern medical treatment a fatal outcome would be extremely rare.[16] Many older books mistakenly list it as deadly, giving the impression that it is far more toxic than it really is.[17] The North American Mycological Association has stated there are no reliably documented fatalities in the past 100 years.[18] The vast majority (90% or more) of mushroom poisoning deaths are from having eaten either the greenish to yellowish death cap (Amanita phalloides) or one of the several white Amanita species known as destroying angels.[19]

The active constituents of this species are water soluble, and boiling and then discarding the cooking water will at least partly detoxify A. muscaria.[20] However, drying may increase potency as the process facilitates the conversion of ibotenic acid to the more potent muscimol.[21] According to some sources, once detoxified, the mushroom becomes edible.[22]

PharmacologyEdit

File:Muscimol-lg.png
File:Ibotenic acid2.png

Muscarine, discovered in 1869,[23] 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,[24] 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.[25]

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.[26][27] Researchers in England,[28] Japan,[29] and Switzerland[27] showed that the effects produced were due mainly to ibotenic acid and muscimol, not muscarine.[30][26] 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.[10]

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[31] 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.[4][11]

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.[32] Muscazone is of minor pharmacological activity compared with the other agents.[4] 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.[33] Vanadium is present in fruit-bodies as an organometallic compound called amavadine.[33] However, the biological importance of the accumulation process is unknown.[34]

SymptomsEdit

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.[5][6][11][14]

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.[6][11] Symptoms typically appear after around 30 to 90 minutes and peak within three hours, but certain effects can last for a number of days.[8][10] In the majority of cases recovery is complete within 12 to 24 hours.[20] The effect is highly variable between individuals with similar doses potentially causing quite different reactions.[5][10][35] Some cases of intoxication have exhibited headaches up to ten hours afterwards.[10] Retrograde amnesia and somnolence frequently result following recovery.[11]

TreatmentEdit

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.[36] Inducing vomiting with syrup of ipecac is no longer recommended in any poisoning situations.[37]

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.[38] 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.[5] However, small doses of benzodiazepines should be used as they may worsen the respiratory depressant effects of muscimol.[39] Recurrent vomiting is rare but if present may lead to fluid and electrolyte imbalances; intravenous rehydration or electrolyte replacement may be required.[11][40] Serious cases may develop loss of consciousness or coma, and may necessitate intubation and artificial ventilation.[6][41] Hemodialysis can remove the toxins, although this intervention is generally considered unnecessary.[20] With modern medical treatment the prognosis is typically good following supportive treatment.[16][20]

Psychoactive useEdit

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.[42]

SiberiaEdit

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.[43] 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.[43] In eastern Siberia, the shaman would consume the mushrooms, and others would drink his urine.[44] 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.[45]


Other reports of entheogenic useEdit

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.[46] 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.[47] 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.[48][49] This information was enthusiastically received by Wasson, although evidence from other sources was lacking.[50] There is also one account of a Euro-American who claims to have been initiated into traditional Tlicho use of Amanita muscaria.[51]

SomaEdit

In 1968, R. Gordon Wasson proposed that A. muscaria was the Soma talked about in the Rig Veda of India,[52] which received widespread publicity and popular support at the time.[53] He noted that descriptions of Soma omitted description of roots, stems or seeds, which suggested a mushroom,[54] and used the adjective hári "dazzling" or "flaming" which the author interprets as red.[55] 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.[56] 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.[57] 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.[58]. 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. [59]


ChristianityEdit

File:Aquileia mushrooms.jpg

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,[60] 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.[61] 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.[62][63]


