From: honig@buckaroo.ICS.UCI.EDU (David Honig)
Subject: Updated LSD FAQ
Message-ID: <9408091330.aa03614@paris.ics.uci.edu>
Newsgroups: alt.drugs
Date: 9 Aug 94 20:30:57 GMT


The following large (200K) file is the updated LSD FAQ incorporating
various posts that I've collected since this faq first came out.
There is a "Changes" section near the top.  This also contains
info on other tryptamine psychedelics, viz. DMT and psilocybin.

(c) 1994 The reproduction for nonprofit use of this file is encouraged.


		The Usenet alt.drugs LSD FAQ



Last Update: 9 Aug 94
    Subject: LSD
       Size: Now 200K, 80K gzip'd

Formatting Info:

       topic break:	******************************
within-topic break:	..............................

Special DMT FAQ insert: ++++++++++++++++++++++++++++++


******************************
	Caveat:

[NB: This FAQ provided to reduce the Net's bandwidth / confusion /
misinformation, as an informational resource ONLY.  There are some
very informed, and some very clueless people on the Net.  This
FAQ tries to shift the balance.  The truth shall set you free,
as they say.]


******************************

	Changes since Previous Version

- added synthesis notes, MAPS
- merged misc. files and references, organizations, the baseball
story, recipes I'm not competent to judge
- added scholarly section on creativity
- include more info on related active tryptamine derivatives
- traded off half-a-decibel of signal-to-noise for wider scope
- added mycological horticultural note
- added postscript stereoimage of structure

******************************

	Synopsis / Table of Contents:

LSD 		(definition, introduction)
Delysid 	(medical fact sheet for pharmaceutical LSD) (pharmacology)

	Cautions, Real And Imagined:

Addiction Potential (none)
Adulterants 	(including the strychnine myth, manufacturing impurities, etc.)
Bad Trips 	(what they are, how to avoid, what to do)
Myths 		(stamps for children, staring at the sun..)
Dangers 	(LSD isn't for morons...)
Flashbacks 	(what they are ---post-traumatic stress syndrome)
Insomnia 	(common, what to do)
Tolerance 	(aquired and lost quickly (3 days) harmlessly, no withdrawal)

	Backround:

Anthropology 		(and history)
Botany 			(sources in nature: mushrooms, ergot, morning glories,
				hawaiian baby woodrose, tropical plants)
Chemistry 		(structure)
Mechanism of Action 	(uncertain)
Related Compounds 	(indoles: psilocybin, DiMethylTryptamine (DMT) )
Manufacture 		(forget it)

Drug Testing 	 	(don't worry)
Legal Scheduling (sched. 1, no medical uses in US (despite past effective use))

	Pragmatics:

Set and Setting 	(how to have a positive experience; lsd != beer)
Storage 			(keep in a cool dark dry place)
Synergies, Bad Combinations 	(cannabis is good, otherwise be careful)

	References & Further Reading:

(Recommended)
 	_Psychedelic Encyclopedia_ by Peter Stafford
	_LSD: My Problem Child_  by Albert Hofmann
	_Licit & Illicit Drugs_ (Consumer Reports)
	_Storming heaven : LSD and the American dream_  by Jay Stevens

******************************



LSD
	Generic name for the hallucinogen lysergic acid
	diethylamide-25.  Discovered by Dr. Albert Hofmann in 1938, LSD is one
	of the most potent mind-altering chemicals known.  A white, odorless
	powder usually taken orally, its effects are highly variable and begin
	within one hour and generally last 8-12 hours, gradually tapering off.
	It has been used experimentally in the treatment of alcoholics and
	psychiatric patients.  [Where it showed some success.] It
	significantly alters perception, mood, and
	psychological processes, and can impair motor coordination and skills.
	During the 1950s and early 1960s, LSD experimentation was legally
	conducted by psychiatrists and others in the health and mental health
	professions.  Sometimes dramatic, unpleasant psychological reactions
	occur, including panic, great confusion, and anxiety.  Strongly
	affected by SET and SETTING.  Classification: hallucinogens.  Slang
	names: acid, sugar.  See also appendix B.  (RIS 27:211-52 entries)

	-- Research Issues 26, Guide to Drug Abuse Research Terminology,
		   available from NIDA or the GPO, page 54.

