Newsgroups: alt.drugs
From: [an 135054] at [anon.penet.fi]
Date: Thu, 24 Nov 1994 03:51:21 UTC
Subject: PALARIS FAQ (1/1) work damnit!
Hope this post attempt works. Thanx for the help and feedback!
XXXXXXXXX INITIAL NOTES XXXXXXXXXXX
This author assumes absolutely no responsibility for
anything you do, as a result of reading this material, or for any
other reason. I make no claims as to accuracy. Always assume your
own responsibility for research and for your actions. Read all
the warnings. Read the articles. Decide what you may be willing
and unwilling to put in your head.
The following alkaloids are discussed and abbreviated as
indicated: N,N-dimethyltryptamine (DMT), 5-Hydroxy-N,N-
Dimethyltryptamine (5-Me-DMT) and 5-Hydroxy-N,N-
Dimethyltryptamine (5-OH-DMT or bufotenine).
XXXXXXXXXX THE DRUGS IN QUESTION XXXXXXXXXX
The main drug of interest here is DMT. DMT causes intense
visual hallucinations and other psychedelic phenomena. It has
been mostly encountered in the technologically developed world as
a crystalline powder, which was smoked or injected. This caused
nearly instant, brief, and intense trips. Peaks occur immediately
and last around 10 minutes, with another 30 or so minutes of mild
effects.
5-Me-DMT is a close relative of DMT. 5-Me-DMT is reported to
be about 4 times as potent as DMT and is often regarded as
preferable to DMT. 5-Me-DMT has most of the psychedelic qualities
as DMT but does not cause visual hallucinations.
Bufotenine (5-OH-DMT) is another DMT relative. This compound
is vaguely referred to as "noxious" by Jonathan Ott. Apparently
10mg of pure 5-OH-DMT injected is enough to cause "dramatic
circulatory crises." Other DMT relatives exist, but are not of
great importance here.
DMT in the past has only been used by smoking or injecting.
Oral use was completely ineffective. It turns out that ancient
tribal cultures solved that problem aeons ago, and have been
dosing up the whole time. Now THAT'S technology. By combining
plants that contained MAOIs (monoamine oxidase inhibitors) and
other plants containing DMT, the DMT would become active orally.
MAOIs block the destruction of DMT in the digestive track and in
the brain. So, with MAOIs, DMT can be eaten and also becomes more
potent. MAOIs also increase the potency of smoked DMT. The effect
of the orally administered DMT with MOAI lengthens in time and
decreases in intensity. Typical plateau period is 10-40 minutes,
after a hour delay with low buzz for an hour. Great for people
who don't like the time investment of most psychedelics.
MAOIs are reported to work for psilocybin ('shrooms) and
mescaline. Subjective reports are that MAOIs double their
potency. I hypothesize that it will also potentiate lysergic acid
(woodrose and morning-glories). LSD does not interact with
MAOIs.
The ancient solution mentioned above is the ayahuasca
potion. This potion has been produced, in one form and name or
another, throughout Central America and South America for quite
some time. The most commonly referred to potion is made by
combining ayahuasca, a jungle vine, and yopo, leaves from a small
bush. The ayahuasca provides the MAOIs and the yopo provides DMT.
Occasional, mescaline bearing cacti are added. The potion was
usually used ceremonial for healing, divining, and teaching.
Often there are reports of blue glows and jaguars, a holy animal
in many endogenous South American cultures.
MAOIs are a class of drugs that all do the same thing:
prevent the destruction of monoamines (like DMT). One MAOI is
harmaline. Harmaline is easily obtained. Syrian rue is an
excellent source. Three grams of seed, extracted with the DMT or
eaten alone should suffice. Doses over three grams do not add
more potency. Caution should be used with MAOIs. Large doses are
hallucinogenic in and of themselves. Large doses are unpleasant
and sometimes fatal.
The remainder of this section is information cited directly
from "Legal Highs" by Twentieth Century Alchemists. They just did
a better job than I could do. I have seen this posted around the
net and is highly recommended. This information pertains to
precautions for MAO inhibitors. READ THEM, KNOW THEM ! You will
notice several discrepancies: Legal Highs says that MAOI and
mescaline combinations are very dangerous, which contradicts
Ott's later reports on the subject; Legal Highs suggests that 5-
Me-DMT is a MAOI, which I cannot substantiate.
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!!DANGEROUS COMBINATIONS!!
READ THIS!! VERY IMPORTANT. IGNORING THIS COULD LEAD TO SERIOUS
MEDICAL PROBLEMS (like death...)
