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Discussion => Drug safety => Topic started by: DMtryptamine285 on August 02, 2013, 09:32 pm
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Galbulimima belgraveana is an hallucinogenic plant. Its common names include white magnolia.[1] It is native to northeastern Australia, Malaysia, and Papua New Guinea. Papuans (who tend to use this drug the most) boil the bark and the leaves together with another plant, called Homalomena[2], in order to make tea. This tea leads to a deep sleep, in which it is said that vivid dreams and visions occur. The plant itself grows to about 90 feet, it has no petals and its flower are a yellow-brown colour. It is similar to strong marijuana which induces a similar slumber like feeling.The tree is also used for its wood. (from wikipedia.)[1]
The use of Galbulimima belgraveana in Papua New Guinea has been reported in several popular books on psychoactive plants (BOCK in press; EMBODEN 1972; 1979; OTT 1993; 1996; RATSCH 1998; SCHULTES & HOFMANN 1979; 1980). The bark of Galbulimima belgraveana has been chewed with the leaves of an unidentified Homalomena sp. [Araceae] by the people of the Okapa region, Eastern Highlands (BARRAU 1958). The chewing of Galbulimima belgraveana bark (agara) and Homalomena sp. leaves (ereriba) has been reported to induce visions and a dream-like state (BARRAU 1958; HAMILTON 1960). Physical effects of chewing agara and eririba include violent tremor and miosis (DE SMET 1983:296; 1985). The violent tremors last for about an hour followed by a sense of calmness, euphoria and then drowsiness (DE SMET 1983:296; 1985). Galbulimima belgraveana has also been used without Homalomena sp. leaves for divination and to produce trance-like states and visions among the Gimi people of the Eastern Highlands (GLICK 1963; 1967). The bark and also the leaves of Galbulimima belgraveana have been used among other groups of the Eastern Highlands to make young men fierce (POWELL 1976:150; WEBB 1960). The people of Aseki in the south of Morobe Province use waga, the bark of Galbulimima belgraveana, as an analgesic by chewing the bark, spitting it out into a bowl, mixing salt with it and then swallowing it again to relieve pain (WOODLEY 1991). The Oksapmin of the West Sepik Province use alusa, shredded Galbulimima belgraveana bark mixed with wild ginger (Zingiber sp. [Zingiberaceae]), in the treatment of diseases caused by sorcery and witchcraft (eg. fever, skin conditions and poisoning) (SKINGLE 1970). The Bimin-Kiskusmin of the West Sepik Province have also used Galbulimima belgraveana in ritual (POOLE 1984).
CHEMISTRY AND ACTIVITY: The phytochemistry of Galbulimima belgraveana has been extensively studied and well documented (BINNS et al. 1965; BROWN et al. 1956; CHOO et al. 1990; COLLINS et al. 1990; RITCHIE & TAYLOR 1967; 1971; WEBB 1955). The pioneering research of Australian scientists Leonard J. Webb, Ernest Ritchie and Walter C. Taylor on the phytochemistry of Australian flora identified the chemical constituents of Galbulimima belgraveana (RITCHIE & TAYLOR 1967; 1971; WEBB 1945-1965; 1955; 1960). Galbulimima belgraveana is rich in alkaloids (WEBB 1955) and twenty-eight alkaloids have been isolated (RITCHIE & TAYLOR 1967:531): himbacine (C22H35NO2), himbeline (C21H33NO2), himandravine (C21H33NO2), himgravine (C22H33NO2), himbosine (C35H41NO10), himandridine (C30H37NO7), himandrine (C30H37NO6), G.B. 1 (C33H39NO9), G. B. 2 (C30H39NO10), G. B. 3 (C26H35NO8), G. B. 4 (C31H37NO8), G. B. 5 (C24H33NO7), G. B. 