Dan Quan
Ryan Kelly
Greg Pisotti
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Once upon time…. There was a princess who kissed a lowly little
frog who then became a prince.
Familiar story right?
After investigating into this mere
children’s story, we have come up with a
possible scientific explanation.
As it turns out, upon kissing this frog the
princess unknowingly ingested a
potentially potent psychedelic toxin by
the name of bufotenine.
With the ingestion of this toxin, her slimy
frog appeared to have transformed into what the princess
perceived as a handsome prince.
This is the story of bufotenine and how it could have possibly been
the source of this well-known bedtime story…
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Many organisms have evolved the ability to produce toxins.
One member of the toad family Bufo bufo gargarizans and another
organism, a plant species known as Anedenathera colubrina.
Robert Most led the movement with his pamphlet entitled Bufo
alvarius: The Psychedelic Toad of the Desert.
Chinese maps from Fei, L. 1999. Atlas of Amphibians of China
Russian maps from Kuzmin, S.L. 1999. The amphibians of the former Soviet Union.
Paratoid Gland
Femoral
Pores
http://upload.wikimedia.org/wikipedia/commons/4/43/B
ufo_gargarizans_profile.jpg
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Ch’an su is a traditional Chinese medicine (TCM) that is derived
from the venom of various toad species. Eg: Bufo bufo gargarizans.
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Ch’an su was ingested orally or applied topically to reduce
swelling and alleviate pain.
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Ch’an su is still known today as powerful
aphrodisiac which can be applied
topically to an area of interest.
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Also claims to “expel summer heat,
open the orifices, and awaken the spirit”
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It acts as a CNS stimulant and exerts
cardiopulmonary effects.
Anadenanthera colubrina is a plant found mostly in
South America and seen in early mesoamerican art.
 The people in Meso America used the beans of this
plant, which contains high concentrations of
bufotenine.
 Psychedelic snuff was then created by the
inhabitants through a long process.
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• They would pop the beans like popcorn and ground them up
with mortar and pestle.
• The powder was then mixed with a lime and was moistened
into a dough.
• Bufotenine constitutes 12.4% of the substance and is the active
ingredient.
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Shamans used to use snuff as ways to transcend this
realm and enter another.
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A closely related compound to bufotenine has been shown
to produce psychedelic effects in humans.
The worship of this species, Bufo alvarious, resulted in the
religious movement known as The Church of the Toad of
Light.
It also led to the a drug movement in the 1970’s commonly
referred to as “Toad Licking”
Toad licking is impractical and the real effects came from
smoking extracted bufotenine, This is how you do it…
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Hold toad with one hand and with the thumb and forefinger of
your other hand.
Squeeze near the base of the gland until the venom squirts out the
pores and onto a smooth pore-less surface, such as a glass plate.
The venom is a milky-white in color when first squeezed from the
glands.
The substance is very viscous and begins to
evaporate immediately, leaving behind the
dried smokeable portion.
Scrape off the substance and store in an
airtight container until ready to smoke.
tryptamine
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The DEA has classified tryptamines which are chemical compounds with
the general structure in the above picture, and chemical similarity to the
amino acid tryptophan, as schedule I hallucinogenic substances.
Some tryptamines in this catergory are psilocybin (certain mushrooms),
DMT (dimethyltryptamine, and our toxin that we are researching,
bufotenine. Bufotenine as well as other tryptamines are labeled as
schedule I hallucinogenic because “as pure chemicals at doses of 10 to 20
mg, these hallucinogens produce muscle relaxation, dilation of pupils,
vivid visual and auditory distortions, and emotional disturbances” (DEA).
psilocybin
Dimethyltryptamine (Found
In many plants)
Drugs that are classified as schedule I are considered so because:
• The drug or other substance has a high potential for abuse.
•
The drug or other substance has no currently
accepted medical use in treatment in the United
States
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There is a lack of accepted safety for use of the
drug or other substance under medical
supervision. (DEA)
•
Some well known schedule I substances are heroin, ecstacy, PCP,
and marijuana.