..............................

Common Drug Slang Terms (NB: many of these refer to the carrier, ie, "Blotter"
	or "Sugar Cubes".  Often the local names will refer to patterns printed
	on the blotter, eg, "Blue unicorn".):

	Acid, 'Cid, Sid, Bart Simpsons, Barrels, Tabs, Blotter, Heavenly blue,
	"L", Liquid, Liquid A, Lucy in the sky with diamonds, Microdots,
	Mind detergent, Orange cubes, Orange micro,  Owsley, Hits,
	Paper acid,  Sacrament, Sandoz,  Sugar, Sugar lumps,
	Sunshine, Tabs, Ticket, Twenty-five, Wedding bells, Windowpane,
	etc.

..............................

from the data sheet accompanying product:
(see also Physician's Desk Reference from mid-60's)

                      Delysid (LSD 25)

           D-lysergic acid diethylamide tartrate

	Sugar-coated tablets containing 0.025 mg. (25 ug.)

	Ampoules of 1 ml. containing 0.1  mg.  (100  ug.)  for  oral
administration.

     The solution may also be injected  s.c.  or  i.v.   The
effect  is  identical  with  that of oral administration but
sets in more rapidly.

                         PROPERTIES

     The administration  of  very  small  doses  of  Delysid
(1/2-2  ug./kg.  body  weight) results in transitory distur-
bances of affect, hallucinations, depersonalization,  reliv-
ing  of  repressed memories, and mild neuro-vegetative symp-
toms.  The effect sets in after 30 to 90  minutes  and  gen-
erally  lasts  5 to 12 hours.  However, intermittent distur-
bances of affect may occasionally persist for several days.

                  METHOD OF ADMINISTRATION

     For oral administration the contents of  1  ampoule  of
Delysid  are  diluted with distilled water, a 1% solution of
tartaric acid or halogen-free tap water.

     The absorption of the solution is somewhat  more  rapid
and more constant that that of the tablets.

     Ampoules which have not been opened,  which  have  been
protected  against  light  and  stored  in  a cool place are
stable for an unlimited period.  Ampoules  which  have  been
opened or diluted solutions retain their effectiveness for 1
to 2 days, if stored in a refrigerator.

                   INDICATIONS AND DOSAGE

a)   Analytical  psychotherapy,   to   elicit   release   of
     repressed  material and provide mental relaxation, par-
     ticularly in anxiety states and obsessional neuroses.
     The initial dose is 25 ug. (1/4  of  an  ampoule  or  1
     tablet).   This  dose is increased at each treatment by
     25 ug. until the optimum dose (usually between 50  and
     200  ug.) is found.  The individual treatments are best
     given at intervals of one week.

b)   Experimental studies on the nature  of  psychoses:   By
     taking  Delysid  himself,  the  psychiatrist is able to
     gain an insight in the world of ideas and sensations of
     mental  patients.   Delysid can also be used to induced
     model psychoses of short duration in  normal  subjects,
     this facilitating studies on the pathogenesis of mental
     disease.

     In normal subjects, doses of 25 to 75 ug. are generally
     sufficient  to produce a hallucinatory psychosis (on an
     average 1 ug./kg. body weight).  In  certain  forms  of
     psychosis  and  in chronic alcoholism, higher doses are
     necessary (2 to 4 ug./kg. body weight).

                        PRECAUTIONS

     Pathological mental conditions may  be  intensified  by
Delysid.  Particular caution is necessary in subjects with a
suicidal tendency and  in  those  cases  where  a  psychotic
development appears imminent.  The psycho-affective lability
and the tendency to commit impulsive acts  may  occasionally
last for some days.

     Delysid should only be administered under strict  medi-
cal supervision.  The supervision should not be discontinued
until the effects of the drug have completely worn off.

                          ANTIDOTE

     The mental effects of Delysid can be  rapidly  reversed
by the i.m.  administration of 50 mg. chlorpromazine.

              Literature available on request.

              SANDOZ LTD., BASLE, SWITZERLAND

9792*-Z1540 e.-sp./d.-fr.
Printed in Switzerland.

..............................

From: An Introduction to Pharmacology  3rd edition, JJ Lewis, 1964   (p 385)

Peripheral Actions

These include an oxytocic action and constriction of the blood vessels
of isolated vascular beds.  In intact animals LSD causes a fall in
blood pressure, but its adrenergic blocking potency is low.