6 (C32H39NO8), G. B. 7 (C32H39NO8), G. B. 8 (C23H33NO5), G. B. 9 (C25H35NO6), G. B. 10 (C27H37NO7), G. B. 11 (C24H33NO6), G. B. 12 (C28H37NO8), himgaline (C20H31NO2), himbadine (C21H31NO2), G. B. 13 (C20H29NO2), himgrine (C22H33NO3), G. B. 14 (C24H33NO5), G. B. 15 (C22H35NO3), G. B. 16 (C20H27NO2), G. B. 17 (C21H31NO3) and G. B. 18 (C22H33NO2). There is considerable variation in the presence of these alkaloids in samples of Galbulimima begraveana collected in Papua New Guinea and North Queensland. Samples of Galbulimima bark collected in Papua New Guinea have isolated the alkaloids himbacine, himbeline, himandravine, himgravine, himbosine, himandridine, himandrine, G. B. 1, G. B. 2, G. B. 3, G. B. 4, G. B. 5, G. B. 8, G. B. 9, G. B. 10, G. B. 11, G. B. 12, himgaline, himgrine, G. B. 14, G. B. 15, and G. B. 16 (BROWN et al. 1955; RITCHIE & TAYLOR 1967:531). North Queensland samples of Galbulimima bark analysed contain himbacine, himgravine, himbosine, himandridine, himandrine, G. B. 1, G. B. 2, G. B. 4, G. B. 5, G. B. 6, G. B. 7, himgaline, himbadine, G. B. 13, G. B. 17 and G. B. 18 (RITCHIE & TAYLOR 1967:531). The alkaloids himbacine, himbeline, himandravine and himgravine are tetracyclic lactones and himbacine has been successfully synthesised (ADAMSON et al. 1997; MANDER & WELLS 1997; NEUMANN 1998). The total synthesis of himgravine (NEUMANN 1998) and other Galbulimima alkaloids is currently under investigation (ADAMSON et al. 1997). Himbosine, himanridine, himandrine and alkaloids G. B. 1 - G. B. 12 are oxygentated heterocyclic esters (RITCHIE & TAYLOR 1967:530). The alkaloid himgaline is a hexacyclic base. Himbadine and G. B. 13 are pentacyclic bases. The alkaloids himgrine and alkaloids G. B. 14 - G. B. 18 have been considered to have miscellaneous structures (RITCHIE & TAYLOR 1967:530).
The Galbulimima alkaloids have become a focus of attention in Western biomedical research as a potential source of new pharmaceutical drugs (ADAMSON et al. 1997; CHOO et al. 1990; COBBIN 1955; COBBIN & THORP 1957; COLLINS et al. 1990; MANDER & WELLS 1997; NEUMANN 1998). The pharmacology of the Galbulimima alkaloid himbacine has been evaluated in laboratory research and clinical trials (ANWAR et al. 1986; EGLEN et al. 1988; GILANI & COBBIN 1984; LAI et al. 1990; LAI et al. 1991; SHEN et al. 1993; WEI et al. 1994; ZHOLOS & BOLTON 1997). The pharmacological activity of himbacine and other Galbulimima alkaloids is a result of these alkaloids actions on muscarine cholinergic receptors (parasympathetic nervous system). Himbacine is a muscarinic receptor antagonist with affinity for the M2 receptor (ZHOLOS & BOLTON 1997). Galbulimima alkaloids like himbacine have been proposed as pharmaceutical treatments of Alzheimer's Disease (NEUMANN 1998), cardiac brachycardias (ANWAR et al. 1986) and to reduce intraocular pressure (ALLERGAN 1998). It remains to be seen if the entheogenic activity of Galbulimima belgraveana is a result of the muscarinic (M2) receptor antagonist activity of the Galbulimima alkaloids.
Copyright Haight Ashbury Publications Mar 2005
[Headnote]
Abstract-There are several reports that the bark of the rainforest tree Galbulimima belgraveana (F. Muell.) Sprague has been chewed for its psychoactive properties in Papua New Guinea. Twenty-eight alkaloids have been isolated from Galbulimima bark. There is no direct pharmacological evidence that any of these alkaloids are psychoactive. Two different pharmacological explanations for the reported psychoactive properties of Galbulimima bark are offered.