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Two main receptors associated with causing
a hallucinogenic response in an individual.
They are named the 5-HT2A and 5-HT2C
receptors.
It is believed that the “5-HT2A receptors
may predominantly mediate the stimulus
properties of hallucinogens, while the 5HT2C receptors play a modulatory role”
(McBride 324).
Bufotenine activity on these two receptors
mimics results produced by known
hallucigens LSD and 5-MeO-DMT proving
that it does possess psychoactive abilities.
Thus if bufotenine toxin is able to
accumulate at a sufficient concentration in
the brain, then it should elicit the same
responses as LSD, 5-MeO-DMT, or psilocin
(psychoactive mushrooms).
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It is well known that “a drug’s degree of lipid
solubility generally correlates to ability to cross
the BBB and other biological membranes if an
active transport mechanism is lacking” (McBride
326).
To measure the ability of a drug to cross the
blood-brain barrier, partition coefficients are
used. The coefficients are the ratio
of concentration of a compound in two phases of
a mixture of two immiscible
solvents at equilibrium. The coefficients are thus
a measure of solubility of the compound
between two solvents.
It has been proposed through research that a
partition coefficient of 1.40 is the minimum
required to activate a hallucinogenic response
with 3.14 being the most optimum.
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Two known psychedelics, 5-Me0-DMT and psilocin have partition
coefficients of 3.30 and 3.30, further supporting these two toxins
ability to bring about a psychoactive response.
Bufotenine on the other hand only has a partition
coefficient of 0.06. This low number is the reason
that scientists do not believe in the ability of
bufotenine to produce hallucinogenic activity.
•The exact mechanism of action of bufotenine still eludes scientists.
•Unlike its very close relative 5-MeO-DMT, Bufotenine is a very polar
compound. Because of its polarity, it has very low lipid solubility, and
thus has difficulty crossing the Blood Brain Barrier.
•With its inability to penetrate the Blood Brain Barrier effectively, it has
been proposed that bufotenine cannot ilicit a psychoactive response.
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It is not easy to do research into drugs of this category
(schedule I) in the US, therefore many times American
researchers must leave the country.
The effects of “licking toads” or more generally
ingesting bufotenine can have widely varying effects.
As with any drug these effects vary from person to
person.
These effects can range from mostly physical to mildly
or intensely hallucinogenic.
Usage or prevalence in today’s society is low do to the
more readily available substances that are much easier
to obtain such as LSD or DMT, which can both have
similar effects.
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There have been seven ways of ingesting this toxin that have been
tested.
Intranasal, intrarectal, sublingual, intravenous, intramuscularly,
intraoral and vapor inhalation.
Each of these various ways of ingesting bufotenine required a
different dose to discern any “hallucinogenic” effects.
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Intravenous: 1-16mg
Intramuscular: 10-12.5
Intranasal: 40-100mg -yes this is a very large dose but it is what
was discovered by John Ott while doing research in South America
to cause a hallucinogenic effect
Sublingual: 50mg before effects were felt
Intra-orally: 100mg before effects were felt
Vapor inhalation: 2-8 mg -arguably the most effective way of using
the drug
Intra-rectally: 50mg -this method has been used by shamans in
native tribes of South America
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Tests have shown that various responses to the toxin have
been elicited.
Most notably it almost always comes with some form of
physiological symptom
These can be a heavy feeling in the chest
Shortness of breath
A mild to intense purpling of the face
Nausea/vomiting
Increased heart rate
Rarely have any of these symptoms, or any symptom of
ingesting bufotenine proven to be fatal.
Obviously it must be noted that “EVERYTHING IS TOXIC”
and of coarse there is a dose that can be lethal but there is
not enough research to discover the lethal dose
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In 1956 research was done on prisoners
to determine the effects of injected
bufotenine (Fabing)
Each prisoner was given a different
dose and saw a mildly different yet
similar response
Most reported some sort of “trip” in
which they saw various colors or
patterns.
