Shamanism

"Shaman" redirects here. For other uses, see Shaman (disambiguation).

Russian postcard based on a photo taken in 1908 by S. I. Borisov, showing a woman shaman likely of the Turkic Khakasethnicity.[1]

Shamanism is an anthropological term referencing a range of beliefs and practices regarding communication with the spiritual world.[2] A practitioner of shamanism is known as a shaman (pronounced /ˈʃɑːmən/ "SHAH-men"or /ˈʃeɪmən/ "SHAY-men").[3]

Shamanism encompasses the belief that shamans are intermediaries or messengers between the human world and the spirit worlds. Shamans are said to treat ailments/illness by mending the soul. Alleviating traumas affecting the soul/spirit restores the physical body of the individual to balance and wholeness. The shaman also enters supernatural realms or dimensions to obtain solutions to problems afflicting the community. Shamans may visit other worlds/dimensions to bring guidance to misguided souls and to ameliorate illnesses of the human soul caused by foreign elements. The shaman operates primarily within the spiritual world, which in turn affects the human world. The restoration of balance results in the elimination of the ailment.[4]

Etymology

The term "shaman" is a loan from the Turkic[5][6][7][8] word šamán, the term for such a practitioner, which also gained currency in the wider Turko-Mongol and Tungusic cultures in ancient Siberia. Shamanism played an important role in Altaic mythology.Tengriism which was the major belief of Xiongnu, Turkic, Hungarian and Bulgar peoples in ancient times incorporates elements of shamanism.

Sociology

Shamanism in sociology applies to various empirical investigative methods and critical analysis to develop and refine a body of knowledge about shamanic social structure and activity, often with the goal of applying such knowledge to the pursuit of social welfare.[clarification needed]

Role

The shaman’s social role may be defined by a set of connected behaviors, rights and obligations as conceptualized by actors in a social situation and the expected behavior in a given individual within their cultural social status and social position.

Shamanism is a ‘calling’. Individuals who are ‘called’ typically experience an illness of some sort over a prolonged period of time. This illness will prompt the individual to seek out spiritual guidance and other shamanic healers. Such illnesses are usually not healed/curable by physicians and western medicine. The shaman heals through spiritual means that consequently affect the human world by bringing about restored health.

Cultural anthropology approaches shamanism as an integral part of the study of culture, belief, and practice.

Healer

Shamans gain knowledge and the power to heal by entering into the spiritual world or dimension. The shaman may have, or acquire many spirit guides in the spirit world, these often guide and direct the shaman in his/her travels. These spirit guides are always present within the shaman though others only encounter them when the shaman is in a trance. The spirit guide energizes the shaman, enabling him/her to enter the spiritual dimension. The shaman heals within the spiritual dimension by returning ‘lost’ parts of the human soul from wherever they have gone. The shaman also cleanses excess negative energies which confuse or pollute the soul. [citation needed]

Mediator

Shaman act as "mediators" in their culture.[9][10] The shaman communicates with the spirits on behalf of the community, including the spirits of the deceased. The shaman communicates with both living and dead to alleviate unrest, unsettled issues, and to deliver gifts to the spirits.

Often, unsettled issues can be resolved with money. Paper money can be burnt to transfer its value to the spirits.

Among the Selkups, the sea duck is a spirit animal because ducks fly in the air, and dive in the water. Thus ducks belong to both the upper world and the world below.[11] Among other Siberian peoples these characteristics are attributed to water fowl in general.[12] Among many Native Americans, the jaguar is a spirit animal because jaguars walk on earth, swim in water, and climb in trees. Thus jaguars belong to all three worlds, Sky, Earth, Underworld.

Function

Shamans perform a variety of functions depending upon their respective cultures:[13] healing;[14][15] leading a sacrifice;[16]preserving the tradition by storytelling and songs;[17] fortune-telling;[18] acting as a psychopomp (literal meaning, “guide of souls”).[19] In some cultures, a shaman may fulfill several functions in one person.[13]

The functions of a shaman may include either guiding to their proper abode the souls of the dead (which may be guided either one-at-a-time or in a cumulative group, depending on culture), and/or curing (healing) of ailments. The ailments may be either purely physical afflictions—such as disease, which may be cured by gifting, flattering, threatening, or wrestling the disease-spirit (sometimes trying all these, sequentially), and which may be completed by displaying some supposedly extracted token of the disease-spirit (displaying this, even if "fraudulent", is supposed to impress the disease-spirit that it has been, or is in the process of being, defeated, so that it will retreat and stay out of the patient’s body) –, or else mental (including psychosomatic) afflictions—such as persistent terror (on account of some frightening experience), which may be likewise cured by similar methods. Usually in most languages a different term other than the one translated "shaman" is applied to a religious official leading sacrificial rites ("priest"), or to a raconteur ("sage") of traditional lore; there may be more of an overlap in functions (with that of a shaman), however, in the case of an interpreter of omens or of dreams.

To quote Mircea Eliade: "A first definition of this complex phenomenon, and perhaps the least hazardous, will be: shamanism =technique of ecstasy."[20]

[edit]Distinct types of shaman

In some cultures there may be additional types of shaman, who perform more specialized functions. For example, among theNanai people, a distinct kind of shaman acts as a psychopomp.[21] Other specialized shaman may be distinguished according to the type of spirits, or realms of the spirit world, with which the shaman most commonly interacts. These roles vary among theNenets, Enets, and Selkup shaman (paper;[22] online[23]). Among the Huichol,[24] there are two categories of shaman. This demonstrates the differences among shaman within a single tribe.

Amongst the Hmong people, the shaman or the "shi yi", acts as healer. The Shi Yi also performs rituals/ceremonies designed to call upon the soul from its many travels back to the physical human body. A Shi Yi may use several shamanistic tools such as swords, divinity horns, a gong (drum), or finger bells/jingles. All tools serve to protect the spirits from the eyes of the unknown, thus enabling the Shi Yi to deliver souls back to their proper owner. The Shi Yi may wear a white, red, or black veil to disguise the soul from its attackers in the spiritual dimension.

Soul and spirit concepts

The variety of functions described above may seem distinct tasks, but they may be united by underlying soul and spirit concepts.

Soul
This concept can generally explain more, seemingly unassociated phenomena in shamanism:[25][26][27]
Healing
This concept may be based closely on the soul concepts of the belief system of the people served by the shaman (online[14]). It may consist of the retrieving the lost soul of the ill person.[28] See also the soul dualism concept.
Scarcity of hunted game
This problem can be solved by “releasing” the souls of the animals from their hidden abodes. Besides that, many taboosmay prescribe the behavior of people towards game, so that the souls of the animals do not feel angry or hurt, or the pleased soul of the already killed prey can tell the other, still living animals, that they can allow themselves to be caught and killed.[29][30] For the ecological aspects of shamanistic practice, and related beliefs, see above.
Infertility of women
This problem can be cured by obtaining the soul of the expected child.
Spirits
Beliefs related to spirits can explain many different phenomena,[31] for example, the importance of storytelling, or acting as a singer, can be understood better if we examine the whole belief system. A person who can memorize long texts or songs, and play an instrument, may be regarded as the beneficiary of contact with the spirits (eg. Khanty people).[32]
Ecological aspect

Resources for human consumption are easily depletable in tropical rainforests. Among Tucano, a sophisticated system exists for resource management, and for avoiding resource depletion through overhunting. This system is conceptualized mythologically and symbolically by the belief that breaking hunting restrictions may cause illness. As the primary teacher of tribal symbolism, the shaman may have a leading role in this ecological management, actively restricting hunting and fishing. The shaman is able to “release” game animals, or their souls, from their hidden abodes,[33] The Desana shaman negotiates with mythological beings for the souls of game.[34] Not only Tucanos, but the Piaroa have ecological concerns related to shamanism.[35] Among theEskimo, shamans fetch the souls of game from remote places,[36][37] or soul travel to ask for game from mythological beings like the Sea Woman.[38]

Economics

The way shamans get sustenance and take part in everyday life varies among cultures. In many Eskimo groups, they provide services for the community and get a “due payment” (some cultures believe the payment is given to the helping spirits[39]), but these goods are only “welcome addenda.” They are not enough to enable shamanizing as a full-time activity. Shamans live like any other member of the group, as hunter or housewife.[39][40]

Beliefs

There are many variations of shamanism throughout the world; and several common beliefs are shared by all forms of shamanism. Common beliefs identified by Eliade (1964)[4] are the following:

  • Spirits exist and they play important roles both in individual lives and in human society.
  • The shaman can communicate with the spirit world.
  • Spirits can be good or evil.
  • The shaman can treat sickness caused by evil spirits.
  • The shaman can employ trance inducing techniques to incite visionary ecstasy and go on "vision quests."
  • The shaman’s spirit can leave the body to enter the supernatural world to search for answers.
  • The shaman evokes animal images as spirit guides, omens, and message-bearers.
  • The shaman can tell the future, scry, throw bones/runes, and perform other varied forms of divination

Shamanism is based on the premise that the visible world is pervaded by invisible forces or spirits which affect the lives of the living.[41] Shamans require individualized knowledge and special abilities. Many shamans operate alone, although some take on an apprentice. Shamans can gather into associations, as Indian tantric practitioners have done.[citation needed]

Although the causes of disease lie in the spiritual realm, inspired by malicious spirits or witchcraft, both spiritual and physical methods are used to heal. Commonly, a shaman "enters the body" of the patient to confront the spiritual infermity and heals by banishing the infectious spirit. Many shamans have expert knowledge of medicinal plants native to their area, and an herbal treatment is often prescribed. In many places shamans learn directly from the plants, harnessing their effects and healing properties, after obtaining permission from the indwelling or patron spirits. In the Peruvian Amazon Basin, shamans and curanderos use medicine songs called icaros to evoke spirits. Before a spirit can be summoned it must teach the shaman its song.[41] The use of totemic items such as rocks with special powers and an animating spirit is common. Such practices are presumably very ancient. Plato wrote in his Phaedrus that the "first prophecies were the words of an oak", and that those who lived at that time found it rewarding enough to "listen to an oak or a stone, so long as it was telling the truth".

Belief in witchcraft and sorcery, known as brujeria in Latin America, exists in many societies. Some societies distinguish shamans who cure from sorcerers who harm. Other societies assert all shamans have the power to both cure and kill. Shamanic knowledge usually enjoys great power and prestige in the community,[citation needed] but it may also be regarded suspiciously or fearfully as potentially harmfull to others.

By engaging in the work, a shaman is exposed to significant personal risk. Risks may emerge from the spirit world, from enemy shamans, or from the means employed to alter the shaman’s state of consciousness. Some of the plant materials used by shamans are toxic or fatal if misused. Failure to return from an out-of-body journey can lead to physical death. Spells are commonly used to protect against these dangers, and the use of more dangerous plants is often very highly ritualized.

Knowledge

Boundaries between shaman and laity are not always clearly defined.


Among the Barasana [of Brazil], there is no absolute difference between those men recognized as shamans and those who are not. At the lowest level, most adult men have some abilities as shamans and will carry out some of the same functions as those men who have a widespread reputation for their powers and knowledge.

The Barasana shaman knows more myths and understands their meaning better, nonetheless the majority of adult men also know many myths.[42]

Among Eskimo peoples the laity have experiences which are commonly attributed to the shamans of those Eskimo groups.Daydream, reverie, and trance are not restricted to shamans.[43] Control over helping spirits is the primary characteristic attributed to shamans. The laity usually employ amulets, spells, formulas, songs.[43][44] Among the Greenland Inuit, some of the laity have greater capacity to relate with spiritual beings. These people are often apprentice shamans who failed to complete their initiations.[40]

The assistant of an Oroqen shaman (called jardalanin, or "second spirit") knows many things about the associated beliefs. He or she accompanies the rituals and interprets the behavior of the shaman.[45] Despite these functions, the jardalanin is not a shaman. For this interpretative assistant, it would be unwelcome to fall into trance.[46]

[edit]Initiation and learning

In some societies, shamanic powers are inherited, whereas shamans are normally "called" by dreams or signs which require lengthy training.

Shamanic illness

Turner and colleagues[47] mention a phenomenon called shamanistic initiatory crisis. A rite of passage for shamans-to-be, commonly involving physical illness and/or psychological crisis. The significant role of initiatory illnesses in the calling of a shaman can be found in the detailed case history of Chuonnasuan, the last master shaman among the Tungus peoples in Northeast China.[48]

Cognitive, semiotic, hermeneutic approaches

As mentioned, a (debated) approach explains the etymology of word “shaman” as meaning “one who knows”.[49][50] Really, the shaman is a person who is an expert in keeping together the multiple codes through which this complex belief system appears, and has a comprehensive view on it in their mind with certainty of knowledge.[51] The shaman uses (and the audience understands) multiple codes. Shaman express meanings in many ways: verbally, musically, artistically, and in dance. Meanings may be manifested in objects, such as amulets.[50]

The shaman knows the culture of his or her community well,[52][53][54] and acts accordingly. Thus, their audience knows the used symbols and meanings—that is why shamanism can be efficient: people in the audience trust it.[54] Such belief systemcan appear to its members with certainty of knowledge—this explains the above described etymology for the word “shaman”.[55]

Sami shaman with his drum

There are semiotic theoretical approaches to shamanism,[56][57][58](“ethnosemiotics”). The symbols on the shaman’s costume and drum can refer toPower animals, or to the rank of the shaman.

There are also examples of “mutually opposing symbols”, distinguishing a “white” shaman who contacts sky spirits for good aims by day, from a “black” shaman who contacts evil spirits for bad aims by night.[59] (Series of such opposing symbols referred to a world-view behind them. Analogously to the way grammar arranges words to express meanings and convey a world, also this formed a cognitive map?).[51][60]Shaman’s lore is rooted in the folklore of the community, which provides a “mythological mental map”.[61][62] Juha Pentikäinen uses the concept “grammar of mind”.[62][63] Linking to a Sami example, Kathleen Osgood Dana writes:[64]


Juha Pentikäinen, in his introduction to Shamanism and Northern Ecology, explains how the Sámi drum embodies Sámi worldviews. He considers shamanism to be a ‘grammar of mind’ (10), because shaman need to be experts in the folklore of their cultures (11)

.

Armin Geertz coined and introduced the hermeneutics,[65] “ethnohermeneutics”,[60]approaches to the practice of interpretation. Hoppál extended the term to include not only the interpretation of oral or written texts, but also that of “visual texts as well (including motions, gestures and more complex ritual, and ceremonies performed for instance by shamans)”.[66] It can not only reveal the animistic views hiding behind shamanism, but also convey their relevance for the recent world, where ecological problems made paradigms about balance and protection valid.[62]

Ecological approaches, systems theory

Other fieldworks use systems theory concepts and ecological considerations to understand the shaman’s lore. Desana andTucano Indians have developed a sophisticated symbolism and concepts of “energy” flowing between people and animals in cyclic paths. Gerardo Reichel-Dolmatoff relates these concepts to the changes how modern science (systems theory, ecology, some new approaches in anthropology and archeology) treats causality in a less linear way.[33] He suggests also a cooperation of modern science and indigenous lore (online[67])

Practice

Generally, the shaman traverses the axis mundi and enters the spirit world by effecting a transition of consciousness, entering into an ecstatic trance, either autohypnotically or through the use of entheogens. The methods employed are diverse, and are often used together. Some of the methods for effecting such trances:

Plants (often psychoactive)
Other

Shamans will often observe dietary or customary restrictions particular to their tradition. Sometimes these restrictions are more than just cultural. For example, the diet followed by shamans and apprentices prior to participating in an Ayahuasca ceremony includes foods rich in tryptophan (a biosynthetic precursor to serotonin) as well as avoiding foods rich in tyramine, which could induce hypertensive crisis if ingested with MAOIs such as are found in Ayahuasca brews.[41]

Music, songs

See also: Shamanic music and Imitation of sounds in shamanism

Just like shamanism itself,[68] music and songs related to it in various cultures are diverse, far from being alike. In some cultures and several instances, some songs related to shamanism intend to imitate also natural sounds, sometimes viaonomatopoiea.[69]

Of course, in several cultures, imitation of natural sounds may serve other functions, not necessarily related to shamanism: practical goals as luring game in the hunt;[70] or entertainment (katajjaqs of Inuit).[70][71]

Paraphernalia

Goldes shaman priest in his regalia

Shamans may have various kinds of paraphernalia in different cultures.

Shaman’s drum

Drum – The Drum is used by shamans of several peoples in Siberia; the same holds for many Eskimo groups,[72] although its usage for shamanistic seances may be lacking among the Inuit of Canada.[73]

The beating of the drum allows the shaman to achieve an altered state of consciousness or to travel on a journey. The drum is for example referred to as, “‘horse’ or ‘rainbow-bridge’ between the physical and spiritual worlds”.[74] The journey mentioned is one in which the shaman establishes a connection with one or two of the spirit worlds. With the beating of the drum come neurophysiological effects. Much fascination surround the role that the acoustics of the drum play to the shaman.Siberian shamans’ drums are generally constructed of an animal-skin stretched over a bent wooden hoop, with a handle across the hoop.

The three worlds, the upper, the human, and the lower worlds.

The upper world, including sky spirits is often represented by images such as “climbing a mountain, tree, cliff, rainbow, or ladder; ascending into the sky on smoke; flying on an animal, carpet, or broom and meeting a teacher or guide”,[74] are typical.

The human world consists of what is visible and known to ordinary senses and people.

The lower world consists of underworld or underwater spirits and is often represented by images including, “entering into the earth through a cave, hollow tree stump, a water hole, a tunnel, or a tube”.[74] By being able to interact with the appropriate world in an altered and aware state, the Shaman can then exchange information between the world in which he lives and that to which he has traveled.

Feathers – In numerous cultures, birds are seen as messengers of the spirits. Feathers are often used in ceremonies.

Rattle – Found mostly among South American[75] and African peoples. Also used in ceremonies among the Navajo and in traditional ways in their blessings and ceremonies.

Gong – Often found through South East Asia, Far Eastern peoples.

Pipe Pipe used for smoking various psychoactive herbs (e.g. tobacco in South America, cannabis in India).

Sword – In the Hmong culture, a holly sword will always be used in the practice to protect the shaman from wondering "evil" spirits as he travel to the spirit world.

Shake – Found mostly in the Hmong culture, the shaman begins his practice by rattling, which turns into a shake. It is the process of communicating with his shamanistic spirits to guide him to the spirit world.

Long Table – A flexible wooden table approximately at a size of 9X2. Found in the Hmong Culture, the long table transforms into a "flying horse and boat" in the spirit world.

Rooster – A rooster is often used in the Hmong culture. A shaman uses a rooster when he journeys to the unknown. It is said that the rooster shields the shaman from wandering "evil" spirits by making him invisible, thus the evil spirits only see a worthless rooster’s spirit.

History

Hypotheses on origins

Shamanic practices may originate as early as the paleolithic, predating all organized religions,[76][77] and certainly as early as the Neolithic period.[77]

Archaeological evidence exists for Mesolithic shamanism. In November 2008, researchers announced the discovery of a 12,000-year-old site in Israel that they regard as one of the earliest known shaman burials. The elderly woman had been arranged on her side, with her legs apart and folded inward at the knee. Ten large stones were placed on the head, pelvis and arms. Among her unusual grave goods were 50 complete tortoise shells, a human foot, and certain body parts from animals such as a cow tail and eagle wings. Other animal remains came from a boar, leopard, and two martens. "It seems that the woman … was perceived as being in a close relationship with these animal spirits," researchers noted. The grave was one of at least 28 at the site, located in a cave in lower Galilee and belonging to the Natufian culture, but is said to be unlike any other among the Natufians or in the Paleolithic period.[78]

Decline and revitalization / tradition-preserving movements

A recent photograph: shaman doctor ofKyzyl, 2005. (Details missing). Attempts are being made to preserve and revitalize Tuvanshamanism:[79] some former authentic shamans have begun to practice again, and young apprentices are being educated in an organized way.[80]

In many areas, former shamans ceased to fill the functions in the community they used to, as they felt mocked by their own community,[81] or regarded their own past as a deprecated thing, sometimes even unwilling to talk about it to an ethnographer.[82]

Moreover, besides personal communications of former shamans, even some folklore texts narrate directly about a deterioration process. For example, a Buryat epic text details the wonderful deeds of the ancient “first shaman” Kara-Gürgän:[83] he could even compete with God, create life, steal back the soul of the sick from God without his consent. A subsequent text laments that shamans of older times were stronger, possessing capabilities like omnividence,[84] fortune-telling even for decades in the future, moving as fast as bullet; the texts contrast them to the recent heartless, unknowing, greedy shamans.[85]

In most affected areas, shamanistic practices ceased to exist, with authentic shamans died and their personal experiences following. The loss of memories is not always lessened by the fact the shaman is not always the only person in a community who knows the beliefs and motifs related to the local shamanhood (laics know myths as well, among Barasana, even though less;[42] there are former shaman apprentices unable to complete the learning among some Greenlandic Inuit peoples,[40] moreover, even laics can have trance-like experiences among Eskimos;[43] the assistant of a shaman can be extremely knowledgeable amongOroqen[45][46]). Although the shaman is often believed and trusted exactly because he/she "accommodates" to the "grammar" of the beliefs of the community,[54] but several parts of the knowledge related to the local shamanhood consist of personal experiences of the shaman (illness), or root in his/her family life (the interpretation of the symbolics of his/her drum),[86] thus, these are lost with his/her death. Besides of this, in many cultures, the entire traditional belief system has become endangered (often together with a partial or total language shift), the other people of the community remembering the associated beliefs and practices (or the language at all) became old or died, many folklore memories (songs, texts) went forgotten—this may threaten even such peoples which could preserve their isolation until the middle of the 20th century, like the Nganasan.[87]

Some areas could enjoy a prolonged resistance due to their remoteness.

  • Variants of shamanism among Eskimo peoples were once a widespread (and very diverse) phenomenon, but today are rarely practiced, and they were already in the decline among many groups even in the times when the first major ethnological researches were done,[88] e.g. among Polar Eskimos, in the end of 19th century, Sagloq died, the last shaman who was believed to be able to travel to the sky and under the sea—and many other former shamanic capacities were lost in that time as well, like ventriloquism and sleight-of-hand.[89]
  • The isolated location of Nganasan people allowed shamanism to be a living phenomenon among them even in the beginning of 20th century,[90] the last notable Nganasan shaman’s séances could be recorded on film in the 1970s.[91]

After exemplifying the general decline even in the most remote areas, let us mention that there are some revitalization or tradition-preserving efforts as a response. Besides collecting the memories,[92] there are also some tradition-preserving[93] and even revitalization efforts,[94] sometimes led by authentic former shamans (for example among Sakha people[95] and Tuvans[80]). However, according to Richard L. Allen, Research & Policy Analyst for the Cherokee Nation, they are overwhelmed withfraudulent Shaman. "One may assume that anyone claiming to be a Cherokee "shaman, spiritual healer, or pipe-carrier," is equivalent to a modern day medicine show and snake-oil vendor."[96] In fact, there is no Cherokee word for Shaman or Medicine Man. The Cherokee word for "medicine" is Nvowti which means "power".

Besides tradition-preserving efforts, there are also neoshamanistic movements, these may differ from many tradtitional shamanistic practice and beliefs in several points.[97] Admittedly, several traditional beliefs systems indeed have ecological considerations (for example, many Eskimo peoples), and among Tukano people, the shaman indeed has directly resource-protecting roles, see details in section Ecological aspect.

Today, shamanism survives primarily among indigenous peoples. Shamanic practices continue today in the tundras, jungles, deserts, and other rural areas, and even in cities, towns, suburbs, and shantytowns all over the world. This is especially true for Africa and South America, where "mestizo shamanism" is widespread.

Regional variations

Gender and sexuality

While male shamans are predominant in many cultures, native Korean and some African Nguni cultures have had a preference for females. Recent archaeological evidence suggests that the earliest known shamans—dating to the Upper Paleolithic era in what is now the Czech Republic—were women.[98]

Shamans may exhibit a two-spirit identity, assuming the dress, attributes, role or function of the opposite sex, gender fluidity and/or same-sex sexual orientation. This practice is common, and found among the Chukchi, Sea Dayak, Patagonians,Araucanians, Arapaho, Cheyenne, Navajo, Pawnee, Lakota, and Ute, as well as many other Native American tribes. Indeed, these two-spirited shamans were so widespread as to suggest a very ancient origin of the practice. See, for example, Joseph Campbell‘s map in his The Historical Atlas of World Mythology [Vol I: The Way of the Animal Powers: Part 2: p. 174] Such two-spirit shamans are thought to be especially powerful, and Shamanism so important to ancestral populations that it may have contributed to the maintenance of genes for transgendered individuals in breeding populations over evolutionary time through the mechanism of "kin selection". [see final chapter of E.O. Wilson’s "Sociobiology: The New Synthesis] They are highly respected and sought out in their tribes, as they will bring high status to their mates.

Duality and bisexuality are also found in the shamans of the Dagara people of Burkina Faso (Africa). References to this can be found in several works of Malidoma Somé, a writer who was born and initiated there.

Siberia

Main article: Shamanism in Siberia

Ainu bear sacrifice. Japanese scroll painting, circa 1870.

Among the Siberian Chukchis peoples, a shaman is interpreted as someone who is possessed by a spirit who demands that someone assume the shamanic role for their people. Among the Buryat, there is a ritual known as "shanar" whereby a candidate is consecrated as shaman by another, already-established shaman.

Siberia is regarded as the locus classicus of shamanism.[99] It is inhabited by many different ethnic groups. Many of its Uralic, Altaic, and Paleosiberianpeoples observe shamanistic practices even in modern times. Many classical ethnographic sources of “shamanism” were recorded among Siberian peoples.

Among several Samoyedic peoples shamanism was a living tradition also in modern times, especially at groups living in isolation until recent times (Nganasans).[100] The last notable Nganasan shaman’s seances could be recorded on film in the 1970s.[100][101]

When the People’s Republic of China was formed in 1949 and the border with Russian Siberia was formally sealed, many nomadic Tungus groups that practiced shamanism were confined in Manchuria and Inner Mongolia. These include the Ewenki and the Oroqen. The last shaman of the Oroqen, Chuonnasuan (Meng Jin Fu), died in October 2000.

In many other cases, shamanism was in decline even at the beginning of 20th century (Selkups).[102]

Europe

Sami shamanic drum in the Arctikum museum, in Rovaniemi, Finland

Main articles: Noaide and Sami shamanism

Main article: Finnish mythology

Main articles: Astuvansalmi and Astuvansalmi rock paintings

Main article: shamanistic remnants in Hungarian folklore

While shamanism had a strong tradition in Europe before the rise of monotheism, shamanism remains as a traditional, organized religion in Uralic, Altaic people andHuns; and also in Mari-El and Udmurtia, two semi-autonomous provinces of Russiawith large Finno-Ugric minority populations. Shamanism in Scandinavia may be represented in rock art dating to the Neolithic era[103] and was practiced throughout the Iron Age by the various Teutonic tribes and the Baltic-Finnic peoples.[104] Some peoples, which used to live in Siberia, have wandered to their present locations since then. For example, many Uralic peoples live now outside Siberia, however the original location of the Proto-Uralic peoples (and its extent) is debated. Combinedphytogeographical and linguistic considerations (distribution of various tree species and the presence of their names in various Uralic languages) suggest that this area was north of Central Ural Mountains and on lower and middle parts of Ob River.[105]The ancestors of Hungarian people or Magyars have wandered from their ancestral proto-Uralic area to the Pannonian Basin. Shamanism played an important role inAltaic mythology. Tengriism, the major belief among Xiongnu, Turkic peoples, Magyars and Bulgars in ancient times incorporates elements of shamanism.

There are currently no known historically verifiable accounts that compare the practices of the Druids of Britain to Shamanistic practices though some research has been undertaken regarding the bog bodies [106] in regard to the bodies being shamans and also to Norse seiðr[107] . Shamanism is no more a living practice among Hungarians, but some remnants have been reserved as fragments of folklore, in folktales, customs.[108]

Asia
China

Main article: Wu (shaman)

Chinese shamanism has the longest recorded history in the world. The word wu "shaman; spirit medium; healer" first appeared on oracle bones from the late Shang Dynasty (ca. 1600-1046 BCE). Chinese classics from the Zhou Dynasty (1045-256 BCE) provide details about male and female shamans serving as exorcists, healers, rainmakers, oneiromancers, soothsayers, and officials. Ever since Emperor Wu of Han (r. 141-87 BCE) established Confucianism as the "state religion", the male-dominated Confucian ruling class has marginalized shamanism, especially female shamans. Shamanic practices continue in present day Chinese culture.

Korea

Main article: Korean shamanism

Shamanism is still practiced in South Korea, where the role of a shaman is most frequently taken by women known asmudangs, while male shamans (rare) are called baksoo mudangs. Korean shamans are considered to be from a low class.

A person can become a shaman through hereditary title or through natural ability. Shamans are consulted in contemporary society for financial and marital decisions.

Japan

Main article: Shinto

The Japanese call Shamansim "Shinto," the distinction is that Shinto is Shamanism for agricultural society. Today Shinto has morphed with Buddhism and other Japanese folk culture. The book "Occult Japan: Shinto, Shamanism and the Way of the Gods" by Percival Lowell delves further into researching Japanese Shamanism or Shintoism.[109] It is generally accepted that the vast majority of Japanese people take part in Shinto rituals. The book "Japan Through the Looking Glass: Shaman to Shinto" uncovers the extraordinary aspects of Japanese beliefs[110][111]

Cyprus

The modern-day folk dances of the Middle Eastern island of Cyprus have been argued to originate from ancient shamanist ceremonies and "early religious and incantational worship".[112] The country was one of the last centres of ancient female-lead shamanistic Goddess rites in the Mediterranean, where the so-called Double Goddesses were worshiped.[113] Ancient Cypriot healers used special rituals, charms and incantations in their practices, as well as herbs and spices including frankincense,myrrh, olive oil. Medicine was also linked to the Phoenician gods Astarte and Baal. Healers and magi still exist in Cyprus today,[114][115] and a study by Harvard University suggests that, during Biblical times, "the island of Cyprus was in fact reputed for magia", a variant which was relatively "more recent" than the Persian (Zoroastrian) and Jewish traditions which would have influenced the island.[116] Additionally, Gypsies, who first arrived in Cyprus between 1322 and 1400 from the Levantine mainland, are known for fortune telling by palm reading.[117]

Other Asian traditions

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There is a strong shamanistic influence in the Bön religion of some Central Asians, and in Tibetan Buddhism. Buddhism became popular with shamanic peoples such as the Tibetans, Mongols, and Manchu beginning in the eighth century. Forms of shamanistic ritual combined with Tibetan Buddhism became institutionalized as a major religion under the Mongolian Yuan dynasty and the Manchurian Qing dynasty. However, in the shamanic cultures still practiced by various ethnic groups in areas such as Nepal and northern India, shamans are not necessarily considered enlightened, and often are even feared for their ability to use their power to carry out malicious intent.[citation needed]

Kipchak stone statues of Pontic steppes. The nomadic Kipchak Turks followed a Shamanist religion.

In Tibet, the Nyingma schools in particular, had a Tantric tradition that had married "priests" known as Ngakpas or Ngakmas/mos (fem.). The Ngakpas were often employed or commissioned to rid the villages of demons or disease, creations of protective amulets, the carrying out of religious rites etc. The Ngakpas should however, have been grounded in Buddhist philosophy and not simply another form of shaman, but sadly,[citation needed] this was most often not the case. There have always been, however, highly realised and accomplished ngakpas. They were in their own right great lamas who were of equal status as lamas with monastic backgrounds. The monasteries, as in many conventional religious institutions, wished to preserve their own traditions, sometimes at the expense of others. The monasteries depended upon the excesses of patrons for support. This situation often led to a clash between the more grassroots and shamanic character of the travelling Chödpa and Ngakpaculture and the more conservative religious monastic system.[118][not in citation given]

Shamanism is still widely practiced in the Ryukyu Islands (Okinawa), where shamans are known as ‘Noro’ (all women) and ‘Yuta’. ‘Noro’ generally administer public or communal ceremonies while ‘Yuta’ focus on civil and private matters. Shamanism is also practiced in a few rural areas in Japan proper. It is commonly believed that theShinto religion is the result of the transformation of a shamanistic tradition into a religion. Forms of practice vary somewhat in the several Ryukyu islands, so that there is, e.g., a distinct Miyako shamanism.

Some practices also seem to have been preserved in the Catholic religious traditions of aborigines in Taiwan[119] and someKazakhs.

In Vietnam, shamans conduct rituals in many of the religious traditions that co-mingle in the majority and minority populations. In their rituals, music, dance, special garments and offerings are part of the performance that surround the spirit journey.[120]

Inuit and Eskimo cultures

Yup’ik shaman exorcising evil spirits from a sick boy, Nushagak, Alaska, 1890s.[121]Nushagak, located on Nushagak Bay of the Bering Sea in southwest Alaska, is part of the territory of the Yup’ik, speakers of theCentral Alaskan Yup’ik language

Main article: Shamanism among Eskimo peoples

Eskimo groups comprise a huge area stretching from Eastern Siberia through Alaskaand Northern Canada (including Labrador Peninsula) to Greenland. Shamanistic practice and beliefs have been recorded at several parts of this vast area crosscutting continental borders.[30][43][122]

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When speaking of “shamanism” in various Eskimo groups, we must remember that (as mentioned above) the term “shamanism” can cover certain characteristics ofvarious different cultures.[51] Mediation is regarded often as an important aspect of shamanism in general.[123] Also in most Eskimo groups, the role of mediator is known well:[124] the person filling it in is actually believed to be able to contact the beings who populate the belief system. Term “shaman” is used in several English-language publications also in relation to Eskimos.[43][122][125][126] Also the [aˈliɣnalʁi]of the Asian Eskimos is translated as “shaman” in the Russian[127] and English[124]literature.

The belief system assumes specific links between the living people, the souls of hunted animals, and those of dead people.[128] The soul concepts of several groups are specific examples of soul dualism (showing variability in details in the various cultures).

Unlike the majority of shamanisms the careers of most Eskimo shamans lack the motivation of force: becoming a shaman is usually a result of deliberate consideration, not a necessity forced by the spirits.[40]

Diversity, with some similarities

Another possible concern: do the belief systems of various Eskimo groups have such common features at all, that would justify any mentioning them together? There was no political structure above the groups, their languages were relative, but differed more or less, often forming language continuums (online[129]).

There are some similarities in the cultures of the Eskimo groups[130][131][132][133][134]together with diversity, far from homogeneity.[135]

The Russian linguist Меновщиков, an expert of Siberian Yupik and Sireniki Eskimo languages (while admitting that he is not a specialist in ethnology[136]) mentions, that the shamanistic seances of those Siberian Yupik and Sireniki groups he has seen have many similarities to those of Greenland Inuit groups described by Fridtjof Nansen,[137] although a large distance separates Siberia and Greenland. There may be certain similarities also in Asiatic groups with some North American ones.[138] Also the usage of a specific shaman’s language is documented among several Eskimo groups, used mostly for talking to spirits.[139][140]Also the Ungazighmiit (belonging to Siberian Yupiks) had a special allegoric usage of some expressions.[141]

The local cultures showed great diversity. The myths concerning the role of shaman had several variants, and also the name of their protagonists varied from culture to culture. For example, a mythological figure, usually referred to in the literature by the collective term Sea Woman, has factually many local names: Nerrivik “meat dish” among Polar Inuit, Nuliayuk “lubricous” amongNetsilingmiut, Sedna “the nether one” among Baffin Land Inuit.[142] Also the soul conceptions, e.g. the details of the soul dualismshowed great variability, ranging from guardianship to a kind of reincarnation. Conceptions of spirits or other beings had also many variants (see e.g. the tupilaq concept).[143]

Africa

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Main article: African traditional religion

Some forms of African traditional religion are sometimes also subsumed under "shamanism".[citation needed] In central Mali, Dogon sorcerers (both male and female) claim to have communication with a head deity named Ama, who advises them on healing and divination practices.

In the early 19th century traditional healers in parts of Africa were often referred to in a derogatory manner as "witch doctors"practicing Juju by early European settlers and explorers.The San or Bushmen ancestors who were primarily scattered in Southern Africa before the 19th century, are reported to have practiced a practice similar to shamanism. In areas in Eastern Free State and Lesotho, where they co-existed with the early Sotho tribes, local folklore describes them to have lived in caves where they drew pictures on cave walls during a trance and were also reputed to be good rain makers.

  • The classical meaning of "shaman" as a person who, after recovering from a mental "illness" (of "insanity") takes up the professional calling of socially recognized religious practitioner, is exemplified among the Sisala (of northern Gold Coast) : "the fairies “seized” him and made him insane for several months. Eventually, though, he learned to control their power, which he now uses to divine."[144]
  • The term "sangoma", as employed in Zulu and congeneric languages, is effectively equivalent to ‘shaman’.
  • The term "inyanga" also employed by the nguni cultures is equivalent to ‘herbalist’ as used by the Zulu people and a variation used by the Karanga, among whom remedies for ailments are discovered by the inyanga being informed in a dream, of the herb able to effect the cure and also of where that herb is to be found. The majority of the herbal knowledge base is passed down from one inyanga to the next, often within a particular family circle in any one village.
  • Shamanism is known among the Nuba of Kordofan in Sudan.[145][146]
Americas
North America

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Native American "conjuror" in a 1590 engraving

Hamatsa ritualist, 1914

Native American and First Nations cultures have diverse religious beliefs. There was never one universal Native American religion or spiritual system. Though many Native American cultures have traditional healers, ritualists, singers, mystics, lore-keepers and "Medicine People", none of them ever used, or use, the term "shaman" to describe these religious leaders. Rather, like other indigenous cultures the world over, their spiritual functionaries are described by words in their own languages, and in many cases are not taught to outsiders.