Keywords-alkaloids, bark, Galbulimima belgraveana, GB. 18, himbacine, Papua New Guinea
Reports on the psychoactive properties of Galbulimima belgraveana (F. Muell.) Sprague bark have corne from several places in Papua New Guinea (Benjamin 1999; Woodley 1991; Poole 1987; Hayano 1982; Click 1967; Barrau 1962, 1958; Hamilton 1960). The chewing of Galbulimima bark is reported to produce a destructive frenzy (Woodley 1991 : 75) often accompanied by violence (Hamilton 1960: 1617). Physical restraint is sometimes required (Hamilton 1960: 17). This is usually, but not always, followed by deep sleep during which visions are experienced (Schultes & Hofmann 1979: 43; Hamilton 1960: 17). These visions are of men and animals to be killed (Schultes & Hofmann 1979: 67; Hamilton 1960: 17). The physical effects of chewing Galbulimima bark include violent tremor that lasts about an hour and miosis (De Smet 1983: 296; Hamilton 1960: 16). This is followed by calmness, euphoria, and drowsiness (De Smet 1983: 296; Hamilton 1960: 17).
Galbulimima belgraveana is a large aromatic evergreen tree that grows in thick mountain rainforests and often contributes to the canopy of these rainforests (Croft 1978). This tree is most common in the highlands of Papua New Guinea but can also be found in the rainforests of North Queensland (Australia) and in some areas of Indonesia (West Papua). It is a tall tree (up to about 35 metres) with a trunk up to 60 centimeters in diameter. A buttress root is sometimes present and may be three metres high, one metre wide and five to 20 centimeters thick. The leaves are round or oval shaped with copper coloured scales all over them, giving the leaves a coppery-green appearance. Each leaf has a conspicuous network of veins. The flowers are large and white, cream or brown. A small pink or red fleshy fruit appears after flowering. The outer bark is grey or greyish brown and is scaly and pimply. This bark has a resinous smell and a bitter taste (Benjamin 1999).
In 1957 a pharmacological study of himandrine, one of the Galbulimima alkaloids, found that this alkaloid had spasmolytic activity comparable to papaverine (Cobbin & Thorp 1957). This study also demonstrated that himandrine produced a blood pressure fall of central origin along with brachycardia which was partly of central and direct origin (Collins et al. 1990: 102; Cobbin & Thorp 1957). Cobbin and Thorp (1957) suggested that himandrine suppressed the sympathetic centers of the hypothalamus (Collins et al. 1990: 102). These findings on the properties of himandrine were supported by research conducted by the Smith, Kline and French (SKF) pharmaceutical company (Collins et al. 1990: 102). SKF extended research with himandrine to 11 other Galbulimima alkaloids: himbacine, himgravine, himbosine, himbadine, himandravine, himandridine, himbeline, himgaline, alkaloid GB.7, alkaloid GB. 18 and alkaloid GB. 5. Of these 12 Galbulimima alkaloids, SKF considered the alkaloid himbacine to be the most active and the alkaloid most likely to be of clinical benefit. The most significant activities of himbacine were observed to be cardiovascular and antispasmodic (Collins et al. 1990: 102). As an antispasmodic, himbacine was similar to atropine in activity and potency (Collins et al. 1990: 102). However, as a mydriatic, himbacine was 50 (oral) or 100 (i.p.) times less potent than atropine (Collins et al. 1990: 102). Himbacine acts as an antagonist to the effects of the parasympathetic nervous stimulation and is more effective on the heart than on any other organ. Himbacine is of potential clinical benefit in the treatment of abnormally slow heart rate with minimal side effects (Collins et al. 1990: 102). The pharmacology of himbacine has recently been evaluated in laboratory research (Meloy et al. 2001; Shen & Mitchelson 2001). The pharmacological activity of himbacine is a result of this alkaloid's action on muscarine cholinergic receptors in the parasympathetic nervous system (Darroch et al. 1990). Himbacine is a muscarinic receptor antagonist with affinity for the M2 receptor (Broadley & Kelly 2001). It has been proposed as a pharmaceutical treatment for Alzheimer's Disease (Neumann 1998), cardiac brachycardias (Gilani & Cobbin 1986) and to reduce intraocular pressure (Allergan 1998).