LSD causes mydriasis in man and other species.  It also causes
hyperglycaemia and mydriasis, has a hyperthermic action and causes
piloerection.  These effects are sympathetic in nature and are
abolished by ganglion blocking or adrenergic blocking agents.
Parasympathetic effects include salivation, lachyrmation, vomiting,
hypotension, and brachycardia.  Low doses stimulate respiration but
larger doses depress it.

(nb: mydriasis = pupillary dilation)
..............................

Hoffman thought the diethylamide version of the lysergic acid molecule
might be a respiratory stimulant... (see _Problem Child_ by Hoffman)

..............................

The "speedy" quality of unadulterated LSD is due to the pharmacological
actions of LSD itself, and not necessarily due to decomposition or impurities.
LSD typically causes early adrenergic effects such as sweating, nervousness,
jaw grinding and insomnia which are easily confused with the side effects
of amphetamine.

******************************

ADDICTION POTENTIAL:

Zero physical addiction potential.  Not something that makes you want to
do it again immediately.

Essentially zero psychological addiction potential.


Rarely people use it to escape in a negative way or as part of "polydrug
abuse" behavior or pattern of behavior.  Usually in this case other
drugs are causing more harm, and the fundamental problem is a personal
difficulty; the escapism/distraction is a symptom.

******************************

ADULTERANTS:

Several problems are associated with street drugs: their unknown
purity and their unknown strength.  Because of its extreme cheapness
and potency, the purity of LSD in blotter form is not an issue: either
it's lsd or untreated paper.  The purity of powders, pills, and liquids
cannot be assumed as safe.  With regards to uncertain strength, the
strength of hits these days is low, 100 micrograms or so.  One should
be careful and assume that the smallest square in a tiling of a sheet
is a dose, even if a printed pattern covers several.  An experienced
person could judge the strength of a dose, and if it is assumed all
doses on a sheet have been processed equivalently, those doses would
be calibrated for others, much like anything else.

..............................

From _Psychedelic Chemistry_ by M.V.Smith,  2nd edition p 5:

"There is a great deal of superstition regarding purification of
psychedelics.  Actually, any impurities which may be present as a
result of synthetic procedures will almost certainly be without any
effect on the trip.  If there are 200 micrograms of LSD in a tablet,
there could only be 200 mics of impurities present even if the LSD was
originally only 50% pure (assuming nothing else has been added), and
few compounds will produce a significant effect until a hundred to a
thousand times this amount has been ingested.  Even mescaline, which
has a rather specific psychedelic effect, requires about a thousand
thimes this amount."

..............................

Note that: 1) on a piece of paper, vs. a tablet, you can't even add
significant amounts of adulterants 2) adulterants would cost, whereas
blank paper will rip someone off just as well.

LSD itself has some "body-kinks" on some people some times.  Nausea is
one of them.  its usually mild and transient.  It also has speedlike
(ie, adrenergic stimulation) effects, etc.

(It is common for the uninformed to harbor fears (e.g., about adulterants)
instilled by ignorance and the current hysteria/propoganda.  That's why this
FAQ exists.)

..............................

[Referring to strychnine] 15 mg has been fatal, but a more typical fatal
dose is on the order of 50mg.  [Another post indicates 25 mg. as the LD50] 1
mg of strychnine orally probably has no observable pharmacological effects
in a typical adult.  [1 mg being ten times the effective dose of LSD, by the
way.]

From: Handbook of Poisoning, 10th ed, R.H. Dreisbach, M.D., PhD, Lange Med.
Pub. Co. Los Altos, Ca.: strychnine is lethal in 15-30 mg amounts to adult
humans.  (Pure nicotine is fatal at 40 mg./person; cyanide salts are fatal
at about 100 mg./person) Strychnine causes death by respitory failure, via
increased spinal reflex excitability.


Actually, I think the fact that PharmChem analyzed something on the order of
2,000 LSD samples between 1972 and 1979 and never found one with strychnine
in it would be better.  I'm going over all their data with a toothpick and
I'll get back to you on exactly what I find.  It looks like the percent of
LSD with strychnine in it is, however, at least under .05%.  More a little
later.


..............................