Some reported as though they were
looking through literal “rose colored
glasses”
Colors appeared in front of their eyes in
blotches
Some saw patterns, such as lines or
boxes on the walls of the room
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Most hallucinations involved some sort of color display.
No reports of “people’s faces melting or sheep dancing” were
noted.
Meaning that the “trip” or hallucinogenic effect is relatively mild,
when compared to other hallucinogens.
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With its inability to cross the blood-brain barrier through
conventional methods, there must be another mechanism that
allows for the reported psychoactive effects.
“During periods of acute hypertension, the permeability of the
BBB to a number of compounds is increased” (McBride 327).
Therefore it is possible that when the blood-brain barrier is
compromised, a partially effective dose is allowed to enter the
brain along with the natural accumulation, which can cause a
partial hallucinogenic response.
More research needs to be done on the toxin, because in nature,
the toxin is combined with other “bioactive ingredients such as in
the Bufo toad toxin” (McBride 328).
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It has been researched that toad toxins and toad skins comprise of
catecholamines such as epinephrine, and therefore the “potential
effects of high concentrations of epinephrine and other
vasopressors likewise cannot be omitted” (McBride 328).
Therefore to truly test if the accounts of toad licking and toad skin
smoking, or whether any other toxin application actually
produced hallucinogenic responses, research needs to look past
the toxin itself and its inability to penetrate the BBB.
Researchers need to look at the compound bufotenine when it is
mixed naturally in certain species of toads and plant species.
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Bufotenine has been used by ancient cultures for many centuries.
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It can been found in different organisms.
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Anecdotal evidence is the only “proof” that bufotenine elicits a
hallucinogenic response.
Even without conclusive scientific evidence behind the psychoactivity of bufotenine, the DEA realizes the danger behind its
usage and has made it illegal.
So in the end there is no limit to the means a princes will use in
her search for a prince. The princess violated the law and after the
effects wear off she will be left with nothing but a wart covered
frog and a bad tasted in her mouth, or how ever she may chose to
ingest the toxin.
THIS COULD BE YOUR PRINCE
NO FREE LUNCH!!!
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Brawley P., Duffield, J. The Pharmacology of Hallucinogens. 1972 Pharmacological Reviews.
Vol. 24 No 1
Brian K. Roberts, DVM Michael G. Aronsohn, VMD, DACVS Bradley L. Moses, DVM,
DACVIM Ronald L. Burk, DVM, MS, DACVR Jeffrey Toll, VMD, DACVIM
Robert Weeren, DVM, MS, DACVS. Bufo marinus intoxication in dogs: 94 cases (1997-1998) June 2000. Journal of the
American Veterinary Medical Association Vol 216. Issue: 12. Pages 1941-1944
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Fabing, H. D., Hawkins R. J. Intravenous Bufotenine Injection in the Human Being. May 1956.
Science. Vol. 123 Issue: 3203. Pages: 886-887
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McBride, Michael C. “Bufotenine: Toward an Understanding of Possible Psychoactive Mechanisms.” Journal of
Psychoactive Drugs. Jul-Sep 2000:32,3
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McLeod W. R., Sitaram B.R., Bufotenine Reconsidered. 1985 Acta Psychiatrica
Scandinavica Vol 72 Issue: 5 Pages: 447-450
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Ott, Jonathon. 2001. “Pharmanopo-Pyschonautics: Human INtransal, Sublingual, Intrarectal,
Pulmonary and Oral Phamacology of Bufotenine”. Retrieved from
http://www.tacethno.com/info/bufotenine/pharmanopo.html
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Sandoroni, P. M.D. Ph.D. Aphrodisiacs Past and Present: a Historical Review 2000.
Department of Neurology, Mayo Clinic Rochester, Minnesota, USA
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US Drug Enforcement Administration. Retrieved from
http://www.justice.gov/dea/concern/psilocybin.html