It is possible that himbacine may have some muscarinic receptor (Ml) antagonist activity. all of the pharmacological studies of himbacine have observed effects only on the parasympathetic nervous system similar to or weaker than atropine. Atropine is a potent muscarinic receptor (M^sub 1^) antagonist (Broadley & Kelly 2001). The atropine-like activity of himbacine may produce agitation, excitement and hallucinations. This is possible, but a lot of bark would need to be consumed to get similar amounts, supposing that there was activity (Taylor 2000). Reports on the chewing of Galbulimima bark in Papua New Guinea indicate that large amounts have been used: "seven or eight pieces... about the size of a penny" (Hamilton 1960: 16). Large doses of himbacine may produce M^sub 1^ antagonism and psychoactive effects like those of atropine. However, the psychoactive properties of himbacine have not yet been demonstrated.
The second explanation for the reported psychoactive properties of Galbulimima bark is that one of the 28 alkaloids found in this bark may have novel psychoactive activity. This alkaloid may be alkaloid GB.18 (C^sub 22^H^sub 33^NO^sub 2^), also known as alkaloid J. Alkaloid GB. 18 has been reported to have "psychotropic properties" (Collins et al. 1990:105). This has been suggested because of its lack of influence on the pain threshold in mice at a dose of five milligrams per kilogram. Psychotropic activity of centrally active drugs is determined in animal assays that measure analgesia, including hot-plate, light-warmth stimuli and loss of stretch reflex response (Braun, Shulgin & Braun 1980: 193). In all animal assays, alkaloid G.B. 18 was significantly more active as an analgesic than control saline. In larger doses, alkaloid GB. 18 produces central nervous system depression in mice at 50 milligrams per kilogram (oral) and ataxia and death at 500 milligrams per kilogram (oral) (Collins et al. 1990: 105). It has hypotensive activity that is associated with respiratory depression and weak antispasmodic activity. Alkaloid GB. 18 may be responsible for the psychoactive properties of Galbulimima bark. The chemical structure of alkaloid GB. 18 is unknown (Collins et al. 1990). What is known is that alkaloid GB. 18 is structurally distinct from the other types of alkaloids found in Galbulimima bark (Mander 2000). When the structure of alkaloid GB. 18 has been determined, it will be possible to synthesize the compound. The synthesis of alkaloid GB. 18 is currently under investigation (Mander 2000; Taylor 2000). Synthetic alkaloid GB.18 may become a new psychoactive drug with effects like phencyclidine (PCP; see Chen 1958) if its psychotropic properties can be demonstrated. There is one problem with this explanation and that is that there is only a suggestion of psychotropic properties; there is no definite proof at all (Taylor 2000). It is a minor alkaloid in Galbulimima bark from North Queensland, and it is not known if it occurs in Galbulimima bark from Papua New Guinea. If it does, it would only be a minor component and would therefore have to be extremely active if it is alone responsible for the observed effects of Galbulimima bark (Taylor 2000).
It has been suggested that the problem of explaining the psychoactive properties of Galbulimima bark is "a complex one with many aspects to which there are no quick and easy answers" (Taylor 2000). Two different pharmacological explanations have been offered. The first explanation is based on the possibility that himbacine, one of the alkaloids found in Galbulimima bark, has muscarinic receptor (M^sub 1^) antagonist activity like atropine. The second explanation is that another one of the Galbulimima alkaloids (alkaloid GB. 18) may have novel psychotropic properties like phencyclidine (PCP). More research on the psychoactive properties of Galbulimima bark is required in the future.