According to Alexander Shulgin the difinitive answer is that strychnine is
neither used in the synthesis, produced by the synthesis, or a possible
contaminant of the synthesis.  But just look at the structures of strychnine
vs Lysergic acid/LSD/etc and you should be able to understand that readily.



..............................

From "The PharmChem Newsletter" (vol 3, no 3), 1973:

Summary of Street Drug Results - 1973: "Of 189 samples of LSD quantitatively
analyzed, the average dose was 67.25ug LSD.  Of the 32 samples of alleged
mescaline actually containing mescaline, [...stuff about mescaline and
mushrooms deleted...]  It is interesting to note the low incidence of
deception among the less sought after psychotomimetics LSD and PCP."


Most likely "good" acid is N-acetyl-LSD (ALD-52) [according to
_Psychedelic Encyclopedia_ it produces a smoother trip and is somewhat
commonly found in analysis -- references to the latter were provided].  while
"speedy" acid is LSD-25.  You might want to inform her that those "speedy"
effects are also commonly reported side effects of legal drugs which
effect the 5-HT neurotransmitter system.  And ditto on the potency issue --
you'd need mg quantities of strychnine to feel anything.  And what you would
feel (according to descriptions I've read) does not match descriptions of
LSD "speed" effects.  Most significantly because strychnine muscular effects
tend to fade in & out, while LSD "speed" effects are typically reported as
being consistent -- and there are other qualitative differences.

"actual experience"? ... no one here is likely to post descriptions of that
over the net, even in e-mail...  I'm *quite* sure that some people could
though...

> Well, hypothetically speaking, I bought some from her friends, and I could
> probably surrender half a hit or a whole one, maybe, in the interest of
> science.  Does anyone have facilities to perform a REAL (hypothetical)
> analysis of blotter to find out exactly what's in it?

Its been done....

> > Schnoll SH  Vogel WH
> > Analysis of "street drugs".
> > N Engl J Med (1971 Apr 8) 284(14):791

This reference sucks.

> > Brown JK  Shapazian L  Griffin GD
> > A rapid screening procedure for some "street drugs" by thin-layer
> >      chromatography.
> > J Chromatogr (1972 Jan 19) 64(1):129-33

Nope.

There's a LA County analysis of street drugs I've got (Clin Tox ~1984 I think)
that reports LSD as being >96% pure or blank (If I remember correctly) --
the rest most likely is substitutes, but it wasn't reported in the analysis.




..............................

This is the PharmChem analysis of LSD from 1972 (vol 1, no 1) up to the time
that the DEA no longer allowed them to make quantitative measurements (1974-
vol 3, no 2 included).  NOTE:  NO STRYCHNINE! also note that PharmChem found
a sample of Shrooms contaminated with Strychnine in 1972 (vol 1, no 7), and
I would think it safe to assume that they also checked LSD for Strychnine.


******************************

BAD TRIPS:

 A person on LSD who becomes depressed, agitated, or confused may
experience these feelings in an overwhelming manner that grows on
itself.  The best solution is to remove disturbing influences, get to
a safe, comforting environment, and reassure the tripper that things
are alright.  It may comfort those who fear that they are losing their
minds to be reminded that it will end in several hours.

Authorities are fond of administering injections of anti-psychotic
drugs.  Recovery in the presence of authorities, in hospitals or
police stations, is not pleasant.  Sedatives or tranquilizers such as
Valium may help reduce panic and anxiety, but the best solution is
calm talking.  Some claim that niacin (an over the counter vitamin
supplement) can abort a trip, but this may be due to a placebo effect
(niacin produces a flushing effect).

Remember that odd bodily sensations are normal and not harmful.

******************************

From page 8 of Robert Anton Wilson's Sex and Drugs: A Journey Beyond Limits

"The distinction between psycholytic and psychedelic doses of LSD is used in
many scientific publications but seems to be ignored by popularizers who
either preach the "LSD utopia" or warn of the "decline of the West." A
psycholitic does, generally 75 or 100 - or at most 200 - micrograms, causes
a rush of thoughts, a lot of free association, some visualization
(hallucination) and abreaction (memories so vivid that one seems to relive
the experience). A psychedelic dose, around 500 micrograms, produces total
but temporary breakdown of usual ways of perceiving self and world and
(usually) some form of "peak experience" or mystic transcendence of ego.
"Bad trips" usually occur only on psychedelic doses."