Unless one is very experienced in pharmacology it is
unwise to experiment with combinations of drugs. Even when using
a single drug, thought should be given to all substances, both
food and drug, which have been taken recently. Most primitive
people fast or at least abstain from certain substances for
several days prior to taking a sacrament. Substances most
universally avoided are alcohol, coffee, meat, fat and salt. Some
drugs potentiate others. For example, atropine will increase the
potency of mescaline, harmine, cannabis and opiates. Many of the
substances discussed in this book are MAO inhibitors. MAO
(monoamine oxidase) is an enzyme produced in the body which
breaks down amines and renders them harmless and ineffective. A
MAO inhibitors interfere with the protective enzyme and leaves
the body vulnerable to these amines. A common substance such as
tyramine, which is usually metabolized with little or no
pharmacological effect, may become dangerous in the presence of
an MAO inhibitor and cause headache, stiff neck, cardiovascular
difficulties, and even death. MAO inhibitors may intensify and
prolong the effects of other drugs (CNS depressants, narcotic
analgesics, anticholinergics, dibenzazepine antidepressants,
etc.) by interfering with their metabolism. In the presence of an
MAO inhibitor many substances which are ordinarily non-active
because of their swift metabolism may become potent psychoactive
drugs. The phenomenon may create a new series of mind alterants.
However, because of the complex and precarious variables
involved, it is risky and foolish for anyone to experiment with
these possibilities on the non-professional level.
The most commonly used MAO inhibitors include hydrazines
such as iproniazid, Marsilid, Marplan, Niamid, Nardil, Catron;
also non-hydrazines such as propargylamines, cyclopropylamines,
aminopyrazine derivatives, indolealkylamines, and carbolines.
MAO-inhibiting materials discussed in this book include
yohimbine, various tryptamines, especially 5-MeO-DMT and the `-
methyltryptamines, and the various harmala alkaloids. The latter
are especially potent inhibitors but, like yohimbine and the
trytamines, are short-lasting in action (30 minutes to
several hours). Some of the commercial MAO inhibitors listed
above are effective for several days to several weeks.
Among the materials which may be dangerous in
combination with MAO inhibitors are sedatives, tranquilizers,
antihistamines, narcotics and alcohol - any of which can cause
hypotensive crisis (severe blood pressure drop); and amphetamines
(even diet pills), mescaline, asarone, nutmeg (active doses),
macromerine, ephedrine, oils of dill, parsley or wild fennel,
beer, wine, cocoa, aged cheese and other tyrosine-containing
foods (tyrosine is converted into tyramine by bacteria in the
bowel) - any of which can cause hypertensive crises (severe blood
pressure rise).
SYRIAN RUE Peganum harmala. Family Zygophyllaceae (Caltrop
family.)
Material: Seeds of woody perennial native to Middle East.
(Roots also active but seldom used.)
Usage 1 oz. seeds are thoroughly chewed and swallowed. Most
effective when combined with other psychotropic materials,
especially those containing tropanes.
Active Constituents: Harmine, harmaline and harmalol.
Effects and Contraindications: Hallucinogen; see harmine.
HARMINE 7-methoxy-1-methyl-9H-pyrido (3,4-b) indole.
Material: Indole-based alkaloid found in several plants
including Banisteriopsis caapi (from which the South American
hallucinogenic brew yage is prepared), Peganum harmala (Syrian
rue), Zygophyllum fabago, and Passiflora incarnata (Passion
flower).
Usage: 25-750 mg harmine (see effects) is ingested on an
empty
stomach. In its hydrochloride form harmine may be snuffed
(20-200 mg). Injection dosages are smaller: SC 40-70 mg; IV 10-30
mg. Absorbed poorly through stomach.
Effects: Harmine and related alkaloids are serotonin
antagonists, hallucinogens, CNS stimulants, and short-term MAO
inhibitors (100 x MAO inhibition of iproniazid but lasting only
several hours). Small doses (25-50 mg) act as mild and
therapeutic cerebral stimulant, sometimes producing drowsy or
dreamy state for 1-2 hours. Larger doses up to 750 mg may have
hallucinogenic effects, the intensity of which varies widely with
the individual. Doses of 25-250 mg taken with LSD or psilocybin
alter the quality of the experience of the latter. Telepathic
experience have been reported with this combination.
Contraindications: Harmine is a brief MAO inhibitor. It
should not be used with alcohol and certain foods and drugs (see
list at end of file). When snuffed harmine may be slightly
irritating to nasal passages. Large amounts may depress CNS.
Since individual sensitivity varies this may occur with 250-750
mg.
Notes on other harmala alkaloids: Different harmala
alkaloids vary in potency. The equivalent of 100 mg harmine is 50
mg harmaline, 35 mg tetrahydraharman, 25 mg harmalol or harmol, 4
mg methoxyharmalan. Harmal alkaloids are synergistic (mutually
potentiating) and are therefore most effective when combined in
an appropriate balance. Tropines (belladonna alkaloids) also
potentiate harmals. Harmol and harmalol (phenols) in overdoses
can cause progressive CNS paralysis.