See alsoEdit

ReferencesEdit

  1. Furst, Peter T. (1976). Hallucinogens and Culture, 96–108, Chandler & Sharp.
  2. Zeitlmayr L. (1976). Wild mushrooms: an illustrated handbook, Hertfordshire, UK: Garden City Press.
  3. Cite error: Invalid <ref> tag; no text was provided for refs named Geml06
  4. Cite error: Invalid <ref> tag; no text was provided for refs named Michelot03
  5. 5.0 5.1 5.2 5.3 5.4 Benjamin DR. (1992). Mushroom poisoning in infants and children: the Amanita pantherina/muscaria group. Journal of Toxicology: Clinical Toxicology 30 (1): 13–22.
  6. 6.0 6.1 6.2 6.3 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.
  7. Benjamin, Mushrooms: poisons and panaceas, p 303–04.
  8. 8.0 8.1 Brvar, M., Mozina, M.; Bunc, M. (May 2006). Prolonged psychosis after Amanita muscaria ingestion. Wien. Klin. Wochenschr. 118 (9–10): 294–7.
  9. 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)]. Arzneimittelforschung 18 (3): 311–5.
  10. 10.0 10.1 10.2 10.3 10.4 Chilton WS (1975). The course of an intentional poisoning. MacIlvanea 2: 17.
  11. 11.0 11.1 11.2 11.3 11.4 11.5 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.
  12. Benjamin, Mushrooms: poisons and panaceas, p 309.
  13. Cagliari GE. (1897). Mushroom poisoning. Medical Record 52: 298.
  14. 14.0 14.1 Buck, R. W. (August 1963). Toxicity of Amanita muscaria. JAMA 185: 663–4.
  15. Vecchi's death said to be due to a deliberate experiment with poisonous mushrooms. New York Times. URL accessed on 2009-02-02.
  16. 16.0 16.1 Tupalska-Wilczyńska, K.;, Ignatowicz, R.; Poziemski, A.; Wójcik, H.; Wilczyński, G.; (1996). [Poisoning with spotted and red mushrooms--pathogenesis, symptoms, treatment]. Wiad. Lek. 49 (1–6): 66–71.
  17. Arora, Mushrooms demystified, p 894.
  18. Mushroom poisoning syndromes. North American Mycological Association (NAMA) website. NAMA. URL accessed on 2009-03-22.
  19. Benjamin, Mushrooms: poisons and panaceas, p 200.
  20. 20.0 20.1 20.2 20.3 Piqueras, J.. Amanita muscaria, Amanita pantherina and others. IPCS INTOX Databank. URL accessed on 2008-12-08.
  21. Benjamin, Mushrooms: poisons and panaceas, p 310.
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  23. Schmiedeberg O.; Koppe R. (1869). Das Muscarin, das giftige Alkaloid des Fliegenpilzes (in German), Leipzig: F.C.W. Vogel.
  24. Eugster, C. H. (July 1968). [Active substances from the toadstool]. Naturwissenschaften 55 (7): 305–13.
  25. Benjamin, Mushrooms: poisons and panaceas, p 306.
  26. 26.0 26.1 Bowden, K., Drysdale, A. C.; Mogey, G. A. (June 1965). Constituents of Amanita muscaria. Nature 206 (991): 1359–60.
  27. 27.0 27.1 Eugster, C. H., Müller, G. F.; Good, R. (June 1965). [The active ingredients from Amanita muscaria: ibotenic acid and muscazone]. Tetrahedron Lett. 23: 1813–5.
  28. Bowden, K., Drysdale, A. C. (March 1965). A novel constituent of Amanita muscaria. Tetrahedron Lett. 12: 727–8.
  29. Takemoto, T., Nakajima, T.; Yokobe, T. (December 1964). [Structure of ibotenic acid]. Yakugaku Zasshi 84: 1232–33.
  30. Benjamin, Mushrooms: poisons and panaceas, p 306–07.
  31. 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.
  32. Fritz, H., Gagneux, A. R.; Zbinden, R.; Eugster, C. H. (1965). The structure of muscazone.. Tetrahedron Letters 6: 2075–76.
  33. 33.0 33.1 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.
  34. 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.
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  36. 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.
  37. (2004). Position paper: Ipecac syrup. Journal of Toxicology - Clinical Toxicology 42 (2): 133–43.
  38. Dart, R. C. (2004). Medical toxicology, 1719–35, Philadelphia, PA: Lippincott Williams & Wilkins.
  39. 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, 1263–75, Philadelphia, PA: Elsevier Mosby.
  40. Benjamin, Mushrooms: poisons and panaceas, p 313.
  41. 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.
  42. European Monitoring Centre for Drugs and Drug Addiction, p 17.
  43. 43.0 43.1 Nyberg, H. (1992). Religious use of hallucinogenic fungi: A comparison between Siberian and Mesoamerican Cultures. Karstenia 32 (71–80).
  44. Wasson, Soma: Divine Mushroom of Immortality, p 161.
  45. Diaz, J. (1996). How Drugs Influence Behavior: A Neurobehavioral Approach, Upper Saddle River, N.J.: Prentice Hall.
  46. Wasson, Soma: Divine Mushroom of Immortality, p 279.
  47. "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). The Hallucinogens Muscarine and Ibotenic Acid in the Middle Hindu Kush: A contribution on traditional medicinal mycology in Afghanistan. Afghanistan Journal. URL accessed on 2009-02-23.
  48. 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.
  49. (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.
  50. Letcher, p 149.
  51. Larsen, S. (1976). The Shaman's Doorway, New York, NY: Station Hill Press.
  52. Wasson, Soma:Divine Mushroom of Immortality, p 10.
  53. Letcher, p 145.
  54. Wasson, Soma:Divine Mushroom of Immortality, p 18.
  55. Wasson, Soma:Divine Mushroom of Immortality, p 36–37.
  56. Wasson, Soma:Divine Mushroom of Immortality, p 22–24.
  57. Letcher, p 146.
  58. Brough, J. (1971). Soma and Amanita muscaria. Bulletin of the School of Oriental and African Studies (BSOAS) 34: 331–62.
  59. Furst, Peter T. (1976). Hallucinogens and Culture, 96–108, Chandler & Sharp.
  60. 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.
  61. Letcher, p 160.
  62. King, J. C. (1970). A Christian View of the Mushroom Myth, London: Hodder and Stoughton.
  63. Letcher, p 161.

Cited textsEdit

  • Arora, David (1986). Mushrooms demystified: a comprehensive guide to the fleshy fungi, 2nd, Berkeley: Ten Speed Press.
  • Benjamin, Denis R. (1995). Mushrooms: poisons and panaceas—a handbook for naturalists, mycologists and physicians, New York: WH Freeman and Company.
  • European Monitoring Centre for Drugs and Drug Addiction (2006). Hallucinogenic mushrooms: an emerging trend case study, Lisbon, Portugal: European Monitoring Centre for Drugs and Drug Addiction. URL accessed 2009-02-13.
  • Letcher, Andy (2006). Shroom: A Cultural history of the magic mushroom, London: Faber and Faber.
  • Ramsbottom, J. (1953). Mushrooms & Toadstools, Collins.
  • Wasson, R. Gordon (1968). Soma: Divine Mushroom of Immortality, Harcourt Brace Jovanovick.
  • Furst, Peter T. (1976). Hallucinogens and Culture, 98–106, Chandler & Sharp.

External linksEdit

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  • Extensive and detailed webpages on Amanita species by Tulloss & Yang Zhuliang [1]


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