******************************

The best review of this question is Rick Strassman's "Adverse Reactions
to Psychedelic Drugs: a Review of the Literature" in _J. Nerv and Mental
Disease_ 172(10):577-595.  He writes:

The most common adverse reaction is a temporary (less than 24 hours)
episode of panic --the "bad trip".  Symptoms include frightening illusions/
hallucinations (usually visual and/or auditory); overwhelming anxiety
to the point of panic; aggression with possible violent acting-out behavior;
depression with suicidcal ideations, gestures, or attempts; confusion; and
fearfulness to the point of paranoid delusions.

Reactions that are prolonged (days to months) and/or require hospitalization
are often referred to as "LSD psychosis," and include a heterogenous
population and group of symptoms.  Although there are no hard and
fast rules, some trends have been noted in these patients.  There is a
tendency for people with poorer premorbid adjusment, a history of
psychiatric illness and/or treatment, a greater number of exposure to
psychedelic drugs (and correlatively, a great average total
cumulative dosage taken over time), drug-taking in an unsupervised
setting, a history of polydrug abuse, and self-therapeutic and/or
peer-pressure-submission motive for drug use, to suffer these consequences.

In spite of the impressive degree of prior problems noted in many of these
patients, there are occasional reports of severe and prolonged reactions
occuring in basically well adjusted individuals.  In the same vein,
there are many instance of faily poorly adapted individuals who suffer
_no_ ill effects from repeated psychedelic drug use.  In fact, it has been
hypothesized that some schizophrenics do not suffer adverse reactions
because of their familiarity with such acute altered states.  Another
possibility is that there individuals may be "protected" by possible "down-
regulation" of the receptors for LSD, bu the (over-)production of some
endogenous compound.  _Individual_ prediction of adverse reactions,
therefore, is quite difficult...
...

Major "functional" psychosis vs. "LSD psychosis"
-----------------------------------------------

A diagnostic issue dealth with explicitly in only a few papers is that of
LSD-precipitated major functional illnesses, e.g. affective disorders
or schizophrenia.  In other words, many of these so called LSD psychoses
could be other illnesses that were triggered by the stress of a traumatic
psychedelic drug experience.  Some of the same methodological issues
described earlier affect these studies, but they are, on the averagem
better controlled, with more family and past psychiatric history available
for comparison.

Hensala et al. compared LSD-using and non-LSD-using psychiatric inpatients.
They found that this group of patients was generally of a younger age and
contained more characteristically disordered individuals than the non-
LSD-using group.  Patients with specific diagnoses with or without LSD
histories were not compared.  Based on their observations, they concluded
that LSD was basically just another drug of abuse in a population of
frequently hospitalized individuals in the San Francisco area, and that
it was unlikely that psychedelic use could be deemed etiological in the
development of their psychiatric disorders.

Roy, Breakey et al., and Vardy and Kay have attempted to relate LSD use to
the onset and revelopment of a schizophrenia-like syndrome.  A few comments
regarding this conceptual framework seem in order, before their findings
are discussed.  The major factor here is that of choosing schizophrenia,
or in the Vardy and Kay study, schizophreniform disorders, as the
comparison group.  There is an implication here that LSD psychoses are
comparable, phenomenologically, to schizophrenia-like disorders, and that
LSD can "cause" the development of such disorders.  The multiplicity of
symptoms and syndromes described in the "adverse reaction" literature
should make it clear that LSD can cause a number of reactions that can last
for any amount of time--from minutes to, possibly, years.  I believe what
is being studied here is the question of the potential role of LSD in
accelerating or precipitating the onset of an illness that was "programmed"
to develop ultimately in a particular individual--in a manner comparable
to the major physical or emotional stress that often precipitates a bona
fide myocardial infarction in an individual with advanced coronary
atheresclerosis.  The stress did not _cause_ the heart disease; it was
only the stimulus that accelerated the inexorable process to manifest
illness.

In looking at the relevant studies, Breakey et al. found that schizophrenics
who "used drugs" had an earlier onset of symptoms and hospitalization than
non-drug-using schizophrenics, and had possibly better premorbid personal-
ities than non-drug using patients (although Vardy and KAy have challenged
this analysis of Breakey's data).