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XXXXXXXXXX THE PLANTS XXXXXXXXXX
As reports show, there is a great variation in the alkaloid
content of phalaris plants. Within phalaris tuberosa, one study
found that total alkaloid levels ranged from 5 to 178 mg/ 100g
dry plant matter. Thus 100g of phalaris tuberosa could contain
anywhere from 1/10 of a trip to 4 trips. The trick is to find out
(as I have) how to maximize the alkaloid levels. CAUTION: because
alkaloid levels vary so drastically, you should always determine
the potency of any product by starting with low doses.
Most discussion so far on the internet has centered on
Phalaris Arundinacea. However, P. tuberosa also has high alkaloid
levels. Table one reports alkaloid levels of several plants. As
you can see in the table, Phalaris Tuberosa does not have
particularly high DMT levels, but it does have quite a bit of 5-
Me-DMT. It appears that the alkaloid content of Phalaris Tuberosa
is such that one dose of DMT also includes a dose of 5-Me-DMT. So
Phalaris Tuberosa is actually just as strong as the other plants
containing minimal 5-Me-DMT. The DMT in Phalaris Tuberosa should
contribute visual hallucinations to the trip.
The bad news for Phalaris Tuberosa is that it contains
bufotenine. But even a large dose of Phalaris Tuberosa (100g
containing 100mg DMT and 22mg 5-Me-DMT, a full dose of each)
contains 5g of 5-OH-DMT, one half the dose given in the study
cited in Ott. Most phalaris users report that they ingest or
smoke the product. Such an administration route is less sudden
and "shocking" than injection. Perhaps this will temper the
effects of 5-OH-DMT. Caution should still be used with Phalaris
Tuberosa. Phalaris arundinacae and desmanthus illinoesis,
containing no 5-OH-DMT, appear to be safer, but lacking in 5-Me-
DMT.
The phalaris plants are tall grasses. They grow well in
Australia, around the Mediterranean sea, and all over
America. They grow in clumps up to 7 feet tall. Desmanthus
Illinoisis is also called "Illinois Bundlweed." It's a bush that
grows, obviously, in the Illinois area.
Table 1
ALKALOIDS REPORTED AS mg PER 100g RAW DRIED PLANT,
AND AS PERCENT OF TOTAL PLANT SOURCE WEIGHT.
*************************************************
P. Tuberosa:
DMT 100 mg .100%
5-Me-DMT 22 mg .022%
5-OH-DMT 5 mg .005%
P. Arundinacea
DMT ? ?
Desmanthus Illinoisis (root)
DMT 200 .200%
Desmanthus Illinoisis (root bark only)
DMT 340 mg .340%
Psychotria species (averaged)
DMT 200 mg .200%
**************************************************
Unfortunately, sheep herders in Australian desired strains
of low alkaloid phalaris plants. So now most commercially
available phalaris are probably weak. Phalaris can be obtained
through mail order herb companies, some of who advertise high
alkaloid plants. Because I do not wish to associate these fine
suppliers names' with an article on how to prepare a drug, I will
not provide names or addresses. Just ask around on the net.
XXXXXXXXXX DOSES XXXXXXXXXX
There seems to be a variety of dosages suggested in the
literature. Table 2 lists some of the reported dosage levels. It
should be noted that levels that are listed in table two are
within the range reported to cause "phalaris staggers" in sheep
and cause them to.... die.
Table 2 Jonathan Net Peter
REPORTED DOSES Ott Lore Gessner
****************************************************************
DMT 1mg/kg 60mg ---
5-Me-DMT .25mg/kg 5mg 5-10 mg
5-OH-DMT NONE! ? ---
****************************************************************
NOTE: These 'reported doses' are non-lethal dosages given to
humans in the literature and as referenced. THIS AUTHOR MAKES NO
RECOMMENDATIONS! The "mg/kg" means one mg of drug for every kg of
body weight.
Using Ott's levels, .5g of Phalaris Tuberosa per kilogram
body weight should yield one dose of 50% DMT and 50% 5-Me-DMT.
Using the net lore, 25g of Phalaris Tuberosa would yield 1 dose
of 5-Me-DMT with less than 1/2 dose of DMT: still a fairly strong
dose when totaled. These doses are based on plants that have not
had their alkaloid levels boosted.