Many of these indigenous religions have been grossly misrepresented by outside observers and anthropologists, even to the extent of superficial or seriously mistaken anthropological accounts being taken as more authentic than the accounts of actual members of the cultures and religions in question. Often these accounts suffer from "Noble Savage"-type romanticism and racism. Some contribute to the fallacy that Native American cultures and religions are something that only existed in the past, and which can be mined for data despite the opinions of Native communities.[147]

Not all Indigenous communities have roles for specific individuals who mediate with the spirit world on behalf of the community. Among those that do have this sort of religious structure, spiritual methods and beliefs may have some commonalities, though many of these commonalities are due to some nations being closely related, from the same region, or through post-Colonial governmental policies leading to the combining of formerly independent nations on reservations. This can sometimes lead to the impression that there is more unity among belief systems than there was in antiquity.

Navajo medicine men, known as "Hatałii", use several methods to diagnose the patient’s ailments. These may include using special tools such as crystal rocks, and abilities such as hand-trembling and trances, sometimes accompanied by chanting. The Hatałii will select a specific healing chant for that type of ailment. Navajo healers must be able to correctly perform a healing ceremony from beginning to end. If they do not, the ceremony will not work. Training a Hatałii to perform ceremonies is extensive, arduous, and takes many years, and is not unlike priesthood. The apprentice learns everything by watching his teacher, and memorizes the words to all the chants. Many times, a medicine man cannot learn all sixty of the traditional ceremonies, so he will opt to specialize in a select few.

Extirpation of Shamanism in North America

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With the arrival of foreign European settlers and colonial administration, the practice of shamanism was discouraged.

During the late 19th Century a shamanic mass movement, the Ghost Dance, swept through many tribes of Native Americans,First Nations. The belief was that through practicing the shamanic dance a great flood would come and all the invading foreigners would die. Some groups, or perhaps this is from other accounts of this movement, focused more on tapping into a separate world without the invaders. This form of shamanism was brutally suppressed by the United States Government’s military. In the massacre of Wounded Knee, a whole band of Lakota Sioux under Chief Big Foot were gunned down with automatic Hotchkiss guns and left to die in a snow storm.

During the last hundred years, thousands of surviving Native Americans, First Nations youngsters from many cultures were sent into Indian boarding schools to destroy any tribal, shamanic or totemic faith.

South America

Panama: Shamanic healing is found among indigenous the Kuna people of Panama, who rely on sacred talismans. As such, they enjoy a popular position among local peoples.

Peru: The Urarina of the Peruvian Amazonia have an elaborate cosmological system predicated on the ritual consumption ofayahuasca. Urarina ayahuasca shamanism is a key feature of this poorly documented society.[148]

Brazil: Among the Brazilian Tapirape shamans are called to serve in their dreams.

Ecuador: The Shuar, seeking the power to defend their family against enemies, would apprentice themselves to become a shaman.

Santo Daime and União do Vegetal ( abbreviated to UDV) are syncretic religions with elements of shamanism. They use anentheogen called Ayahuasca to connect with the spirit realm and receive divine guidance.[41]

Mesoamerican Shamanism

Main article: Maya priesthood

Further information: Mayan astrology

Further information: Maya religion

Maya priest performing a healing ritual atTikal.

The Maya people of Guatemala, Belize, and Southern Mexico practice a highly sophisticated form of shamanism based upon astrology and a form of divination known as "the blood speaking", in which the shaman is guided in divination and healing by pulses in the veins of his arms and legs.

Main article: Aztec priesthood

Further information: Aztec astrology

Further information: Aztec religion

In contemporary Nahuatl, shamanism is known as cualli ohtli (‘the good path’) leading (during dreaming by ‘friends of the night’) to Tlalocán.

Circumpolar Shamanism

Main article: Shamanism among Eskimo peoples

Shamanic practices are also present in tribes in northern Canada, such the animism and shamanism of the Chipewyan and of the Cree.

Amazonia

Shaman from an equatorial Amazonian forest, June 2006

Urarina shaman, 1988

In the Peruvian Amazon Basin and north coastal regions of the country, the healer shamans are known as curanderos. Ayahuasqueros are Peruvian shamans, such as among the Urarina, who specialize in the use of ayahuasca, a psychedelic herbal potion used for physical and psychological healing, divine revelation, and for the very reproduction of society itself.[148] Ayahuasqueros have become popular among Western spiritual seekers, who claim that the shamans and their ayahuasca brews have cured them of everything from depression to addiction to cancer.[41]

In addition to Peruvian shaman’s (curanderos) use of rattles, and their ritualized ingestion of mescaline-bearing San Pedro cactuses (Trichocereus pachanoi) for thedivinization and diagnosis of sorcery, north-coastal shamans are famous throughout the region for their intricately complex and symbolically dense healing altars called mesas (tables). Sharon (1993) has argued that the mesas symbolize the dualistic ideology underpinning the practice and experience of north-coastal shamanism.[149]For Sharon, the mesas are the, "physical embodiment of the supernatural opposition between benevolent and malevolent energies” (Dean 1998:61).[150]

In the Amazon Rainforest, at several Indian groups the shaman acts also as a manager of scarce ecological resources (paper;[33][35] online[67]). The rich symbolism behind Tukano shamanism has been documented in some in-depth field works[33][151][152] even in the last decades of the 20th century. For variations in shamanism among the several Tukano tribes, see : "Shamans, Prophets, Priests, and Pastors." For individual tribes of the Tukano, separate reports have been published, such as "Desana Shamanism".

The yaskomo of the Waiwai is believed to be able to perform a soul flight. The soul flight can serve several functions:

  • healing
  • flying to the sky to consult cosmological beings (the moon or the brother of the moon) to get a name for a new-born baby
  • flying to the cave of peccaries’ mountains to ask the father of peccaries for abundance of game
  • flying deep down in a river, to achieve the help of other beings.

Thus, a yaskomo is believed to be able to reach sky, earth, water, in short, every element.[153]

Shamanism among the Yąnomamö (of the Venezolano Amazonas and the Brazilian Roraima) is described in Tales of the Yanomami by Jacques Lizot.

There is Asuriní shamanism of Pará, Brazil.

Harakmbut shamanism (of Peru) involves curing by dream-interpretion.

Among other literature on South American tropical forest shamanism are:-

Mapuche

Among the Mapuche people of South America, the community "shaman", usually a woman, is known as the Machi, and serves the community by performing ceremonies to cure diseases, ward off evil, influence the weather and harvest, and by practicing other forms of healing such as herbalism.

Fuegians

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Although Fuegians (the indigenous peoples of Tierra del Fuego) were all hunter-gatherers,[154] they did not share a common culture. The material culture was not homogenous, either: the big island and the archipelago made two different adaptations possible. Some of the cultures were coast-dwelling, others were land-oriented.[155][156]

Both Selk’nam and Yámana had persons filling in shaman-like roles. The Selk’nams believed their /xon/s to have supernatural capabilities, e.g. to control weather.[157][158] The figure of /xon/ appeared in myths, too.[159] The Yámana /jekamuʃ/[160]corresponds to the Selknam /xon/.[161]

Oceania

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On the island of Papua New Guinea, indigenous tribes believe that illness and calamity are caused by dark spirits, or masalai, which cling to a person’s body and "poison" them. Shamans, such as the one pictured to the right, are summoned in order to "purge" the unwholesome spirits from a person.[162][163] Shamans also perform rain-making ceremonies and can allegedly improve a hunter’s ability to catch animals.[164]

In Australia various aboriginal groups refer to their "shamans" as "clever men" and "clever women" also as kadji. These Aboriginal shamans use maban or mabain, the material that is believed to give them their purported magical powers. Besides healing, contact with spiritual beings, involvement in initiation and other secret ceremonies, they are also enforcers of tribal laws, keepers of special knowledge and may "hex" to death one who breaks a social taboo by singing a song only known to the "clever men".

See for example, Umbarra (King Merriman).

Contemporary Western Shamanism

Main article: Neoshamanism

There is an endeavor in some contemporary occult and esoteric circles to reinvent shamanism in a modern form, often drawing from core shamanism — a set of beliefs and practices synthesized by Michael Harner — centered use of ritual drumming and dance, and Harner’s interpretations of various indigenous religions. Harner has faced criticism for taking pieces of diverse religions out of their cultural contexts and synthesising a set of universal shamanic techniques. Some neoshamans focus on the ritual use of entheogens, as well as embrace the philosophies of chaos magic whilst others (such as Jan Fries[165]) have created their own forms of shamanism .

European-based Neoshamanic traditions are focused upon the researched or imagined traditions of ancient Europe, where many mystical practices and belief systems were suppressed by the Christian church. Some of these practitioners express a desire to practice a system that is based upon their own ancestral traditions. Some anthropologists and practitioners have discussed the impact of such "neoshamanism" as ‘giving extra pay’ (Harvey, 1997 and elsewhere) to indigenous American traditions, particularly as many Pagan- or Heathen-‘shamanic practitioners’ do not call themselves shamans, but instead use specific names derived from the European traditions -they work within such as völva or seidkona (seid-woman) of the sagas (see Blain 2002, Wallis 2003).

Many New Age spiritual seekers travel to Peru to work with ayahuasqueros, shamans who engage in the ritual use of ayahuasca, a psychedelic tea which has been documented to cure everything from depression to addiction. When taking ayahuasca, participants frequently report meeting spirits and receiving divine revelations.[41] Shamanistic techniques have also been used in New Age therapies which use enactment and association with other realities as an intervention

Criticism of the term “shaman” or “shamanism”

Certain anthropologists, most notably Alice Kehoe in her book Shamans and Religion: An Anthropological Exploration in Critical Thinking, are highly critical of the term. Part of this criticism involves the notion of cultural appropriation.[citation needed] This includes criticism of New Age and modern Western forms of Shamanism, which may not only misrepresent or ‘dilute’ genuine indigenous practices but do so in a way that, according to Kehoe, reinforces racist ideas such as the Noble Savage.

A tableau presenting figures of various cultures filling in mediator-like roles, often being termed as "shaman" in the literature. The tableau presents the diversity of this concept.

Kehoe is highly critical of Mircea Eliade‘s work. Eliade, being a philosopher and historian of religions rather than an anthropologist, had never done any field work or made any direct contact with ‘shamans’ or cultures practicing ‘shamanism’, though he did spend four years studying at the University of Calcutta in India where he received his doctorate based on his Yoga thesis and was acquainted with Mahatma Gandhi. According to Kehoe, Eliade’s ‘shamanism’ is an invention synthesized from various sources unsupported by more direct research. To Kehoe, what some scholars of shamanism treat as being definitive of shamanism, most notably drumming, trance, chanting, entheogens and hallucinogenics, spirit communication and healing, are practices that

  • exist outside of what is defined as shamanism and play similar roles even in non-shamanic cultures (such as the role of chanting in Judeo-Christian rituals)
  • in their expression are unique to each culture that uses them and cannot be generalized easily, accurately or usefully into a global ‘religion’ such as shamanism.

Because of this, Kehoe is also highly critical of the notion that shamanism is an ancient, unchanged, and surviving religion from the Paleolithic period.

Mihály Hoppál also discusses whether the term “shamanism” is appropriate. He recommends using the term “shamanhood”[168]or “shamanship”[169] for stressing the diversity and the specific features of the discussed cultures. This is a term used in old Russian and German ethnographic reports at the beginning of the 20th century. He believes that this term is less general and places more stress on the local variations,[68] and it emphasizes also that shamanism is not a religion of sacred dogmas, but linked to the everyday life in a practical way.[170] Following similar thoughts, he also conjectures a contemporary paradigm shift.[168] Also Piers Vitebsky mentions, that despite really astonishing similarities, there is no unity in shamanism. The various, fragmented shamanistic practices and beliefs coexist with other beliefs everywhere. There is no record of pure shamanistic societies (although, as for the past, their existence is not impossible).[171]

See books and small online materials on this topic.[172]

See also

Notes

  1. ^ Hoppál, Mihály (2005) (in Hungarian). Sámánok Eurázsiában. Budapest: Akadémiai Kiadó. ISBN 963-05-8295-3 2. pp. 77, 287;Znamensky, Andrei A. (2005). "Az ősiség szépsége: altáji török sámánok a szibériai regionális gondolkodásban (1860–1920)". in Molnár, Ádám (in Hungarian). Csodaszarvas. Őstörténet, vallás és néphagyomány. Vol. I. Budapest: Molnár Kiadó. pp. 117–134.ISBN 963 218 200 6., p. 128
  2. ^ Hoppál 1987: 76
  3. ^ Oxford Dictionary Online. us dict: shâ′·mən, shā′·mən.
  4. ^ a b Mircea Eliade, Shamanism, Archaic Techniques of Ecstacy, Bollingen Series LXXVI, Pantheon Books, NYNY 1964, pp. 3-7.
  5. ^ http://www.sozluk.net/index.php?word=%C5%9Faman&sozluk=turkce
  6. ^ http://books.google.com.br/books?id=cb0p1SqkEcgC&printsec=frontcover&hl=tr&source=gbs_v2_summary_r&cad=0#v=onepage&q=turkic%20word&f=false
  7. ^ http://books.google.com.br/books?id=JenWAAAAMAAJ&q=shaman+etymology+turkic&dq=shaman+etymology+turkic&lr=&hl=tr
  8. ^ http://books.google.com.br/books?id=NDVkAAAAMAAJ&q=shaman+etymology+turkic&dq=shaman+etymology+turkic&lr=&hl=tr
  9. ^ Hoppál 2005: 45
  10. ^ Boglár 2001: 24
  11. ^ Hoppál 2005: 94
  12. ^ Vitebsky 1996: 46
  13. ^ a b Hoppál 2005: 25
  14. ^ a b Sem, Tatyana. "Shamanic Healing Rituals". Russian Museum of Ethnography.
  15. ^ Hoppál 2005: 27–28
  16. ^ Hoppál 2005: 28–33
  17. ^ Hoppál 2005: 37
  18. ^ Hoppál 2005: 34–35
  19. ^ Hoppál 2005: 36
  20. ^ Eliade 1964: 4
  21. ^ Hoppál 2005:36164
  22. ^ Hoppál 2005:87–95
  23. ^ Czaplicka 1914
  24. ^ a b Salak, Kira. ""Lost souls of the Peyote Trail"". National Geographic Adventure.
  25. ^ Merkur 1985: 4
  26. ^ Vitebsky 1996: 11, 12–14, 107
  27. ^ Hoppál 2005:27, 30, 36
  28. ^ Hoppál 2005: 27
  29. ^ Kleivan & Sonne 1985: 7, 19–21
  30. ^ a b Gabus, Jean: A karibu eszkimók. Gondolat Kiadó, Budapest, 1970. (Hungarian translation of the original: Vie et coutumes des Esquimaux Caribous, Libraire Payot Lausanne, 1944.) It describes the life of Caribou Eskimo groups.
  31. ^ Hoppál 2007c: 18
  32. ^ Hoppál 2005: 99
  33. ^ a b c d Reichel-Dolmatoff 1997
  34. ^ Vitebsky 1996:107
  35. ^ a b Boglár 2001:26
  36. ^ Merkur 1985: 5
  37. ^ Vitebsky 1996:108
  38. ^ Kleivan & Sonne: 27–28
  39. ^ a b Merkur 1985: 3
  40. ^ a b c d Kleivan & Sonne 1985: 24
  41. ^ a b c d e f g h Salak, Kira. ""Hell and Back"". National Geographic Adventure.
  42. ^ a b Stephen Hugh-Jones 1980: 32
  43. ^ a b c d e Merkur 1985
  44. ^ Kleivan & Sonne 1985: 8–10
  45. ^ a b Noll & Shi 2004: 10, footnote 10 (see online)
  46. ^ a b Noll & Shi 2004: 8–9 (see online)
  47. ^ Turner et al., page 440
  48. ^ Noll & Shi 2004 (see online)
  49. ^ Diószegi 1962:13
  50. ^ a b Hoppál 2005:14
  51. ^ a b c Hoppál 2005:15
  52. ^ Pentikäinen 1995: 270
  53. ^ Boglár 2001:24
  54. ^ a b c Hoppál 2005:25–26,43
  55. ^ Hoppál 2004:14
  56. ^ Hoppál 2005: 13–15, 58, 197
  57. ^ Hoppál 2006a: 11
  58. ^ Hoppál 2006b: 175
  59. ^ Hoppál 2007c: 24–25
  60. ^ a b Hoppál, Mihály: Nature worship in Siberian shamanism
  61. ^ Hoppál 2007b: 12–13
  62. ^ a b c Hoppál 2007c: 25
  63. ^ Pentikäinen 1995: 270–271
  64. ^ Dana 2004: 18 (see online)
  65. ^ Merkur 1985:v
  66. ^ Hoppál 2007b: 13
  67. ^ a b Gerardo Reichel-Dolmatoff: A View from the Headwaters. The Ecologist, Vol. 29 No. 4, July 1999.
  68. ^ a b Hoppál 2005: 15
  69. ^ Hoppál 2006c: 143
  70. ^ a b Nattiez: 5
  71. ^ Deschênes 2002
  72. ^ Barüske 1969: 24, 50–51
  73. ^ Kleivan & Sonne 1985: 25
  74. ^ a b c Maxfield, Melinda. "The journey of the drum." ReVision 16.4 (1994): 157.
  75. ^ Vitebsky 1996: 49
  76. ^ Jean Clottes. "Shamanism in Prehistory". Bradshaw foundation. Retrieved 2008-03-11.
  77. ^ a b Karl J. Narr. "Prehistoric religion". Britannica online encyclopedia 2008. Retrieved 2008-03-28.
  78. ^ "Earliest known shaman grave site found: study," reported by Reuters via Yahoo! News, November 4, 2008, archived.see.Proceedings of the National Academy of Sciences.
  79. ^ Hoppál 2005: 117
  80. ^ a b Hoppál 2005: 259
  81. ^ Boglár 2001: 19–20
  82. ^ Diószegi 1960: 37–39
  83. ^ Eliade 2001: 76 (= Chpt 3 about obtaining shamanic capabilities)
  84. ^ Omnividence: A word created by Edwin A. Abbott in his book titled Flatland
  85. ^ Diószegi 1960: 88–89
  86. ^ Hoppál 2005: 224
  87. ^ Nagy 1998: 232
  88. ^ Merkur 1985:132
  89. ^ Merkur 1985:134
  90. ^ Hoppál 2005: 92
  91. ^ Hoppál 1994: 62
  92. ^ Hoppál 2005: 88
  93. ^ Hoppál 2005: 93
  94. ^ Hoppál 2005: 111, 117–119, 128, 132, 133–134, 252-263
  95. ^ Hoppál 2005: 257–258
  96. ^ "Pseudo Shamans Cherokee Statement". Retrieved 2008-06-23.
  97. ^ Vitebsky 1996: 150–153
  98. ^ Tedlock, Barbara. 2005. The Woman in the Shaman’s Body: Reclaiming the Feminine in Religion and Medicine. New York: Bantam.
  99. ^ Hoppál 2005:13
  100. ^ a b Hoppál 2005:92–93
  101. ^ Hoppál 1994:62
  102. ^ Hoppál 2005:94
  103. ^ Bolin 2000: 157
  104. ^ A. Asbjorn Jon, Shamanism and the Image of the Teutonic Deity, Óðinn
  105. ^ Hajdú 1975:35
  106. ^ The Quest for the Shaman:Miranda & Stephen Aldhouse-Green ISBN 0-500-05134-8
  107. ^ Nine Worlds of Seid-Magic:Jenny Blain ISBN 0-415-25651-8
  108. ^ Diószegi 1998
  109. ^ Percival Lowell, Occult Japan: Shinto, Shamanism and the Way of the Gods, Inner Traditions International (April 1990), Rochester Vt
  110. ^ Alan Mcfarlane, Japan Through the Looking Glass: Shaman to Shinto, Profile Books Ltd, Aug 2007, London England
  111. ^ http://search.japantimes.co.jp/cgi-bin/fb20071007a1.html
  112. ^ "Cyprus Culture Folk Dancing", Cyprus.com
  113. ^ Noble, Vicki, The Double Goddess: Women Sharing Power, 2003
  114. ^ Gravenore, Kristian, "Magus In Training", Montreal Mirror, April 15, 2004
  115. ^ King, Serge Kahili, Urban Shaman, November 1990
  116. ^ South, Alison, "Elvis Found in Bronze Age Tomb", Harvard University & Cyprus American Archaelogical Research Institute, December 2000
  117. ^ Dr. Williams, G. A., "The Gypsies of Cyprus", Dom Research Center, March 2000
  118. ^ Economy of Excess. George Bataille.
  119. ^ O. Lardenois, Shamanism and Catholic Indigenous Communities in Taiwan
  120. ^ "Journeys to Other Worlds: The Rites of Shamans". American Museum of Natural History.
  121. ^ Fienup-Riordan, Ann. 1994:206
  122. ^ a b Kleivan & Sonne 1985
  123. ^ Hoppál 2005:45–50
  124. ^ a b Menovščikov 1996:442
  125. ^ Vitebsky 1996
  126. ^ Freuchen 1961: 32
  127. ^ Рубцова 1954: 203, 209
  128. ^ Both death of a person and successfully hunted game require that cutting, sewing etc. be tabooed, so that the invisible soul does not get hurt accidentally (Kleivan&Sonne, pp. 18–21). In Greenland, the transgression of death tabu could turn the soul of the dead into a tupilak, a restless ghost which scared game away (Kleivan&Sonne 1985, p. 23). Animals fleed from hunter in case of taboo breaches, e.g. birth taboo, death taboo (Kleivan&Sonne, pp. 12–13)
  129. ^ Lawrence Kaplan: Comparative Yupik and Inuit (found on the site of Alaska Native Language Center)
  130. ^ Kleivan 1985:8
  131. ^ Rasmussen 1965:366 (ch. XXIII)
  132. ^ Rasmussen 1965:166 (ch. XIII)
  133. ^ Rasmussen 1965:110 (ch. VIII)
  134. ^ Mauss 1979
  135. ^ Kleivan 1985:26
  136. ^ Menovščikov 1996 [1968]:433
  137. ^ Menovščikov 1996 [1968]:442
  138. ^ Vitebsky 1996:42 (ch. North America)
  139. ^ Merkur 1985:7
  140. ^ Kleivan & Sonne 1985:14
  141. ^ Rubcova 1954:128
  142. ^ Kleivan & Sonne 1985: 27
  143. ^ Kleivan & Sonne 1985: 30–31
  144. ^ Eugene L. Mendonsa : The Politics of Divination : a Processual View of Reactions to Illness and Deviance among the Sisala. University of California Press, Berkeley, 1982. p. 112
  145. ^ Nadel, S.F. "A Shaman Cult in the Nuba Mountains". Sudan Notes and Records 1941; 24(l): 85-112
  146. ^ Nadel, S.F. "A Study of Shamanism in the Nuba Mountains". Journal of the Royal Anthropological Institute 1946; 76:25-37
  147. ^ Jones, Peter N. 2008 Shamans and Shamanism: A Comprehensive Bibliography of the Terms Use in North America. Boulder, CO: Bauu Press.
  148. ^ a b Dean, Bartholomew 2009 Urarina Society, Cosmology, and History in Peruvian Amazonia, Gainesville: University Press of Florida ISBN 978-081303378 [1]
  149. ^ Joralemen, D and D Sharon 1993 Sorcery and Shamanism: Curanderos and Clients in Northern Peru. Salt Lake City: University of Utah Press.
  150. ^ Dean, Bartholomew 1998 “Review of Sorcery and Shamanism: Curanderos and Clients in Northern Peru” American Ethnologist. 25(1): 61-62.
  151. ^ Christine Hugh-Jones 1980
  152. ^ Stephen Hugh-Jones 1980
  153. ^ Fock 1963: 16
  154. ^ Gusinde 1966, pp. 6–7
  155. ^ Service, Elman: The Hunter. Prentice-Hall, 1966.
  156. ^ Extinct Ancient Societies Tierra del Fuegians
  157. ^ Gusinde 1966:175
  158. ^ About the Ona Indian Culture in Tierra del Fuego
  159. ^ Gusinde 1966:15
  160. ^ Gusinde 1966:156
  161. ^ Gusinde 1966:186
  162. ^ "Amazon.com listing for the "Four Corners: A Journey into the Heart of Papua New Guinea"".
  163. ^ Salak, Kira. "Kira Salak’s official webpage on "Four Corners"".
  164. ^ Salak, Kira. "MAKING RAIN–from Four Corners"".
  165. ^ Visual Magic:A Manual of Freestyle Shamanism:Jan Fries ISBN 1-869928-57-1
  166. ^ ULL – Universidad de La Laguna (Spanish)
  167. ^ Encyclopedia of NLP
  168. ^ a b ISSR, 2001 Summer, abstract online in 2nd half of 2nd paragraph)
  169. ^ Hoppál & Szathmári & Takács 2006: 14
  170. ^ Hoppál 1998:40
  171. ^ Vitebsky 1996:11
  172. ^ Books relating to “shamanhood”, some of them with online abstract:
    • (Online abstract) Pentikäinen, Juha. Shamanhood symbolism and epic. Akadémiai Kiadó, Budapest, 2001. ISBN 963-05-7811-5.
    • Pentikäinen, Juha and Simoncsics, Péter (eds): Shamanhood. An endangered language. The Institute for Comparative Research in Human Culture, 2005. (Series B, 117). ISBN 82-7099-391-3.

    See also similar online abstracts.

References

  • Barüske, Heinz (1969) (in German). Eskimo Märchen. Die Märchen der Weltliteratur. Düsseldorf • Köln: Eugen Diederichs Verlag. The title means: “Eskimo tales”, the series means: “The tales of world literature”.
  • Boglár, Lajos (2001) (in Hungarian). A kultúra arcai. Mozaikok a kulturális antropológia köreiből. TÁRStudomány. Budapest: Napvilág Kiadó. ISBN 963 908294 5. The title means “The faces of culture. Mosaics fom the area of cultural anthropology”.
  • Bolin, Hans. "Animal Magic: The mythological significance of elks, boats and humansin north Swedish rock art.". Journal of Material Culture. Vol. 5(2): 153-176..
  • Czaplicka, M. A. (1914). "Types of shaman". Shamanism in Siberia. Aboriginal Siberia. A study in social anthropology. preface by Marett, R. R.. Sommerville College, University of Oxford, Clarendon Press.
  • Dana, Kathleen Osgood (2004 summer). "Áillohaš and his image drum: the native poet as shaman" (pdf). Nordlit (Faculty of Humanities, University of Tromsø) 15.
  • Deschênes, Bruno (2002). "Inuit Throat-Singing". Musical Traditions. The Magazine for Traditional Music Throughout the World.
  • Diószegi, Vilmos (1960) (in Hungarian). Sámánok nyomában Szibéria földjén. Egy néprajzi kutatóút története. Budapest: Magvető Könyvkiadó. The book has been translated to English: Diószegi, Vilmos (1968). Tracing shamans in Siberia. The story of an ethnographical research expedition. Translated from Hungarian by Anita Rajkay Babó. Oosterhout: Anthropological Publications.
  • Diószegi, Vilmos (1962) (in Hungarian). Samanizmus. Élet és Tudomány Kiskönyvtár. Budapest: Gondolat. The title means: “Shamanism”.
  • Diószegi, Vilmos (1998) [1958] (in Hungarian). A sámánhit emlékei a magyar népi műveltségben (first reprint ed.). Budapest: Akadémiai Kiadó. ISBN 963 05 7542 6. The title means: “Remnants of shamanistic beliefs in Hungarian folklore”.
  • Eliade, Mircea (1983). Le chamanisme et les techniques archaïques de’l extase. Paris: Éditions Payot.
  • Eliade, Mircea (2001) (in Hungarian). A samanizmus. Az extázis ősi technikái. Budapest: Osiris. ISBN 963 379 755 1. Translated from Eliade 1983.
  • Fienup-Riordan, Ann (1994). Boundaries and Passages: Rule and Ritual in Yup’ik Eskimo Oral Tradition. Norman, OK: University of Oklahoma Press.
  • Fock, Niels (1963). Waiwai. Religion and society of an Amazonian tribe. Nationalmuseets skrifter, Etnografisk Række (Ethnographical series), VIII. Copenhagen: The National Museum of Denmark.
  • Freuchen, Peter (1961). Book of the Eskimos. Cleveland • New York: The World Publishing Company.
  • Gusinde, Martin (1966) (in German). Nordwind—Südwind. Mythen und Märchen der Feuerlandindianer.. Kassel: E. Röth. The title means: “Northern wind, southern wind. Myths and tales of Fuegians”.
  • Hajdú, Péter (1975). "A rokonság nyelvi háttere". in Hajdú, Péter (in Hungarian). Uráli népek. Nyelvrokonaink kultúrája és hagyományai. Budapest: Corvina Kiadó. ISBN 963 13 0900 2. The title means: “Uralic peoples. Culture and traditions of our linguistic relatives”; the chapter means “Linguistical background of the relationship”.
  • Hoppál, Mihály (1987), Shamanism: An Archaic and/or Recent System of Beliefs., Nicholson, Shirley, "Shamanism", Quest Books; 1st edition (May 25, 1987), p. 76, ISBN 0835606171
  • Hoppál, Mihály (1994) (in Hungarian). Sámánok, lelkek és jelképek. Budapest: Helikon Kiadó. ISBN 963 208 298 2. The title means “Shamans, souls and symbols”.
  • Hoppál, Mihály (1998). "A honfoglalók hitvilága és a magyar samanizmus" (in Hungarian). Folklór és közösség. Budapest: Széphalom Könyvműhely. pp. 40–45. ISBN 963 9028 142. The title means “The belief system of Hungarians when they entered the Pannonian Basin, and their shamanism”.
  • Hoppál, Mihály (2005) (in Hungarian). Sámánok Eurázsiában. Budapest: Akadémiai Kiadó. ISBN 963-05-8295-3. The title means “Shamans in Eurasia”, the book is published also in German, Estonian and Finnish. Site of publisher with short description on the book (in Hungarian).
  • Hoppál, Mihály (2006a). "Sámánok, kultúrák és kutatók az ezredfordulón". in Hoppál, Mihály & Szathmári, Botond & Takács, András.Sámánok és kultúrák. Budapest: Gondolat. pp. 9–25. ISBN 963 9450 286. The chapter title means “Shamans, cultures and researchers in the millenary”, the book title means “Shamans and cultures”.
  • Hoppál, Mihály (2006b). "Sámánság a nyenyecek között". in Hoppál, Mihály & Szathmári, Botond & Takács, András. Sámánok és kultúrák. Budapest: Gondolat. pp. 170–182. ISBN 963 9450 286. The chapter title means “Shamanhood among the Nenets”, the book title means “Shamans and cultures”.
  • Hoppál, Mihály (2006c). "Music of Shamanic Healing". in Gerhard Kilger. Macht Musik. Musik als Glück und Nutzen für das Leben. Köln: Wienand Verlag. ISBN 3879098654.
  • Hoppál, Mihály (2007b). "Is Shamanism a Folk Religion?". Shamans and Traditions (Vol 13). Bibliotheca Shamanistica. Budapest: Akadémiai Kiadó. pp. 11–16. ISBN 978 963 05 8521 7.
  • Hoppál, Mihály (2007c). "Eco-Animism of Siberian Shamanhood". Shamans and Traditions (Vol 13). Bibliotheca Shamanistica. Budapest: Akadémiai Kiadó. pp. 17–26. ISBN 978 963 05 8521 7.
  • Hugh-Jones, Christine (1980). From the Milk River: Spatial and Temporal Processes in Northwest Amazonia. Cambridge Studies in Social and Cultural Anthropology. Cambridge University Press.
  • Hugh-Jones, Stephen (1980). The Palm and the Pleiades. Initiation and Cosmology in Northwest Amazonia. Cambridge Studies in Social and Cultural Anthropology. Cambridge University Press.
  • Kleivan, Inge; B. Sonne (1985). Eskimos: Greenland and Canada. Iconography of religions, section VIII, "Arctic Peoples", fascicle 2. Leiden, The Netherlands: Institute of Religious Iconography • State University Groningen. E.J. Brill. ISBN 90-04-07160-1.
  • Lawlor, Robert (1991). Voices Of The First Day: Awakening in the Aboriginal dreamtime. Rochester, Vermont: Inner Traditions International, Ltd. ISBN 0-89281-355-5
  • Menovščikov, G. A. (= Г. А. Меновщиков) (1968). "Popular Conceptions, Religious Beliefs and Rites of the Asiatic Eskimoes". in Diószegi, Vilmos. Popular beliefs and folklore tradition in Siberia. Budapest: Akadémiai Kiadó.
  • Merkur, Daniel (1985). Becoming Half Hidden: Shamanism and Initiation among the Inuit. Stockholm: Almqvist & Wiksell. ISBN 91-22-00752-0.
  • Nagy, Beáta Boglárka (1998). "Az északi szamojédok". in Csepregi, Márta (in Hungarian). Finnugor kalauz. Panoráma. Budapest: Medicina Könyvkiadó. pp. 221–234. ISBN 963 243 813 2. The chapter means “Northern Samoyedic peoples”, the title means Finno-Ugric guide.
  • Nattiez, Jean Jacques. Inuit Games and Songs • Chants et Jeux des Inuit. Musiques & musiciens du monde • Musics & musicians of the world. Montreal: Research Group in Musical Semiotics, Faculty of Music, University of Montreal.. The songs are online availablefrom the ethnopoetics website curated by Jerome Rothenberg.
  • Noll, Richard; Shi, Kun. "Chuonnasuan (Meng Jin Fu), The Last Shaman of the Oroqen of Northeast China" (PDF). 韓國宗敎硏究 (Journal of Korean Religions) (Seoul KR: 西江大學校. 宗教硏究所 (Sŏgang Taehakkyo. Chonggyo Yŏnʾguso.)) 6: pp. 135–162. 2004. Retrieved 2008-07-30.. It describes the life of Chuonnasuan, the last shaman of the Oroqen of Northeast China.
  • Pentikäinen, Juha (1995). "The Revival of Shamanism in the Contemporary North". in Tae-gon Kim & Mihály Hoppál. Shamanism in Performing Arts. Bibiotheca Shamanistica (Vol. 1). Budapest: Akadémiai Kiadó. pp. 263–272. ISBN 963 05 6848 9.
  • Reichel-Dolmatoff, Gerardo (1997). Rainforest Shamans: Essays on the Tukano Indians of the Northwest Amazon. Dartington: Themis Books. ISBN 0-9527302-4-3.
  • Reinhard,, Johan (1976) "Shamanism and Spirit Possession: The Definition Problem." In Spirit Possession in the Nepal Himalayas, J. Hitchcock & R. Jones (eds.), New Delhi: Vikas Publishing House, pp. 12–20.
  • Turner, Robert P.; Lukoff, David; Barnhouse, Ruth Tiffany & Lu, Francis G. (1995) Religious or Spiritual Problem. A Culturally Sensitive Diagnostic Category in the DSM-IV. Journal of Nervous and Mental Disease, Vol.183, No. 7, pp. 435–444
  • Vitebsky, Piers (1995). The Shaman (Living Wisdom). Duncan Baird.
  • Vitebsky, Piers (1996) (in Hungarian). A sámán. Bölcsesség • hit • mítosz. Budapest: Magyar Könyvklub • Helikon Kiadó. ISBN 963 208 361 X. Translation of Vitebsky 1995
  • Vitebsky, Piers (2001). The Shaman: Voyages of the Soul – Trance, Ecstasy and Healing from Siberia to the Amazon. Duncan Baird.ISBN 1-903296-18-8.
  • Voigt, Vilmos (1966) (in Hungarian). A varázsdob és a látó asszonyok. Lapp népmesék. Népek meséi. Budapest: Európa Könyvkiadó. The title means: “The magic drum and the clairvoyant women. Sami folktales”, the series means: “Tales of folks”.
  • Voigt, Miklós (2000). "Sámán — a szó és értelme" (in Hungarian). Világnak kezdetétől fogva. Történeti folklorisztikai tanulmányok. Budapest: Universitas Könyvkiadó. pp. 41–45. ISBN 963 9104 39 6. The chapter discusses the etymology and meaning of word “shaman”.

Further reading

  • Joseph Campbell, The Masks of God: Primitive Mythology. 1959; reprint, New York and London: Penguin Books, 1976. ISBN 0-14-019443-6
  • Richard de Mille, ed. The Don Juan Papers: Further Castaneda Controversies. Santa Barbara, CA: Ross-Erikson, 1980.
  • George Devereux, "Shamans as Neurotics", American Anthropologist, New Series, Vol. 63, No. 5, Part 1. (Oct., 1961), pp. 1088–1090.
  • Jay Courtney Fikes, Carlos Castaneda: Academic Opportunism and the Psychedelic Sixties, Millennia Press, Canada, 1993ISBN 0-9696960-0-0
  • Graham Harvey, ed. Shamanism: A Reader. New York and London: Routledge, 2003. ISBN 0-415-25330-6.
  • Åke Hultkrantz (Honorary Editor in Chief): Shaman. Journal of the International Society for Shamanistic Research
  • Philip Jenkins, Dream Catchers: How Mainstream America Discovered Native Spirituality. New York: Oxford University Press, 2004.ISBN 0-19-516115-7
  • Alice Kehoe, Shamans and Religion: An Anthropological Exploration in Critical Thinking. 2000. London: Waveland Press. ISBN 1-57766-162-1
  • Åke Ohlmarks 1939: Studien zum Problem des Schamanismus. Gleerup, Lund.
  • Jordan D. Paper, The Spirits are Drunk: Comparative Approaches to Chinese Religion, Albany, New York: State University of New York Press, 1995. ISBN 0-7914-2315-8
  • Malidoma Patrice Some. Of Water and the Spirit: Ritual, Magi, and Initiaion in the Life of an African Shaman. New York: Penguin Group. 1994. ISBN 0-87477-762-3
  • Barbara Tedlock, Time and the Highland Maya,U. of New Mexico Press, 1992. ISBN 0-8263-1358-2
  • Piers Vitebsky, The Shaman: Voyages of the Soul – Trance, Ecstasy and Healing from Siberia to the Amazon, Duncan Baird, 2001.ISBN 1-903296-18-8
  • Michael Winkelman, (2000) Shamanism: The Neural Ecology of Consciousness and Healing. Westport, CT: Bergin & Garvey.
  • Andrei Znamenski, ed. Shamanism: Critical Concepts, 3 vols. London: Routledge, 2004. ISBN 0-415-31192-6
  • Andrei Znamenski, Shamanism in Siberia: Russian Records of Siberian Spirituality. Dordrech and Boston: Kluwer/Springer, 2003.ISBN 1-4020-1740-5
  • Andrei Znamenski, The Beauty of the Primitive: Shamanism and the Western Imagination.Oxford and New York: Oxford University Press, 2007. ISBN 0-19-517231-0
  • 色音, 东北亚的萨满教:韩中日俄蒙萨满教比较研究(Northeast Asia Shamanism: Compare studies of Shamanism in Korea, China, Japan, Russia and Mongolia).中国社会科学出版社, Mar. 1998. ISBN 7-5004-2193-1

External links

 

 

Amanita muscaria

Amanita muscaria

A. muscaria
showing various growth stages

Scientific classification

Kingdom:
Fungi

Phylum:
Basidiomycota

Class:
Agaricomycetes

Order:
Agaricales

Family:
Amanitaceae

Genus:
Amanita

Species:
Amanita muscaria
(L.:Fr.) Lam.