Bowers compared 12 first-admission patients with psychosis related to LSD
use, requiring hospitalization and phenothiazines, to 26 patients hospital-
ized and treated with phenothiazines with no history of drug use.  Six
of these controls had been previously hospitalized.  Drug-induced psychotic
patients were found to have better premorbib histories and prognostic
indicators than the nondrug groups.  There was no difference in rates of
family history of psychiatric illness.  However, several issues flaw
this study.  One is the poly-drug abusing nature of the "LSD-induced"
psychotic patients, compared to the controls.  The role of LSD, therefore,
in causing or precipitating these symptomatic disorders, is open to dispute.
The other is the lack of an adequate comparison control group, i.e. the
controls were specified only as "psychotic," and did not necessarily
match the LSD group in either symptoms or diagnostic classification.
A follow-up study of the patients occured between 2 and 6 years later.
One half did well and one half did poorly, although the lack of a control
group for a follow-up in a similarly symptomatic control group makes
interpretation of the data difficult.

Roy, in a somewhat different design, compared chronic schizophrenic
patients (diagnosed according to DSM-III criteria) who had used LSD
within the week preceding hospitalization, and found no difference
in age of symptom onset or hospitalization compared to patients without
a history of illicit drug use.

Vardy and Kay, in an elegant study with a 3- and 5- year follow-up period,
demonstrated that patients hospitalized for a schizophrenic picture
that developed within two weeks of LSD use (patients with other diagnoses
were explicitly excluded form comparisons with non-drug-using
schizophrenics) were "fundamentally similar to schizophrenics in
geneology, phenomenology, and course of illness (165, p. 877).  Pre-
morbid adjustment, age of onset of symptoms and hospitalization, family
history of psychosis or suicide, and most cognitive features were also
equal between groups.  Family histories of alcohol abuse were markedly
great in the LSD group.

I believe these data, taken as a whole, limited as they are in terms of
comparing subgroups (i.e. LSD-using vs. non-LSD-using) of "schizophrenia-
like" disorders, point towar, at most, a possible precipitory role in
the development of these disorders, in a non specific and not
etiologically related manner.



MYTHS:

LSD does not form "crystals" that reside in the body to be "dislodged"
later, causing flashbacks.  LSD is a crystalline solid (though it is
unlikely that one would ever have enough to be visible to the naked
eye) but it is easily water soluble, thus cannot form bodily
deposits.  Furthermore, it is metabolized and excreted in hours.  The
bogus "loosened crystal" description in not necessary to explain
flashbacks, which are psychological phenomena (see FLASHBACKS).

LSD does not cause chromosome damage.

In Science 30 April 1972, Volume 172 Number 3982 p. 431-440 there was an
article by Norman I. Dishotsky, William D. Loughman, Robert E. Mogar and
Wendell R. Lipscomb titled "LSD and Genetic Damage - Is LSD chromosome
damaging, carcinogenic, mutagenic, or teratogenic?". They reviewed 68
studies and case reports published 1967-1972, concluding "From our own
work and from a review of literature, we believe that pure LSD ingested
in moderate doses does not damage chromosomes in vivo, does not cause
detectable genetic damage, and is not a teratogen or carcinogen in man."

Well, there's the study by Sidney Cohen which was cited here
recently, Journal of Nervous and Mental Disease, 130, 1960. The
following is from Jay Stevens' Storming Heaven: "Cohen surveyed a sample
of five thousand individuals who had taken LSD twenty-five thousand
times. He found and average of 1.8 psychotic episodes per thousand
ingestions, 1.2 attempted suicides, and 0.4 completed suicides.
'Considering the enormous scope of the psychic responses it induces,'
he concluded, 'LSD is an astonishingly safe drug.'"


Some urban legends: I've heard two "stories" about people blinding
themselves on "drugs". One was revealed as a hoax by the person who
perpetrated it (apparently it was intended to "illustrate" the dangers
of LSD), another is trotted out by anti-drug speakers at high schools:

1) Seven people on LSD stared at the sun and lost 90% of their reading
   vision.

2) A teenager arrested while on LSD plucked out his eyeballs in his
   jail cell, and felt no pain.

While these are bogus, the drug has powerful effects on the mind
and the consumer should be aware of the hazards, and act appropriately.