AGARA (Galbulimima Belgraveana) is a tall forest tree of Malaysia and Australia. In Papua, natives make a drink by boiling the leaves and bark with the leaves of ereriba. When they imbibe it, they become violently intoxicated, eventually falling into a deep sleep during which they experience visions and fantastic dreams. Some 28 alkaloids have been isolated from this tree, and although they are biologically active, the psychoactive principle is still unknown. Agara is one of four species of Galbulimima and belongs to the Himontandraceae, a rare family related to the magnolias (plants of the gods.)
In 1957, the Australian dietician Lucy Hamilton (Mrs. J. Reid) conducted an experiment at Okapa in the Eastern Highlands of Papua New Guinea to observe the effects of eating a substance called "agara" bark, identified as the species Galbulimima belgraveana.
The French ethnobotanist Jacques Barrau was also present at Okapa to observe this experiment (Barrau 1958). A local man called Ogia volunteered to do the bioassay. Seven or eight pieces of "agara" bark about the "size of a penny" were chewed and swallowed. While Ogia masticated the bark, he also smoked some tobacco, chewed some ginger, and additionally ate the dried leaves of a plant called "ereriba" (an unidentified Homalomena species). Following consumption of all this, Ogia waited for the effects, which began shortly thereafter:
[…He] began to tremble, as they say, "like a kuru meri." His arms and body trembled, but not his legs. After a few minutes of this, he suddenly became quite violent. He swept all the things off the table and would have done quite a bit of damage if I hadn’t had a policeman standing by to detain him. I was very thankful for this forethought as I was the only European on the station at the time… He was put in handcuffs and let go outside. He picked up a stick and chased several people with it. He tried to take a bush knife from a workman in the garden. The station women were warned to keep their children inside. I am convinced that his behavior was not an act, as from a pleasant mild little man, he had suddenly become a crazed being. He neither spoke or smiled, and at first did not appear to hear. The pupils of his eyes were mere pinpoints. At the onset of violence the trembling had ceased (Hamilton 1960).
Ogia’s destructive frenzy was followed by calmness, euphoria, drowsiness, and finally a deep sleep that lasted for several hours (Hamilton 1960). It has been suggested that, after eating "agara" bark, one experiences visions while asleep (Schultes & Hofmann 1979; Hamilton 1960). For this reason, the bark has been called "dream man" among the Fore people (Hamilton 1960), although several other substances used by the Fore to produce visions are also known by this term, including the "ereriba" that Ogia had eaten, as well as "maraba" (Kaempferia galangal) (Hamilton 1960). However, Ogia reported no visions related to his experience. He later told Hamilton that the reason he did not experience any visions was because he did not want to. It was also suggested to Hamilton that in this experiment, Ogia had eaten "agara" bark in the morning and not in the evening, which was thought to be the proper time to eat "dream man." The only aftereffect reported by Ogia was a stomach ache (Hamilton 1960).
The following is an experience report I found on the plant.
7:15 pm Begin chewing 10 grams of "agara" bark
7:16 pm Intensely bitter taste
7:20 pm Strong alkaloidal after taste, similar to quinine
7:25 pm Bark is swallowed
7:55 pm First alert, becoming drowsy
7:57 pm Dilated pupils
8:00 pm Difficulty in concentration
8:05 pm Increased pulse and heart rate
8:10 pm Pleasant drowsiness, similar to 0.3 mg dose of hyoscine (scopolamine) hydrobromide, but without changes in perception
8:15 pm Dizziness
8:20 pm Lying down with eyes closed, no eidetic images
8:25 pm Relaxation
8:30 pm Hypnagogic state with no dreams
9:55 pm Drowsiness wearing off
10:05 pm Afterglow, euphoria
10:25 pm Baseline, no aftereffects