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 basidiomycetefungus, one of many in the genus Amanita. Native throughout the temperate andboreal 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. Itassociates 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, andformosa, 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. 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 Wassonproposed the fly agaric was in fact the Soma talked about in the ancient Rig Vedatexts of India; since its introduction in 1968, this theory has gained both detractors and followers in the anthropological literature.[1]

Taxonomy and naming

Amanita muscaria var. formosa

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 vegetabilibussometime 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 botanistCarolus 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] thespecific 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 sanctionedby 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, the 1987 edition of the International Code of Botanical Nomenclature 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 andBiscay is amoroto, further there is Old Danish paddhe stool, Danish paddehat, Dutch padde(n) stoel, Middle Low Germanpaddenstol, 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 var. formosa sensu Thiers, southern Oregon Coast

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 inamyloidspores. Amanita section Amanita includes those species with patchy universal veilremnants, 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. muscariaand its close relatives, including A. pantherina (the panther cap), A. gemmata, A. farinosa, and A. xanthocephala.[22] Modern fungal taxonomists have classifiedAmanita 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 allA. muscaria fitting this description worldwide (cf. Jenkins), others (cf. Tulloss) restrict its use to Eurasian populations.[21][28]

Amanita muscaria var. guessowii has a yellow cap surface.
Middlesex Fells, Massachusetts

  • 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 toTennessee. 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. muscariaby 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. muscariaas 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 gillsare 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 in a Pinus radiata plantation, near Mount Field National Park, Tasmania

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 theSiberianBeringian 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, Tasmaniaand 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 receptorsleading 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 majorneurotransmitters of the central nervous system: glutamic acid and GABArespectively. 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 anorganometallic compound called amavadine.[79] However, the biological importance of the accumulation process is unknown.[80]

Other chemical contents of the fungus:

Bufotenine – 5-HO-DMT (Waser, 1979) Amavadin: a vanadium compound (Kneifel et al., 1986). Stizolobic and Stizolobinic acid: L-DOPA oxidation products (Chilton et al. 1974; Bresinsky and Besl, 1985). Muscaflavin, Muscaurin: colorant principles (Depovere & Moens 1984) Muscarine (Eugster, 1979)

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 andsalivation), 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 amnesiaand 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 atmuscarinic 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 ofconsciousness 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. muscariamushrooms began to be sold and consumed.[88] Professor Marija Gimbutas, the renowned Lithuanian prehistorian, had reported to R. Gordon Wasson on the use down to our own day of Amanita muscaria in the remoter parts of Lithuania at wedding feasts and the like when the mushrooms were mixed with vodka, and also how the Lithuanians used to export quantities of A. muscaria to the Lapps in the Far North for use in their shamanic practices. Here in the Lithuanian festivities was the only report that Wasson had received of the ingestion of the fly-agaric in Eastern Europe for jollification ends.[89]

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.[90] In western Siberia, the use of A. muscariawas 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.[90] In eastern Siberia, the shaman would consume the mushrooms, and others would drink his urine.[91] 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.[92]

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.[93] Among the Koryak, one report held the poor would consume the urine of the wealthy, who could afford to buy the mushrooms.[94]

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.[95] 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.[96] There are also unconfirmed reports of religious use of A. muscaria among two Subarctic Native American tribes. Ojibwa ethnobotanistKeewaydinoquay Peschel reported its use among her people, where it was known as the miskwedo.[97][98] This information was enthusiastically received by Wasson, although evidence from other sources was lacking.[99] There is also one account of a Euro-American who claims to have been initiated into traditional Tlicho use of Amanita muscaria.[100]

Soma

See also: Botanical identity of Soma-Haoma

In 1968, R. Gordon Wasson proposed that A. muscaria was the Soma talked about in the Rig Veda of India,[101] which received widespread publicity and popular support at the time.[102] He noted that descriptions of Soma omitted description of roots, stems or seeds, which suggested a mushroom,[103] and used the adjective hári "dazzling" or "flaming" which the author interprets as red.[104] 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.[105] 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.[106] 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.[107] 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.[1]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 Basilicaof 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 ofethnomycology. 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, andJohn 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 ofA. 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, notablymorels, are toxic unless properly cooked.[69]

Cultural depictions

Children play on Jose de Creeft‘s sculpture Alice in Wonderland inCentral Park, New York. Alice sits atop a mushroom, inviting children to climb up and join her. Whilst the mushroom in the sculpture is not a faithfully reproduced Amanita muscaria, the reference within Lewis Carrol‘s original literary work upon which the sculpture is based is often discussed.[118][119]

Moritz von Schwind‘s 1851 paintingRuebezahl features fly agarics.[120]

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][121] Fly agarics have been featured in paintings since theRenaissance,[122] albeit in a subtle manner. In the Victorian erathey became more visible, even becoming the main topic of some fairy paintings.[123] Two of the most famous uses of the mushroom are in the video game series Super Mario Bros.,[124]and the dancing mushroom sequence in the 1940 Disney filmFantasia.[125]

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.[126] The mushroom had been identified as the fly agaric by this time.[127] 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.[128] 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.[129] 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;[130] fly agaric shamanism is explored more recently in the 2003 novel Thursbitch by Alan Garner.[131]

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.[132] 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.[133] American ethnopharmacologist Scott Hajicek-Dobberstein, researching possible links between religious myths and the red mushroom, notes, "If Santa Claus had but one eye [likeOdin], or if magic urine had been a part of his legend, his connection to the Amanita muscaria would be much easier to believe.".[134]

The connection was reported to a much wider audience with an article in the magazine of The Sunday Times in 1980,[135] andNew Scientist in 1986.[136] Historian Ronald Hutton has since disputed the connection;[137] 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 inyurt roofs. Finally, American awareness of Siberian shamanism postdated the appearance of much of the folklore around Santa.[138]

See also

Karl Johanssvamp, Iduns kokbok.png
Fungi portal

References

  1. ^ a b 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, pp 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.
  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, pp 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). 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. 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 (Mycological Society of America) 91 (4): 610–18.doi:10.2307/3761246. 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.. Retrieved 2009-02-14.
  26. ^ Tulloss RE; Yang Z-L. (2008). "Amanita muscaria subsp. flavivolvata Singer". Studies in the Genus Amanita Pers. (Agaricales, Fungi). 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). 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). 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). 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)" (PDF). Molecular Ecology 15 (1): 225–39. doi:10.1111/j.1365-294X.2005.02799.x.PMID 16367842.
  33. ^ Geml J; Tulloss RE; Laursen GA, et al. (2008). "Evidence for strong inter- and intracontinental phylogeographic structure inAmanita muscaria, a wind-dispersed ectomycorrhizal basidiomycete". Molecular Phylogenetics and Evolution 48 (2): 694–701.doi:10.1016/j.ympev.2008.04.029. PMID 18547823. 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.. 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.. 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.. 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 BotanySupplementary 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.
  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. p. 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.
  51. ^ Keane PJ; Kile GA.; Podger FD (2000). Diseases and pathogens of eucalypts. Canberra: CSIRO Publishing. p. 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. PMID 18568796.
  54. ^ Benjamin, Mushrooms: poisons and panaceas, pp 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" (PDF). New York Times. 19 December1897. 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. 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. 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.
  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. ^ Wasson, R. Gordon. The Wondrous Mushroom: Mycolatry in Mesoamerica, pp43–44
  90. ^ a b Nyberg, H. (1992). "Religious use of hallucinogenic fungi: A comparison between Siberian and Mesoamerican Cultures".Karstenia 32 (71–80).
  91. ^ Wasson, Soma: Divine Mushroom of Immortality, p 161.
  92. ^ Diaz, J. (1996). How Drugs Influence Behavior: A Neurobehavioral Approach. Upper Saddle River, N.J.: Prentice Hall. ISBN 0023287640.
  93. ^ Ramsbottom, p 45.
  94. ^ Wasson, Soma: Divine Mushroom of Immortality, pp 234–35.
  95. ^ Wasson, Soma: Divine Mushroom of Immortality, p 279.
  96. ^ "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. Retrieved 2009-02-23.
  97. ^ 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.
  98. ^ (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.
  99. ^ Letcher, p 149.
  100. ^ Larsen, S. (1976). The Shaman’s Doorway. New York, NY: Station Hill Press. ISBN 0892816724.
  101. ^ Wasson, Soma:Divine Mushroom of Immortality, p 10.
  102. ^ Letcher, p 145.
  103. ^ Wasson, Soma:Divine Mushroom of Immortality, p 18.
  104. ^ Wasson, Soma:Divine Mushroom of Immortality, pp 36–37.
  105. ^ Wasson, Soma:Divine Mushroom of Immortality, pp 22–24.
  106. ^ Letcher, p 146.
  107. ^ Brough, J. (1971). "Soma and Amanita muscaria". Bulletin of the School of Oriental and African Studies (BSOAS) 34: 331–62.
  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 & Stoughton. ISBN 0-340-12875-5.
  111. ^ Letcher, p 160.
  112. ^ King, J. C. (1970). A Christian View of the Mushroom Myth. London: Hodder & 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. ^ Letcher, p 126.
  119. ^ Sacred Weeds: Fly Agaric, BBC documentary presented by Dr Andrew Sherratt, The Reader in European Pre-History at the University of Oxford (prior to his resignation, formerly Professor of Archaeology, University of Oxford). Documentary released 1998-08-10. Relevant material circa 06:30–07:00 minutes. Transcription: I then moved on to the appearance of the fly agaric mushroom in our own culture. This is the famous example from Lewis Carrol’s Alice in Wonderland, the caterpillar sitting on the mushroom. Alice bites a little piece of this to get larger / smaller. So there is some evidence that Lewis Carol himself was aware of some of the properties of eating these mushrooms, and the way in which it altered perception. And so the image of the fly agaric became very common in Victorian literature, especially associated with faeries and little people sitting on mushrooms and toadstools.
  120. ^ "Art Registry: 1750–1850". Mykoweb. Retrieved 2009-02-26.
  121. ^ Benjamin, Mushrooms: poisons and panaceas, p 295.
  122. ^ "The Registry of Mushrooms in Works of Art". Mykoweb. Retrieved 2009-02-16.
  123. ^ "Mushrooms in Victorian Fairy Paintings, by Elio Schachter". Mushroom, the Journal of Wild Mushrooming. Retrieved 2009-02-16.
  124. ^ 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.
  125. ^ Ramsbottom, p 43.
  126. ^ Letcher, p 122.
  127. ^ Letcher, p 123.
  128. ^ Letcher, p 125.
  129. ^ Letcher, p 126.
  130. ^ Letcher, p 127.
  131. ^ Letcher, p 129.
  132. ^ Wasson, Soma:Divine Mushroom of Immortality, p 204.
  133. ^ Wasson, Soma:Divine Mushroom of Immortality, p 238.
  134. ^ 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.
  135. ^ Taylor, R. (21 December 1980). "Who is Santa Claus?". Sunday Times Magazine (London: Times Newspapers Ltd): 13–17.
  136. ^ Morgan, A. (December 1986). "Who put the toad in toadstool?". New Scientist 25: 44–47.
  137. ^ Hutton, R. (1996). The Stations of the Sun: A History of the Ritual Year in Britain. Oxford: Oxford University Press. pp. 118–19.
  138. ^ Letcher, p 139.
Cited texts
  • Arora, David (1986). Mushrooms demystified: a comprehensive guide to the fleshy fungi (2nd ed.). Berkeley: Ten Speed Press. ISBN 0-89815-169-4.
  • Benjamin, Denis R. (1995). Mushrooms: poisons and panaceas—a handbook for naturalists, mycologists and physicians. New York: WH Freeman and Company. ISBN 0-7167-2600-9.
  • European Monitoring Centre for Drugs and Drug Addiction (2006). Hallucinogenic mushrooms: an emerging trend case study. EMCDDA Thematic Papers. Lisbon, Portugal: European Monitoring Centre for Drugs and Drug Addiction. ISBN 92-9168-249-7. Retrieved 2009-02-13.
  • Letcher, Andy (2006). Shroom: A Cultural history of the magic mushroom. London: Faber and Faber. ISBN 0-571-22770-8.
  • Ramsbottom, J. (1953). Mushrooms & Toadstools. Collins. ISBN 1870630092.
  • Wasson, R. Gordon (1968). Soma: Divine Mushroom of Immortality. Harcourt Brace Jovanovick. ISBN 0-88316-517-1.
  • Wasson, R. Gordon (1980). The Wondrous Mushroom: Mycolatry in Mesoamerica. McGraw-Hill. ISBN 007068443X.
  • Furst, Peter T. (1976). Hallucinogens and Culture. Chandler & Sharp. pp. 98–106. ISBN 0-88316-517-1.

External links

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List of Amanita species

The following is a list of some notable species of the agaric genus Amanita. This genus contains over 500 named species and varieties, so the list is far from exhaustive. The list follows the classification of subgenera and sections of Amanita outline by Corner and Bas (1962) and Bas (1969), as used by Tulloss (2007). Bolding of the species name and an asterisk (*) following indicates the species is the type species of that section, with a double asterisk (**) indicating the type species of the entire genus. Use of common names follows Tuloss (2007), Holden (2003), Arora (1986), and Lincoff (1981).

subgenus Amanita

section Amanita

A. muscaria

section Vaginatae

A.vaginata

section Caesareae

A. caesarea

subgenus Lepidella

section Lepidella

A. abrupta

section Amidella
section Phalloideae

A. phalloides

section Validae

A. flavoconia

References

 

DMT

Dimethyltryptamine

Dimethyltryptamine

File:DMT.svg

Systematic (IUPAC) name

2-(1H-indol-3-yl)-N,N-dimethylethanamine

Identifiers

CAS number
61-50-7

ATC code
None

PubChem
CID 6089

IUPHAR ligand ID
141

ChemSpider
5864

Chemical data

Formula
C12H16N2

Mol. mass
188.269 g/mol

SMILES
eMolecules & PubChem

Physical data

Density
1.099g/ml g/cm³

Melt. point
40–59 °C (104–138 °F)

Therapeutic considerations

Pregnancy cat.
?

Legal status
Prohibited (S9) (AU) Schedule III(CA) CD Lic (UK) Schedule I (US)

Routes
Oral (with an MAOI), Insufflated,Rectal, Smoked (or vaporized),IM, IV

N,N-Dimethyltryptamine (DMT) is a naturally occurring hallucinogenic drug of the tryptamine family. This drug is found not only in many plants[1], but also in trace amounts in the human body, where its natural function remains undetermined. Structurally, it is analogous to the neurotransmitter serotonin (5-HT) and other hallucinogenic tryptamines such as 5-MeO-DMT, bufotenin (5-OH-DMT), and psilocin (4-HO-DMT). DMT is created in small amounts by the human body during normal metabolism[2] by the enzyme tryptamine-N-methyltransferase. Many cultures, indigenous and modern, ingest DMT as a psychedelic, in either extracted or synthesized forms.[3] When refined, DMT is a clear to white, crystalline solid. However, DMT found on the illicit market is commonly impure and may appear yellow, orange, or salmon in color, unless special care has been taken to remove these impurities. Such impurities result from degradation or originate from plant matter from which the DMT may have been extracted.

Biosynthesis

Biosynthetic pathway for N-N,dimethyltryptamine

Dimethyltryptamine is an indole-alkaloid derived from the shikimate pathway. Its biosynthesis is relatively simple and summarized in the picture to the left. In plants, the tryptophan is produced endogenously where in animals the tryptophan used comes from diet. No matter the source of tryptophan, the biosynthesis begins with the decarboxylation of L-tryptophan (step 1). Once decarboxylated, tryptamine (step 2) is dimethylated by S-adenosyl-methionine (SAM) via nucleophilic attack. This reaction is mediated by tryptamine-N-methyltransferase enzyme. This produces the product (step 3). The mechanism has been proven by radio labelling of SAM with carbon-14.[4] The study found that various mammal tissues contained enzymes capable of performing the above transformation.

Chemistry

DMT Crystals

DMT is a derivative of tryptamine with two additional methyl groups at the amine nitrogen atom. DMT was first synthesized by Canadian chemist Richard Manske in 1931.[1] It was first extracted from the plant roots of Mimosa hostilis in 1946 by Brazilian ethnobotanist and chemist Gonçalves de Lima who named it Nigerine. DMT is commonly handled and stored as a fumarate as other DMT acid salts are generally veryhygroscopic and will not readily crystallize. Its freebase form, although less stable than DMT fumarate, is favored by recreational users choosing to vaporize (smoke) the chemical because it has a lower boiling point. In contrast to DMT’s base, its salts are water-soluble. DMT in solution degrades relatively quickly and should be stored protected from air, light, and heat in a freezer.[citation needed]

Pharmacology

DMT acts as a non-selective agonist at most or all of the serotonin receptors (including 5-HT2A and 5-HT2C),[5][6][7][8] and has also been shown to possess affinity for the D1, α1-adrenergic, α2-adrenergic,imidazoline-1, sigma-1, and trace amine-associated receptors.[5][6][9] At the trace amine-associated receptor (TAAR) and the sigma-1 receptor it acts as an agonist,[9][10] whereas its efficacies at the other sites are unclear. It has also been shown to bind to the SERT and VMAT2 as a substrate (instead of inhibitor), and may act as a serotonin releasing agent.[11] The psychedelic effects of DMT can likely largely be attributed to activation of the 5-HT2A receptor,[12][13] though it cannot be ruled out whether other receptors such as 5-HT2C, sigma-1, and TAAR may also play a role.[9][10][13]

It was speculated that DMT could be an endogenous ligand for the sigma-1 receptor. In this report, the concentration of DMT needed for sigma-1 activation is about 9.4 mg/L (50 µM). This concentration is higher than the average concentration measured in brain tissue or plasma, and is also about two orders of magnitude higher than that needed to activate the 5-HT2A receptor in vitro. In humans, effective hallucinogenic doses produce peak DMT plasma concentrations ranging between 12 and 90 µg/L and with an apparent volume of distribution of 36 to 55 L.[14][15][16]

The corresponding average molar plasma concentration of DMT is therefore in the range of 0.060–0.500 µM. However, the relatively high volume of distribution of DMT indicates significant movement of the drug from plasma into tissues and several reports have described the active accumulation of DMT and other tryptamines into rat brain following peripheral administration.[17][18][19][20][21] Similar active uptake processes in human brain may plausibly concentrate DMT within neurons by several-fold or more, resulting in local concentrations in the micromolar or higher range. Interestingly, the concentrations of DMT required to occupy a significant fraction of any of its known receptor binding sites are between 1,000 and 1,000,000-fold lower than the calculated synaptic concentration of other neurotransmitters. For example, using amperometric measurements, the synaptic concentration of dopamine was estimated to reach about 75 mM.[22] DMT also activated the trace amine associated receptor TAAR1, at the tested high concentration.[23]

Psychedelic properties

DMT occurs naturally in many species of plants often in conjunction with its close chemical relatives 5-MeO-DMT and bufotenin (5-OH-DMT).[24] DMT-containing plants are commonly used in South American Shamanic practices. It is usually one of the main active constituents of the drink ayahuasca[3], however ayahuasca is sometimes brewed without plants that produce DMT. It occurs as the primary psychoactive alkaloid in several plants including Mimosa hostilis, Diplopterys cabrerana, andPsychotria viridis. DMT is found as a minor alkaloid in snuff made from Virola bark resin in which 5-MeO-DMT is the main active alkaloid.[24] DMT is also found as a minor alkaloid in the beans of Anadenanthera peregrina and Anadenanthera colubrina used to make Yopo and Vilca snuff in which bufotenin is the main active alkaloid.[24][25] Psilocybin and psilocin, active chemicals in many psychedelic mushrooms, are structurally very similar to DMT.[26]

The psychotropic effects of DMT were first studied scientifically by the Hungarian chemist and psychologist Dr. Stephen Szára who performed research with volunteers in the mid-1950s. Szára, who later worked for the US National Institutes of Health, had turned his attention to DMT after his order for LSD from the Swiss company Sandoz Laboratories was rejected on the grounds that the powerful psychotropic could be dangerous in the hands of a communist country.[27]

DMT during various stages of purification in an illegal drug laboratory in Los Angeles

DMT can produce powerful entheogenic experiences including intense visuals, euphoria, even true hallucinations (perceived extensions of reality). DMT is generally not active orally unless it is combined with an monoamine oxidase inhibitor (MAOI) such as a reversible inhibitor of monoamine oxidase A (RIMA), e.g., harmaline. Uninhibited, the human body metabolizes DMT too rapidly for oral administration to be effective. Other means of ingestion such as smoking or injecting the drug can produce powerful hallucinations and entheogenic activity for a short time (usually less than half an hour), as the DMT reaches the brain before it can be metabolized by the body’s natural monoamine oxidase. Taking a MAOI prior to smoking or injecting DMT prolongs and potentiates the effects.[28]

Inhalation

A standard dose for smoked DMT is between 15–60 mg. This is generally smoked in a few successive breaths. The effects last for a short period of time, usually 5 to 15 minutes, dependent on the dose. The onset after inhalation is very fast (less than 45 seconds) and peak effects are reached within a minute. In the 1960s, some reportedly referred to DMT as "the businessman’s trip"[29] because of the relatively short duration of vaporized, insufflated, or injected DMT. DMT is commonly vaporized in glass pipes also suitable for use with crack cocaine and methamphetamine. Improvised smoking devices can be constructed from light bulbs. The vapor is sometimes described as harsh, and some users even compare its flavor to that of burning plastic. Some users elect to combine it with cannabis, parsley, mullein, or other plants in an attempt to improve flavor and reduce harshness. Combining DMT with plant matter or depositing it upon a substrate of ash also facilitates use of an ordinary pipe, a bong, or a vaporizer.Insufflation

Insufflating DMT (commonly as a freebase or fumarate) requires a higher dose than does inhalation. The duration is markedly increased, and some users report diminished euphoria but an intensified otherworldly experience[citation needed].Injection

Injected DMT produces an experience that is similar to inhalation in duration, intensity, and characteristics.

In a study conducted from 1990 through 1995, University of New Mexico psychiatrist Rick Strassman found that some volunteers injected with high doses of DMT had experiences with a perceived alien entity. Usually, the reported entities were experienced as the inhabitants of a perceived independent reality the subjects reported visiting while under the influence of DMT.[27] In a September, 2009, interview with Examiner.com, Strassman described the effects on participants in the study: "Subjectively, the most interesting results were that high doses of DMT seemed to allow the consciousness of our volunteers to enter into non-corporeal, free-standing, independent realms of existence inhabited by beings of light who oftentimes were expecting the “volunteers,” and with whom the volunteers interacted. While “typical” near-death and mystical states occurred, they were relatively rare."Oral ingestion

DMT is broken down by the digestive enzyme monoamine oxidase and is practically inactive if taken orally, unless combined with a MAOI. The traditional South American ayahuasca, or yage, is a tea mixture containing DMT and a MAOI.[3] There are a variety of recipes to this brew, but most commonly it is simply the leaves of Psychotria viridis (the source of DMT) and the vine Banisteriopsis caapi (the source of MAOI). It has often puzzled researchers how the natives managed to find this combination without modern analytical chemistry[citation needed]. Other DMT containing plants, including Diplopterys cabrerana, are sometimes used in ayahuasca in different areas of South America. Two common sources in the western US are Reed canary grass(Phalaris arundinacea) and Harding grass (Phalaris aquatica). These invasive grasses contain low levels of DMT and other alkaloids. In addition, Jurema (Mimosa hostilis) shows evidence of DMT content: the pink layer in the bark of this vine contains a high concentration of N,N-DMT.

Taken orally with an appropriate MAOI, DMT produces a long lasting (over 3 hour), slow, deep metaphysical experience similar to that of psilocybin mushrooms, but more intense.[3] MAOIs should be used with extreme caution as they can have lethal complications with some prescription drugs such as SSRI antidepressants, some over-the-counter drugs,[30] and many common foods.[31]

Induced DMT experiences can include profound time-dilation, visual and auditory illusions, and other experiences that, by most firsthand accounts, defy verbal or visual description. Some users report intense erotic imagery and sensations and utilize the drug in a ritual sexual context.[3][32][33]

Rectal Administration

DMT can also be taken rectally. Dosage started at 200 mg without a MAOI. Effects last 2 hours.[34]

Distinguish from 5-MeO-DMT

5-MeO-DMT, a psychedelic drug structurally similar to N,N-DMT, is sometimes referred to as DMT through ignorance or by abbreviation. As a white, crystalline solid, it is also similar in appearance to DMT. However, it is considerably more potent (5-MeO-DMT typical smoked dose: 5–20 mg), and care should be taken to clearly differentiate between the two drugs to avoid accidental overdose.[35]

Side effects

When DMT is vaporized, the inhaled vapor feels harsh to a minority of users. According to a "Dose-response study of N,N-dimethyltryptamine in humans" by Rick Strassman, "Dimethyltryptamine dose slightly elevated blood pressure, heart rate, pupil diameter, and rectal temperature, in addition to elevating blood concentrations of beta-endorphin, corticotropin, cortisol, and prolactin. Growth hormone blood levels rose equally in response to all doses of DMT, and melatonin levels were unaffected."[36]

Speculation

DMT crystal at 400x magnification.

Several speculative and yet untested hypotheses suggest that endogenous DMT, produced in the human brain, is involved in certain psychological and neurological states. DMT is naturally produced in small amounts in the brain and other tissues of humans and other mammals.[37] It may play a role in mediating the visual effects of natural dreaming, and also near-death experiences, religious visions and other mystical states.[38] A biochemical mechanism for this was proposed by the medical researcher J. C. Callaway, who suggested in 1988 that DMT might be connected with visual dream phenomena, where brain DMT levels are periodically elevated to induce visual dreaming and possibly other natural states of mind.[39] A new hypothesis proposed is that in addition to being involved in altered states of consciousness, endogenous DMT may be involved in the creation of normal waking states of consciousness. It is proposed that DMT and other endogenous hallucinogens mediate their neurological abilities by acting as neurotransmitters at a sub class of the trace amine receptors; a group of receptors found in the CNS where DMT and other hallucinogens have been shown to have activity. Wallach further proposes that in this way waking consciousness can be thought of as a controlled psychedelic experience. It is when the control of these systems becomes loosened and their behavior no longer correlates with the external world that the altered states arise.[40]

Dr. Rick Strassman, while conducting DMT research in the 1990s at the University of New Mexico, advanced the theory that a massive release of DMT from the pineal gland prior to death or near death was the cause of the near death experience (NDE) phenomenon. Several of his test subjects reported NDE-like audio or visual hallucinations. His explanation for this was the possible lack of panic involved in the clinical setting and possible dosage differences between those administered and those encountered in actual NDE cases. Several subjects also reported contact with ‘other beings’, alien like, insectoid or reptilian in nature, in highly advanced technological environments[27] where the subjects were ‘carried’, ‘probed’, ‘tested’, ‘manipulated’, ‘dismembered’, ‘taught’, ‘loved’ and even ‘raped’ by these ‘beings’. This is most likely due to the setting of the experiments. Strassman has speculated that DMT is made in the pineal gland, largely because the necessary constituents (see methyltransferases) needed to make DMT are found in the pineal gland in substantially greater concentrations than any other part of the body. However, there is no scientific proof of this.

In the 1950s, the endogenous production of psychoactive agents was considered to be a potential explanation for the hallucinatory symptoms of some psychiatric diseases as the transmethylation hypothesis[41] (see also adrenochrome), though this hypothesis does not account for the natural presence of endogenous DMT in otherwise normal humans, rats and other laboratory animals.

Writers on DMT include Terence McKenna, Jeremy Narby and Graham Hancock. In his writings and speeches, Terence McKenna recounts encounters with entities he sometimes describes as "Self-Transforming Machine Elves" among other phrases. McKenna believed DMT to be a tool that could be used to enhance communication and allow for communication with other-worldly entities. Other users report visitation from external intelligences attempting to impart information. These Machine Elf experiences are said to be shared by only a minority of DMT users and some people report never seeing or experiencing anything of that nature.

Legal status

International Law

DMT is classified as a Schedule I drug under the UN 1971 Convention on Psychotropic Substances, meaning that use of DMT is supposed to be restricted to scientific research and medical use and international trade in DMT is supposed to be closely monitored. Natural materials containing DMT, including ayahuasca, are explicitly not regulated under the 1971 Psychotropic Convention.[42]

United States

DMT is classified in the United States as a Schedule I drug under the Controlled Substances Act of 1970.

In December 2004, the Supreme Court lifted a stay thereby allowing the Brazil-based União do Vegetal (UDV) church to use a decoction containing DMT in their Christmas services that year. This decoction is a "tea" made from boiled leaves and vines, known as hoasca within the UDV, and ayahuasca in different cultures. In Gonzales v. O Centro Espirita Beneficente Uniao do Vegetal, the Supreme Court heard arguments on November 1, 2005 and unanimously ruled in February 2006 that the U.S. federal government must allow the UDV to import and consume the tea for religious ceremonies under the 1993 Religious Freedom Restoration Act.

In September, 2008, the three Santo Daime churches filed suit in federal court to gain legal status to import DMT-containing ayahuasca tea. The case, Church of the Holy Light of the Queen v. Mukasey[43], presided over by Judge Owen M. Panner, was ruled in favor of the Santo Daime church. As of March 21, 2009 a federal judge says members of the church in Ashland can import, distribute and brew ayahuasca. U.S. District Judge Owen Panner issued a permanent injunction barring the government from prohibiting or penalizing the sacramental use of "Daime tea." Panner’s order said activities of The Church of the Holy Light of the Queen are legal and protected under freedom of religion. His order prohibits the federal government from interfering and prosecuting church members who follow a list of regulations set out in his order.[44][45]

Canada

DMT is classified in Canada as a Schedule III drug.

France

DMT, along with most of its plant sources, is classified in France as a stupéfiant (Narcotic).

United Kingdom

DMT is classified in the United Kingdom as a Class A drug.

New Zealand

DMT is classified as a Class A drug in New Zealand.

Culture

In South America there are a number of indigenous traditions and more recent religious movements based on the use of ayahuasca, usually in an animistic context that may be mixed with Christian imagery. There are four main branches using DMT-MAOI based sacraments in South America:

  • Amazonian Peoples. There are many indigenous cultures in South America, mostly in the Upper Amazonn Basin whose traditional religious practices include the use of ayahuasca. These are the oldest cultures in the whole of South America that continue to use ayahuasca or analogue brews, such as the ones made from Jurema in the Pernambuco, near Recife or Iquitos in Peru.
  • Santo Daime ("Saint Give Unto Me") and Barquinha ("Little Boat"). A syncretic religion from Brazil. The former was founded by Raimundo Irineu Serra in the early 1930s, as an esoteric Christian religion with shamanic tendencies. The Barquinha was derived from this one.
  • União do Vegetal (Union of Vegetal or UDV). Another Christian ayahuasca religion from Brazil, is a single unified organization with a democratic structure.
  • Neo-shamans. There are some self-styled shamanic facilitators in Brazil and other South American countries that use ayahuasca or analogous brews in their rituals and séances.

See also

References

  1. ^ a b Jeremy Bigwood and Jonathan Ott (1977): "DMT", Head Magazine
  2. ^ Barker SA, Monti JA, Christian ST (1981). "N, N-dimethyltryptamine: an endogenous hallucinogen". Int. Rev. Neurobiol. 22: 83–110. doi:10.1016/S0074-7742(08)60291-3. PMID 6792104.
  3. ^ a b c d e Salak, Kira. ""HELL AND BACK"". National Geographic Adventure.
  4. ^ Mandel LR, Prasad R, Lopez-Ramos B, Walker RW (January 1977). "The biosynthesis of dimethyltryptamine in vivo". Res. Commun. Chem. Pathol. Pharmacol. 16 (1): 47–58. PMID 14361.
  5. ^ a b Ray TS (2010). "Psychedelics and the human receptorome". Plos One 5 (2): e9019. doi:10.1371/journal.pone.0009019. PMID 20126400. PMC 2814854.
  6. ^ a b Pierce PA, Peroutka SJ (1989). "Hallucinogenic drug interactions with neurotransmitter receptor binding sites in human cortex". Psychopharmacology 97 (1): 118–22. PMID 2540505.
  7. ^ McKenna DJ, Peroutka SJ (October 1989). "Differentiation of 5-hydroxytryptamine2 receptor subtypes using 125I-R-(-)2,5-dimethoxy-4-iodo-phenylisopropylamine and 3H-ketanserin". The Journal of Neuroscience : the Official Journal of the Society for Neuroscience 9 (10): 3482–90. PMID 2795135.
  8. ^ Smith RL, Canton H, Barrett RJ, Sanders-Bush E (November 1998). "Agonist properties of N,N-dimethyltryptamine at serotonin 5-HT2A and 5-HT2C receptors". Pharmacology, Biochemistry, and Behavior 61 (3): 323–30. PMID 9768567.
  9. ^ a b c Wallach JV (January 2009). "Endogenous hallucinogens as ligands of the trace amine receptors: a possible role in sensory perception". Medical Hypotheses 72 (1): 91–4. doi:10.1016/j.mehy.2008.07.052. PMID 18805646.
  10. ^ a b Fontanilla D, Johannessen M, Hajipour AR, Cozzi NV, Jackson MB, Ruoho AE (February 2009). "The hallucinogen N,N-dimethyltryptamine (DMT) is an endogenous sigma-1 receptor regulator". Science (New York, N.Y.) 323 (5916): 934–7.doi:10.1126/science.1166127. PMID 19213917.
  11. ^ Cozzi NV, Gopalakrishnan A, Anderson LL, et al. (December 2009). "Dimethyltryptamine and other hallucinogenic tryptamines exhibit substrate behavior at the serotonin uptake transporter and the vesicle monoamine transporter". Journal of Neural Transmission (Vienna, Austria : 1996) 116 (12): 1591–9. doi:10.1007/s00702-009-0308-8. PMID 19756361.
  12. ^ Vollenweider FX, Vollenweider-Scherpenhuyzen MF, Bäbler A, Vogel H, Hell D (December 1998). "Psilocybin induces schizophrenia-like psychosis in humans via a serotonin-2 agonist action". Neuroreport 9 (17): 3897–902. PMID 9875725.
  13. ^ a b Nichols DE (February 2004). "Hallucinogens". Pharmacology & Therapeutics 101 (2): 131–81. doi:10.1016/j.pharmthera.2003.11.002. PMID 14761703.
  14. ^ Callaway JC, McKenna DJ, Grob CS, et al. (June 1999). "Pharmacokinetics of Hoasca alkaloids in healthy humans". J Ethnopharmacol 65 (3): 243–56. doi:10.1016/S0378-8741(98)00168-8. PMID 10404423.
  15. ^ Riba J, Valle M, Urbano G, Yritia M, Morte A, Barbanoj MJ (July 2003). "Human pharmacology of ayahuasca: subjective and cardiovascular effects, monoamine metabolite excretion, and pharmacokinetics". J. Pharmacol. Exp. Ther. 306 (1): 73–83.doi:10.1124/jpet.103.049882. PMID 12660312.
  16. ^ Yritia M, Riba J, Ortuño J, et al. (November 2002). "Determination of N,N-dimethyltryptamine and beta-carboline alkaloids in human plasma following oral administration of Ayahuasca". J. Chromatogr. B Analyt. Technol. Biomed. Life Sci. 779 (2): 271–81.doi:10.1016/S1570-0232(02)00397-5. PMID 12361741.
  17. ^ Barker SA, Beaton JM, Christian ST, Monti JA, Morris PE (August 1982). "Comparison of the brain levels of N,N-dimethyltryptamine and alpha, alpha, beta, beta-tetradeutero-N-N-dimethyltryptamine following intraperitoneal injection. The in vivo kinetic isotope effect". Biochem. Pharmacol. 31 (15): 2513–6. doi:10.1016/0006-2952(82)90062-4. PMID 6812592.
  18. ^ Sangiah S, Gomez MV, Domino EF (December 1979). "Accumulation of N,N-dimethyltryptamine in rat brain cortical slices". Biol. Psychiatry 14 (6): 925–36. PMID 41604.
  19. ^ Sitaram BR, Lockett L, Talomsin R, Blackman GL, McLeod WR (May 1987). "In vivo metabolism of 5-methoxy-N,N-dimethyltryptamine and N,N-dimethyltryptamine in the rat". Biochem. Pharmacol. 36 (9): 1509–12. doi:10.1016/0006-2952(87)90118-3.PMID 3472526.
  20. ^ Takahashi T, Takahashi K, Ido T, et al. (December 1985). "[11C]-labeling of indolealkylamine alkaloids and the comparative study of their tissue distributions". Int J Appl Radiat Isot 36 (12): 965–9. doi:10.1016/0020-708X(85)90257-1. PMID 3866749.
  21. ^ Yanai K, Ido T, Ishiwata K, et al. (1986). "In vivo kinetics and displacement study of a carbon-11-labeled hallucinogen, N,N-[11C]dimethyltryptamine". Eur J Nucl Med 12 (3): 141–6. PMID 3489620.
  22. ^ Colliver TL, Pyott SJ, Achalabun M, Ewing AG (July 2000). "VMAT-Mediated changes in quantal size and vesicular volume". J. Neurosci. 20 (14): 5276–82. PMID 10884311.
  23. ^ Bunzow JR, Sonders MS, Arttamangkul S (2001). "Amphetamine, 3,4-methylenedioxymethamphetamine, lysergic acid diethylamide, and metabolites of the catecholamine neurotransmitters are agonists of a rat trace amine receptor.". Mol. Pharmacol. 60 (6): 1181–8. PMID 11723224.
  24. ^ a b c Anadenanthera: Visionary Plant Of Ancient South America By Constantino Manuel Torres, David B. Repke, 2006, ISBN 0789026422
  25. ^ Pharmanopo-Psychonautics: Human Intranasal, Sublingual, Intrarectal, Pulmonary and Oral Pharmacology of Bufotenine by Jonathan Ott, The Journal of Psychoactive Drugs, September 2001
  26. ^ Relation between DMT and other related compounds http://deoxy.org/t_thc.htm
  27. ^ a b c R.J. Strassman. "Chapter summaries". DMT: The Spirit Molecule. Retrieved 2007-01-13.
  28. ^ http://www.erowid.org/chemicals/dmt/dmt.shtml
  29. ^ Haroz, R; Greenberg, M (2005). "Emerging Drugs of Abuse". Medical Clinics of North America 89: 1259. doi:10.1016/j.mcna.2005.06.008.
  30. ^ Callaway J.C. and Grob C.S. (1998). Ayahuasca preparations and serotonin reuptake inhibitors: a potential combination for adverse interaction. Journal of Psychoactive Drugs 30(4): 367-369.
  31. ^ "MAOIs and Diet". http://www.mayoclinic.com. Retrieved 2009-02-22.
  32. ^ "2C-B, DMT, You and Me". Maps. Retrieved 2007-01-13.
  33. ^ "Entheogens & Visionary Medicine Pages". Miqel.com. Retrieved 2007-08-17.
  34. ^ NeuroSoup. "DMT: The Shamic Colonic Video". Retrieved 2009-10-05.
  35. ^ http://www.erowid.org/chemicals/5meo_dmt/5meo_dmt_dose.shtml
  36. ^ R.J. Strassman and C.R. Qualls (February 1994). "Dose-response study of N,N-dimethyltryptamine in humans". Arch Gen Psychiatry 51 (2): 85–97. PMID 8297216.
  37. ^ "Erowid DMT Vault: Journal Articles & Abstracts". Retrieved 2007-09-05.
  38. ^ http://www.npr.org/templates/story/story.php?storyId=104240746&sc=fb&cc=fp
  39. ^ Callaway J (1988). "A proposed mechanism for the visions of dream sleep". Med Hypotheses 26 (2): 119–24. doi:10.1016/0306-9877(88)90064-3. PMID 3412201.
  40. ^ Wallach J (2008). "Endogenous hallucinogens as ligands of the trace amine receptors: A possible role in sensory perception". Med Hypotheses in print (in print): in print. doi:10.1016/j.mehy.2008.07.052. PMID 18805646.
  41. ^ Osmund H and Smythies JR (1952). Schizophrenia: A new approach. Journal of Mental Science 98:309-315.
  42. ^ Erowid
  43. ^ Church of the Holy Light of the Queen v. Mukasey
  44. ^ Pharma-Law E-News
  45. ^ Portland Tribune

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κOR Agonists

2-EMSB2-MMSBAlazocineBremazocineButorphanolCyclazocineCyprenorphineDextrallorphanDezocineEnadolineHerkinorinHZ-2IbogaineKetazocineMetazocineNalbuphineNalorphineNoribogainePentazocinePhenazocineSalvinorin ASpiradolineTifluadomU-50,488U-69,593

σR Agonists

DextrallorphanDextromethorphanDextrorphanNoscapine (Narcotine)

Others

EfavirenzGlaucineIsoaminile

Adrenergics

Receptor
Ligands

α1

Agonists: 5-FNE6-FNEAmidephrineAnisodamineAnisodineCirazolineDipivefrineDopamineEphedrineEpinephrine (Adrenaline) • EtilefrineEthylnorepinephrineIndanidineLevonordefrinMetaraminolMethoxamineMethyldopaMidodrineNaphazolineNorepinephrine (Noradrenaline) • OctopamineOxymetazolinePhenylephrinePhenylpropanolaminePseudoephedrineSynephrineTetrahydrozoline
Antagonists: AbanoquilAdimololAjmalicineAlfuzosinAmosulalolArotinololAtiprosinBenoxathianBuflomedilBunazosinCarvedilolCI-926CorynanthineDapiprazoleDL-017DomesticineDoxazosinEugenodilolFenspirideGYKI-12,743GYKI-16,084IndoraminKetanserinL-765,314LabetalolMephendioxanMetazosinMonatepilMoxisylyte (Thymoxamine) • NaftopidilNantenineNeldazosinNicergolineNiguldipinePelanserinPhendioxanPhenoxybenzaminePhentolaminePiperoxanPrazosinQuinazosinRitanserinRS-97,078SGB-1,534SilodosinSL-89.0591SpiperoneTalipexoleTamsulosinTerazosinTibalosinTiodazosinTipentosinTolazolineTrimazosinUpidosinUrapidilZolertine
* Note that many TCAs, TeCAs, antipsychotics, ergolines, and some piperazines like buspirone, trazodone, nefazodone, etoperidone, and mepiprazole all antagonize α1-adrenergic receptors as well, which contributes to their side effects such as orthostatic hypotension.