XXXXXXXXXX BOOSTING ALKALOIDS XXXXXXXXXXX
The scientific literature, intended to solve the problem of
"Phalaris staggers" in sheep has revealed the growth parameters
that will optimize the alkaloid content of Phalaris Tuberosa
It is not known if the information applies to other Phalaris
plants. It is my own personal feeling that it will. The nutrient
solutions suggested for phalaris resembles in some respects other
formulas designed to boost tryptamine levels in morning glories,
woodrose, and peyote.
This discussion is based on the works of Oram & Williams,
1967; Baxtor & Slaytor, 1972; and Moore, Williams & Joice, 1967.
The following factors have been shown to influence alkaloid
levels in phalaris tuberosa: shading, nitrogen uptake, and
temperature. It seems that shading causes increased (yes,
increased) levels of alkaloids in Phalaris Tuberosa. The optimal
amount of shading appears to be 15-25% the strength of full
sunlight. Unfortunately, this also causes a significant decrease
in growth. Enough plant mass is lost to almost make up for the
alkaloid gains. However, one might grow the plant in full
sunlight/growlight until a few weeks before harvest, then reduce
the light or shade the plant. I see no reason why alkaloid levels
would not peak during this time.
Increasing temperatures to 21C for day and 16C for night not
only caused an increase in the proportion of alkaloids per
weight, but it also increased the growth rate of the plant.
Temperature regimes of 9c/4c and 15c/10c resulted in much less
weight and fewer alkaloids. The data suggest that even higher
temperatures may be better.
Increased nitrogen supply in the plant's nutrients increased
the plant alkaloids. Nitrogen content of solutions were 0.05,
0.5, and 5.0 times the nitrogen levels of "Hoagland's nutrient
solution (whatever that is). Just go with the principle "more is
good."
Day length does NOT influence alkaloid levels.
Unfortunately, the data provided by the article do not
specify how much the total increase in alkaloids were. However,
examination of the data suggest the alkaloid content more than
doubled as a result of the boosting treatments. Interestingly,
the levels of 5-OH-DMT did not increase significantly. Thus
boosting the alkaloid levels appears to also decrease the
relative concentration of this problematic alkaloid!
Precursors to DMT, 5-Me-DMT, and 5-OH-DMT can be fed
directly to the plants. No one precursor will boost one plant
alkaloid level; all alkaloid levels rise regardless of the
precursor. The precursors are: tryptophan (NH2-Co2), tryptamine
(NH2), and MMT (NHMe). I am unable to translate exactly what the
feeding levels were from this study, but again: "More is good."
Unfortunately, I believe all of these substances are regulated.
XXXXXXXXXXX PREPARATION XXXXXXXXXX
The simplest way to prepare phalaris is to use a wheat juice
extractor. This device presses the juice out of the leaves and
stalks. Of course dosage becomes harder to gauge. One report on
the internet suggested 1 teaspoon as a good dose and 2 teaspoons
as an extreme overdose, resulting in one freaky trip.
Extraction of alkaloids can be performed on dry plant
materials (based on Dr. Jonathan Ott's reports). An acid is used
to exact the alkaloids of both the DMT and the MAOI containing
plants. A solution of 1/3 lemon juice and 2/3 water is used to
quickly boil the plant material. Pour off and repeat two more
times. The dose is easier to determine because it is based on dry
plant material. Three grams of Syrian rue per dose of DMT
provides the required MAOI. Again, increasing the dosage of
Syrian rue beyond 3g does not increase the potency of the DMT
significantly more than 3g.
The liquid form can serve as an oral dose, or it can be
evaporated GENTLY AND SLOWLY to a goo. This goo can then be
smoked for a very intense dose of DMT. Or the goo can be saved
for oral doses. I recommend refrigeration.
XXXXXXXXXX IN CLOSING XXXXXXXXXX
This article, as noted in opening, is probably not totally
accurate or complete. If new or more accurate information arises,
or if a topic has been missed, I would appreciate it if new
chapters are written, and notes are made. Please type in the text
"(See note ##)" and add your note to the END of the text. Stick
new chapters where appropriate. I consider this a public work.
XXXXXXXXXX UNANSWERED QUESTIONS XXXXXXXXXX
Why are human recreational doses of DMT fatal to sheep?
Just what exactly happens at what doses of 5-OH-DMT?
What is the alkaloid level of PA?
XXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXX
Baxtor, C. & Slaytor, M. (1972). Phytochemisty, 11, pp.2767-73.
Gessner, P K. In D. H. Efron (editor) Psychotomimetic Drugs.
1970. Raven Press.
Moore, R. M., Williams, J. D., Chia, J. (1967). Australian
Journal of Biological Science, 20, 1131-40.
Oram, R. N., Williams, J. D. (1967). Nature, March 4, pp.946-7.
Ott, J. Ayahuasca Analogues: Panthaen Ethnogens. 1994. Natural
Products Co.
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