α2

Agonists: (R)-3-Nitrobiphenyline4-NEMD6-FNEAmitrazApraclonidineBrimonidineClonidineDetomidineDexmedetomidineDihydroergotamineDipivefrineDopamineEphedrineErgotamineEpinephrine (Adrenaline) • EsproquinEtilefrineEthylnorepinephrineGuanabenzGuanfacineGuanoxabenzLevonordefrinLofexidineMedetomidineMethyldopaMivazerolNaphazolineNorepinephrine (Noradrenaline) • PhenylpropanolaminePiperoxanPseudoephedrineRilmenidineRomifidineTalipexoleTetrahydrozolineTizanidineTolonidineUrapidilXylazineXylometazoline
Antagonists: 1-PPAdimololAtipamezoleBRL-44408BuflomedilCirazolineEfaroxanEsmirtazapineFluparoxanGYKI-12,743GYKI-16,084IdazoxanMianserinMirtazapineMK-912NAN-190OlanzapinePhentolaminePhenoxybenzaminePiperoxanPiribedilRauwolscineRotigotineSB-269,970SetiptilineSpiroxatrineSunepitronTolazolineYohimbine
* Note that many atypical antipsychotics and azapirones like buspirone and gepirone (via metabolite 1-PP) antagonize α2-adrenergic receptors as well.

β

Agonists: 2-FNE5-FNEAmibegronArbutamineArformoterolArotinololBAAMBambuterolBefunololBitolterolBroxaterolBuphenineCarbuterolCimaterolClenbuterolDenopamineDeterenolDipivefrineDobutamineDopamineDopexamineEphedrineEpinephrine (Adrenaline) • EtafedrineEtilefrineEthylnorepinephrineFenoterolFormoterolHexoprenalineHigenamineIndacaterolIsoetarineIsoprenaline (Isoproterenol) • IsoxsuprineLabetalolLevonordefrinLevosalbutamolMabuterolMethoxyphenamineMethyldopaN-IsopropyloctopamineNorepinephrine (Noradrenaline) • OrciprenalineOxyfedrinePhenylpropanolaminePirbuterolPrenalterolRactopamineProcaterolPseudoephedrineReproterolRimiterolRitodrineSalbutamol (Albuterol) • SalmeterolSolabegronTerbutalineTretoquinolTulobuterolXamoterolZilpaterolZinterol
Antagonists: AcebutololAdaprololAdimololAfurololAlprenololAlprenoximeAmosulalolAncarololArnololArotinololAtenololBefunololBetaxololBevantololBisoprololBopindololBormetololBornaprololBrefonalolBucindololBucumololBufetololBuftiralolBufuralolBunitrololBunololBupranololBurocrololButaxamineButidrineButofilololCapsinololCarazololCarpindololCarteololCarvedilolCeliprololCetamololCicloprololCinamololCloranololCyanopindololDalbraminolDexpropranololDiacetololDichloroisoprenalineDihydroalprenololDilevalolDiprafenoneDraquinololDropranololEcastololEpanololEricololErsentilideEsatenololEsmololEsprololEugenodilolExaprololFalintololFlestololFlusoxololHydroxycarteololHydroxytertatololICI-118,551IdropranololIndenololIndopanololIodocyanopindololIprocrololIsoxaprololIsamoltaneLabetalolLandiololLevobetaxololLevobunololLevocicloprololLevomoprololMedroxalolMepindololMetalolMetipranololMetoprololMoprololNadololNadoxololNafetololNebivololNeraminolNifenalolNipradilolOberadilolOxprenololPacrinololPafenololPamatololPargololParodilolPenbutololPenirololPhQA-33PindololPirepololPractololPrimidololProcinololPronethalolPropafenonePropranololRidazololRonactololSoquinololSotalolSpirendololSR 59230ASulfinalolTA-2005TalinololTazololTeoprololTertatololTerthianololTienoxololTilisololTimololTiprenololTolamololToliprololTribendilolTrigevololXibenololXipranolol

Reuptake
Inhibitors

NET

Selective Norepinephrine Reuptake Inhibitors: Atomoxetine (Tomoxetine) • CiclazindolEsreboxetineMazindolNisoxetineReboxetineTalopramTalsupramTandamineViloxazine; Norepinephrine-Dopamine Reuptake Inhibitors: AmineptineBupropion(Amfebutamone) • FencamineFencamfamineLefetamineLevophacetoperaneLR-5182ManifaxineMethylphenidateNomifensineO-2172Radafaxine; Serotonin-Norepinephrine Reuptake Inhibitors: BicifadineDesvenlafaxineDuloxetineLevomilnacipranMilnacipranSibutramineVenlafaxine; Serotonin-Norepinephrine-Dopamine Reuptake Inhibitors: BrasofensineDiclofensineDOV-102,677DOV-21,947DOV-216,303JNJ-7925476JZ-IV-10MethylnaphthidateNaphyroneNS-2359PRC200-SSSEP-225,289SEP-227,162Tesofensine; Tricyclic Antidepressants: AmitriptylineButriptylineCianopramineClomipramineDesipramineDosulepinDoxepinImipramineLofepramineNortriptylineProtriptylineTrimipramine; Tetracyclic Antidepressants: AmoxapineMaprotilineMianserinOxaprotilineSetiptiline; Others: CocaineCP-39,332EXP-561FezolamineNefazodoneNefopamPridefrineTapentadolTramadolZiprasidone

VMAT

IbogaineReserpineTetrabenazine

Releasing
Agents

Morpholines: FenbutrazateMorazonePhendimetrazinePhenmetrazine; Oxazolines: 4-MethylaminorexAminorexClominorexCyclazodoneFenozoloneFluminorexPemolineThozalinone; Phenethylamines (also Amphetamines, Cathinones, Phentermines, etc): 2-OH-PEA4-CAB4-FA4-FMA4-MA4-MMAAlfetamineAmfecloralAmfepentorexAmfepramoneAmphetamine (Dextroamphetamine, Levoamphetamine) • Amphetaminilβ-Me-PEABDBBenzphetamineBOHBuphedroneButyloneCathineCathinoneClobenzorexClortermineD-DeprenylDimethylamphetamineDimethylcathinone (Dimethylpropion, Metamfepramone) • DMADMMAEBDBEphedrineEthcathinoneEthylamphetamineEthyloneFenethyllineFenproporexFlephedroneFludorexFurfenorexHordenineIAPIMPL-Deprenyl(Selegiline) • LisdexamfetamineLophophineMBDBMDA (Tenamfetamine) • MDEAMDMAMDMPEAMDOHMDPEAMefenorexMephedroneMephentermineMethamphetamine (Dextromethamphetamine, Levomethamphetamine) • MethcathinoneMethedroneMethyloneNAPOrtetamineParedrinepBApCAPentorex (Phenpentermine) • PhenethylaminePholedrinePhenpromethaminePhenterminePhenylpropanolaminepIAPrenylaminePropylamphetaminePseudoephedrineTiflorexTyramineXylopropamineZylofuramine;Piperazines: 2C-B-BZPBZPMBZPmCPPMDBZPMeOPPpFPP; Others: 2-Amino-1,2-dihydronaphthalene2-Aminoindane2-Aminotetralin2-Benzylpiperidine4-Benzylpiperidine5-IAIClofenciclanCyclopentamineCypenamineCyprodenateFeprosidnineGilutensinHeptaminolHexacyclonateIndanorexIsomethepteneMethylhexanamineOctodrinePhthalimidopropiophenonePropylhexedrine (Levopropylhexedrine) • Tuaminoheptane

Enzyme
Inhibitors

Anabolism

PAH

3,4-Dihydroxystyrene

TH

3-IodotyrosineAquayamycinBulbocapnineMetirosineOudenone

AAAD

BenserazideCarbidopaGenisteinMethyldopa

DBH

BupicomideDisulfiramDopastinFusaric AcidNepicastatPhenopicolinic AcidTropolone

PNMT

CGS-19281ASKF-64139SKF-7698

Catabolism

MAO

Nonselective: BenmoxinCaroxazoneEchinopsidineFurazolidoneHydralazineIndantadolIproclozideIproniazidIsocarboxazidIsoniazidLinezolidMebanazineMetfendrazineNialamideOctamoxinParaxazonePhenelzinePheniprazinePhenoxypropazinePivalylbenzhydrazineProcarbazineSafrazineTranylcypromine; MAO-A Selective: AmiflamineBazinaprineBefloxatoneBefolBrofaromineCimoxatoneClorgilineEsuproneHarmala alkaloids (Harmine, Harmaline,Tetrahydroharmine, Harman, Norharman, etc) • Methylene BlueMetralindoleMinaprineMoclobemidePirlindoleSercloremineTetrindoleToloxatoneTyrima; MAO-B Selective: D-DeprenylL-Deprenyl (Selegiline) • LadostigilLazabemideMilacemideMofegilinePargylineRasagiline
* Note that MAO-B inhibitors also influence norepinephrine/epinephrine levels since they inhibit the breakdown of their precursor dopamine.

COMT

EntacaponeTolcapone

Others

Precursors

L-PhenylalanineL-TyrosineL-DOPA (Levodopa) → DopamineL-DOPS (Droxidopa)

Cofactors

Ferrous Iron (Fe2+) • S-Adenosyl-L-MethionineVitamin B3 (Niacin, NicotinamideNADPH) • Vitamin B6 (Pyridoxine, Pyridoxamine, PyridoxalPyridoxal Phosphate) • Vitamin B9 (Folic AcidTetrahydrofolic Acid) • Vitamin C (Ascorbic Acid) • Zinc (Zn2+)

Others

Activity Enhancers: BPAPPPAP; Release Blockers: BethanidineBretyliumGuanadrelGuanazodineGuanclofineGuanethidineGuanoxan; Toxins: Oxidopamine (6-Hydroxydopamine)

Dopaminergics

Receptor
Ligands

Agonists

Adamantanes: AmantadineMemantineRimantadine; Aminotetralins: 7-OH-DPAT8-OH-PBZIRotigotineUH-232; Benzazepines: 6-Br-APBFenoldopamSKF-38,393SKF-77,434SKF-81,297SKF-82,958SKF-83,959; Ergolines: BromocriptineCabergolineDihydroergocryptineLisurideLSDPergolide; Dihydrexidine-derivatives: 2-OH-NPAA-86,929CiladopaDihydrexidineDinapsolineDinoxylineDoxanthrine; Others: A-68,930A-77,636A-412,997ABT-670ABT-724AplindoreApomorphineAripiprazoleBifeprunoxBP-897CY-208,243DizocilpineEtilevodopaFlibanserinKetamineMelevodopaModafinilPardoprunoxPhencyclidinePD-128,907PD-168,077PF-219,061PiribedilPramipexolePropylnorapomorphinePukateineQuinagolideQuineloraneQuinpiroleRDS-127Ro10-5824RopiniroleRotigotineRoxindoleSalvinorin ASKF-89,145SumaniroleTergurideUmespironeWAY-100,635

Antagonists

Typical Antipsychotics: AcepromazineAzaperoneBenperidolBromperidolClopenthixolChlorpromazineChlorprothixeneDroperidolFlupentixolFluphenazineFluspirileneHaloperidolLoxapineMesoridazineMethotrimeprazineNemonapridePenfluridolPerazinePericiazinePerphenazinePimozideProchlorperazinePromazineSulforidazineSulpirideSultoprideThioridazineThiothixeneTrifluoperazineTriflupromazineTrifluperidolZuclopenthixol; Atypical Antipsychotics: AmisulprideAsenapineBlonanserinClozapineGevotrolineIloperidoneLurasidoneMelperoneMolindoneMosapramineOcaperidoneOlanzapinePaliperidonePerospironePiquindoneQuetiapineRemoxiprideRisperidoneSertindoleTiospironeZiprasidoneZotepine; Antiemetics: AS-8112AlizaprideBromoprideCleboprideDomperidoneMetoclopramideThiethylperazine; Others: AmoxapineBuspironeButaclamolEcopipamEEDQEticloprideFananserinL-745,870NafadotrideNuciferinePNU-99,194RacloprideSarizotanSB-277,011-ASCH-23,390SKF-83,566SKF-83,959SonepiprazoleSpiperoneSpiroxatrineStepholidineTetrahydropalmatineTiaprideUH-232Yohimbine

Reuptake
Inhibitors

Plasmalemmal

DAT Inhibitors

Piperazines: DBL-583GBR-12,935NefazodoneVanoxerine; Piperidines: BTCPDesoxypipradrolDextromethylphenidateDifemetorexEthylphenidateMethylnaphthidateMethylphenidatePhencyclidinePipradrol; Pyrrolidines:DiphenylprolinolMethylenedioxypyrovalerone (MDPV) • NaphyroneProlintanePyrovalerone; Tropanes: β-CPPITAltropaneBrasofensineCFTCocaineDichloropaneDifluoropineFE-β-CPPITFP-β-CPPITIoflupane (123I)IometopaneRTI-112RTI-113RTI-121RTI-126RTI-150RTI-177RTI-229RTI-336TenocyclidineTesofensineTroparilTropoxaneWF-11WF-23WF-31WF-33; Others: AdrafinilArmodafinilAmfonelic AcidAmineptineBenzatropine(Benztropine) • BromantaneBTQBTS-74,398Bupropion (Amfebutamone) • CiclazindolDiclofensineDimethocaineDiphenylpyralineDizocilpineDOV-102,677DOV-21,947DOV-216,303Etybenzatropine (Ethylbenztropine) • EXP-561FencamineFencamfamineFezolamineGYKI-52,895IndatralineKetamineLefetamineLevophacetoperaneLR-5182ManifaxineMazindolMedifoxamineMesocarbModafinilNefopamNomifensineNS-2359O-2172PridefrinePropylamphetamineRadafaxineSEP-225,289SEP-227,162SibutramineTametralineTripelennamine

Vesicular

VMAT Inhibitors

DeserpidineIbogaineReserpineTetrabenazine

Releasing
Agents

Morpholines: FenbutrazateMorazonePhendimetrazinePhenmetrazine; Oxazolines: 4-Methylaminorex (4-MAR, 4-MAX) • AminorexClominorexCyclazodoneFenozoloneFluminorexPemolineThozalinone; Phenethylamines (also Amphetamines, Cathinones, Phentermines, etc): 2-Hydroxyphenethylamine (2-OH-PEA) • 4-CAB4-Methylamphetamine (4-MA) • 4-Methylmethamphetamine (4-MMA) • AlfetamineAmfecloralAmfepentorexAmfepramoneAmphetamine (Dextroamphetamine, Levoamphetamine) • Amphetaminilβ-Methylphenethylamine (β-Me-PEA) • Benzodioxolylbutanamine (BDB) • Benzodioxolylhydroxybutanamine (BOH) • BenzphetamineBuphedroneButyloneCathineCathinoneClobenzorexClortermineD-DeprenylDimethoxyamphetamine (DMA) • Dimethoxymethamphetamine (DMMA) • DimethylamphetamineDimethylcathinone (Dimethylpropion, Metamfepramone) • Ethcathinone (Ethylpropion) • EthylamphetamineEthylbenzodioxolylbutanamine (EBDB) • EthyloneFenethyllineFenproporexFlephedroneFludorexFurfenorexHordenineLophophine (Homomyristicylamine) • MefenorexMephedroneMethamphetamine (Desoxyephedrine, Methedrine; Dextromethamphetamine, Levomethamphetamine) • Methcathinone (Methylpropion) • MethedroneMethoxymethylenedioxyamphetamine (MMDA) • Methoxymethylenedioxymethamphetamine (MMDMA) •Methylbenzodioxolylbutanamine (MBDB) • Methylenedioxyamphetamine (MDA; Tenamfetamine) • Methylenedioxyethylamphetamine (MDEA) • Methylenedioxyhydroxyamphetamine (MDOH) • Methylenedioxymethamphetamine (MDMA) • Methylenedioxymethylphenethylamine (MDMPEA; Homarylamine) • Methylenedioxyphenethylamine (MDPEA; Homopiperonylamine) • MethyloneOrtetamineParabromoamphetamine (PBA) • Parachloroamphetamine (PCA) • Parafluoroamphetamine (PFA) • Parafluoromethamphetamine (PFMA) • Parahydroxyamphetamine (PHA) •Paraiodoamphetamine (PIA) • Paredrine (Norpholedrine, Oxamphetamine) • Phenethylamine (PEA) • PholedrinePhenpromethaminePrenylaminePropylamphetamineTiflorex (Flutiorex) • Tyramine (TRA) • XylopropamineZylofuramine; Piperazines:2,5-Dimethoxy-4-bromobenzylpiperazine (2C-B-BZP) • Benzylpiperazine (BZP) • Methoxyphenylpiperazine (MeOPP; Paraperazine) • Methylbenzylpiperazine (MBZP) • Methylenedioxybenzylpiperazine (MDBZP; Piperonylpiperazine); Others: 2-Amino-1,2-dihydronaphthalene (2-ADN) •2-Aminoindane (2-AI) • 2-Aminotetralin (2-AT) • 4-Benzylpiperidine (4-BP) • 5-IAIClofenciclanCyclopentamineCypenamineCyprodenateFeprosidnineGilutensinHeptaminolHexacyclonateIndanylaminopropane (IAP) • IndanorexIsomethepteneMethylhexanamineNaphthylaminopropane (NAP) • OctodrinePhthalimidopropiophenonePropylhexedrine (Levopropylhexedrine) • Tuaminoheptane (Tuamine)

Enzyme
Inhibitors

Anabolism

PAH Inhibitors

3,4-Dihydroxystyrene

TH Inhibitors

3-IodotyrosineAquayamycinBulbocapnineMetirosineOudenone

AAAD / DDC Inhibitors

BenserazideCarbidopaGenisteinMethyldopa

Catabolism

MAO Inhibitors

Nonselective: BenmoxinCaroxazoneEchinopsidineFurazolidoneHydralazineIndantadolIproclozideIproniazidIsocarboxazidIsoniazidLinezolidMebanazineMetfendrazineNialamideOctamoxinParaxazonePhenelzinePheniprazinePhenoxypropazinePivalylbenzhydrazineProcarbazineSafrazineTranylcypromine; MAO-A Selective: AmiflamineBazinaprineBefloxatoneBefolBrofaromineCimoxatoneClorgilineEsuproneHarmala alkaloids(Harmine, Harmaline, Tetrahydroharmine, Harman, Norharman, etc) • Methylene BlueMetralindoleMinaprineMoclobemidePirlindoleSercloremineTetrindoleToloxatoneTyrima; MAO-B Selective: D-DeprenylL-Deprenyl (Selegiline) •LadostigilLazabemideMilacemideMofegilinePargylineRasagiline

COMT Inhibitors

EntacaponeTolcapone

DBH Inhibitors

BupicomideDisulfiramDopastinFusaric AcidNepicastatPhenopicolinic AcidTropolone

Others

Precursors

L-PhenylalanineL-TyrosineL-DOPA (Levodopa)

Cofactors

Ferrous Iron (Fe2+) • TetrahydrobiopterinVitamin B3 (Niacin, NicotinamideNADPH) • Vitamin B6 (Pyridoxine, Pyridoxamine, PyridoxalPyridoxal Phosphate) • Vitamin B9 (Folic AcidTetrahydrofolic Acid) • Vitamin C (Ascorbic Acid) • Zinc (Zn2+)

Others

Activity Enhancers: Benzofuranylpropylaminopentane (BPAP) • Phenylpropylaminopentane (PPAP); Toxins: Oxidopamine (6-Hydroxydopamine)

Serotonergics

Receptor
ligands

5-HT1A

Agonists: Azapirones: AlnespironeBinospironeBuspironeEnilospironeEptapironeGepironeIpsapironePerospironeRevospironeTandospironeTiospironeUmespironeZalospirone; Antidepressants: EtoperidoneNefazodoneTrazodone; Antipsychotics:AripiprazoleAsenapineClozapineQuetiapineZiprasidone; Ergolines: DihydroergotamineErgotamineLisurideMethysergideLSD; Tryptamines: 5-CT5-MeO-DMT5-MTBufoteninDMTPsilocinPsilocybin; Others: 8-OH-DPATAdatanserinBefiradolBMY-14802DimemebfeEbalzotanEltoprazineF-11,461F-12,826F-13,714F-14,679F-15,063F-15,599FlesinoxanFlibanserinLesopitronLu AA21004LY-293,284LY-301,317MKC-242NBUMPOsemozotanOxaflozanePardoprunoxPiclozotanRauwolscineRepinotanRoxindoleRU-24969S-15535SarizotanSSR-181,507SunepitronU-92016AUrapidilVilazodoneXaliprodenYohimbine
Antagonists: Antipsychotics: IloperidoneRisperidoneSertindole; Beta Blockers: AlprenololCyanopindololIodocyanopindololOxprenololPindobindPindololPropranololTertatolol; Others: AV965BMY-7378DotarizineFlopropioneGR-46611IsamoltaneLecozotanMetitepine/MethiothepinMPPFNAN-190PRX-00023RobalzotanS-15535SB-649915SDZ 216-525SpiperoneSpiramideSpiroxatrineUH-301WAY-100,135WAY-100,635Xylamidine

5-HT1B

Agonists: Lysergamides: DihydroergotamineErgotamineMethysergide; Piperazines: EltoprazineTFMPP; Triptans: AvitriptanEletriptanSumatriptanZolmitriptan; Tryptamines: 5-CT5-MT; Others: CGS-12066ACP-93,129CP-94,253CP-135,807RU-24969
Antagonists: Lysergamides: Metergoline; Others: AR-A000002ElzasonanGR-127,935IsamoltaneMetitepine/MethiothepinSB-216,641SB-224,289SB-236,057Yohimbine

5-HT1D

Agonists: Lysergamides: DihydroergotamineMethysergide; Triptans: AlmotriptanAvitriptanEletriptanFrovatriptanNaratriptanRizatriptanSumatriptanZolmitriptan; Tryptamines: 5-CT5-MT; Others: CP-135,807CP-286,601GR-46611L-694,247L-772,405PNU-109,291PNU-142,633
Antagonists: Lysergamides: Metergoline; Others: AlniditanBRL-15572ElzasonanGR-127,935KetanserinLY-310,762LY-367,642LY-456,219LY-456,220Metitepine/MethiothepinRitanserinYohimbineZiprasidone

5-HT1E

Agonists: Lysergamides: Methysergide; Triptans: Eletriptan; Tryptamines: Tryptamine
Antagonists: Metitepine/Methiothepin

5-HT1F

Agonists: Triptans: EletriptanNaratriptanSumatriptan; Tryptamines: 5-MT; Others: LY-334,370
Antagonists: Metitepine/Methiothepin

5-HT2A

Agonists: Lysergamides: ALD-52ErgonovineLisurideLA-SS-AzLSDLSD-PipLysergic acid 2-butyl amideMethysergide; Phenethylamines: 25I-NBMD25I-NBOH25I-NBOMe2C-B2C-B-FLY2CB-Ind2C-E2C-I2C-T-22C-T-72C-T-212CBCB-NBOMe2CBFly-NBOMeBromo-DragonFLYDOBDOCDOIDOMMDAMDMAMescalineTCB-2TFMFly; Piperazines: BZPQuipazineTFMPP; Tryptamines: 5-CT5-MeO-α-ET5-MeO-α-MT5-MeO-DET5-MeO-DiPT5-MeO-DMT5-MeO-DPT5-MTα-ETα-Methyl-5-HTα-MTBufoteninDETDiPTDMTDPTPsilocinPsilocybin; Others: AL-34662AL-37350ADimemebfeMedifoxamineOxaflozanePNU-22394RH-34
Antagonists: Atypical Antipsychotics: AmperozideAripiprazoleClozapineGevotrolineIloperidoneMelperoneOlanzapinePaliperidonePimozideQuetiapineRisperidoneSertindoleZiprasidoneZotepine; Typical Antipsychotics: LoxapinePipamperone;Antidepressants: AmitriptylineAmoxapineEtoperidoneMianserinMirtazapineNefazodoneTrazodone; Others: 5-I-R91150AC-90179AdatanserinAltanserinAMDAAPD-215BlonanserinCinanserinCyproheptadineDeramciclaneDotarizineEplivanserinEsmirtazapineFananserinFlibanserinKetanserinKML-010LubazodoneMepiprazoleMetitepine/MethiothepinNanteninePimavanserinPizotifenPruvanserinRauwolscineRitanserinSarpogrelateSetoperoneSpiperoneSpiramideSR-46349BVolinanserinXylamidineYohimbine

5-HT2B

Agonists: Oxazolines: 4-MethylaminorexAminorex; Phenethylamines: ChlorphentermineCloforexDOBDOCDOIDOMFenfluramineMDAMDMANorfenfluramine; Tryptamines: 5-CT5-MTα-Methyl-5-HT; Others: BW-723C86CabergolinemCPPPergolidePNU-22394Ro60-0175
Antagonists: AgomelatineAsenapineEGIS-7625KetanserinLisurideLY-272,015Metitepine/MethiothepinRauwolscineRitanserinRS-127,445SarpogrelateSB-200,646SB-204,741SB-206,553SB-215,505SB-221,284SB-228,357SDZ SER-082TegaserodYohimbine

5-HT2C

Agonists: Phenethylamines: 2C-B2C-E2C-I2C-T-22C-T-72C-T-21DOBDOCDOIDOMMDAMDMAMescaline; Piperazines: AripiprazolemCPPTFMPP; Tryptamines: 5-CT5-MeO-α-ET5-MeO-α-MT5-MeO-DET5-MeO-DiPT5-MeO-DMT5-MeO-DPT5-MTα-ETα-Methyl-5-HTα-MTBufoteninDETDiPTDMTDPTPsilocinPsilocybin; Others: A-372,159AL-38022ACP-809,101DimemebfeLorcaserinMedifoxamineMK-212ORG-37,684OxaflozanePNU-22394Ro60-0175VabicaserinWAY-629WAY-161,503YM-348
Antagonists: Atypical Antipsychotics: ClozapineIloperidoneMelperoneOlanzapinePaliperidonePimozideQuetiapineRisperidoneSertindoleZiprasidoneZotepine; Typical Antipsychotics: ChlorpromazineLoxapinePipamperone; Antidepressants:AgomelatineAmitriptylineAmoxapineEtoperidoneFluoxetineMianserinMirtazapineNefazodoneNortriptylineTrazodone; Others: AdatanserinCinanserinCyproheptadineDeramciclaneDotarizineEltoprazineEsmirtazapineFR-260,010KetanserinKetotifenLatrepirdineLu AA24530Metitepine/MethiothepinMethysergidePizotifenRitanserinRS-102,221SB-200,646SB-206,553SB-221,284SB-228,357SB-242,084SB-243,213SDZ SER-082Xylamidine

5-HT3

Agonists: Piperazines: BZPQuipazine; Tryptamines: 2-Methyl-5-HT5-CT; Others: ChlorophenylbiguanideButanolEthanolHalothaneIsofluraneRS-56812SR-57,227SR-57,227-ATolueneTrichloroethaneTrichloroethanolTrichloroethyleneYM-31636
Antagonists: Antiemetics: AS-8112AlosetronAzasetronBatanoprideBemesetronCilansetronDazoprideDolasetronGranisetronLerisetronOndansetronPalonosetronRamosetronRenzaprideTropisetronZacoprideZatosetron; Atypical Antipsychotics: ClozapineOlanzapineQuetiapine; Tetracyclic Antidepressants: AmoxapineMianserinMirtazapine; Others: ICS-205,930Lu AA21004Lu AA24530MDL-72,222MemantineNitrous OxideRicasetronSevofluraneThujone  • Xenon

5-HT4

Agonists: Gastroprokinetic Agents: CinitaprideCisaprideDazoprideMetoclopramideMosapridePrucaloprideRenzaprideTegaserodZacopride; Others: 5-MTBIMU-8CJ-033,466PRX-03140RS-67333RS-67506SL65.0155TD-5108
Antagonists: GR-113,808GR-125,487L-LysinePiboserodRS-39604RS-67532SB-203,186

5-HT5A

Agonists: Lysergamides: ErgotamineLSD; Tryptamines: 5-CT; Others: Valerenic Acid
Antagonists: AsenapineLatrepirdineMetitepine/MethiothepinRitanserinSB-699,551
* Note that the 5-HT5B receptor is not functional in humans.

5-HT6

Agonists: Lysergamides: DihydroergotamineErgotamineLisurideLSDMesulergineMetergolineMethysergide; Tryptamines: 2-Methyl-5-HT5-BT5-CT5-MTBufoteninE-6801E-6837EMD-386,088EMDTLY-586,713N-Methyl-5-HTTryptamine; Others:WAY-181,187WAY-208,466
Antagonists: Antidepressants: AmitriptylineAmoxapineClomipramineDoxepinMianserinNortriptyline; Atypical Antipsychotics: AripiprazoleAsenapineClozapineFluperlapineIloperidoneOlanzapineTiospirone; Typical Antipsychotics: ChlorpromazineLoxapine; Others: BGC20-760BVT-5182BVT-74316EGIS-12233GW-742,457KetanserinLatrepirdineLu AE58054Metitepine/MethiothepinMS-245PRX-07034RitanserinRo 04-6790Ro 63-0563SB-258,585SB-271,046SB-357,134SB-399,885SB-742,457

5-HT7

Agonists: Lysergamides: LSD; Tryptamines: 5-CT5-MTBufotenin; Others: 8-OH-DPATAS-19BifeprunoxLP-12LP-44RU-24,969Sarizotan
Antagonists: Lysergamides: 2-Bromo-LSDBromocriptineDihydroergotamineErgotamineMesulergineMetergolineMethysergide; Antidepressants: AmitriptylineAmoxapineClomipramineImipramineMaprotilineMianserin; Atypical Antipsychotics: AmisulprideAripiprazoleClozapineOlanzapineRisperidoneSertindoleTiospironeZiprasidoneZotepine; Typical Antipsychotics: ChlorpromazineLoxapine; Others: ButaclamolEGIS-12233KetanserinLY-215,840Metitepine/MethiothepinPimozideRitanserinSB-258,719SB-258,741SB-269,970SB-656,104SB-656,104-ASB-691,673SLV-313SLV-314SpiperoneSSR-181,507

Reuptake
Inhibitors

SERT

Selective Serotonin Reuptake Inhibitors (SSRIs): AlaproclateCitalopramDapoxetineDesmethylcitalopramDesmethylsertralineEscitalopramFemoxetineFluoxetineFluvoxamineIndalpineIfoxetineLitoxetineLu AA21004LubazodoneParoxetinePirandamineRTI-353SeproxetineSertralineVilazodoneZimelidine; Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs): BicifadineDesvenlafaxineDuloxetineLevomilnacipranMilnacipranSibutramineVenlafaxine; Serotonin-Norepinephrine-Dopamine Reuptake Inhibitors (SNDRIs): BrasofensineDiclofensineDOV-102,677DOV-21,947DOV-216,303NS-2359SEP-225,289SEP-227,162Tesofensine; Tricyclic Antidepressants (TCAs): AmitriptylineButriptylineCianopramineClomipramineDesipramineDosulepinDoxepinImipramineLofepramineNortriptylinePipofezineProtriptylineTrimipramine; Tetracyclic Antidepressants (TeCAs): Amoxapine; Piperazines: NefazodoneTrazodone; Antihistamines: BrompheniramineChlorpheniramineDiphenhydramineMepyramine/PyrilaminePheniramineTripelennamine; Opioids: Meperidine (Pethidine) • MethadonePropoxyphene; Others: CocaineCP-39,332CyclobenzaprineDextromethorphanDextrorphanEXP-561FezolamineMesembrineNefopamPIM-35PridefrineRoxindoleSB-649,915Ziprasidone

VMAT

IbogaineReserpineTetrabenazine

Releasing
Agents

Aminoindanes: 5-IAIETAIMDAIMDMAIMMAITAI; Aminotetralins: 6-CAT8-OH-DPATMDATMDMAT; Oxazolines: 4-MethylaminorexAminorexClominorexFluminorex; Phenethylamines (also Amphetamines, Cathinones, Phentermines, etc): 2-Methyl-MDA4-CAB4-FA4-FMA4-HA4-MTA5-APDB5-Methyl-MDA6-APDB6-Methyl-MDAAmiflamineBDBBOHBrephedroneButyloneChlorphentermineCloforexDiethylcathinoneDimethylcathinoneDMADMMAEBDBEDMAEthyloneEtolorexFenfluramine(Dexfenfluramine) • FlephedroneIAPIMPLophophineMBDBMDAMDEAMDHMAMDMAMDMPEAMDOHMDPEAMephedroneMethedroneMethyloneMMAMMDAMMDMANAPNorfenfluraminepBApCApIAPMAPMEAPMMATAP; Piperazines:2C-B-BZPBZPMBZPmCPPMDBZPMeOPPMepiprazolepFPPTFMPP; Tryptamines: 4-Methyl-αET4-Methyl-αMT5-CT5-MeO-αET5-MeO-αMT5-MTαETαMTDMTTryptamine (itself); Others: IndeloxazineTramadolViqualine

Enzyme
Inhibitors

Anabolism

TPH

AGN-2979Fenclonine

AAAD

BenserazideCarbidopaGenisteinMethyldopa

Catabolism

MAO

Nonselective: BenmoxinCaroxazoneEchinopsidineFurazolidoneHydralazineIndantadolIproclozideIproniazidIsocarboxazidIsoniazidLinezolidMebanazineMetfendrazineNialamideOctamoxinParaxazonePhenelzinePheniprazinePhenoxypropazinePivalylbenzhydrazineProcarbazineSafrazineTranylcypromine; MAO-A Selective: AmiflamineBazinaprineBefloxatoneBefolBrofaromineCimoxatoneClorgilineEsuproneHarmala alkaloids (Harmine, Harmaline,Tetrahydroharmine, Harman, Norharman, etc) • Methylene BlueMetralindoleMinaprineMoclobemidePirlindoleSercloremineTetrindoleToloxatoneTyrima

Others

Precursors

L-Tryptophan5-HTP

Cofactors

Ferrous iron (Fe2+) • Magnesium (Mg2+) • TetrahydrobiopterinVitamin B3 (Niacin, NicotinamideNADPH) • Vitamin B6 (Pyridoxine, Pyridoxamine, PyridoxalPyridoxal phosphate) • Vitamin B9 (Folic AcidTetrahydrofolic acid) • Vitamin C (Ascorbic acid) • Zinc (Zn2+)

Others

Activity Enhancers: BPAPPPAP; Reuptake Enhancers: Tianeptine

Sigmaergics

Receptor
Ligands

Agonists

3-PPP4-IBP4-PPBPAfobazoleAllylnormetazocineAmitriptylineAmphetamineBerberineCitalopramClorgylineCocaineCyclazocineDextrallorphanDextromethorphanDextrorphanDTGBD-1,008DesipramineDHEADimethyltryptamineDimemorfanDitolylguanidineEMD-57,445EscitalopramFluoxetineFluvoxamineHeroinIgmesineImipramineJO-1,784L-687,384LamotrigineLu 28-179MDMAMethamphetamineMorphineNoscapineOPC-14,523OpipramolPB-28PD-144,415PentazocinePentoxyverinePhencyclidinePRE-084PregnenoloneRTI-55SA-4503SertralineSiramesineVenlafaxine

Antagonists

BD-1,047BD-1,063BMY-14,802E-5,842HaloperidolNE-100ProgesteroneRimcazoleSM-21

Unknown

Gevotroline

Tryptamines

2-Methyl-5-HT4-Acetoxy-DET4-Acetoxy-DIPT4-Acetoxy-DMT4-HO-αMT4-HO-DIPT4-HO-MET4-MeO-DMT4-Methyl-αET4-Methyl-αMT5-Benzyloxytryptamine5-Bromo-DMT5-Carboxamidotryptamine5-Fluoro-αMT5-HO-αMT5-HTP5-Fluoro-DMT5-Methyl-DMT5-Methoxytryptamine5-MeO-7,N,N-TMT5-MeO-αET  • 5-MeO-αMT5-MeO-DALT5-MeO-DET5-MeO-DIPT5-MeO-DMT5-MeO-DPT5-MeO-MIPT5,7-Dihydroxytryptamine7-Methyl-αET7-Methyl-DMTαETαMTAeruginascinAL-37350ABW-723C86BaeocystinBufotenidineBufoteninDALTDesformylflustrabromineDETDiPTDMTDPTEthocybinEiPTEMDTEthocinFGIN-127FGIN-143IbogaineIprocinMETMiPTMiprocinMelatoninMS-245NASNMTNorbaeocystinNormelatoninOxypertinePiPTPsilocinPsilocybinRizatriptanSerotoninSumatriptanTryptamineTryptophanYohimbineYuremamineZolmitriptan

Drugs from TiHKAL

AL-LADDBTDETDiPT5-MeO-α-MTDMT2,α-DMTα,N-DMTDPTEiPTα-ETETH-LADHarmalineHarmine4-HO-DBT4-HO-DET4-HO-DiPT4-HO-DMT5-HO-DMT4-HO-DPT4-HO-MET4-HO-MiPT4-HO-MPT4-HO-pyr-TIbogaineLSDMBT4,5-MDO-DiPT5,6-MDO-DiPT4,5-MDO-DMT5,6-MDO-DMT5,6-MDO-MiPT2-Me-DET2-Me-DMTMelatonin5-MeO-DET5-MeO-DiPT5-MeO-DMT4-MeO-MiPT5-MeO-MiPT5,6-MeO-MiPT5-MeO-NMT5-MeO-pyr-T6-MeO-THH5-MeO-TMT5-MeS-DMTMiPTα-MTNETNMTPRO-LADpyr-TTryptamineTetrahydroharmineα,N,O-TMS

5-MeO-DMT

5-MeO-DMT

Systematic (IUPAC) name

2-(5-methoxy-1H-indol-3-yl)-N,N-dimethylethanamine

Identifiers

CAS number
1019-45-0

ATC code
?

PubChem
CID 1832

IUPHAR ligand ID
145

ChemSpider
1766

Chemical data

Formula
C13H18N2O

Mol. mass
218.298 g/mol

SMILES
eMolecules & PubChem

Therapeutic considerations

Pregnancy cat.
?

Legal status
? (UK) Unscheduled(US)

Routes
Smoked, Insufflated

5-MeO-DMT (5-methoxy-dimethyltryptamine) is a powerful psychedelic tryptamine. It is found in a wide variety of plant and psychoactive toad species, and like its close relatives DMT and bufotenin (5-OH-DMT), it has been used as an entheogen by South American shamans for thousands of years.

Chemistry

5-MeO-DMT was first synthesized in 1936, and in 1959 it was isolated as one of the psychoactive ingredients of Anadenanthera peregrina seeds used in preparing yopo snuff. It was once believed to be a major component of the psychoactive effects of the snuff. It occurs in many organisms that contain bufotenin(e) (5-hydroxy-DMT), and is the O-methyl analogue of that compound.

History

Traditionally 5-MeO-DMT has been used in psychedelic snuff made from virola bark resin, and may be a trace constituent of ayahuasca when plants such as Diplopterys cabrerana are used as an admixture. 5-MeO-DMT is also found in the venom of theColorado River toad (Bufo alvarius), although there is no direct evidence this was used as a hallucinogen until recent times.

Religious Use

Traditional

Modern

5-MeO-DMT is a sacrament of the Church of the Tree of Life. From approximately 1971 to the late 1980s 5-MeO-DMT was discreetly available to members of the Church of the Tree of Life from Inner Center and after 1986 was also available to some other religious groups from Inner Center.[1] Between 1970 and 1990 smoking of 5-MeO-DMT on parsley was probably one of the two most common forms of ingestion in the United States.[1] A member of the Church of the Tree of Life estimates there were less than 6000 active members in 1979.[2]

Use and effects

Bufo alvarius, which has 5-MeO-DMT in its venom and skin.

When used as a drug in its purified form, 5-MeO-DMT is smoked, insufflated, or injected and is active at a dose of as little as 2 mg. 5-MeO-DMT is also active orally, when taken with a monoamine oxidase inhibitor, but according to numerous reports, the combination with MAOI is extremely unpleasant and has a strong body load. According to the researcher Jonathan Ott, 5-MeO-DMT is active orally with doses over 30 mg without aid of an MAOI.

The onset of effects occurs within seconds after smoking/injecting, or minutes after insufflating, and the experience is sometimes described as similar to a near-death experience. Peak effects last for approximately 5-10 minutes when smoked. When insufflated, the peak effects are considerably less intense, but last for 15-25 minutes on average.

Although similar in many respects to its close relatives DMT and bufotenin (5-OH-DMT), the effects are typically not as visual. Some users report experiencing no visual effects from it even at very high doses.[3]
Some report the effects to be unpleasant causing nausea and the feeling of being "sat on by an elephant".[4]

Erowid lists the following effects for smoked 5-MeO-DMT:[3]

Positive
  • immersive experiences
  • powerful "rushing" sensation
  • radical perspective shifting
  • profound life-changing spiritual experiences
  • some people experience erotic / sensual enhancement
  • occasional euphoria
  • internal visions (actual visual effects not as common)
  • journey into mind
Neutral
  • short duration
  • change in perception of time
  • experience of "the void"
  • lack of memory of experience
  • muscle jerking, twitching, abnormal vocalizations
  • unconsciousness / nonresponsiveness lasting 5-20 minutes
  • dissociation
[edit]Negative
  • overly-intense experiences
  • nausea[4]
  • sense of pressure in the body[4]
  • hard on the lungs to smoke
  • difficulty integrating experiences
  • fear, terror and panic
  • dysphoria (bad feelings)
  • fast onset and intensity can lead to problems if not prepared (dropped pipe, knocking things over, falling & hitting head, etc)

[edit]Legality

[edit]International Law
[edit]Denmark

As of December 1, 2004, 5-MeO-DMT is legally restricted to "medical or scientific purposes". See EMCDDA.

[edit]Germany

Schedule I / Highest level of control, unable to be prescribed, manufactured, or possessed as of Sep, 1999. (listed as [2-(5-Methoxyindol-3-yl)ethyl]dimethylazan) (see Deutsche BtMG or http://www.silicium-sensei.de/projecte/drugs/news/news.html)

[edit]Greece

5-MeO-DMT became a controlled substance in Greece on Feb 18, 2003 [EU Legal Database].

[edit]New Zealand

5-MeO-DMT is Schedule I (Class A) in New Zealand.

[edit]Sweden

Controlled in Sweden as of Oct 1, 2004 (see notisum.se)

[edit]Switzerland

5-MeO-DMT is Schedule I in Switzerland. [unconfirmed]

[edit]Romania

5-MeO-DMT is illegal in Romania since feb 2010.

[edit]US Federal Law

On August 21, 2009, the DEA issued a Notice of Proposed Rulemaking to initiate placing 5-MeO-DMT into Schedule I of the Controlled Substances Act (the most restrictive category).[5] Comment DEA-2009-0008-0007.1 requested a 180 day extension of the period for public comment and requests for hearings, objected to the proposed rule on multiple grounds including Constitutional issues, identified the submitter as a person who would be "adversely affected and aggrieved by the proposed ruling" and requested an exemption for religious use if DEA did place 5-MeO-DMT in Schedule I "as an attempt to define and clarify some legal issues."[2]

On September 29 and 30, 2009, the DEA posted the Supporting & Related Materials for the NPRM while retaining the September 21, 2009 Due date for comments.[6]

On October 28, 2009 DEA reopened the period for public comment because it had not posted two Supporting & Related Materials documents online during the original period for public comment. Documents and comments were split between Docket ID: DEA-2009-0008 and Docket ID: DEA-2009-0013 in a manner which creates difficulty and in viewing all documents and determining where and how to submit comments online. The two Supporting & Related Materials documents were not posted to Docket ID: DEA-2009-0013 until November 3, 2009 but the 30 day period for public comment was not changed from November 27, 2009.[7]

[edit]US State Law
[edit]Nebraska

Schedule I[8]

[edit]Oklahoma

Schedule I[9]

[edit]S. Dakota

Schedule I[10]

[edit]See also

[edit]References

  1. ^ a b Erowid. "Erowid 5-Meo-DMT Timeline".
  2. ^ a b "DEA-2009-0008-0007.1".
  3. ^ a b Erowid. "Effects".
  4. ^ a b c Psychedelic Chemistry by Michael Valentine Smith, Page 40, ISBN 0915179105
  5. ^ DEA-2009-0008. "Placement of 5-Methoxy-N,N-Dimethyltryptamine Into Schedule I of the Controlled Substances Act by DEA, August 2009".
  6. ^ http://www.regulations.gov/search/Regs/home.html#docketDetail?R=DEA-2009-0008
  7. ^ http://www.regulations.gov/search/Regs/home.html#docketDetail?R=DEA-2009-0013
  8. ^ "Statutes Relating to Pharmacy" (PDF). Nebraska Health and Human Services System. 2005. Retrieved 2008-07-04.
  9. ^ "Section 2-204 – Schedule I".
  10. ^ "SB 25 revise the schedule of certain controlled…".

[edit]External links

Bufotenin

From Wikipedia, the free encyclopedia

Bufotenin

Systematic (IUPAC) name

3-(2-dimethylaminoethyl)-1H-indol-5-ol

Identifiers

CAS number
487-93-4

ATC code
None

PubChem
CID 10257

IUPHAR ligand ID
144

ChemSpider
9839

Chemical data

Formula
C12H16N2O

Mol. mass
204.268 g/mol

SMILES
eMolecules & PubChem

Synonyms
N,N-dimethyl-5-hydroxytryptamine, 5-hydroxy-dimethyltryptamine, bufotenine, cebilcin

Physical data

Melt. point
146–147 °C (295–297 °F)

Boiling point
320 °C (608 °F)

Therapeutic considerations

Pregnancy cat.
?

Legal status
Schedule I (US)

Routes
Parenteral

Bufotenin (also known as bufotenine and cebilcin), or 5-hydroxy-dimethyltryptamine (5-HO-DMT or 5-OH-DMT), is a tryptamine related to the neurotransmitter serotonin. It is an alkaloid found in the skin of some species of toads; in mushrooms, higher plants, and mammals.[1]

The name bufotenin originates from the Bufo genus of toads, which includes several species of psychoactive toads (such as Bufo alvarius and Bufo marinus) that secrete bufotoxins from their parotoid glands.[2]Bufotenin is similar in chemical structure to the psychedelics psilocin (4-HO-DMT), 5-MeO-DMT, and DMT, chemicals which also occur in some of the same plant and animal species as bufotenin. Psychedelic effects of bufotenin in humans have been observed in some studies.

Contents

[hide]

[edit]Nomenclature

Bufotenin (bufotenine) is also known by the chemical names 5-hydroxy-dimethyltryptamine (5-HO-DMT), N,N-dimethyl-5-hydroxytryptamine, dimethyl serotonin,[3] and mappine.[3]

[edit]History

Bufotenine was first isolated, from toad skin, and named by the Austrian chemist Handovsky at the University of Prague during World War I.[4] The structure of bufotenine was first confirmed in 1934 by Heinrich Wieland’s laboratory in Munich, and the first reported synthesis of bufotenine was by Toshio Hoshino in 1936.[4]

[edit]Sources

[edit]Toads

See also: Psychoactive toad

Bufotenin is a chemical constituent in the venom and eggs of several species of toads belonging to the Bufo genus, including Bufo alvarius and Bufo marinus. Extracts of toad venom, containing bufotenin and other bioactive compounds, have been used in some traditional medicines such as ch’an su (probably derived from Bufo gargarizans), which has been used medicinally for centuries in China.[5]

The toad was "recurrently depicted in Mesoamerican art,"[6] which some authors have interpreted as indicating that the effects of ingesting Bufo secretions have been known in Mesoamerica for many years; however, others doubt that this art provides sufficient "ethnohistorical evidence" to support the claim. [5]

In addition to bufotenine, Bufo venoms also contain digoxin-like cardiac glycosides, and ingestion of the venom can be fatal. Ingestion of Bufo toad venom and eggs by humans has resulted in several reported cases of poisoning,[7][8][9] some of which resulted in death.[9][10][11]

Contemporary reports indicate that bufotenine-containing toad venom has been used as a street drug; that is, as an aphrodisiac, ingested orally in the form of ch’an su,[9] and as a psychedelic, by smoking or orally ingesting Bufo toad venom or dried Bufoskins. The use of chan’su and love stone (a related toad venom preparation used as an aphrodisiac in the West Indies) has resulted in several cases of poisoning and at least one death.[9][12] The practice of orally ingesting toad venom has been referred to in popular culture and in the scientific literature as toad licking and has drawn media attention[13][14]. Albert Most, founder of the Church of the Toad of Light and a proponent of recreational use of Bufo alvarius venom, published a booklet titled Bufo alvarius: The Psychedelic Toad of the Sonoran Desert[15][16] in 1983 which explained how to extract and smoke the secretions.

Bufotenin is also present in the skin secretion of three arboreal amphibian species of the Osteocephalus genus (Osteocephalus taurinus, Osteocephalus oophagus, and Osteocephalus langsdorffii) from the Amazon and Atlantic rain forests.[17]

[edit]Anadenanthera seeds

Bufotenin is a constituent of the seeds of Anadenanthera colubrina and Anadenanthera peregrina trees. Anadenanthera seeds have been used as an ingredient in psychedelic snuff preparations by indigenous cultures of Central and South America.[18]

[edit]Mushrooms

Bufotenine is also found in several species of Amanita mushrooms, including Amanita muscaria(disputed), Amanita citrina, and Amanita porphyria.[4]

[edit]Other sources

Bufotenin has been identified as a component in the latex of the takini (Brosimum acutifolium) tree, which is used as a psychedelic by South American shamans,[19] and in the seeds of Mucuna pruriens [20]

[edit]Pharmacology

[edit]Uptake and elimination

In rats, subcutaneously administered bufotenin (1–100 μg/kg) distributes mainly to the lungs, heart, and blood, and to a much lesser extent, the brain (hypothalamus, brain stem, striatum, and cerebral cortex) and liver. It reaches peak concentrations at 1 hour and is nearly completely eliminated within 8 hours.[21] In humans, bufotenine is rapidly absorbed following intravenous administration and is excreted in the urine predominantly (70%) in the form of 5-HIAA, an endogenous metabolite of serotonin, while roughly 4% is eliminated unmetabolized in the urine. Orally administered bufotenine undergoes extensive first-pass metabolism by the enzyme monoamine oxidase.

[edit]Lethal dose

The acute toxicity (LD50) of bufotenin in rodents has been estimated at 200 to 300 mg/kg. Death occurs by respiratory arrest.[18]

[edit]Effects in humans
[edit]Fabing & Hawkins (1955)

In 1955, Fabing and Hawkins administered bufotenin intravenously at doses of up to 16 mg to prison inmates at Ohio State Penitentiary. [22] A troubling toxic blood circulation effect causing a purpling of the face was seen in these tests.

A subject given 1 mg reported “a tight feeling in the chest” and prickling “as if he had been jabbed by needles.” This was accompanied by a “fleeting sensation of pain in both thighs and a mild nausea.” [22]

Another subject given 2 mg reported “tightness in his throat”. He had tightness in the stomach, tingling in pretibial areas, and developed a purplish hue in the face indicating blood circulation problems. He vomited after 3 minutes. [22]

Another subject given 4 mg complained of “chest oppression” and that “a load is pressing down from above and my body feels heavy.” The subject also reported “numbness of the entire body” and “a pleasant Martini feeling-my body is taking charge of my mind”. The subject reported he saw red spots passing before his eyes and red-purple spots on the floor, and the floor seemed very close to his face. Within 2 minutes these visual effects were gone, and replaced by a yellow haze, as if he were looking through a lens filter. [22]

Fabing and Hawkins commented that bufotenin’s psychedelic effects were "reminiscent of LSD and mescaline but develop and disappear more quickly, indicating rapid central action and rapid degradation of the drug".

[edit]Isbell (1956)

In 1956, Dr. Harris S. Isbell at the Public Health Service Hospital in Lexington, Kentucky experimented with bufotenine as a snuff. He reported “no subjective or objective effects were observed after spraying with as much as 40 mg bufotenine”; however subjects who received 10-12 mg injected intramuscularly reported “elements of visual hallucinations consisting of a play of colors, lights, and patterns”.[4]

[edit]Turner & Merlis (1959)

Turner and Merlis (1959) [23] experimented with intravenous administration of bufotenine (as the water soluble creatinine sulfate salt) to schizophrenics at a New York state hospital. They reported that when one subject received 10 mg during a 50-second interval, “the peripheral nervous system effects were extreme: at 17 seconds, flushing of the face, at 22 seconds, maximal inhalation, followed by maximal hyperventilation for about 2 minutes, during which the patient was unresponsive to stimuli; her face was plum-colored". Finally, Turner and Merlis reported that:

“on one occasion, which essentially terminated our study, a patient who received 40 mg intramuscularly, suddenly developed an extremely rapid heart rate; no pulse could be obtained; no blood pressure measured. There seemed to have been an onset of auricular fibrillation…extreme cyanosis developed. Massage over the heart was vigorously executed and the pulse returned to normal…shortly thereafter the patient, still cyanotic, sat up saying: ‘Take that away. I don’t like them’.”

After pushing doses to the morally admissible limit without producing visuals, Turner and Merlis conservatively concluded: “We must reject bufotenine…as capable of producing the acute phase of Cohoba intoxication”.[4]

[edit]McLeod and Sitaram (1985)

A 1985 study by McLeod and Sitaram in humans reported that bufotenine administered intranasally at a dose of 1-16 mg had no effect, other than intense local irritation. When given intravenously at low doses (2-4 mg), bufotenine oxalate caused anxiety but no other effects; however, a dose of 8 mg resulted in profound emotional and perceptual changes, involving extreme anxiety, a sense of imminent death, and visual disturbance associated with color reversal and distortion, and intense flushing of the cheeks and forehead. [24]

[edit]Ott (2001)

In 2001, ethnobotanist Jonathan Ott published the results of a study in which he self-administered free base bufotenine via insufflation (5-100 mg), sublingually (50 mg), intrarectally (30 mg), orally (100 mg) and via vaporization (2-8 mg).[25] Ott reported “visionary effects" of intranasal bufotenine and that the "visionary threshold dose" by this route was 40 mg, with smaller doses eliciting perceptibly psychoactive effects. He reported that "intranasal bufotenine is throughout quite physically relaxing; in no case was there facial rubescence, nor any discomfort nor disesteeming side effects".

At 100 mg, effects began within 5 minutes, peaked at 35-40 minutes, and lasted up to 90 minutes. Higher doses produced effects that were described as psychedelic, such as "swirling, colored patterns typical of tryptamines, tending toward the arabesque". Free base bufotenin taken sublingually was found to be identical to intranasal use. The potency, duration, and psychedelic action was the same. Ott found vaporized free base bufotenin active from 2-8 mg with 8 mg producing "ring-like, swirling, colored patterns with eyes closed". He noted that the visionary effects of insufflated bufotenine were verified by one colleague, and those of vaporized bufotenine by several volunteers.

Ott concluded that free base bufotenin taken intranasally and sublingually produced effects similar to those of Yopo without the toxic peripheral symptoms, such as facial flushing, observed in other studies in which the drug was administered intravenously.

[edit]Association with schizophrenia and other mental disorders

A study conducted in the late 1960s reported the detection of bufotenin in the urine of schizophrenic subjects;[26] however, subsequent research has failed to confirm these findings.[27][28][29][30]

Studies have detected endogenous bufotenin in urine specimens from individuals with other psychiatric disorders,[31] such as infant autistic patients.[32] Another study indicated that paranoid violent offenders or those who committed violent behaviour towards family members have higher bufotenin levels in their urine than other violent offenders.[33]

A 2010 study utilized a mass spectrometry approach to detect levels of bufotenin in the urine of individuals with severe autism spectrum disorder (ASD), schizophrenia, and asymptomatic subjects. Their results indicate significantly higher levels of bufotenin in the urine of the ASD and schizophrenic groups when compared to asymptomatic individuals.[34]

[edit]Legal status

Bufotenine is regulated as a Schedule I drug (ID number 7403) by the U.S. Drug Enforcement Agency.[3] It is classified as a Schedule I controlled substance according to the Criminal Code Regulations of the Government of the Commonwealth of Australia.[35]

[edit]See also

[edit]References

  1. ^ CID 10257. PubChem. Accessed on May 6, 2007.
  2. ^ Bufo Alvarius. AmphibiaWeb. Accessed on May 6, 2007.
  3. ^ a b c "DEA Drug Scheduling". U.S. Drug Enforcement Agency. Retrieved 2007-08-11.
  4. ^ a b c d e Chilton WS, Bigwood J, Jensen RE (1979). "Psilocin, bufotenine and serotonin: historical and biosynthetic observations". J Psychedelic Drugs. 11 (1-2): 61–9. PMID 392119.
  5. ^ a b Davis W, Weil A (1992). "Identity of a New World Psychoactive Toad". Ancient Mesoamerica 3: 51–9.
  6. ^ Kennedy AB (1982). "Ecce Bufo: The Toad in Nature and in Olmec Iconography". Current Anthropology 23: 273–90. doi:10.1086/202831.
  7. ^ Hitt M, Ettinger DD (1986). "Toad toxicity". N Engl J Med 314 (23): 1517–8. PMID 3702971.
  8. ^ Ragonesi DL (1990). "The boy who was all hopped up". Contemporary Pediatrics 7: 91–4.
  9. ^ a b c d Brubacher JR, Ravikumar PR, Bania T, Heller MB, Hoffman RS (1996). "Treatment of toad venom poisoning with digoxin-specific Fab fragments". Chest 110 (5): 1282–8. doi:10.1378/chest.110.5.1282. PMID 8915235.
  10. ^ Gowda RM, Cohen RA, Khan, IA (2003). "Toad venom poisoning: resemblance to digoxin toxicity and therapeutic implications". Heart 89 (4): e14. doi:10.1136/heart.89.4.e14. PMID 12639891. PMC 1769273.
  11. ^ Lever, Christopher (2001). The Cane Toad: The History and Ecology of a Successful Colonist. Westbury Academic & Scientific Publishing. ISBN 1-84103-006-6.
  12. ^ Centers for Disease Control and Prevention (CDC) (1995). "Deaths associated with a purported aphrodisiac—New York City, February 1993-May 1995". MMWR Morb Mortal Wkly Rep 44 (46): 853–5, 861. PMID 7476839.
  13. ^ The Dog Who Loved to Suck on Toads. NPR. Accessed on May 6, 2007.
  14. ^ Psychoactive toad: Cultural references
  15. ^ Most, A. "Bufo avlarius: The Psychedelic Toad of the Sonoran Desert". http://www.erowid.org. Retrieved 2007-08-12.
  16. ^ http://www.smokymountainnews.com/issues/11_06/11_01_06/out_naturalist.html How ‘bout them toad suckers? Ain’t they clods?] Smoky Mountain News. Accessed on May 6, 2007
  17. ^ Costa TO, Morales RA, Brito JP, Gordo M, Pinto AC, Bloch C Jr. (2005). "Occurrence of bufotenin in the Osteocephalus genus (Anura: Hylidae)". Toxicon 46 (4): 371–5. doi:10.1016/j.toxicon.2005.02.006. PMID 16095048.
  18. ^ a b Repke, David B.; Torres, Constantino Manuel (2006). Anadenanthera: visionary plant of ancient South America. New York: Haworth Herbal Press. ISBN 0-7890-2642-2.
  19. ^ Moretti C, Gaillard Y, Grenand P, Bévalot F, Prévosto JM (2006). "Identification of 5-hydroxy-tryptamine (bufotenine) in takini (Brosimumacutifolium Huber subsp. acutifolium C.C. Berg, Moraceae), a shamanic potion used in the Guiana Plateau". J Ethnopharmacol106 (2): 198–202. doi:10.1016/j.jep.2005.12.022. PMID 16455218.
  20. ^ Chamakura RP (1994). "Bufotenine—a hallucinogen in ancient snuff powders of South America and a drug of abuse on the streets of New York City". Forensic Sci Rev 6 (1): 2–18.
  21. ^ Fuller RW, Snoddy HD, Perry KW (1995). "Psilocin Tissue distribution, metabolism and effects of bufotenine administered to rats". Neuropharmacology 34 (7): 799–804. doi:10.1016/0028-3908(95)00049-C. PMID 8532147.
  22. ^ a b c d Fabing HD, Hawkins, JR (1956). "Intravenous bufotenine injection in the human being". Science 123 (3203): 886–7. doi:10.1126/science.123.3203.886. PMID 13324106.
  23. ^ Turner WJ, Merlis S (1959). "Effects of some indolealkylamines on man". Arch Neurol Psychiatr 81: 121–9.
  24. ^ McLeod WR, Sitaram BR (1985). "Bufotenine reconsidered". Acta Psychiatrica Scandinavica 72 (5): 447–50. doi:10.1111/j.1600-0447.1985.tb02638.x.
  25. ^ Ott J (2001). "Pharmanopo-psychonautics: human intranasal, sublingual, intrarectal, pulmonary and oral pharmacology of bufotenine". J Psychoactive Drugs 33 (4): 403–7. PMID 11824699.
  26. ^ [Faurbye A, Pind K (November 1968). "Occurrence of bufotenin in the urine of schizophrenic patients and normal persons". Nature 220 (5166): 489. doi:10.1038/220489a0. PMID 5686166.
  27. ^ Siegel M (October 1965). "A sensitive method for the detection of n,n-dimethylserotonin (bufotenin) in urine; failure to demonstrate its presence in the urine of schizophrenic and normal subjects". J Psychiatr Res 3 (3): 205–11. doi:10.1016/0022-3956(65)90030-0. PMID 5860629.
  28. ^ Pomilio AB, Vitale AA, Ciprian-Ollivier J, Cetkovich-Bakmas M, Gómez R, Vázquez G. (1999). "Ayahoasca: an experimental psychosis that mirrors the transmethylation hypothesis of schizophrenia". J Ethnopharmacol 65 (1): 29–51. doi:10.1016/S0378-8741(98)00163-9. PMID 10350367.
  29. ^ Ciprian-Ollivier J, Cetkovich-Bakmas MG (1997). "Altered consciousness states and endogenous psychoses: a common molecular pathway?". Schizophrenia Research 28 (2-3): 257–65. doi:10.1016/S0920-9964(97)00116-3. PMID 9468359.
  30. ^ Carpenter WT Jr, Fink EB, Narasimhachari N, Himwich HE (1975). "A test of the transmethylation hypothesis in acute schizophrenic patients". Am J Psychiatry 132 (10): 1067–71. PMID 1058643.
  31. ^ Takeda N, Ikeda R, Ohba K, Kondo M (November 1995). "Bufotenine reconsidered as a diagnostic indicator of psychiatric disorders". Neuroreport 6 (17): 2378–80. doi:10.1097/00001756-199511270-00024. PMID 8747157.
  32. ^ Takeda N (February 1994). "Serotonin-degradative pathways in the toad (Bufo bufo japonicus) brain: clues to the pharmacological analysis of human psychiatric disorders". Comp Biochem Physiol Pharmacol Toxicol Endocrinol 107 (2): 275–81.doi:10.1016/1367-8280(94)90051-5. PMID 7749594.
  33. ^ Räisänen MJ, Virkkunen M, Huttunen MO, Furman B, Kärkkäinen J (September 1984). "Increased urinary excretion of bufotenin by violent offenders with paranoid symptoms and family violence". Lancet 2 (8404): 700–1. doi:10.1016/S0140-6736(84)91263-7.PMID 6147728.
  34. ^ Emanuele E, Colombo R, Martinelli V, Brondino N, Marini M, Boso M, Barale F, Politi P (2010). "Elevated urine levels of bufotenine in patients with autistic spectrum disorders and schizophrenia.". Neuro Endocrinol Lett 31 (1): 117-21. PMID 20150873.
  35. ^ (rtf) Criminal Code Regulation 2005 (SL2005-2). Australian Capital Territory. May 1, 2005. Retrieved 2007-08-12.

 

Ayahuasca

 

  (Redirected from Hoasca)

Ayahuasca being prepared in the Naporegion of Ecuador.

Freshly harvested caapi vine ready for preparation

Banisteriopsis caapi preparation

Beaten caapi ready for boiling

Caapi cooking over an open fire

This entry focuses on the Ayahuasca brew; for information on the vine of the same name, see Banisteriopsis caapi

Ayahuasca (ayawaska pronounced [ajaˈwaska] in the Quechua language) is any of various psychoactive infusions or decoctions prepared from the Banisteriopsis spp. vine, usually mixed with the leaves ofdimethyltryptamine-containing species of shrubs from the Psychotria genus. The brew, first described academically in the early 1950s by Harvard ethnobotanist Richard Evans Schultes, who found it employed for divinatory and healing purposes by Amerindians of Amazonian Colombia, is known by a number of different names (see below).

Preparation

Sections of B. caapi vine are macerated and boiled alone or with leaves from any of a number of other plants, including Psychotria viridis (chacruna) or Diplopterys cabrerana (also known as chaliponga). The resulting brew contains the powerful hallucinogenic alkaloid N,N-dimethyltryptamine (DMT), and MAO inhibiting harmala alkaloids, which are necessary to make the DMT orally active. Though B. caapi is a central ingredient in traditional ayahuasca brews, harmala-containing plants from other plant-medicine cultures, such as Syrian Rue, can be used instead of the vine to make an ayahuasca analogue, yet it isn’t considered ayahuasca, as Caapi vine is considered the main plant in the brew.[citation needed]

Brews can also be made with no DMT-containing plants; Psychotria viridis being substituted by plants such as Justicia pectoralis, Brugmansia, or sacred tobacco, also known as Mapacho (Nicotiana rustica), or sometimes left out with no replacement. The potency of this brew varies radically from one batch to the next, both in potency and psychoactive effect, based mainly on the skill of the shaman or brewer, as well as other admixtures sometimes added and the intent of the ceremony.[citation needed] Natural variations in plant alkaloid content and profiles also affect the final concentration of alkaloids in the brew, and the physical act of cooking may also serve to modify the alkaloid profile of harmala alkaloids.[1][2]

Individual polymorphisms in the cytochrome P450-2D6 enzyme affect the ability of individuals to metabolize harmine.[3] Some natural tolerance to habitual use of ayahuasca (roughly once weekly) may develop through upregulation of the serotonergic system.[4] A phase 1 pharmacokinetic study on Ayahuasca (as Hoasca) with 15 volunteers was conducted in 1993, during the Hoasca Project.[5] A review of the Hoasca Project has been published.[6]

Names

  • "cipó" (generic vine, liana), "caapi", "hoasca", "vegetal", "daime" or "santo daime" in Brazil
  • "yagé" or "yajé" (both pronounced [jaˈhe]) in Tucanoan; popularized in English by the beat generation writers William S. Burroughs and Allen Ginsberg in The Yage Letters.
  • "ayahuasca" or "ayawaska" ("Spirit vine" or "vine of the souls": in Quechua, aya means "spirit" while huasca or waska means "vine") in Ecuador, Bolivia and Peru, and to a lesser extent in Brazil. The spellingayahuasca is the hispanicized version of the name; many Quechua or Aymara speakers would prefer the spelling ayawaska. The name is properly that of the plant B. caapi, one of the primary sources of beta-carbolines for the brew.
  • "natem" amongst the indigenous Shuar people of Peru.
  • "Grandmother"
  • "Shori"

Molecular structure of Harmine.

Molecular structure of Harmaline.

Molecular structure of Tetrahydroharmine.

Chemistry

Harmine compounds are of beta-carboline origin. The three most studied beta-carboline compounds found in the B. caapi vine are harmine, harmaline and tetrahydroharmine. Harmine and harmaline are selective and reversible inhibitors of MAO-A, while tetrahydroharmine is a weak serotonin uptake inhibitor. This inhibition of MAO-A allows DMT to diffuse unmetabolized past the membranes in the stomach and small intestine and eventually get through the blood-brain barrier to activate receptor sites in the brain. Without RIMAs or the MAOI of MAO-A, DMT would be metabolized in the digestive tract and would not have an effect when taken orally[7].

Usage

Urarina shaman, 1988

Ayahuasca is used largely as a religious sacrament. Those whose usage of ayahuasca is performed in non-traditional contexts often align themselves with the philosophies and cosmologies associated with ayahuasca shamanism, as practiced among indigenous peoples like the Urarina of Peruvian Amazonia.[8] The religion Santo Daime uses it.

While non-native users know of the spiritual applications of ayahuasca, a less well-known traditional usage[specify] focuses on the medicinal properties of ayahuasca. Its purgative properties are highly important (many refer to it as la purga, "the purge"). The intense vomiting and occasional diarrhea it induces can clear the body of worms and other tropical parasites,[9] and harmala alkaloids themselves have been shown to be anthelmintic[10] Thus, this action is twofold; a direct action on the parasites by these harmala alkaloids (particularly harmine in ayahuasca) works to kill the parasites, and parasites are expelled through the increased intestinal motility that is caused by these alkaloids.

Dietary taboos are often associated with the use of Ayahuasca[11]. In the rainforest, these tend towards the purification of one’s self – abstaining from spicy and heavily-seasoned foods, excess fat, salt, caffeine, acidic foods (such as citrus) and sex before, after, or both before and after a ceremony. A diet low in foods containing tyramine has been recommended, as the speculative interaction of tyramine and MAOIs could lead to a hypertensive crisis. However, evidence indicates that harmala alkaloids act only on MAO-A, in a reversible way similar to moclobemide (an antidepressant that does not require dietary restrictions).Psychonautic experiments and the absence of dietary restrictions in the highly urban Brazilian ayahuasca church União do Vegetal also suggest that the risk is much lower than perceived, and probably non-existent.[11]

The name ‘ayahuasca’ specifically refers to a botanical decoctions that contains Banisteriopsis caapi. A synthetic version, known as pharmahuasca is a combination of an appropriate MAOI and typically DMT. In this usage, the DMT is generally considered the main psychoactive active ingredient, while the MAOI merely preserves the psychoactivity of orally ingested DMT, which would otherwise be destroyed in the gut before it could be absorbed in the body. Thus, ayahuasqueros and most others working with the brew maintain that the B. caapi vine is the defining ingredient, and that this beverage is not ayahuasca unless B. caapi is in the brew. The vine is considered to be the "spirit" of ayahuasca, the gatekeeper and guide to the otherworldly realms.

In some areas[specify], it is even said that the chakruna or chaliponga admixtures are added only to make the brew taste sweeter. This is a strong indicator of the often wildly divergent intentions and cultural differences between the native ayahuasca-using cultures and psychedelics enthusiasts in other countries.

In modern Europe and North America, ayahuasca analogues are often prepared using non-traditional plants which contain the same alkaloids. For example, seeds of the Syrian rue plant can be used as a substitute for the ayahuasca vine, and the DMT-rich Mimosa hostilis is used in place of chakruna. Australia has several indigenous plants which are popular among modern ayahuasqueros there, such as various DMT-rich species of Acacia.

Ayahuasca cooking in the Napo region ofEcuador.

In modern Western culture, entheogen users sometimes base concoctions on Ayahuasca. When doing so, most often Rue or B. caapi is used with an alternative form of the DMT molecule, such as psilocin, or a non-DMT based hallucinogen such as mescaline.[citation needed] Nicknames such as Psilohuasca, Mush-rue-asca, or ‘Shroom-a-huasca, for mushroom based mixtures, or Pedrohuasca (from the San Pedro Cactus, which contains mescaline) are often given to such brews. The psychedelic experimentalist trappings of such concoctions bear little resemblance to the medicinal use of Ayahuasca in its original cultural context[citation needed], where ayahuasca is usually ingested only by experienced entheogen users who are more familiar with the chemicals and plants being used.

Introduction to Europe and North America

Ayahuasca is mentioned in the writings of some of the earliest missionaries to South America, but it only became commonly known in Europe and North America much later.[specify] The early missionary reports generally claim it as demonic, and great efforts were made by the Roman Catholic Church to stamp it out.[citation needed] When originally researched in the 20th century, the active chemical constituent of B. caapiwas called telepathine, but it was found to be identical to a chemical already isolated from Peganum harmala and was given the name harmaline. The original botanical description done was the Harvard ethnobotanist Richard Evans Schultes.[citation needed] Having read Schultes’s paper, Beat writer William Burroughs sought yagé (still referred to as "telepathine") in the early 1950s while traveling through South America in the hopes that it could relieve or cure opiate addiction (see The Yage Letters). Ayahuasca became more widely known when the McKenna brothers published their experience in the Amazon in True Hallucinations. Dennis later studied the pharmacology, botany, and chemistry of ayahuasca and oo-koo-he, which became the subject of his master’s thesis.

In Brazil, a number of modern religious movements based on the use of ayahuasca have emerged, the most famous of them being Santo Daime and the União do Vegetal (or UDV), usually in an animistic context that may be shamanistic or, more often (as with Santo Daime and the UDV), integrated with Christianity. Both Santo Daime and União do Vegetal now have members and churches throughout the world. Similarly, the US and Europe have started to see new religious groups develop in relation to increased ayahuasca use.[12]. PaDeva, an American Wiccan group, has become the first incorporated legal church which holds the use of ayahuasca central to their beliefs.[citation needed] Some Westerners have teamed up with shamans in the Amazon rainforest regions, forming Ayahuasca healing retreats that claim to be able to cure mental and physical illness and allow communication with the spirit world. Anecdotal reports and scientific studies affirm that ritualized use of ayahuasca may improve mental and physical health.[13]

Several notable celebrities have publicly discussed their use of ayahuasca, including Sting (detailed in his 2003 memoir Broken Music), David Icke, Tori Amos, and Paul Simon (who wrote the song "Spirit Voices" about his experience with the brew in the Amazon).[citation needed]

Recent years have seen notable media attention to the position of the UDV church in the United States. After having their importation and use of Hoasca tea challenged by the U.S. Department of Justice, and then having the issue settled in their favor by the U.S. Supreme Court, the church gained some notoriety. This mirrors in some ways the experiences of UDV and Santo Daime churches in Europe, where legal authorities have taken interest in their activities in France, Germany, Holland and Spain.

Holland was an early Western context for the spread of ayahuasca use. Supporting a large Brazilian population, Santo Daime members in particular made efforts to spread the philosophy of ritualized ayahuasca use. In the mid-to-late 1990s one group, the Amsterdam-based Friends of the Forest, was formed by Santo Daime members to introduce ayahuasca to Europeans and others with "allergies to Christianity."[citation needed] They did this by introducing "New Age" rituals incorporating basic ritual structure, celebrating with songs in the Daime tradition (Portuguese waltzes), English language songs, ambient music and mantras and kirtan. They existed at least until the Dutch authorities raided a Santo Daime ritual in progress, and other ayahuasca-oriented groups sensed that an obvious public profile was not in their best interest. Amsterdam is also among the few cities in Europe where one can find, in addition to cannabis, psilocybin mushrooms and peyote, ayahuasca vine, chacruna leaves, and plants for ayahuasca analogues in the tradition of Jonathan Ott’s so-called "ayahuasca borealis."[citation needed]

Ayahuasca tourism

"Ayahuasca tourist" refers to a tourist wanting a taste of an exotic ritual or who partakes in modified services geared specifically towards non-indigenous persons. Some seek to clear emotional blocks and gain a sense of peace. Other participants includeexplorers of consciousness, writers, medical doctors, journalists, anthropologists, ethnobotanists, philosophers and spiritual seekers. Ayahuasca tourism is greatest in Peru, and attracts visitors from all over the world, especially from Europe, USA, Australia, and South Africa, but also from other Latin American countries like Argentina, Chile, Costa Rica, Colombia and Mexico.

Initiation

Usually a visitor who wishes to become a "dietero" or "dietera", that is, a male or female apprentice-shaman learning the way of the teacher plants, undergoes a rigorous initiation. This can involve spending up to a year or more in the jungle. This initiation challenges and trains the initiate through extreme circumstances involving a special diet and numerous different plant medicines to complement the Ayahuasca, the lack of western food and conveniences, the harsh environmental conditions of heavy rains, storms, intense heat, insects, and poisonous animals. The initiate is also tested for their unwavering commitment to Ayahuasca and the shaman who oversees the training.

Modern descriptions

Wade Davis (author of The Serpent and The Rainbow [non-fiction][14][15]) describes the traditional mixture as tough in his book One River: "The smell and acrid taste was that of the entire jungle ground up and mixed with bile." [p. 194]

Chilean novelist Isabel Allende told The Sunday Telegraph in London that she once took the drug in an attempt to "punch through" writer’s block.[16]
Writer Kira Salak describes her personal experiences with ayahuasca at Blue Morpho Ayahuasca center in Peru in the March 2006 issue of National Geographic Adventure magazine[18][19] The article includes a candid description of how ayahuasca cured her depression, as well as provides detailed information about the brew. Here is an excerpt from the article about Dr. Charles Grob’s landmark findings[20]: The taking of ayahuasca has been associated with a long list of documented cures: the disappearance of everything from metastasized colorectal cancer to cocaine addiction, even after just a ceremony or two. It has been medically proven to be nonaddictive and safe to ingest. Yet Western scientists have all but ignored it for decades, reluctant to risk their careers by researching a substance containing the outlawed DMT. Only in the past decade, and then only by a handful of researchers, has ayahuasca begun to be studied. At the vanguard of this research is Charles Grob, M.D., a professor of psychiatry and pediatrics at UCLA’s School of Medicine. In 1993 Dr. Grob directed the Hoasca Project, the first in-depth study of the physical and psychological effects of ayahuasca on humans. He and his team went to Brazil, where the plant mixture can be taken legally, to study members of a church, the União do Vegetal (UDV), who use ayahuasca as a sacrament, and compared them to a control group that had never ingested the substance. The studies found that all the ayahuasca-using UDV members had experienced remission without recurrence of their addictions, depression, or anxiety disorders. Unlike most common anti-depressants, which Grob says can create such high levels of serotonin that cells may actually compensate by losing many of their serotonin receptors, the Hoasca Project showed that ayahuasca strongly enhances the body’s ability to absorb the serotonin that’s naturally there [4]. ‘Ayahuasca is perhaps a far more sophisticated and effective way to treat depression than SSRIs [antidepressant drugs],’ Grob concludes, adding that the use of SSRIs is ‘a rather crude way’ of doing it. And ayahuasca, he insists, has great potential as a long-term solution in maintaining abstinence.

Related phenomena

There have been reports that a phenomenon similar to folie à deux had been induced most recently by anthropologists in the South American rainforest by consuming ayahuasca[17] and by military experiments for chemical warfare in the late 60’s using theincapacitating agent BZ. In both incidents there were very rare claims of shared visual hallucinations.

Plant constituents

Traditional

Traditional Ayahuasca brews are always made with Banisteriopsis caapi as a MAOI[citation needed], although DMT sources and other admixtures vary from region to region. There are several varieties of caapi, often known as different "colors", with varying effects, potencies, and uses.

DMT admixtures:

Other common admixtures:

MAOI:

DMT admixture sources:

Common admixtures with their associated ceremonial values and spirits:

Dead Head Tree. Provides protection and is used in healing susto (soul loss from spiritual fright or trauma). Head spirit is a headless giant.

Provides cleansing and protection. It is noted for its smooth bark, white flowers, and hard wood. Head spirits look Caucasian.

Provides cleansing to the physical body. Used to transcend physical body ailments. Head spirits look Caucasian.

Provides protection. Head spirits take the form of giants.

Yellow Punga. Provides protection. Used to pull or draw out negative spirits or energies. Head spirit is the yellow anaconda.

Oar Tree. Used to move dense or dark energies. Head spirit is a native warrior.

Air Tree. Used to create purging, transcend gastro/intestinal ailments, calm the mind, and bring tranquility. Head spirit looks African.

Brings purple medicine to the ceremony. Provides healing and protection.

Head spirit comes in the form of a large dark skinned giant. He provides medicine and protection in the form of warding off dark and demonic spirits.

Head spirit looks like an old Asian warrior with a long white wispy beard. He carries a staff and manages thousands of spirits to protect the ceremony and send away energies that are purged from the participants.

Head of the sanango plants. Provides power, strength, and protection. Head doctor spirit is a grandfather with a long, gray-white beard.

Giant tree of the amazon with very hard bark. Its head spirits come in the form of Amazonian giants and provide a strong grounding presence in the ceremony.

[edit]Legal status

Internationally, DMT is a Schedule I drug under the Convention on Psychotropic Substances. The Commentary on the Convention on Psychotropic Substances notes, however, that the plant itself is excluded from international control:[18]

The cultivation of plants from which psychotropic substances are obtained is not controlled by the Vienna Convention. . . . Neither the crown (fruit, mescal button) of the Peyote cactus nor the roots of the plant Mimosa hostilis nor Psilocybe mushrooms themselves are included in Schedule 1, but only their respective principles, mescaline, DMT and psilocin.

A fax from the Secretary of the International Narcotics Control Board to the Netherlands Ministry of Public Health sent in 2001 goes on to state that "Consequently, preparations (e.g.decoctions) made of these plants, including ayahuasca, are not under international control and, therefore, not subject to any of the articles of the 1971 Convention."[19]

The legal status in the United States of DMT-containing plants is somewhat questionable. Ayahuasca plants and preparations are legal, as they contain no scheduled chemicals. However, brews made using DMT containing plants are illegal since DMT is a Schedule I drug. That said, some people are challenging this, using arguments similar to those used by peyotist religious sects, such as the Native American Church. A court case allowing União do Vegetal to use the tea for religious purposes in the United States, Gonzales v. O Centro Espirita Beneficente Uniao do Vegetal, was heard by the U.S. Supreme Court on November 1, 2005; the decision, released February 21, 2006, allows the UDV to use the tea in its ceremonies pursuant to the Religious Freedom Restoration Act. In a similar case an Ashland, Oregon based Santo Daime church sued for their right to import and consume ayahuasca tea. In March 2009, U.S. District Court Judge Panner ruled in favor of the Santo Daime, acknowledging its protection from prosecution under the Religious Freedom Restoration Act.[20]

Religious use in Brazil was legalized after two official inquiries into the tea in the mid-1980s, which concluded that ayahuasca is not a recreational drug and has valid spiritual uses.[21]

In France, Santo Daime won a court case allowing them to use the tea in early 2005; however, they were not allowed an exception for religious purposes, but rather for the simple reason that they did not perform chemical extractions to end up with pure DMT and harmala and the plants used were not scheduled. Four months after the court victory, the common ingredients of Ayahuasca as well as harmala were declared stupéfiants, or narcotic schedule I substances, making the tea and its ingredients illegal to use or possess.[citation needed]

In Peru, the government is undergoing the legislation process of legalizing and regulating Ayahuasca usage and monitoring Ayahuasca centers. Currently (April 2010) the use of Ayahuasca is not technically legal but since it is an accepted practice of its indigenous cultures the Peruvian government is going through of the process maintaining the continuity of its culture whilst avoiding international issues.

International research

The Institute of Medical Psychology at the University Hospital in Heidelberg, Germany has set up a Research Department Ayahuasca / Santo Daime [22], which in May 2008 held a 3-day conference under the title The globalization of Ayahuasca – An Amazonian psychoactive and its users[23]. There are also the investigations of the human pharmacology of ayahuasca done by the team of Doctor Jordi Riba, in Barcelona, Spain [7],[24],[25],[26],[27],[28],[29],[30],[31],[32], and the work of Rafael G. dos Santos and collaborators, in Brazil [33],[34],[35],[36]. And there are also the studies (i.e. Hoasca Project and others) by Dr. Charles Grob and collaborators (e.g., Dr. Callaway and Dr. McKenna), already cited, done in Brazil, United States and Finland. In Brazil, the University of São Paulo is doing a study led by psychiatrist Dartiu Xavier da Silveira to establish the risks of ayahuasca, e.g serpent visitation.

See also

References

Bibliography
Nonfiction
Fiction
Documentaries
  • Alistair Appleton, The Man Who Drank the Universe, 30 min. 2005
  • Dean Jefferys; Shamans of the Amazon, 52 min. Australia 2001
  • Jan Kounen, Autres mondes
  • Glenn Switkes, Night of the Liana, 45 min. Brazil 2002
  • Armand BERNARDI, L’Ayahuasca, le Serpent et Moi, 52 min. France 2003
  • Anna Stevens, Woven Songs of the Amazon, 54 min. 2006
  • Rudolf Pinto do Amaral & Harald Scherz, ["Heaven Earth"], 60 min. Peru/Austria 2008
  • Keith Aronowitz "METAMORPHOSIS" 95 min. / 2009 Official website
  • Madventures Season 3 Episode 1: Riku & Tunna venture deep into the Amazon to find themselves and drink ayahuasca with a shaman.
  • Piers Gibbon, Jungle Trip – Channel 4 UK from Google Video
  • Richard Meech, Vine of the Soul: Encounters with Ayahuasca, 58 min. Canada 2010
  • BBC – Bruce Parry’s Amazon, Peru, 2008, Episode 2
Fictional films
Notes
  1. ^ Callaway JC (2005). Various alkaloid profiles in decoctions of Banisteriopsis caapi. Journal of Psychoactive Drugs 37(2): 151–155
  2. ^ Callaway JC, Brito GS & Neves ES (2005). Phytochemical analyses of Banisteriopsis caapi and Psychotria viridis. Journal of Psychoactive Drugs 37(2): 145–150.
  3. ^ Callaway JC (2005). Fast and slow metabolizers of hoasca. Journal of Psychoactive Drugs 37(2): 157–161.
  4. ^ Callaway JC, Airaksinen MM, McKenna DJ, Brito GS & Grob CS (1994). Platelet serotonin uptake sites increased in drinkers of ayahuasca. Psychopharmacology 116(3): 385–387.
  5. ^ Callaway JC, McKenna DJ, Grob CS, Brito GS, Raymon LP, Poland RE, Andrade EN, Andrade EO (1999). Pharmacology of hoasca alkaloids in healthy humans. Journal of Ethnopharmacology 65(3): 243–256.
  6. ^ McKenna DJ, Callaway JC, Grob CS (1998). The scientific investigation of ayahuasca: A review of past and current research. The Heffter Review of Psychedelic Research 1: 65–77.
  7. ^ a b RIBA, J. Human Pharmacology of Ayahuasca. Doctoral Thesis: Universitat Autònoma de Barcelona, 2003.
  8. ^ Dean, Bartholomew 2009 Urarina Society, Cosmology, and History in Peruvian Amazonia, Gainesville: University Press of Florida ISBN 978-081303378 [1]
  9. ^ Andritzky, W. (1989). Sociopsychotherapeutic functions of ayahuasca healing in Amazonia. Journal of Psychoactive Drugs. 21(1), 77-89.
  10. ^ Hassan, I. 1967. Some folk uses of Peganum harmala in India and Pakistan. Economic Botany 21: 384.
  11. ^ a b Ott, J. Jonathan Ott. Ayahuasca Analogues: Pangaean Entheogens. Kennewick, WA: Natural Books, 1994.
  12. ^ LABATE, B.C.; ROSE, I.S. & SANTOS, R.G. Ayahuasca Religions: a comprehensive bibliography and critical essays. Santa Cruz: Multidisciplinary Association for Psychedelic Studies – MAPS. 2008.
  13. ^ See research by Doctor John Halpern in New Scientist
  14. ^ There is a 1988 American horror film, directed by Wes Craven and starring Bill Pullman. The film is very loosely based on a non-fiction book by ethnobotanist Wade Davis. Statement by Mr. Davis: ”Davis has frequently voiced his displeasure with the final film. "When I wrote my first book, ‘The Serpent and the Rainbow’, it was made into one of the worst Hollywood movies in history. I tried to escape the hysteria and the media by going to Borneo."
  15. ^ http://www.ed.psu.edu/icik/2004Proceedings/section7-davis.pdf
  16. ^ Elsworth, Catherine (2008-03-21). "Isabel Allende: kith and tell". The Daily Telegraph (London). Retrieved 2010-04-26.
  17. ^ Ayahuasca: Human Consciousness and the Spirits of Nature, edited by Ralph Metzner, Thunder’s Mouth Press, NY
  18. ^ MAPS: DMT – UN report
  19. ^ Erowid Ayahuasca Vault : Law : UNDCP’s Ayahuasca Fax, Jan 17 2001
  20. ^ Ruling by District Court Judge Panner in Santo Daime case in Oregon
  21. ^ More on the legal status of ayahuasca can be found in the Erowid vault on the legality of ayahuasca.
  22. ^ ‘Research Department Ayahuasca / Santo Daime’ at the University Hospital in Heidelberg, Germany
  23. ^ Conference schedule "The globalization of Ayahuasca" (May 2008, Heidelberg, Germany)
  24. ^ RIBA, J. & BARBANOJ, M.J. Bringing ayahuasca to the clinical research laboratory. Journal of Psychoactive Drugs, 37 (2): 219-230. 2005.
  25. ^ RIBA, J. & BARBANOJ, M.J. Ayahuasca. In: PERIS, J.C., ZURIÁN, J.C., MARTÍNEZ, G.C. & VALLADOLID, G.R. (eds.). Tratado SET de Transtornos Adictivos. Madrid: Ed. Médica Panamericana, 2006. pp. 321-324.
  26. ^ RIBA, J., RODRIGUEZ–FORNELLS, A., STRASSMAN, R.J. & BARBANOJ, M.J. Psychometric assessment of the Hallucinogen Rating Scale. Drug and Alcohol Dependence, 62 (3): 215-223. 2001a.
  27. ^ RIBA, J., RODRIGUEZ–FORNELLS, A., URBANO, G., MORTE, A., ANTONIJOAN, R., MONTEIRO, M., CALLAWAY, J.C. & BARBANOJ, M.J. Subjective effects and tolerability of the South American psychoactive beverage Ayahuasca in healthy volunteers. Psychopharmacology (Berl), 154 (1): 85-95. 2001b.
  28. ^ RIBA, J., ANDERER, P., MORTE, A., URBANO, G., JANE, F., SALETU, B. & BARBANOJ, M.J. Topographic pharmaco–EEG mapping of the effects of the South American beverage ayahuasca in healthy volunteers. British Journal of Clinical Pharmacology, 53 (6): 613-628. 2002a.
  29. ^ RIBA, J., RODRIGUEZ–FORNELLS, A., & BARBANOJ, M.J. Effects of ayahuasca sensory and sensorimotor gating in humans as measured by P50 suppression and prepulse inhibition of the startle reflex, respectively. Psychopharmacology (Berl), 165 (1): 18-28. 2002b.
  30. ^ RIBA, J., VALLE, M., URBANO, G., YRITIA, M., MORTE, A. & BARBANOJ, M.J. Human pharmacology of ayahuasca: subjective and cardiovascular effects, monoamine metabolite excretion, and pharmacokinetics. Journal of Pharmacology and Experimental Therapeutics, 306 (1): 73-83. 2003.
  31. ^ RIBA, J., ANDERER, P., JANÉ, F., SALETU, B. & BARBANOJ, M.J. Effects of the South American psychoactive beverage Ayahuasca on regional brain electrical activity in humans: a functional neuroimaging study using low–resolution electromagnetic tomography. Neuropsychobiology, 50 (1): 89-101. 2004.
  32. ^ RIBA, J., ROMERO, S., GRASA, E., MENA, E., CARRIÓ, I. & BARBANOJ, M.J. Increased frontal and paralimbic activation following ayahuasca, the pan-amazonian inebriant. Psychopharmacology (Berl), 186 (1): 93-98. 2006.
  33. ^ SANTOS, R.G., MORAES, C.C. & HOLANDA, A. Ayahuasca e redução do uso abusivo de psicoativos: eficácia terapêutica? Psicologia: Teoria e Pesquisa, 22 (3): 363-370. 2006.http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0102-37722006000300014&lng=en&nrm=iso&tlng=pt.
  34. ^ SANTOS, R.G. AYAHUASCA: Neuroquímica e Farmacologia. SMAD – Revista Eletrônica Saúde Mental Álcool e Drogas, 3 (1). 2007. http://pepsic.bvs-psi.org.br/scielo.php?script=sci_arttext&pid=S1806-69762007000100007&lng=pt&nrm=iso&tlng=pt.
  35. ^ SANTOS, R.G., LANDEIRA-FERNANDEZ, J., STRASSMAN, R.J., MOTTA, V. & CRUZ, A.P.M. Effects of ayahuasca on psychometric measures of anxiety, panic-like and hopelessness in Santo Daime members. Journal of Ethnopharmacology, 112 (3): 507-513. 2007.http://www.maps.org/w3pb/new/2007/2007_Santos_22932_1.pdf.
  36. ^ SANTOS, R.G. & STRASSMAN, R.J. Ayahuasca and Psychosis (eLetter). British Journal of Psychiatry (online), 3 December 2008.http://bjp.rcpsych.org/cgi/eletters/190/1/81-a#22556.

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LSD

Lysergic acid diethylamide

Lysergic acid diethylamide

Systematic (IUPAC) name

(6aR,9R)- N,N– diethyl- 7-methyl- 4,6,6a,7,8,9- hexahydroindolo- [4,3-fg] quinoline- 9-carboxamide

Identifiers

CAS number
50-37-3

ATC code
?

PubChem
CID 5761

IUPHAR ligand ID
17

DrugBank
DB04829

ChemSpider
5558

Chemical data

Formula
C20H25N3O

Mol. mass
323.43 g/mol

SMILES
eMolecules & PubChem

Synonyms
LSD, LSD-25,
lysergide,
D-lysergic acid diethyl amide,
N,N– diethyl- D- lysergamide

Physical data

Melt. point
80 °C (176 °F)

Pharmacokinetic data

Metabolism
Hepatic

Half-life
3–5 hours[1][2]

Excretion
Renal

Therapeutic considerations

Pregnancy cat.
C(US)

Legal status
Prohibited (S9) (AU) Schedule III(CA) ? (UK) Schedule I (US)

Routes
Oral, Intravenous

Yes(what is this?) (verify)

Lysergic acid diethylamide, abbreviated LSD or LSD-25, also known as lysergide and colloquially as acid, is a semisynthetic psychedelic drug of the ergoline family. LSD is non-addictive and well known for its psychological effects which can include altered thinking processes, closed and open eye visuals, synaesthesia, a sense of time distortion, ego death and spiritual experiences, as well as for its key role in1960s counterculture. It is used mainly as an entheogen, recreational drug and as an agent in psychedelic therapy.

LSD was first synthesized by Albert Hofmann in 1938 from ergot, a grain fungus that typically grows on rye. The short form LSD comes from its early code name LSD-25, which is an abbreviation for the German "Lysergsäure-diethylamid" followed by a sequential number.[3][4] LSD is sensitive to oxygen, ultraviolet light, and chlorine, especially in solution, though its potency may last for years if it is stored away from light and moisture at low temperature. In pure form it is a colorless, odorless, and mildly bitter solid.[5] LSD is typically delivered orally, usually on a substrate such as absorbent blotter paper, a sugar cube, or gelatin. In its liquid form, it can also be administered by intramuscular or intravenous injection. LSD is very potent, with 20–30 µg (micrograms) being the threshold dose.[6]

Introduced by Sandoz Laboratories, with trade-name Delysid, as a drug with various psychiatric uses in 1947, LSD quickly became a therapeutic agent that appeared to show great promise. However, the emerging recreational use of the drug by youth culture in the Western world during the 1960s led to a political firestorm that resulted in its prohibition.[7] A number of organizations—including the Beckley Foundation, MAPS, Heffter Research Institute and the Albert Hofmann Foundation—exist to fund, encourage and coordinate research into its medicinal and spiritual uses.[8]

Contents

[hide]

[edit]Chemistry and structure

The four possible stereoisomers of LSD. Only LSD is psychoactive.

LSD is an ergoline derivative. It is commonly synthesised by reacting diethylamine with an activated form of lysergic acid. Activating reagents include phosphoryl chloride[9] and peptide coupling reagents.[10]Lysergic acid is made by alkaline hydrolysis of lysergamides like ergotamine, a substance derived from the ergot fungus on rye, or from ergine (lysergic acid amide, LSA), a compound that is found in morning glory (Ipomoea tricolor) and hawaiian baby woodrose (Argyreia nervosa) seeds.

LSD is a chiral compound with two stereocenters at the carbon atoms C-5 and C-8, so that theoretically four different optical isomers of LSD could exist. LSD, also called (+)-D-LSD, has the absolute configuration(5R,8R). The C-5 isomers of lysergamides do not exist in nature and are not formed during the synthesis from D-lysergic acid. Retrosynthetically, the C-5 stereocenter could be analysed as having the same configuration of the alpha carbon of the naturally occuring amino acid L-tryptophan, the precursor to all biosynthetic ergoline compounds.

However, LSD and iso-LSD, the two C-8 isomers, rapidly interconvert in the presence of base, as the alpha proton is acidic and can be deprotonated and reprotonated. Non-psychoactive iso-LSD which has formed during the synthesis can be separated by chromatography and can be isomerized to LSD.

A totally pure salt of LSD will emit small flashes of white light when shaken in the dark.[4] LSD is strongly fluorescent and will glow bluish-white under UV light.

[edit]Reactivity and degradation

"LSD," writes the chemist Alexander Shulgin, "is an unusually fragile molecule."[4] It is stable for indefinite time if stored as a solid salt or dissolved in water, at low temperature and protected from air and light exposure.

LSD has two labile protons at the tertiary stereogenic C5 and C8 positions, rendering these centres prone to epimerisation. The C8 proton is more labile due to the electron-withdrawing carboxamide attachment, but removal of the chiral proton at the C5 position (which actually was once also an alpha proton of the parent molecule tryptophan) is assisted by the inductively-withdrawing nitrogen and pi electron delocalisation with the indole ring.

LSD also has enamine-type reactivity because of the electron-donating effects of the indole ring. Because of this, chlorine destroys LSD molecules on contact; even though chlorinated tap water typically contains only a slight amount of chlorine, because a typical LSD solution only contains a small amount of LSD, dissolving LSD in tap water is likely to completely eliminate the substance.[4] The double bond between the 8-position and the aromatic ring, being conjugated with the indole ring, is susceptible to nucleophilic attacks by water or alcohol, especially in the presence of light. LSD often converts to "lumi-LSD", which is totally inactive in human beings (to the best of current knowledge).

A controlled study was undertaken to determine the stability of LSD in pooled urine samples.[11] The concentrations of LSD in urine samples were followed over time at various temperatures, in different types of storage containers, at various exposures to different wavelengths of light, and at varying pH values. These studies demonstrated no significant loss in LSD concentration at 25 °C for up to four weeks. After four weeks of incubation, a 30% loss in LSD concentration at 37 °C and up to a 40% at 45 °C were observed. Urine fortified with LSD and stored in amber glass or nontransparent polyethylene containers showed no change in concentration under any light conditions. Stability of LSD in transparent containers under light was dependent on the distance between the light source and the samples, the wavelength of light, exposure time, and the intensity of light. After prolonged exposure to heat in alkaline pH conditions, 10 to 15% of the parent LSD epimerized to iso-LSD. Under acidic conditions, less than 5% of the LSD was converted to iso-LSD. It was also demonstrated that trace amounts of metal ions in buffer or urine could catalyze the decomposition of LSD and that this process can be avoided by the addition of EDTA.

[edit]Dosage

White on White blotters (WoW)

Pink Elephant Blotters Containing 150μg of LSD

A single dose of LSD may be between 100 and 500 micrograms—an amount roughly equal to one-tenth the mass of a grain of sand. Threshold effects can be felt with as little as 25 micrograms of LSD.[6][6][12]Dosages of LSD are measured in micrograms (µg), or millionths of a gram. By comparison, dosages of most drugs, both recreational and medicinal, are measured in milligrams (mg), or thousandths of a gram. For example, an active dose of mescaline, roughly 0.2 to 0.5g, has effects comparable to 100 µg or less of LSD.[3]

Typical doses in the 1960s ranged from 200 to 1000 µg while street samples of the 1970s contained 30 to 300 µg. By the 1980s, the amount had reduced to between 100 to 125 µg, lowering more in the 1990s to the 20–80 µg range.[13]

Estimates for the lethal dosage (LD50) of LSD range from between 200 µg/kg to more than 1 mg/kg of human body mass, though most sources report that there are no known human cases of such an overdose. Other sources note one report of a suspected fatal overdose of LSD occurring in November 1975 in Kentucky in which there were indications that ~1/3 of a gram (320 mg or 320,000 µg) had been injected intravenously. (This is a very extraordinary amount, particularly when compared to the average LSD dosage of ~100 µg).[14][15] Experiments with LSD have also been done on animals; in 1962, an elephant namedTusko died shortly after being injected with 297 mg, but whether the LSD was the cause of his death is controversial (due, in part, to a plethora of other medicines administered simultaneously).[16]

[edit]History

Main article: History of LSD

LSD was first synthesized on November 16, 1938[17] by Swiss chemist Dr. Albert Hofmann at the Sandoz Laboratories in Basel, Switzerland as part of a large research program searching for medically useful ergot alkaloid derivatives. LSD’s psychedelic properties were discovered 5 years later when Hofmann accidentally ingested an unknown quantity of the chemical.[18] The first intentional ingestion of LSD occurred at 4:20 PM on April 19, 1943[19], when Dr. Hofmann ingested 250 µg of LSD. He hypothesized this would be a threshold dose based on the dosages of other ergot alkaloids. Hofmann found the effects to be much stronger than he anticipated.[20] Sandoz Laboratories introduced LSD as a psychiatric drug in 1947.[21]

Beginning in the 1950s the US Central Intelligence Agency began a research program code named Project MKULTRA. Experiments included administering LSD to CIA employees, military personnel, doctors, other government agents, prostitutes, mentally ill patients, and members of the general public in order to study their reactions, usually without the subject’s knowledge. The project was revealed in the US congressional Rockefeller Commission report in 1975.

In 1963 the Sandoz patents expired on LSD.[13] Also in 1963, the US Food and Drug Administration classified LSD as an Investigational New Drug, which meant new restrictions on medical and scientific use.[13]Several figures, including Aldous Huxley, Timothy Leary, and Al Hubbard, began to advocate the use of LSD. LSD became central to the counterculture of the 1960s, although some members of the counterculture, such as Meher Baba, opposed the use of LSD[22]. On October 24, 1968, possession of LSD was made illegal in the United States.[23] The last FDA approved human study with LSD, for use in dying cancer patients, ended in 1980. Legally approved and regulated psychiatric use of LSD continued in Switzerland until 1993.[24] Today, medical research is resuming around the world.[25]

[edit]Effects

[edit]Physical

LSD reliably causes pupil dilation, reduced appetite, and wakefulness. Other physical reactions to LSD are highly variable and nonspecific, and some of these reactions may be secondary to the psychological effects of LSD. The following symptoms have been reported: numbness, weakness, nausea, hypothermia or hyperthermia (decreased or increased body temperature), elevated blood sugar, goose bumps, increase in heart rate, jaw clenching, perspiration, saliva production, mucus production,sleeplessness, hyperreflexia, and tremors. Uterine contractions have been reported in animals.[citation needed] Some users, including Albert Hofmann, report a strong metallic taste for the duration of the effects.[26]

LSD is not considered addictive by the medical community.[27] Rapid tolerance build-up prevents regular use, and there is cross-tolerance shown between LSD, mescaline[28] and psilocybin.[29] This tolerance diminishes after a few days without use and is probably caused by downregulation of 5-HT2A receptors in the brain.[citation needed]

[edit]Psychological

LSD’s psychological effects (colloquially called a "trip") vary greatly from person to person, depending on factors such as previous experiences, state of mind and environment, as well as dose strength. They also vary from one trip to another, and even as time passes during a single trip. An LSD trip can have long-term psychoemotional effects; some users cite the LSD experience as causing significant changes in their personality and life perspective. Widely different effects emerge based on what Timothy Leary called set and setting; the "set" being the general mindset of the user, and the "setting" being the physical and social environment in which the drug’s effects are experienced. Diablo Valley College Professor Dr. Ken Kesey once told a group of students that LSD changed his life forever after dropping (consuming) acid for the first time, he realized that the intense psychological impact to his brain led the inspiration for his novel, "One Flew Over the Cuckoo’s Nest".[citation needed]

Some psychological effects may include an experience of radiant colors, objects and surfaces appearing to ripple or "breathe," colored patterns behind the eyes, a sense of time distorting (time seems to be stretching, repeating itself, changing speed or stopping), crawling geometric patterns overlaying walls and other objects, morphing objects, a sense that one’s thoughts are spiraling into themselves, loss of a sense of identity or the ego (known as "ego death"), and other powerful psycho-physical reactions.[30] Many users experience a dissolution between themselves and the "outside world".[31] This unitive quality may play a role in the spiritual and religious aspects of LSD. The drug sometimes leads to disintegration or restructuring of the user’s historical personality and creates a mental state that some users report allows them to have more choice regarding the nature of their own personality.

If the user is in a hostile or otherwise unsettling environment, or is not mentally prepared for the powerful distortions in perception and thought that the drug causes, effects are more likely to be unpleasant than if he or she is in a comfortable environment and has a relaxed, balanced and open mindset.[32]

[edit]Sensory and perception

LSD causes expansion and an altered experience of senses, emotions, memories, time, and awareness for 6 to 14 hours, depending on dosage and tolerance. Generally beginning within thirty to ninety minutes after ingestion, the user may experience anything from subtle changes in perception to overwhelming cognitive shifts. Changes in auditory and visual perception are typical.[31][33] Visual effects include the illusion of movement of static surfaces ("walls breathing"), after image-like trails of moving objects ("tracers"), the appearance of moving colored geometric patterns (especially with closed eyes), an intensification of colors and brightness ("sparkling"), new textures on objects, blurred vision, and shape suggestibility. Users commonly report that the inanimate world appears to animate in an unexplained way; for instance, objects that are static in three dimensions can seem to be moving relative to one or more additional spatial dimensions.[34] Many of the basic visual effects resemble thephosphenes seen after applying pressure to the eye and have also been studied under the name "form constants". The auditory effects of LSD may include echo-like distortions of sounds, changes in ability to discern concurrent auditory stimuli, and a general intensification of the experience of music. Higher doses often cause intense and fundamental distortions of sensory perception such as synaesthesia, the experience of additional spatial or temporal dimensions, and temporary dissociation.

[edit]Potential use

LSD has been used in psychiatry for its perceived therapeutic value, in the treatment of alcoholism, pain and cluster headache relief, for spiritual purposes, and to enhance creativity. However, government organizations like the United States Drug Enforcement Administration maintain that LSD "produces no aphrodisiac effects, does not increase creativity, has no lasting positive effect in treating alcoholics or criminals, does not produce a ‘model psychosis’, and does not generate immediate personality change."[35]

[edit]Psychotherapy

In the 1950s and 1960s LSD was used in psychiatry to enhance psychotherapy. Some psychiatrists believed LSD was especially useful at helping patients to "unblock" repressed subconscious material through other psychotherapeutic methods,[36] and also for treating alcoholism. One study concluded, "The root of the therapeutic value of the LSD experience is its potential for producing self-acceptance and self-surrender,"[37] presumably by forcing the user to face issues and problems in that individual’s psyche.

In December 1968, a survey was made of all 74 UK doctors who had used LSD in humans, 73 replied, 1 had moved overseas and was unavailable. Of the 73 replies, the majority of UK doctors with clinical experience with LSD felt that LSD was effective and had acceptable safety: 41 (56%) continued with clinical use of LSD, 11 (15%) had stopped because of retirement or other extraneous reasons, 9 (12%) had stopped because they found LSD ineffective, and 5 (7%) had stopped because they felt LSD was too dangerous.[38]

[edit]Alcoholism

Some studies in the 1950s that used LSD to treat alcoholism professed a 50% success rate,[39] five times higher than estimates near 10% for Alcoholics Anonymous.[40] These studies were criticized for methodological flaws, and different groups had inconsistent results. M. Mangini’s 1998 paper reviewed this history. She concluded that the efficacy of LSD in treating alcoholism remains an open question.[41]

[edit]Pain

LSD was studied in the 1960s by Eric Kast as an analgesic for serious and chronic pain caused by cancer or other major trauma.[42] Even at low (sub-psychedelic) dosages, it was found to be at least as effective as traditional opiates, while being much longer lasting pain reduction (lasting as long as a week after peak effects had subsided). Kast attributed this effect to a decrease in anxiety. This reported effect is being tested (though not using LSD) in an ongoing (as of 2006) study of the effects of thepsychedelic tryptamine psilocybin on anxiety in terminal cancer patients.

[edit]Cluster headaches

LSD has been used as a treatment for cluster headaches, an uncommon but extremely painful disorder. Researcher Peter Goadsby describes the headaches as "worse than natural childbirth or even amputation without anesthetic."[43] Although the phenomenon has not been formally investigated, case reports indicate that LSD and psilocybin can reduce cluster pain and also interrupt the cluster-headache cycle, preventing future headaches from occurring. Currently existing treatments include variousergolines, among other chemicals, so LSD’s efficacy may not be surprising. A dose-response study testing the effectiveness of both LSD and psilocybin was planned at McLean Hospital, although the current status of this project is unclear. A 2006 study by McLean researchers interviewed 53 cluster-headache sufferers who treated themselves with either LSD or psilocybin, finding that a majority of the users of either drug reported beneficial effects.[44] Unlike use of LSD or MDMA in psychotherapy, this research involves non-psychological effects and often sub-psychedelic dosages.[45]

[edit]Spiritual

LSD is considered an entheogen because it can catalyze intense spiritual experiences, during which users may feel they have come into contact with a greater spiritual or cosmic order. Users claim to experience lucid sensations where they have "out of body" experiences. Some users report insights into the way the mind works, and some experience permanent shifts in their life perspective. LSD also allows users to view their life from an introspected point of view. From this point of view, a user can travel back in time to a specific moment or memory and relive that moment again. Some users report using introspection to resolve unresolved or negative feelings towards an individual or incident that occurred in the past. Some users consider LSD a religious sacrament, or a powerful tool for access to the divine. Dr. Stanislav Grof has written that religious and mystical experiences observed during LSD sessions appear to be phenomenologically indistinguishable from similar descriptions in the sacred scriptures of the great religions of the world and the secret mystical texts of ancient civilizations.[46]

[edit]Creativity

In the 1950s and 1960s, psychiatrists like Oscar Janiger explored the potential effect of LSD on creativity. Experimental studies attempted to measure the effect of LSD on creative activity and aesthetic appreciation.[47][48][49][50] 70 professional artists were asked to draw two pictures of a Hopi Indian kachina doll, one before ingesting LSD and one after.[51]

[edit]Dangers

Chart of dependence potential and effective dose/lethal dose of some psychoactive drugs. Data was taken from [52] via [53]

LSD may temporarily impair the ability to make sensible judgments and understand common dangers, thus making the user more susceptible to accidents and personal injury and cause signs of organic brain damage-impaired memory and attention span, mental confusion or difficulty with abstract thinking.[54] However LSD is physiologically well tolerated and there is no evidence for long-lasting effects on the brain or other parts of the human organism.[55]

[edit]Adverse drug interactions

There is some indication that LSD may trigger a dissociative fugue state in individuals who are taking certain classes of antidepressants such as lithium salts andtricyclics. In such a state, the user has an impulse to wander, and may not be aware of his or her actions, which can lead to physical injury. Anonymous anecdotal reports have attributed seizures and one death to the combination of LSD with lithium.[56] SSRIs noticeably reduce LSD’s subjective effects.[57] MAOIs are also reported to reduce the effects of LSD.[56]

[edit]Panic and anxiety

LSD may bring out panic attacks or feelings of extreme anxiety, colloquially referred to as a "bad trip".[58]

[edit]Suggestibility

While publicly available documents indicate that the CIA and Department Of Defense have discontinued research into the use of LSD as a means of mind control,[59]research from the 1960s suggests there exists evidence that both mentally ill and healthy are more suggestible while under its influence.[60][61]

[edit]Psychosis

There are some cases of LSD inducing a psychosis in people who appeared to be healthy prior to taking LSD.[62] In most cases, the psychosis-like reaction is of short duration, but in other cases it may be chronic. It is difficult to determine whether LSD itself induces these reactions or if it triggers latent conditions that would have manifested themselves otherwise. The similarities of time course and outcomes between putatively LSD-precipitated and other psychoses suggest that the two types of syndromes are not different and that LSD may have been a nonspecific trigger.

Estimates of the prevalence of LSD-induced prolonged psychosis lasting over 48 hours have been made by surveying researchers and therapists who had administered LSD:

  • Cohen (1960) estimated 0.8 per 1,000 volunteers (the single case among approximately 1250 study volunteers was the identical twin of a schizophrenic and he recovered within 5 days) and 1.8 per 1,000 psychiatric patients (7 cases among approximately 3850 patients, of which 2 cases were "preschizophrenic" or had previous hallucinatory experience, 1 case had unknown outcome, 1 case had incomplete recovery, and 5 cases recovered within up to 6 months).[63]
  • Malleson (1971) reported no cases of psychosis among experimental subjects (170 volunteers who received a total of 450 LSD sessions) and estimated 9 per 1,000 among psychiatric patients (37 cases among 4300 patients, of which 8 details are unknown, 10 appeared chronic, and 19 recovered completely within up to 3 months).[38]

However, in neither survey study was it possible to compare the rate of lasting psychosis in these volunteers and patients receiving LSD with the rate of psychosis found in other groups of research volunteers or in other methods of psychiatric treatment (for example, those receiving placebo).

Cohen (1960) noted:[63]

"The hallucinogenic experience is so striking that many subsequent disturbances may be attributed to it without further justification. The highly suggestible or hysterical individual would tend to focus on his LSD experience to explain subsequent illness. Patients have complained to Abramson that their LSD exposure produced migraine headaches and attacks of influenza up to a year later. One Chinese girl became paraplegic and ascribed that catastrophe to LSD. It so happened that these people were all in the control group and had received nothing but tap water."
[edit]Flashbacks and HPPD

See also: Flashback (psychological phenomenon)

"Flashbacks" are a reported psychological phenomenon in which an individual experiences an episode of some of LSD’s subjective effects long after the drug has worn off, usually in the days after typical doses. In some rarer cases, flashbacks have lasted longer, but are generally short-lived and mild compared to the actual LSD "trip". Flashbacks can incorporate both positive and negative aspects of LSD trips, and are typically elicited by triggers such as alcohol or cannabis use, stress, or sleepiness. Flashbacks have proven difficult to study and are no longer officially recognized as a psychiatric syndrome. However, colloquial usage of the term persists and usually refers to any drug-free experience reminiscent of psychedelic drug effects, with the typical connotation that the episodes are of short duration.

No definitive explanation is currently available for these experiences. Any attempt at explanation must reflect several observations: first, over 70 percent of LSD users claim never to have "flashed back"; second, the phenomenon does appear linked with LSD use, though a causal connection has not been established; and third, a higher proportion of psychiatric patients report flashbacks than other users.[64] Several studies have tried to determine how likely a user of LSD, not suffering from known psychiatric conditions, is to experience flashbacks. The larger studies include Blumenfeld’s in 1971[65] and Naditch and Fenwick’s in 1977,[66] which arrived at figures of 20% and 28%, respectively.

Although flashbacks themselves are not recognized as a medical syndrome, there is a recognized syndrome called Hallucinogen Persisting Perception Disorder (HPPD) in which LSD-like visual changes are not temporary and brief, as they are in flash-backs, but instead are persistent, and cause clinically significant impairment or distress. The syndrome is a DSM-IV diagnosis. Several scientific journal articles have described the disorder.[67]

HPPD differs from flashbacks in that it is persistent and apparently entirely visual (although mood and anxiety disorders are sometimes diagnosed in the same individuals). A recent review suggests that HPPD (as defined in the DSM-IV) is rare and affects only a distinctly vulnerable subpopulation of users.[68] However, it is possible that the prevalence of HPPD is underestimated because most of the diagnoses are applied to people who are willing to admit to their health care practitioner that they have previously used psychotropics, and presumably many people are reluctant to admit this.[69]

There is no consensus regarding the nature and causes of HPPD (or flashbacks). A study of 44 HPPD subjects who had previously ingested LSD showed EEG abnormalities.[70] Given that some symptoms have environmental triggers, it may represent a failure to adjust visual processing to changing environmental conditions. There are no explanations for why only some individuals develop HPPD. Explanations in terms of LSD physically remaining in the body for months or years after consumption have been discounted by experimental evidence.[64] Some say HPPD is a manifestation of post-traumatic stress disorder, not related to the direct action of LSD on brain chemistry, and varies according to the susceptibility of the individual to the disorder. Many emotionally intense experiences can lead to flashbacks when a person is reminded acutely of the original experience. However, not all published case reports of HPPD appear to describe an anxious hyper-vigilant state reminiscent of post-traumatic stress disorder. Instead, some cases appear to involve only visual symptoms.[64]

[edit]Uterine contractions

Early pharmacological testing by Sandoz in laboratory animals showed that LSD can stimulate uterine contractions, with efficacy comparable to ergobasine, the active uterotonic component of the ergot fungus. (Hofmann’s work on ergot derivatives also produced a modified form of ergobasine which became a widely accepted medication used in obstetrics, under the trade name Methergine.) Therefore, LSD use by pregnant women could be dangerous and is contraindicated.[3] However, the relevance of these animal studies to humans is unclear, and a 2008 medical reference guide to drugs in pregnancy and lactation stated, "It appears unlikely that pure LSD administered in a controlled condition is an abortifacient."[71]

[edit]Genetic

Beginning in 1967, studies raised concerns that LSD might produce genetic damage[72] or developmental abnormalities in fetuses. However, these initial reports were based on in vitro studies or were poorly controlled and have not been substantiated. In studies of chromosomal changes in human users and in monkeys, the balance of evidence suggests no increase in chromosomal damage. For example, white blood cells of people who had been given LSD in a clinical setting were examined for visible chromosomal abnormalities; overall, there appeared to be no lasting changes.[72] Several studies have been conducted using illicit LSD users and provide a less clear picture. Interpretation of this data is generally complicated by factors such as the unknown chemical composition of street LSD, concurrent use of other psychoactive drugs, and diseases such as hepatitis in the sampled populations. It seems possible that the small number of genetic abnormalities reported in users of street LSD is either coincidental or related to factors other than a toxic effect of pure LSD.[72] A 2008 medical review concluded, "The available data suggest that pure LSD does not cause chromosomal abnormalities, spontaneous abortions, or congenital malformations."[71]

[edit]Antidotes

Adverse effects of psychotropics are often treated with fast-acting benzodiazepines like diazepam or triazolam that have calming and antianxiety effects but do not directly affect the specific actions of psychotropics. Theoretically, specific 5-HT2A receptorantagonists, which most commonly means atypical antipsychotics (quetiapine, olanzapine, risperidone, etc.) or other 5-HT2A antagonist such as trazodone or mirtazapine, would be direct antidotes, although some anecdotal reports claim otherwise.[73]Also, some people have reported that taking an SSRI such as fluoxetine will counteract the effects of LSD.[74] Some reports indicate that although administration of chlorpromazine (Thorazine) or similar typical antipsychotic tranquilizers will not end an LSD trip, it will either lessen the intensity or immobilize and numb the patient, a side effect of the medication.[75] While it also may not end an LSD trip, the best chemical treatment for a "bad trip" is an anxiolytic agent such as diazepam (Valium) or anotherbenzodiazepine. As the effect of the drug is psychological as well as physical, any treatment should focus on calming the patient. Limiting stimuli such as bright lights and loud noises can help in the event of an ill reaction.

Many rumors about home remedies to counteract psychedelic effects are circulated, including vanilla essence, and anti-histamines. These may have a placebo effect, working by making the taker think they have done something to make it better.[76]

[edit]Pharmacokinetics

LSD’s effects normally last from 6–12 hours depending on dosage, tolerance, body weight and age.[4] The Sandoz prospectus for "Delysid" warned: "intermittent disturbances of affect may occasionally persist for several days."[3] Contrary to early reports and common belief, LSD effects do not last longer than the amount of time significant levels of the drug are present in the blood. Aghajanian and Bing (1964) found LSD had an elimination half-life of only 175 minutes.[1] However, using more accurate techniques, Papac and Foltz (1990) reported that 1 µg/kg oral LSD given to a single male volunteer had an apparent plasma half-life of 5.1 hours, with a peak plasma concentration of 5 ng/mL at 3 hours post-dose.[2]

[edit]Detection in biological fluids

LSD may be quantified in urine as part of a drug abuse testing program, in plasma or serum to confirm a diagnosis of poisoning in hospitalized victims or in whole blood to assist in a forensic investigation of a traffic or other criminal violation or a case of sudden death. Both the parent drug and its major metabolite are unstable in biofluids when exposed to light, heat or alkaline conditions and therefore specimens should be protected from light, stored at the lowest possible temperature and analyzed quickly to minimize losses.[77]

[edit]Pharmacodynamics

Affinity of LSD for various receptors. The lower the affinity, the more strongly LSD binds to that receptor. The horizontal line represents an approximate value for human plasma concentrations of LSD, and hence, receptor affinities that are above the line are unlikely to be involved in LSD’s effect. Data averaged from data from the Ki Database

LSD affects a large number of the G protein coupled receptors, including all dopamine receptor subtypes, and all adrenoreceptor subtypes, as well as many others. LSD binds to most serotonin receptor subtypes except for 5-HT3 and 5-HT4. However, most of these receptors are affected at too low affinity to be sufficiently activated by the brain concentration of approximately 10–20 nM.[78] In humans, recreational doses of LSD can affect 5-HT1A, 5-HT2A, 5-HT2C, 5-HT5A, and 5-HT6 receptors.[1][79] 5-HT5B receptors, which are not present in humans, also have a high affinity for LSD.[80]The psychedelic effects of LSD are attributed to its strong partial agonist effects at 5-HT2A receptors as specific 5-HT2A agonists are psychedelics and largely 5-HT2A specific antagonists block the psychedelic activity of LSD.[78] Exactly how this produces the drug’s effects is unknown, but it is thought that it works by increasing glutamate release in the cerebral cortex and therefore excitationin this area, specifically in layers IV and V.[81] LSD, like many other drugs, has been shown to activate DARPP-32-related pathways.[82]

[edit]Production

Glassware seized by the DEA

Because an active dose of LSD is very minute, a large number of doses can be synthesized from a comparatively small amount of raw material. Beginning withergotamine tartrate, for example, one can manufacture roughly one kilogram of pure, crystalline LSD from five kilograms of the ergotamine salt. Five kilograms of LSD—25 kilograms of ergotamine tartrate—could provide 100 million doses, according to the DEA, more than enough to meet what is believed to be the entire annual U.S. demand. Since the masses involved are so small, concealing and transporting illicit LSD is much easier than smuggling other illegal drugs like cocaineor cannabis.[83]

Manufacturing LSD requires laboratory equipment and experience in the field of organic chemistry. It takes two to three days to produce 30 to 100 grams of pure compound. It is believed that LSD is not usually produced in large quantities, but rather in a series of small batches. This technique minimizes the loss of precursor chemicals in case a step does not work as expected.[83]

[edit]Forms

LSD Blotter

LSD is produced in crystalline form and then mixed with excipients or redissolved for production in ingestible forms. Liquid solution is either distributed in small vials or, more commonly, sprayed onto or soaked into a distribution medium. Historically, LSD solutions were first sold on sugar cubes, but practical considerations forced a change to tablet form. Appearing in 1968 as an orange tablet measuring about 6 mm across, "Orange Sunshine" acid was the first largely available form of LSD after its possession was made illegal. Tim Scully, a prominent chemist, made some of it, but said that most "Sunshine" in the USA came by way of Ronald Stark, who imported approximately thirty-five million doses from Europe.[84]

Over a period of time, tablet dimensions, weight, shape and concentration of LSD evolved from large (4.5–8.1 mm diameter), heavyweight (≥150 mg), round, high concentration (90–350 µg/tab) dosage units to small (2.0–3.5 mm diameter) lightweight (as low as 4.7 mg/tab), variously shaped, lower concentration (12–85 µg/tab, average range 30–40 µg/tab) dosage units. LSD tablet shapes have included cylinders, cones, stars, spacecraft and heart shapes. The smallest tablets became known as "Microdots".[85]

After tablets came "computer acid" or "blotter paper LSD", typically made by dipping a preprinted sheet of blotting paper into an LSD/water/alcohol solution.[84][85] More than 200 types of LSD tablets have been encountered since 1969 and more than 350 blotter paper designs have been observed since 1975.[85] About the same time as blotter paper LSD came "Windowpane" (AKA "Clearlight"), which contained LSD inside a thin gelatin square a quarter of an inch across.[84] LSD has been sold under a wide variety of often short-lived and regionally restricted street names including Acid, Trips, Uncle Sid, Blotter, Lucy, Alice and doses, as well as names that reflect the designs on the sheets of blotter paper.[86][87] Authorities have encountered the drug in other forms—including powder or crystal, and capsule.[88]

[edit]Modern distribution

LSD manufacturers and traffickers in the United States can be categorized into two groups: A few large-scale producers, and an equally limited number of small, clandestine chemists, consisting of independent producers who, operating on a comparatively limited scale, can be found throughout the country.[89] As a group, independent producers are of less concern to the Drug Enforcement Administration than the larger groups, as their product reaches only local markets.[90]

[edit]Mimics

LSD blotter acid mimic actually containing DOC

Different Blotters possibly mimics

In recent years, law enforcement in the United States and elsewhere has seized several chemicals and combinations of chemicals in blotter paper which were sold as LSD mimics, including DOB,[91][92] 2C-I,[93][94]DOC,[94] a mixture of DOC and DOI,[95] and a mixture of DOC and DOB.[96] Street users of LSD are often under the impression that blotter paper which is actively hallucinogenic can only be LSD because that is the only chemical with low enough doses to fit on a small square of blotter paper. While it is true that LSD requires lower doses than most other hallucinogens, blotter paper is capable of absorbing a much larger amount of material. The DEA performed a chromatographic analysis of blotter paper containing 2C-C which showed that the paper contained a much greater concentration of the active chemical than typical LSD doses, although the exact quantity was not determined.[97] Blotter LSD mimics can have relatively small dose squares; a sample of blotter paper containing DOC seized by Concord, California police had dose markings approximately 6 mm apart.[94]

[edit]Legal status

The United Nations Convention on Psychotropic Substances (adopted in 1971) requires its parties to prohibit LSD. Hence, it is illegal in all parties to the convention, which includes the United States, Australia, New Zealand, and most of Europe. However, enforcement of extant laws varies from country to country. Medical and scientific research with LSD in humans is permitted under the 1971 UN Convention.

[edit]Canada

In Canada, LSD is a controlled substance under Schedule III of the Controlled Drugs and Substances Act.[98] Every person who seeks to obtain the substance, without disclosing authorization to obtain such substances 30 days prior to obtaining another prescription from a practitioner, is guilty of an indictable offense and liable to imprisonment for a term not exceeding 3 years. Possession for purpose of trafficking is an indictable offense punishable by imprisonment for 10 years.

[edit]United Kingdom

In the United Kingdom, LSD is a class A drug. This means that possession of the drug without a license is punishable with 7 years imprisonment and/or an unlimited fine, and trafficking is punishable with life imprisonment and an unlimited fine (see main article on drug punishments Misuse of Drugs Act 1971).

In 2000, after consultation with members of the Royal College of Psychiatrists‘ Faculty of Substance Misuse, the UK Police Foundation issued the Runciman Report which recommended "the transfer of LSD from Class A to Class B".[99]

In Nov 2009, the UK Transform Drug Policy Foundation released in the House of Commons a guidebooks to the legal regulation of drugs, After the War on Drugs: Blueprint for Regulation, which details options for regulated distribution and sale of LSD and other psychedelics.[100]

[edit]United States

LSD is Schedule I in the United States, according to the Controlled Substances Act of 1970.[101] This means LSD is illegal to manufacture, buy, possess, process, or distribute without a DEA license. By classifying LSD as a Schedule I substance, theDrug Enforcement Administration holds that LSD meets the following three criteria: it is deemed to have a high potential for abuse; it has no legitimate medical use in treatment; and there is a lack of accepted safety for its use under medical supervision. There are very few or no documented deaths due to chemical toxicity; most LSD deaths are a result of behavioral toxicity.[102]

There can also be substantial discrepancies between the amount of chemical LSD that one possesses and the amount of possession with which one can be charged in the U.S. This is because LSD is almost always present in a medium (e.g. blotter or neutral liquid), and the amount that can be considered with respect to sentencing is the total mass of the drug and its medium. This discrepancy was the subject of 1995 United States Supreme Court case, Neal v. U.S.[103]

Lysergic acid and lysergic acid amide, LSD precursors, are both classified in Schedule III of the Controlled Substances Act. Ergotamine tartrate, a precursor to lysergic acid, is regulated under the Chemical Diversion and Trafficking Act.

[edit]Notable individuals

Some notable individuals have commented publicly on their experiences with LSD.[104][105] Some of these comments date from the era when it was legally available in the US and Europe for non-medical uses, and others pertain to psychiatric treatment in the 1950s and 60s. Still others describe experiences with illegal LSD, obtained for philosophic, artistic, therapeutic, spiritual, or recreational purposes.

[edit]See also

[edit]References

  1. ^ a b c Aghajanian, George K.; Bing, Oscar H. L. (1964). "Persistence of lysergic acid diethylamide in the plasma of human subjects" (PDF). Clinical Pharmacology and Therapeutics 5: 611–614. PMID 14209776. Retrieved 2009-09-17.
  2. ^ a b Papac, DI; Foltz, RL (May/June 1990). "Measurement of lysergic acid diethylamide (LSD) in human plasma by gas chromatography/negative ion chemical ionization mass spectrometry" (PDF). Journal of Analytical Toxicology 14 (3): 189–190.PMID 2374410. Retrieved 2009-09-17.
  3. ^ a b c d Hofmann, Albert. LSD—My Problem Child (McGraw-Hill, 1980). ISBN 0-07-029325-2.
  4. ^ a b c d e Alexander and Ann Shulgin. "LSD", in TiHKAL (Berkeley: Transform Press, 1997). ISBN 0-9630096-9-9.
  5. ^ Shulgin, Alexander; Shulgin, Ann (1991). "Burt". PiHKAL (1st ed.). Transform Press. p. 21. ISBN 978-0-9630096-0-9.
  6. ^ a b c Greiner T, Burch NR, Edelberg R (1958). "Psychopathology and psychophysiology of minimal LSD-25 dosage; a preliminary dosage-response spectrum". AMA Arch Neurol Psychiatry 79 (2): 208–10. PMID 13497365.
  7. ^ "LSD: cultural revolution and medical advances". Royal Society of Chemistry. Retrieved 2007-09-27.
  8. ^ "The Albert Hofmann Foundation". Hofmann Foundation. Retrieved 2007-09-27.
  9. ^ Monte AP, Marona-Lewicka D, Kanthasamy A, Sanders-Bush E, Nichols DE (March 1995). "Stereoselective LSD-like activity in a series of d-lysergic acid amides of (R)- and (S)-2-aminoalkanes". J. Med. Chem. 38 (6): 958–66. doi:10.1021/jm00006a015.PMID 7699712.
  10. ^ Nichols DE, Frescas S, Marona-Lewicka D, Kurrasch-Orbaugh DM (September 2002). "Lysergamides of isomeric 2,4-dimethylazetidines map the binding orientation of the diethylamide moiety in the potent hallucinogenic agent N,N-diethyllysergamide (LSD)". J. Med. Chem. 45 (19): 4344–9. doi:10.1021/jm020153s. PMID 12213075.
  11. ^ Li Z., McNally A. J., Wang H., Salamone S. J. (October 1998). "Stability study of LSD under various storage conditions.". J. Anal. Toxicol. 22 (6): 520–5. PMID 9788528.
  12. ^ Stoll, W.A. (1947). Ein neues, in sehr kleinen Mengen wirsames Phantastikum. Schweiz. Arch. Neur. 60,483.
  13. ^ a b c Henderson, Leigh A.; Glass, William J. (1994). LSD: Still with us after all these years. San Francisco: Jossey-Bass. ISBN 978-0787943790.
  14. ^ "LSD Vault: Dosage". 2006-07-06. Retrieved 2007-01-31.
  15. ^ "LSD Toxicity: A Suspected Cause of Death". Journal of the Kentucky Medical Association. Retrieved 2007-11-26.
  16. ^ Erowid & R. Stuart (2002). "LSD Related Death of an Elephant – Controversy surrounding the 1962 death of an elephant after an injection of LSD". Erowid. Retrieved 2008-07-28.
  17. ^ Dr. Albert Hofmann; translated from the original German (LSD Ganz Persönlich) by J. Ott. MAPS-Volume 6 Number 69 Summer 1969
  18. ^ Nichols, David (2003-05-24). "Hypothesis on Albert Hofmann’s Famous 1943 "Bicycle Day"". Hofmann Foundation. Retrieved 2007-09-27.
  19. ^ Dr. Albert Hofmann. "LSD My Problem Child". Retrieved 2010-04-19.
  20. ^ Hofmann, Albert. "History Of LSD". Retrieved 2007-09-27.
  21. ^ LSD: The Drug
  22. ^ ^ Brecher, Edward M; et al. (1972). "How LSD was popularized". Consumer Reports/Drug Library. http://www.druglibrary.org/schaffer/Library/studies/cu/CU50.html. Retrieved 2008-07-14.
  23. ^ United States Congress (1968-10-24). "Staggers-Dodd Bill, Public Law 90-639". Retrieved 2009-09-08.
  24. ^ Gasser, Peter (1994). "Psycholytic Therapy with MDMA and LSD in Switzerland". Retrieved 2009-09-08.
  25. ^ MAPS Psychedelic Research
  26. ^ Albert Hofmann. "LSD: My Problem Child". ""taste of metal on the palate""
  27. ^ Lüscher C, Ungless MA (November 2006). ["http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.0030437" "The mechanistic classification of addictive drugs"]. PLoS Med. 3 (11): e437. doi:10.1371/journal.pmed.0030437. PMID 17105338.PMC 1635740.
  28. ^ Wolbach AB Jr, Isbell H, Miner EJ (1962). "Cross tolerance between mescaline and LSD-25, with a comparison of the mescaline and LSD reactions". Psychopharmacologia 3: 1–14. doi:10.1007/BF00413101. PMID 14007904.
  29. ^ Isbell H, Wolbach AB, Wikler A, Miner EJ (1961). "Cross Tolerance between LSD and Psilocybin". Psychopharmacologia 2: E353. doi:10.1007/BF00407974. PMID 13717955.
  30. ^ The Good Drugs Guide. "LSD psychedelic effects". Retrieved 2008-03-03.
  31. ^ a b Linton, Harriet B. and Langs, Robert J. "Subjective Reactions to Lysergic Acid Diethylamide (LSD-25)". Arch. Gen. Psychiat. Vol. 6 (1962): 352–68.
  32. ^ "LSD dangers". The Good Drugs Guide. Retrieved 2008-10-20.
  33. ^ Katz MM, Waskow IE, Olsson J (1968). "Characterizing the psychological state produced by LSD". J Abnorm Psychol 73 (1): 1–14. doi:10.1037/h0020114. PMID 5639999.
  34. ^ See, e.g., Gerald Oster’s article "Moiré patterns and visual hallucinations". Psychedelic Rev. No. 7 (1966): 33–40.
  35. ^ DEA – Publications – LSD in the US – The Drug
  36. ^ Cohen, S. (1959). The therapeutic potential of LSD-25. A Pharmacologic Approach to the Study of the Mind, p251–258.
  37. ^ Chwelos N, Blewett D.B., Smith C.M., Hoffer A. (1959). "Use of d-lysergic acid diethylamide in the treatment of alcoholism". Quart. J. Stud. Alcohol 20: 577–90. PMID 13810249.
  38. ^ a b Malleson, Nicholas (1971). "Acute Adverse Reactions to LSD in Clinical and Experimental Use in the United Kingdom" (PDF). Br J Psychiatry 118 (543): 229–30. doi:10.1192/bjp.118.543.229. PMID 4995932.
  39. ^ Maclean, J.R.; Macdonald, D.C.; Ogden, F.; Wilby, E., "LSD-25 and mescaline as therapeutic adjuvants." In: Abramson, H., Ed., The Use of LSD in Psychotherapy and Alcoholism, Bobbs-Merrill: New York, 1967, pp. 407–426; Ditman, K.S.; Bailey, J.J., "Evaluating LSD as a psychotherapeutic agent," pp.74–80; Hoffer, A., "A program for the treatment of alcoholism: LSD, malvaria, and nicotinic acid," pp. 353–402.
  40. ^ Minogue SJ (May 1948). "Alcoholics Anonymous". Med. J. Aust. 1 (19): 586. PMID 18868217.
  41. ^ Mangini M (1998). "Treatment of alcoholism using psychedelic drugs: a review of the program of research". J Psychoactive Drugs 30 (4): 381–418. PMID 9924844.
  42. ^ Kast, Eric (1967). "Attenuation of anticipation: a therapeutic use of lysergic acid diethylamide" (PDF). Psychiat. Quart. 41 (4): 646–57. doi:10.1007/BF01575629. PMID 4169685.
  43. ^ Dr. Goadsby is quoted in "Research into psilocybin and LSD as cluster headache treatment", and he makes an equivalent statement in an Health Report interview on Australian Radio National (August 9, 1999). Pages accessed 2007-01-31.
  44. ^ Sewell, R. A.; Halpern, J. H.; Pope, H. G. Jr. (2006-06-27). "Response of cluster headache to psilocybin and LSD". Neurology 66 (12): 1920–2. doi:10.1212/01.wnl.0000219761.05466.43. PMID 16801660.
  45. ^ Summarized from "Research into psilocybin and LSD as cluster headache treatment" and the Clusterbusters website. Pages accessed 2007-01-31.
  46. ^ Grof, Stanislav; Joan Halifax Grof (1979). Realms of the Human Unconscious (Observations from LSD Research). London: Souvenir Press (E & A) Ltd. pp. 13–14. ISBN 0 285 64882 9.
  47. ^ Sessa, B. (2008). "Is it time to revisit the role of psychedelic drugs in enhancing human creativity?". J Psychopharmacol 22 (8): 821–7. doi:10.1177/0269881108091597. PMID 18562421.
  48. ^ Janiger, O.; Dobkin de Rios M. (1989). "LSD and creativity". J Psychoactive Drugs 21 (1): 129–34. PMID 2723891.
  49. ^ Stafford, Peter G.; B. H. Golightly (1967). LSD, the problem-solving psychedelic.
  50. ^ McGlothlin, W.; Cohen S, McClothlin MS (1967). "Long lasting effects of LSD on normals". Arch Gen Psychiat 17 (5): 521–532. PMID 6054248.
  51. ^ Whalen, John (1998-07-09). "The Trip: Cary Grant on acid, and other stories from the LSD Studies of Dr. Oscar Janiger". LA Weekly.
  52. ^ Fish, Jefferson M. (2006). Drugs and Society: U.S. Public Policy. Lanham, MD: Rowman & Littlefield. pp. 149–162. ISBN 0742542459.
  53. ^ http://web.cgu.edu/faculty/gabler/drug_toxicity.htm
  54. ^ LSD AND ORGANIC BRAIN IMPAIRMENT S Cohen, AE Edwards – Drug dependence, 1969
  55. ^ http://www.maps.org/research/cluster/psilo-lsd/cns-neuroscience+therapeutics_2008-passie.pdf
  56. ^ a b "LSD and Antidepressants" (2003) via Erowid.
  57. ^ Kit Bonson, "The Interactions between Hallucinogens and Antidepressants" (2006).
  58. ^ http://www.erowid.org/chemicals/lsd/lsd_health1.shtml
  59. ^ "Is Military Research Hazardous to Veterans Health? Lessons Spanning Half A Century, part F. HALLUCINOGENS". December 8, 1994 John D. Rockefeller IV, West Virginia. 1994-12-08.
  60. ^ Middlefell R (March 1967). "The effects of LSD on body sway suggestibility in a group of hospital patients" (PDF). Br J Psychiatry 113 (496): 277–80. PMID 6029626.
  61. ^ Sjoberg BM, Hollister LE (November 1965). "The effects of psychotomimetic drugs on primary suggestibility". Psychopharmacologia 8 (4): 251–62. PMID 5885648.
  62. ^ [Rick Strassman (1984). "Adverse reactions to psychedelic drugs. A review of the literature". J Nerv Ment Dis 172 (10): 577–95. doi:10.1097/00005053-198410000-00001. PMID 6384428.
  63. ^ a b Cohen, Sidney (January 1960). "Lysergic Acid Diethylamide: Side Effects and Complications" (PDF). Journal of Nervous and Mental Disease 130 (1): 30–40. doi:10.1097/00005053-196001000-00005. PMID 13811003.
  64. ^ a b c David Abrahart (1998). "A Critical Review of Theories and Research Concerning Lysergic Acid Diethylamide (LSD) and Mental Health". Retrieved 2007-02-02.
  65. ^ Blumenfield M (1971). "Flashback phenomena in basic trainees who enter the US Air Force". Military Medicine 136 (1): 39–41. PMID 5005369.
  66. ^ Naditch MP, Fenwick S (1977). "LSD flashbacks and ego functioning". Journal of Abnormal Psychology 86 (4): 352–9. doi:10.1037/0021-843X.86.4.352. PMID 757972.
  67. ^ See, for example, Abraham HD, Aldridge AM (1993). "Adverse consequences of lysergic acid diethylamide". Addiction 88 (10): 1327–34. doi:10.1111/j.1360-0443.1993.tb02018.x. PMID 8251869.
  68. ^ Halpern JH, Pope HG Jr (2003). "Hallucinogen persisting perception disorder: what do we know after 50 years?". Drug Alcohol Depend 69 (2): 109–19. doi:10.1016/S0376-8716(02)00306-X. PMID 12609692.; Halpern JH (2003). "Hallucinogens: an update".Curr Psychiatry Rep 5 (5): 347–54. doi:10.1007/s11920-003-0067-4. PMID 13678554. [1]
  69. ^ Baggott et al. (2006). "Prevalence of chronic flashbacks in hallucinogen users: a web-based questionnaire" (PDF). Retrieved 2009-09-25.
  70. ^ Abraham, H. D., & Duffy, F. H. ((1996)). "Stable quantitative EEG difference in post-LSD visual disorder by split-half analysis: Evidence for disinhibition". Psychiatry Research 67 (3): 173–187. doi:10.1016/0925-4927(96)02833-8. PMID 8912957.
  71. ^ a b Gerald G. Briggs,Roger K. Freeman,Sumner J. Yaffe (2008). Drugs in pregnancy and lactation. Lippincott Williams & Wilkins. ISBN 9780781778763.
  72. ^ a b c Dishotsky NI, Loughman WD, Mogar RE, Lipscomb WR (1971). "LSD and genetic damage" (PDF). Science 172 (982): 431–40. doi:10.1126/science.172.3982.431. PMID 4994465.
  73. ^ Huxley, Aldous The Doors of Perception and Heaven & Hell, Harper & Row, 1954.
  74. ^ Bonson, Kit (1994). "The Interactions between Hallucinogens and Antidepressants – Summary of Results from Online Survey and Online Interviews". Erowid. Retrieved 2008-07-28.
  75. ^ Gilberti, F. and Gregoretti, L. L. (1955). "Prime esperienze di antaonismo psicofarmacologico" (PDF). Sistema Nervoso 4: 301–309.
  76. ^ RaveSafe (1999). "RaveSafe Q&A – Can you actually end an acid trip?". Retrieved 2008-07-28.
  77. ^ R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 871-874.
  78. ^ a b Nichols, David E. (2004). "Psychotropics". Pharmacology & Therapeutics 101 (2): 131–81. doi:10.1016/j.pharmthera.2003.11.002. PMID 14761703.
  79. ^ "PDSP database". Retrieved 2009-11-02.
  80. ^ Nelson, DL (February 2004). "5-HT5 receptors". Current drug targets. CNS and neurological disorders 3 (1): 53–8. doi:10.2174/1568007043482606. PMID 14965244.
  81. ^ BilZ0r. "The Neuropharmacology of Hallucinogens: a technical overview". Erowid, v3.1 (August 2005).
  82. ^ Svenningsson P. , Nairn A. C., Greengard P. (2005). "DARPP-32 Mediates the Actions of Multiple Drugs of Abuse.". AAPS Journal 07 (02): E353–E360. doi:10.1208/aapsj070235. PMID 16353915. PMC 2750972.
  83. ^ a b DEA (2007). "LSD Manufacture – Illegal LSD Production". LSD in the United States. U.S. Department of Justice Drug Enforcement Administration. Archived from the original on 2007-08-29.
  84. ^ a b c Stafford, Peter (1992). "Chapter 1 – The LSD Family". Psychedelics Encyclopaedia (Third Expanded ed.). Ronin Publishing Inc. p. 62. ISBN 0-914171-51-8.
  85. ^ a b c Laing, Richard R.; Barry L. Beyerstein, Jay A. Siegel (2003). "Chapter 2.2 – Forms of the Drug". Hallucinogens: A Forensic Drug Handbook. Academic Press. pp. 39–41. ISBN 0124339514.
  86. ^ Honig, David. Frequently Asked Questions via Erowid
  87. ^ "Street Terms: Drugs and the Drug Trade". Office of National Drug Control Policy. 2005-04-05. Retrieved 2007-01-31.
  88. ^ DEA (2008). "Photo Library (page 2)". US Drug Enforcement Administration. Retrieved 2008-06-27.
  89. ^ ^ Maclean, J.R.; Macdonald, D.C.; Ogden, F.; Wilby, E., "LSD-25 and mescaline as therapeutic adjuvants." In: Abramson, H., Ed., The Use of LSD in Psychotherapy and Alcoholism, Bobbs-Merrill: New York, 1967, pp. 407–426; Ditman, K.S.; Bailey, J.J., "Evaluating LSD as a psychotherapeutic agent," pp.74–80; Hoffer, A., "A program for the treatment of alcoholism: LSD, malvaria, and nicotinic acid," pp. 353–402.
  90. ^ ^ LSD: The Drug
  91. ^ United States Drug Enforcement Administration (October 2005). Microgram Bulletin 38 (10). http://www.usdoj.gov/dea/programs/forensicsci/microgram/mg1005/mg1005.html. Retrieved 2009-08-20.
  92. ^ United States Drug Enforcement Administration (November 2006). Microgram Bulletin 39 (11). http://www.usdoj.gov/dea/programs/forensicsci/microgram/mg1106/mg1106.html. Retrieved 2009-08-20.
  93. ^ United States Drug Enforcement Administration (February 2007). Microgram Bulletin 40 (2). http://www.usdoj.gov/dea/programs/forensicsci/microgram/mg0207/mg0207.html. Retrieved 2009-08-20.
  94. ^ a b c United States Drug Enforcement Administration (December 2007). Microgram Bulletin 40 (12). http://www.usdoj.gov/dea/programs/forensicsci/microgram/mg1207/mg1207.html. Retrieved 2009-08-20.
  95. ^ United States Drug Enforcement Administration (March 2008). Microgram Bulletin 41 (3). http://www.usdoj.gov/dea/programs/forensicsci/microgram/mg0308/mg0308.html. Retrieved 2009-08-20.
  96. ^ United States Drug Enforcement Administration (March 2009). Microgram Bulletin 42 (3). http://www.usdoj.gov/dea/programs/forensicsci/microgram/mg0309/mg0309.html. Retrieved 2009-08-20.
  97. ^ United States Drug Enforcement Administration (November 2005). Microgram Bulletin 38 (11). http://www.usdoj.gov/dea/programs/forensicsci/microgram/mg1105/mg1105.html. Retrieved 2009-08-20.
  98. ^ Canadian government (1996). "Controlled Drugs and Substances Act". Justice Laws. Canadian Department of Justice. Retrieved 2007-07-05.
  99. ^ Drugs and the law: Report of the inquiry into the Misuse of Drugs Act 1971 London: Police Foundation, 2000, Runciman Report
  100. ^ After the War on Drugs: Blueprint for Regulation Transform Drug Policy Foundation 2009
  101. ^ From [2]: LSD is a Schedule I substance under the Controlled Substances Act.
  102. ^ Toxicity, Hallucinogens – LSD
  103. ^ Neal v. United States, U.S. 284 ., originating from U.S. v. Neal, 46 F.3d 1405 (7th Cir. 1995)
  104. ^ "Famous LSD users". The Good Drugs Guide. Retrieved 2008-10-20.
  105. ^ Publicly expressed thoughts and ideas about the effects of psychedelic drugs.

LSA Ergine

Ergine

Systematic (IUPAC) name

(8β)-9,10-didehydro-6-methyl-
ergoline-8-carboxamide

Identifiers

CAS number
478-94-4

ATC code
None

PubChem
CID 442072

ChemSpider
390611

Chemical data

Formula
C16H17N3O

Mol. mass
267.326 g/mol

Synonyms
LSA, d-lysergic acid amide, d-lysergamide, Ergine, and LA-111

Pharmacokinetic data

Metabolism
hepatic

Excretion
renal

Therapeutic considerations

Pregnancy cat.
X [1]

Legal status
? (UK) Schedule III (US)

Routes
Oral, Intramuscular

LSA, also known as d-lysergic acid amide, d-lysergamide, ergine, and LA-111, is an alkaloid of the ergoline family that occurs in various species of vines of the Convolvulaceae and some species of fungi. As the dominant alkaloid in the hallucinogenic seeds of Rivea corymbosa (ololiuhqui), Argyreia nervosa (Hawaiian baby woodrose) and Ipomoea tricolor (morning glories, tlitliltzin), it is often stated that ergine and/or isoergine (its epimer) is responsible for the psychedelic activity. In fact, the effects of synthetic LSA and iso-LSA are not particularly psychedelic, see Mixing the Kykeon below for a summary of human trials, and Chapter 17 and entry #26 of TiHKAL for further discussion. As a precursor to LSD, ergine is a DEA schedule III drug in the United States.

History

A traditional use of morning glory seeds by Mexican Native Americans was first described by Richard Schultes in 1941 in a short report documenting their use going back to Aztec times (cited in TiHKAL byAlexander Shulgin). Further research was published in 1960, when Don Thomes MacDougall reported that the seeds of Ipomoea tricolor were used as sacraments by certain Zapotecs, sometimes in conjunction with the seeds of Rivea corymbosa, another species which has a similar chemical composition, with lysergol instead of ergometrine. Ergine was assayed for human activity by Albert Hofmann in self-trials in 1947, well before it was known to be a natural compound. Intramuscular administration of a 500 microgram dose led to a tired, dreamy state, with an inability to maintain clear thoughts. After a short period of sleep the effects were gone, and normal baseline was recovered within five hours.[2] .

In 1956 the Central Intelligence Agency conducted research on the psychedelic properties of the ergine in the seeds of Rivea corymbosa, as Subproject 22 of MKULTRA.

[edit]Natural occurrence

Ergine has been found in high concentrations of 20 µg/g dry weight in the grass Stipa robusta (sleepygrass) infected with an Acremonium endophytic fungus together with other ergot alkaloids.[3]

It is also found in the seeds of several varieties of Morning Glories in concentrations of approximately 10 µg per seed, as well as Hawaiian Baby Woodrose seeds, at a concentration of around .3%.

Extraction

LSA can be extracted from morning glory (Ipomoea spp.) seeds[4] or Hawaiian baby woodrose[5].

See also

References

Smith, Sydney; Timmis, Geoffrey M. (1932). "98. The Alkaloids of Ergot. Part III. Ergine, a New Base obtained by the Degradation of Ergotoxine and Ergotinine". J. Chem. Soc. 1932: 763–766.doi:10.1039/JR9320000763.

Powell, William (2002). The Anarchist Cookbook. Ozark Press,LLC. pp. 44. ISBN 0848811305.

References

This article needs additional citations for verification.
Please help improve this article by adding reliable references. Unsourced material may be challenged and removed. (July 2007)

  1. ^ Erowid (04-15-07). "Erowid Morning Glory Basics".
  2. ^ Alexander Shulgin. "TiHKAL #26".
  3. ^ Petroski RJ, Powell RG, Clay K (1992). "Alkaloids of Stipa robusta (sleepygrass) infected with an Acremonium endophyte". Nat. Toxins 1 (2): 84–88. doi:10.1002/nt.2620010205. PMID 1344912.
  4. ^ "Ask Erowid".
  5. ^ "LSA Extraction".

Mescaline

From Wikipedia, the free encyclopedia

Mescaline

Systematic (IUPAC) name

2-(3,4,5-trimethoxyphenyl)ethanamine

Identifiers

CAS number
54-04-6

ATC code
None

PubChem
CID 4076

ChemSpider
3934

Chemical data

Formula
C11H17NO3

Mol. mass
211.257 g/mol

SMILES
eMolecules & PubChem

Synonyms
3,4,5-trimethoxyphenethylamine

Physical data

Melt. point
183–186 °C (361–367 °F) (Sulfate dihydrate)

Pharmacokinetic data

Half-life
6 hours

Therapeutic considerations

Pregnancy cat.
C(US)

Legal status
Prohibited (S9) (AU) Schedule III(CA) ? (UK) Schedule I (US)

Routes
Oral, Intravenous

Yes(what is this?) (verify)

Mescaline or 3,4,5-trimethoxyphenethylamine is a naturally-occurring psychedelic alkaloid of the phenethylamine class. It is mainly used as an entheogen, and as a tool to supplement various practices fortranscendence, including in meditation, psychonautics, art projects, and psychedelic psychotherapy.

It occurs naturally in the peyote cactus (Lophophora williamsii),[1] the San Pedro cactus (Echinopsis pachanoi) and the Peruvian Torch cactus (Echinopsis peruviana), and in a number of other members of theCactaceae plant family. It is also found in small amounts in certain members of the Fabaceae (bean) family, including Acacia berlandieri.[2] Mescaline was first isolated and identified in 1897 by the GermanArthur Heffter and first synthesized in 1919 by Ernst Späth.

Naturally derived mescaline powder extract.

Contents

[hide]

[edit]History and usage

Peyote has been used for over 3000 years by Native Americans in Mexico.[1] Europeans noted use of peyote in Native American religious ceremonies upon early contact, notably by the Huichols in Mexico. Other mescaline-containing cacti such as the San Pedro have a long history of use in South America, from Peru to Ecuador.

In traditional peyote preparations the top of the cactus is cut at ground level, leaving the large tap roots to grow new ‘Heads’. These ‘Heads’ are then dried to make disk-shaped buttons. Buttons are chewed to produce the effects or soaked in water for an intoxicating drink. However, the taste of the cactus is bitter, so users will often grind it into a powder and pour it in capsules to avoid having to taste it. The usual human dosage is 200–400 milligrams of mescaline sulfate or 178–356 milligrams of mescaline hydrochloride[3]. The average 3 inch button contains about 25 mg mescaline.[4]

Aldous Huxley described his experience with mescaline in The Doors of Perception. Aleister Crowley reported using mescaline in his diary. The sex psychologist Havelock Ellis also tried mescaline. Mescaline may have played a part in the development of the Cubist school of abstract art, when George Braque and Pablo Picasso published the "Cubist Manifesto" they described design paradigms which were similar to visual experiences induced by mescaline and other rare drugs known to the South American Islanders.[5] Hunter S. Thompson recounted his use of mescaline in Fear and Loathing in Las Vegas.

[edit]Pharmacokinetics

Tolerance builds with repeated usage, lasting for a few days. Mescaline causes cross-tolerance with LSD and other psychedelics.

About half the initial dosage is excreted after 6 hours, but some studies suggest that it is not metabolized at all before excretion.

Mescaline appears to not be subject to metabolism by CYP2D6[6] and between 20 and 50% of mescaline is excreted in the urine unchanged, and the rest being excreted as the carboxylic acid form of mescaline, a likely result of MAO degradation.[7]

The LD50 of mescaline has been measured in various animals: 212 mg/kg i.p. (mice), 132 mg/kg i.p. (rats), and 328 mg/kg i.p. (guinea pigs).

[edit]Behavioral and non-behavioral effects

The visual distortions produced by mescaline are somewhat different from those of LSD. The subjective "visuals" are not true Hallucinations as they are consistent with actual experience and typically intensifications of the different stimulus (objects and sounds), not the appearance of non existent fanciful objects or actions that the user believes are real. Prominence of color is distinctive, appearing brilliant and intense. Placing a strobing light in front of closed eyelids can produce brilliant visual effects at the peak of the experience. Recurring visual patterns observed during the mescaline experience include stripes, checkerboards, angular spikes, multicolored dots, and very simple fractals which turn very complex. Aldous Huxley described these self transforming amorphous shapes as like animated stained glass illuminated from light coming through the eyelids. Like LSD, mescaline induces distortions of form and kaleidoscopic experiences but which manifest more clearly with eyes closed and under low lighting conditions; however, all of these visual descriptions are purely subjective. Research into the root causes for the patterns associated with mescaline, LSD and DMT have given rise to mathematical theories that explain the biological processes that are disrupted by molecules like mescaline. [8]

As with LSD, synesthesia can occur especially with the help of music.[9] An unusual but unique characteristic of mescaline use is the "geometricization" of three-dimensional objects. The object can appear flattened and distorted, similar to the presentation of a Cubist painting.[10]

Mescaline elicits a pattern of sympathetic arousal, with the peripheral nervous system being a major target for this drug.[9] Effects last for up to 12 hours.[9]

[edit]Mode of action

Mescaline acts similarly to other psychedelic agents.[11] It binds to and activates the serotonin 5-HT2A receptor with a high affinity as a partial agonist.[12] How activating the 5-HT2A receptor leads to psychedelia is still unknown, but it likely somehow involves excitation of neurons in the prefrontal cortex.[13]

[edit]Legality

In the US, mescaline was made illegal in 1970 by the Comprehensive Drug Abuse Prevention and Control Act.[14] It was prohibited internationally by the 1971 Convention on Psychotropic Substances[15] and is categorized as a Schedule I hallucinogen by the CSA. Mescaline is only legal for certain religious groups (such as the Native American Church) and in scientific and medical research. In 1990, the Supreme Court ruled that the state of Oregon could bar the use of mescaline in Native American religious ceremonies. The Religious Freedom Restoration Act in 1993 allowed the use of peyote in religious ceremony but in 1997, the Supreme Court ruled that RFRA was unconstitutional when applied against states. However, a subsequent ruling in 2006 held that RFRA was constitutional when applied against the federal government.[16] Thus, the current state of the law is that, while the federal government may not restrict use of peyote in ceremony, individual states do have a right to restrict it.[17]Penalties for manufacture or sale can be as high as five years in prison and a fine of $15,000, with a penalty of up to one year and fine of $5000 for possession.

In the UK, mescaline is a Class A drug (in purified powder form, although dried cactus can be bought and sold legally, unlike raw "magic" mushrooms, which are now illegal),[18] and so carries the following penalties. For possession: up to seven years in prison or an unlimited fine or both. For dealing: up to life in prison or an unlimited fine or both.

In Canada, mescaline in raw form is considered an illegal drug. However, anyone may grow and use peyote, or Lophophora williamsii, without restriction, as it is specifically exempt from legislation.[1]

[edit]See also

[edit]References

  1. ^ a b c Drug Identification Bible. Grand Junction, CO: Amera-Chem, Inc.. 2007. ISBN 0-9635626-9-X.
  2. ^ Chemistry of Acacia’s from South Texas
  3. ^ http://www.erowid.org/library/books_online/pihkal/pihkal096.shtml
  4. ^ AJ Giannini, AE Slaby, MC Giannini. Handbook of Overdose and Detoxification Emergencies.New Hyde Park, NY. Medical Examination Publishing/Excerpta Medica Company,1982.
  5. ^ AJ Giannini. Drugs of Abuse—Second Edition. Los Angeles, Practice Management Information Corp., 1997.
  6. ^ Wu D, Otton SV, Inaba T, Kalow W, Sellers EM (June 1997). "Interactions of amphetamine analogs with human liver CYP2D6". Biochem. Pharmacol. 53 (11): 1605–12. doi:10.1016/S0006-2952(97)00014-2. PMID 9264312.
  7. ^ Cochin J, Woods LA, Seevers MH (February 1951). "The absorption, distribution and urinary excretion of mescaline in the dog". J. Pharmacol. Exp. Ther. 101 (2): 205–9. PMID 14814616.
  8. ^ http://www.math.pitt.edu/~bard/pubs/Ermentrout-Cowan79b.pdf],Biological Cybernetics 1979.
  9. ^ a b c Diaz, Jaime. How Drugs Influence Behavior. Englewood Cliffs: Prentice Hall, 1996
  10. ^ AJ Giannini, AE Slaby. Drugs of Abuse. Oradell, NJ. Medical Economics Books,1989, pp.207-239.
  11. ^ Nichols DE (February 2004). "Hallucinogens". Pharmacol. Ther. 101 (2): 131–81. doi:10.1016/j.pharmthera.2003.11.002. PMID 14761703.
  12. ^ Monte AP, Waldman SR, Marona-Lewicka D, et al. (September 1997). "Dihydrobenzofuran analogues of hallucinogens. 4. Mescaline derivatives". J. Med. Chem. 40 (19): 2997–3008. doi:10.1021/jm970219x. PMID 9301661.
  13. ^ Béïque JC, Imad M, Mladenovic L, Gingrich JA, Andrade R (June 2007). "Mechanism of the 5-hydroxytryptamine 2A receptor-mediated facilitation of synaptic activity in prefrontal cortex". Proc. Natl. Acad. Sci. U.S.A. 104 (23): 9870–5.doi:10.1073/pnas.0700436104. PMID 17535909.
  14. ^ United States Department of Justice. "Drug Scheduling". Retrieved 2007-11-02.
  15. ^ "List of psychotropic substances under international control". International Narcotics Control Board. Retrieved 2008-01-27.
  16. ^ [http://caselaw.lp.findlaw.com/cgi-bin/getcase.pl?court=US&navby=case&vol=000&invol=04-1084 GONZALES, ATTORNEY GENERAL, et al. v. O CENTRO ESPIRITA BENEFICENTE UNIAO DO VEGETAL et al.]
  17. ^ "Uses Drugs of Abuse—Origins and Effects – Hallucinogens".
  18. ^ "2007 U.K. Trichocereus Cacti Legal Case Regina v. Saul Sette".

MDA

3,4-Methylenedioxyamphetamine

 

3,4-Methylenedioxyamphetamine

Systematic (IUPAC) name

(R) 1-(benzo[1,3]dioxol-5-yl)propan-2-amine

Identifiers

CAS number
4764-17-4
51497-09-7 61614-60-665620-66-8

ATC code
?

PubChem
CID 1614

ChemSpider
1555

Chemical data

Formula
C10H13NO2

Mol. mass
179.22 g/mol

SMILES
eMolecules & PubChem

Pharmacokinetic data

Metabolism
Hepatic, CYP extensively involved

Half-life
dose dependent 6–10 hours

Excretion
Renal

Therapeutic considerations

Pregnancy cat.
?

Legal status
Prohibited (S9) (AU) Schedule III(CA) ? (UK) Schedule I (US)

Routes
Oral, Sublingual

3,4-Methylenedioxyamphetamine (MDA), also known as tenamfetamine (INN), is a psychedelic, stimulant, and empathogen-entactogen of the phenethylamine and amphetamine chemical classes. It is mainly used as a recreational drug, an entheogen, and a tool in use to supplement various types of practices for transcendence, including in meditation, psychonautics, and illegal psychedelic psychotherapy, whether self administered or not. It was first synthesized by G. Mannish and W. Jacobson in 1910. There are about 20 different synthetic routes described in the literature for its preparation.

Contents

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[edit]Medical use

There are no currently accepted medical uses for MDA. However, researchers have investigated many possible uses in the past. It was first ingested in July of 1930 by Gordon Alles who then licensed the drug toSmith Kline and French.[1]. MDA was first used in animal tests in 1939, and human trials began in 1941 in the exploration of possible therapies for Parkinson’s disease. From 1949 to 1957, more than 500 human subjects were given MDA in an investigation of its potential use as an antidepressant and/or anorectic by Smith, Kline & French. The United States Army also experimented with the drug, code named EA-1298, while working to develop a truth drug or incapacitating agent. One human subject[2] died in January 1953 after being intravenously injected with 450mg of the drug. MDA was patented as a cough suppressant by H. D. Brown in 1958, as an ataractic by Smith, Kline & French in 1960, and as an anorectic under the trade name “Amphedoxamine” in 1961. Several researchers, including Claudio Naranjo and Richard Yensen, have explored MDA in the field of psychotherapy.

[edit]Synthesis

One method of MDA synthesis is to turn safrole into isosafrole via isomerization. The isosafrole is then oxidized, using a peroxyacid, to produce MDP2P (methylenedioxyphenylacetone). Finally, it is converted to MDA via reductive amination with ammonia. This synthesis is very similar to that of MDMA (Ecstasy) and of MDEA. The most common route is by starting from piperonal, and condensing it with nitroethane. The resulting nitro-isosafrole can then be reduced to MDA with a suitable reducing agent.

[edit]Recreational use

MDA began to appear on the recreational drug scene around 1963 to 1964. It was then inexpensive and readily available as a research chemical from several scientific supply houses. Although now illegal, MDA continues to be bought, sold, and used for recreational purposes, often in the form of tablets purporting to contain MDMA (Ecstasy). It is also sold in powder form, referred to as "Sass", "Pink", or "Yop", derived from the urban street vocabulary of the Atlanta gang culture.

[edit]Effects

The MDA molecule

A recreational dose of MDA is commonly between 100 and 160mg. The “S” optical isomer of MDA is more potent than the “R” optical isomer as a psychostimulant, possessing greater affinity for the threemonoamine transporter proteins (SERT, NET and DAT). Although there is some debate, the duration of the drug is now generally believed to be roughly 6 to 10 hours; but most individuals report the duration of the drug’s effects to be around 5–6 hours, slightly longer than that of MDMA. (In the late 1990s, Alexander Shulgin changed his opinion of the duration to 3–6 hours).

MDA is thought to be similar in pharmacological mechanism of action and phenomenological effects to its more widely used N-methyl analogue MDMA (Ecstasy). Like MDMA, MDA causes serotonin and dopamine release by acting as a substrate at the SERT and DAT, respectively. This may explain the similar euphoric and empathogenic effects of the two compounds. However, (S)-MDA has a higher efficacy in stimulating the 5-HT2A receptor than (R)-MDMA; thus MDA tends to cause more psychedelic-like effects, such as visual hallucinations. MDMA can also produce psychedelic-like visual effects, though these are generally less pronounced than those of MDA, or require a heavier dose to become apparent.

MDA is said to share the empathogen/entactogenic effects of MDMA. While it is generally similar to MDMA, users report that MDA has more stimulant, or psychedelic hallucinogenic qualities and slightly less intense empathogen/entactogenic effects than MDMA. MDA is also considered less predictable than MDMA, with effects varying greatly from person to person. However, no properly controlled experiments have compared these drugs in humans.

MDA also differs from its methylated cousin MDMA in its acute toxicity—it is clearly more toxic, with toxicity indicative of overstimulation of the central nervous system and the cardiovascular system.[3]Symptoms of acute toxicity may include agitation, sweating, increased blood pressure and heart rate, dramatic increase in body temperature, convulsions, and death. Death is usually caused by cardiac effects and subsequent hemorrhaging in the brain (stroke).[3] The website erowid.org lists the fatality rate at roughly 2 in 100,000 users, assuming it has similar rates as MDMA.[4] The LD50 (median lethal dose) in mice has been reported as 92mg/kg by intraperitoneal injection.

[edit]Legality

In 1970, the Controlled Substances Act was enacted in the United States, placing MDA into Schedule I. It is similarly controlled in other nations. In Canada MDA is a Schedule III drug. Internationally, MDA is a Schedule I drug under the Convention on Psychotropic Substances. The US has also essentially banned any drug with (methylenedioxy) in its structure, as well as several other phenethylamine-based compounds. This means that all unscheduled MDXX chemicals can be prosecuted under theFederal Analog Act.[5]

[edit]Notes

Question book-new.svg

This article needs additional citations for verification.
Please help improve this article by adding reliable references. Unsourced material may be challenged and removed. (December 2007)

  1. ^ The First MDA trip and the measurement of ‘mystical experience’ after MDA, LSD, and Psilocybin http://psychedelicresearch.org/?p=45
  2. ^ The History Channel documented details of his death here http://www.youtube.com/watch?v=ySw-0uY4CUA See minute 2:38 onward.
  3. ^ a b Diaz, Jaime. How Drugs Influence Behavior. Englewood Cliffs: Prentice Hall, 1996.
  4. ^ Erowid.org
  5. ^ Incb.org

[edit]References

  • Lee, M.A. and Shlain, B., Acid Dreams: The CIA, LSD, and the Sixties Rebellion. Grove, 1985.
  • Stafford, P. Psychedelics Encyclopedia. Ronin, 1992.
  • Pihkal: A Chemical Love Story, Transform Press, Alexander Shulgin, Ann Shulgin.

MMDA (drug)

From Wikipedia, the free encyclopedia

  (Redirected from 3-Methoxy-4,5-methylendioxyamphetamine)

MMDA (drug)

Identifiers

CAS number
13674-05-0

ATC code
None

PubChem
CID 26175

ChemSpider
24386

Chemical data

Formula
C11H15NO3

Mol. mass
209.24 g/mol

SMILES
eMolecules & PubChem

Therapeutic considerations

Pregnancy cat.
?

Legal status
Schedule I (US)

Routes
Oral, Insufflation, Rectal

3-Methoxy-4,5-methylenedioxyamphetamine (MMDA; 5-Methoxy-MDA) is a psychedelic and entactogen drug of the amphetamine class. It is an analogue of lophophine, MDA, and MDMA, and also bears resemblance to the essential oil myristicin found in nutmeg.

MMDA was described by Alexander Shulgin in his book PiHKAL. Shulgin lists the dosage range of MMDA as 100-250 mg. The first symptoms appear within 30–60 minutes following oral administration. MMDA produces euphoria and loving warmth, and attenuates feelings such as anxiety and loneliness. MMDA also produces eyes-closed visuals, a state of drowsiness muscle relaxation, and time dilation. Side effectsinclude moderate mydriasis, dizziness, sensations of heat or cold, and trembling. The imagery is generally realistic, and often related to everyday perception of people, landscapes, or objects. The effects of MMDA usually reach a peak after the first hour following the initial symptoms, and begin to wane during the second hour, and usually completely disappear by the end of the fifth hour.

Contents

[hide]

[edit]Psychotherapuetic actions

In his 1973 book, "The Healing Journey", Claudio Naranjo explored the psychotherapeutic potential of MMDA. Like MDA, he found that MMDA facilitates communication and suggested it has potential applications in psychotherapy. Worldwide as of 2005, MMDA has not been approved for any human applications.

[edit]Pharmacology

MMDA has been shown to act as a non-neurotoxic serotonin releasing agent with no effects on dopamine release and probably norepinephrine release as well,[1] and as a 5-HT2A receptor agonist.[2] The latter property is responsible for its psychedelic effects, whereas the former mediates its mood-lifting and empathogenic effects.

[edit]Legality

MMDA is classified as a Schedule 1 substance in the United States, and is similarly controlled in other parts of the world. Internationally, MMDA is a Schedule I drug under the Convention on Psychotropic Substances[1].

[edit]See also

[edit]References

  1. ^ McKenna DJ, Guan XM, Shulgin AT (March 1991). "3,4-Methylenedioxyamphetamine (MDA) analogues exhibit differential effects on synaptosomal release of 3H-dopamine and 3H-5-hydroxytryptamine". Pharmacology, Biochemistry, and Behavior 38 (3): 505–12.PMID 1829838.
  2. ^ Zhang Z, An L, Hu W, Xiang Y (April 2007). "3D-QSAR study of hallucinogenic phenylalkylamines by using CoMFA approach". Journal of Computer-aided Molecular Design 21 (4): 145–53. doi:10.1007/s10822-006-9090-y. PMID 17203365.

Bromo-DragonFLY

From Wikipedia, the free encyclopedia

Bromo-DragonFLY

IUPAC name[hide]

1-(8-Bromobenzo[1,2-b;4,5-b]difuran-4-yl)-2-aminopropane

Other names[hide]

Bromo-benzodifuranyl-isopropylamine

Identifiers

CAS number
502759-67-3

PubChem
10544447

SMILES

[show]

Properties

Molecular formula
C13H12BrNO2

Molar mass
294.14 g/mol

Melting point

decomposes at 240 °C (hydrochloride)

Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)

Infobox references

Bromo-DragonFLY is a psychedelic hallucinogenic drug related to the phenethylamine family. Bromo-DragonFLY is considered an extremely potent hallucinogen, only slightly less potent than LSD with a normal dose in the region of 200 μg to 800 μg, and it has an extremely long duration of action up to several days.[1] It is explicitly illegal only in Sweden[2], Norway and Denmark, although it may be considered a controlled substance analogue under US and Australian drug laws. Bromo-DragonFLY has a stereocenter and R-(-)-bromo-DragonFLY is the more active stereoisomer.

Contents

[hide]

[edit]History

Bromo-DragonFLY was first synthesized by Matthew Parker in the laboratory of David E. Nichols in 1998. It got its name from an earlier and less active dihydrofurane series of compounds nicknamed FLY due to the molecule’s superficial structural resemblance to a fly.

[edit]Pharmacology

The hallucinogenic effect of bromo-DragonFLY is mediated by its agonist activity at the 5-HT2A serotonin receptor. Bromo-DragonFLY also has a high binding affinity for the 5-HT2B and 5-HT2C serotoninreceptors, and is most accurately described as a non-subtype selective 5-HT2 agonist, as it is actually twice as potent an agonist for 5-HT2C receptors as for 5-HT2A, as well as being less than 5x selective for 5-HT2A over 5-HT2B.[3]

[edit]Dosage

The typical dose of Bromo-DragonFLY is not known, however it has varied from 500 μg to 1 mg.[1] It has about 300 times the potency of mescaline, or 1/5th the potency of LSD. It has been sold in the form of blotters, similar to the distribution method of LSD, which has led to confusion, and reports of mistakenly consuming Bromo-DragonFly. It has a much longer duration of action than LSD and can last for up to 2–3 days[1] following a single large dose, with a slow onset of action that can take up to 6 hours before the effects are felt.

[edit]Toxicity

Pink ABDF powder.

The toxicity of Bromo-DragonFLY appears to be fairly high for humans when taken in doses above the therapeutic range, with reports of at least five deaths believed to have resulted from Bromo-DragonFLY reported inNorway,[4] Sweden,[5][6] Denmark[7][8] and the United States. Laboratory testing has confirmed that in October 2009, a batch of Bromo-Dragonfly was distributed, mislabeled as the related compound 2C-B-FLY, which is around 20x less potent than BDF by weight. This mistake is believed to have contributed to several lethal overdoses and additional hospitalizations. The batch implicated in these deaths also contained significant synthesis impurities, which may have contributed to the toxicity.[9]

Also, a Swedish man had to have the front part of his feet and several fingers on one hand amputated after taking a massive overdose. Apparently the compound acted as a long-acting efficacious vasoconstrictor, leading tonecrosis and gangrene which was delayed by several weeks after the overdose occurred. Several other cases have also been reported of severe peripheral vasoconstriction following overdose with Bromo-DragonFLY, and a similar case is also known from DOB. Treatment was of limited efficacy in this case although tolazoline is reportedly an effective treatment where available.[10][11]

Overdoses, disturbing experiences, and Bromo-DragonFLY associated health problems have been described. One case in 2008 in England involved inhalation of vomit, causing nearly fatal asphyxia.[12] Seizures have also been reported.[13]

October 3, 2009 a 22 year old man from Copenhagen died after ingesting Bromo-dragonfly. His friend described the trip saying, "It was like being dragged to hell and back again. Many times. It is the most evil [thing] I’ve ever tried. It lasted an eternity" [14]

[edit]Legal Status

[edit]Sweden

Bromo-DragonFLY was classified as a "health hazard" in Sweden on July 15, 2007, making it illegal to sell or possess there.[15][16]

[edit]Denmark

On December 5, 2007 the drug was banned in Denmark.[17] The substance has been declared illegal by health minister Jakob Axel Nielsen, following recommendations from the Danish Health Ministry. It is currently classified as a dangerous narcotic and therefore its possession, manufacture, importation, supply or usage is strictly prohibited. Anyone involved in such activities can face legal action.[15]

[edit]Norway

Bromo-DragonFLY is currently not on the Norwegian narcotics list,[18] but is affected by Norwegian derivate laws according to state officials.[19] Thus it is effectively a narcotic drug by Norwegian law.

[edit]Romania

The chemical compound has been added as an illegal substance under the Law 143/2000 on February 10, 2010.[20]

See also

Notes

  1. ^ a b c "Erowid Bromo-DragonFly Vault : Dosage".
  2. ^ "Svensk författningssamling (SFS) – Riksdagen".
  3. ^ Parker MA, Marona-Lewicka D, Lucaites VL, Nelson DL, Nichols DE (December 1998). "A novel (benzodifuranyl)aminoalkane with extremely potent activity at the 5-HT2A receptor". Journal of Medicinal Chemistry 41 (26): 5148–9. doi:10.1021/jm9803525.PMID 9857084.
  4. ^ "Erowid Bromo-Dragonfly Vault : Reported GHB-Related Death Involved Bromo-Dragonfly".
  5. ^ "Erowid Bromo-Dragonfly Vault : Information about a death reportedly related to Bromo-Dragonfly".
  6. ^ Kajsa Hallberg (2007-04-03). "Man i 20-årsåldern dog av drogen Dragonfly" (in Swedish). expressen.se (AB Kvällstidningen Expressen). Retrieved 2009-10-30.
  7. ^ Ritzau (2008-08-24). "Nyt stof har slået dansker ihjel" (in Danish). jp.dk. Retrieved 2009-10-30.
  8. ^ Andreasen MF, Telving R, Birkler RI, Schumacher B, Johannsen M. (January 2009). "A fatal poisoning involving Bromo-Dragonfly". Forensic Science International 183 (1-3): 91–6. doi:10.1016/j.forsciint.2008.11.001. PMID 19091499.
  9. ^ "Erowid 2C-B-Fly Vault: Death Report".
  10. ^ Bromo-dragonfly – livsfarlig missbruksdrog (Swedish)
  11. ^ Thorlacius K, Borna C, Personne M. Bromo-dragon fly–life-threatening drug. Can cause tissue necrosis as demonstrated by the first described case. (Swedish). Lakartidningen. 2008 Apr 16-22;105(16):1199-200. PMID 18522262
  12. ^ George, Sallie (2008-03-27). "England | Surrey | ‘I nearly died from taking £5 hit’". BBC News. Retrieved 2010-02-08.
  13. ^ Wood DM, Looker JJ, Shaikh L, Button J, Puchnarewicz M, Davies S, Lidder S, Ramsey J, Holt DW, Dargan PI (December 2009). "Delayed onset of seizures and toxicity associated with recreational use of Bromo-dragonFLY". Journal of Medical Toxicology : Official Journal of the American College of Medical Toxicology 5 (4): 226–9. PMID 19876858.
  14. ^ "| Danish man died after trip on Chinese drug". Jp.dk. Retrieved 2010-02-08.
  15. ^ a b "Erowid Bromo-Dragonfly Vault : Legal Status".
  16. ^ "Statens folkhälsoinstitut – Två nya droger klassas som hälsofarliga".
  17. ^ "Amendment of Executive Order on Euphoriant Substances". Danish Medicines Agency. 2007.
  18. ^ "List of narcotic drugs according to Norwegian law".
  19. ^ "Statens Legemiddelverk about derivates and Bromo-DragonFLY".
  20. ^ "Modified Romanian law 143/2000 on January 10, 2010.". Retrieved February 28, 2010.

2

References

External links

STP or DOM

2,5-Dimethoxy-4-methylamphetamine

From Wikipedia, the free encyclopedia

2,5-Dimethoxy-4-methylamphetamine

IUPAC name[hide]

1-(2,5-Dimethoxy-4-methylphenyl)-2-aminopropane

Other names[hide]

2,5-Dimethoxy-4-methylamphetamine

Identifiers

CAS number
26011-50-7, (R): 43061-13-8
(S): 43061-14-9

SMILES

[show]

Properties

Molecular formula
C12H19NO2

Molar mass
209.29 g/mol

Melting point

61 °C, 334 K, 142 °F

Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)

Infobox references

2,5-Dimethoxy-4-methylamphetamine (DOM or STP, allegedly standing for "Serenity, Tranquility and Peace", but based on the motor oil company STP as named by Owsley Stanley) is a psychedelic(hallucinogenic drug) and a substituted amphetamine. It was first synthesized by Alexander Shulgin, and later reported in his book PiHKAL (Phenethylamines i Have Known And Loved). DOM is classified as aSchedule I substance in the United States, and is similarly controlled in other parts of the world. Internationally, it is a Schedule I drug under the Convention on Psychotropic Substances.[1] It is generally taken orally.

History

In mid-1967, tablets containing 20 mg (later 10 mg) of DOM were widely distributed in the Haight-Ashbury District of San Francisco under the name of STP. This short-lived appearance of DOM on the black market proved disastrous for several reasons. First, the tablets contained an excessively high dose of the chemical. This, combined with DOM’s slow onset of action (which encouraged some users, familiar with drugs that have quicker onsets, such as LSD, to re-dose) and its remarkably long duration, caused many users to panic and sent some to the emergency room. Second, treatment of such overdoses was complicated by the fact that no one at the time knew that the tablets called STP were, in fact, DOM.

Effects

Effects of this drug include substantial perceptual changes such as blurred vision, multiple images, vibration of objects, visual hallucinations, distorted shapes, enhancement of details, slowed passage of time, and increased contrasts. It may also cause pupillary dilation and a rise in systolic blood pressure.[2]

Pharmacology

DOM is a selective 5-HT2A, 5-HT2B, and 5-HT2C receptor partial agonist. Its psychedelic effects are mediated by its agonistic properties at the 5-HT2A receptor. Due to its selectivity, DOM is often used in scientific research when studying the 5-HT2 receptor subfamily. DOM is a chiral molecule, and R-(-)-DOM is the more active enantiomer, functioning as a potent agonist of the serotonin 5-HT family of receptors; mainly of the 5-HT2 subtype.[3]

Analogues and derivatives

The 2,6-dimethoxy positional isomer of DOM, known as Ψ-DOM, is also mentioned in PiHKAL as being active, as is the alpha-ethyl homologue Ariadne. Analogues where the methoxy groups at the 2,5- positions of the aromatic ring have been altered have also been synthesised and tested as part of an effort to identify the binding mode of DOM at the 5-HT2A receptor. Both the 2- and 5- O-desmethyl derivatives 2-DM-DOM and 5-DM-DOM, and the 2- and 5- ethyl analogues 2-Et-DOM and 5-Et-DOM have been tested, but in all cases were significantly less potent than the corresponding methoxy compound, showing the importance of the oxygen lone pairs in 5-HT2A binding.[4][5]

DOM-25-varients.png

Toxicity

Very little is known about the toxicity of DOM. According to Shulgin, the effects of DOM typically last 14 to 20 hours, though other clinical trials indicate a duration of 7 to 8 hours.[2]

See also

References

Text document with red question mark.svg

This article includes a list of references or external links, but its sources remain unclear because it has insufficient inline citations. Please help to improve this article by introducing more precise citations where appropriate. (September 2009)

  1. ^ "List of psychotropic substances under international control". Retrieved 2007-03-30.
  2. ^ a b Snyder, Solomon H.; Louis Faillace and Leo Hollister (November 1967). "2,5-Dimethoxy-4-methyl-amphetamine (STP): A New Hallucinogenic Drug". Science 158 (3801): 669–670.
  3. ^ Sanders-Bush, E; Burris, KD; Knoth, K (1988). "Lysergic acid diethylamide and 2,5-dimethoxy-4-methylamphetamine are partial agonists at serotonin receptors linked to phosphoinositide hydrolysis". The Journal of pharmacology and experimental therapeutics246 (3): 924–928. PMID 2843634.
  4. ^ Eckler JR, Chang-Fong J, Rabin RA, Smith C, Teitler M, Glennon RA, Winter JC (July 2003). "Behavioral characterization of 2-O-desmethyl and 5-O-desmethyl metabolites of the phenylethylamine hallucinogen DOM". Pharmacology, Biochemistry, and Behavior 75(4): 845–52. PMID 12957227.
  5. ^ Michael Robert Braden PhD. Towards a biophysical understanding of hallucinogen action. Purdue University 2007.
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