..............................

There is an occasionally circulated fake warning from some police department
about LSD-laced "tattoos" or stickers (the "blue star tattoo" story) being
given to children.  This probably originated with some hick cop or ignorant
and panicky parent not understanding some children-cartoon (eg, mickey mouse
in sorcerer's garb) printed on a sheet of blotter.

..............................

See also myths about testing in DRUG TESTING


******************************

DANGERS:

Purely psychological hazards, not harmful to body.  May release latent
psychosis or exacerbate depression, leading to irrational behavior.  There
is also a danger of foolish or incautious behavior, e.g, misjudging
distances or thinking one can fly.  Physical overdose is not a hazard,
though one may easily ingest more than one may be able to handle
psychologically.

..............................

Because the "LSD psychosis" is not distinguishable from non-drug-
induced psychosis, we have reasonable evidence to conclude that LSD
was not the sole cause of psychosis.  Instead, it would seem that the
drug brought on the problems in vulnerable individuals.
Interestingly, the rate of parental alcoholism was found to be much
higher in LSD patients than in other patients or in the general
population by one study (Vardy and Kay, Arch-Gen-Psych, 1983 40(8):
877-83).

..............................

Lethal (toxic) doses of LSD are conservatively several tens of
thousands of times as much as a normal dose, making it (in the toxic
sense) one of the safest drugs known.  See section on Pharmacology for
description of bodily  side-effects.

    The LD50 for psilocybin (active ingredient in mushrooms) is 275 mg/kg
i.v. in mice.  Of course, it would take lots more p.o. to kill someone.

    The reported LD50 values for LSD are 46, 16.5, 0.3 mg/kg I.V. for mice,
rats, and rabbits, respectively.  Again, it's hard to accurately translate
these numbers to oral values.

Note that an average human dose is 0.001 mg/kg, ie, 1 microgram/kg, ie,
1 part per billion by weight.

..............................

Never take any drugs while pregnant.  Best to be prudent.

******************************

FLASHBACKS:

   Quoted without permission from 'Licit and Illicit Drugs,' written by
Edward M. Brecher and the editors of Consumer Reports. ISBN: 0-316-15340-0

   A simple explanation of LSD flashbacks, and of their changed character
after 1967, is available.  According to this theory, almost everybody
suffers flashbacks with or without LSD.  Any intense emotional
experience--the death of a loved one, the moment of discovery that one is in
love, the moment of an automobile smashup or of a narrow escape from a
smashup--may subsequently and unexpectedly return vividly to consciousness
weeks or months later.  Since the LSD trip is often an intense emotional
experience, it is hardly surprising that it may similarly "flash back."

   <end quote>

"Post-traumatic stress disorder has been commonly associated with war
veterans, but it also affects victims of disasters and violence... Experts
estimate that 1% of the population suffers from the disorder."
---LA Times, Feb 18 1992, p A3, "Journey For Better Life Hell For Some Women."

..............................


   Can smoking marijuana induce a flashback?
   Also are you more likely to suffer flashbacks from having a bad trip?

Apparently yes and yes.  The following is reproduced without
permission from Lester Grinspoon and James B. Bakalar, "Psychedelic
Drugs Reconsidered," Basic Books, Inc.  New York, 1979. pp. 159-163.
I highly recommend this book, and if you find it please buy me one
too.

I typed this in a while ago and didn't type in the references at the
time (slap!).  If you want them i'll see what i can do.  Typos are
mine.

	-	-	-	-	-	-	-

	... Studies of flashbacks are hard to evaluate because the
term has been used so loosely and variably.  On the broadest
definition, it means the transitory recurrence of emotions and
perceptions originally experienced while under the influence of a
psychedelic drug.  It can last seconds or hours; it can mimic any of
the myriad aspects of a trip; and it can be blissful, interesting,
annoying, or frightening.  Most flashbacks are episodes of visual
distortion, time distortion, physical symptoms, loss of ego
boundaries, or relived intense emotion lasting a few seconds to a few
minutes.  Ordinarily they are only slightly disturbing, especially
since the drug user usually recognizes them for what they are; they
may even be regarded lightheartedly as "free trips."  Occasionally
they last longer, and in a small minority of cases they turn into
repeated frightening images or thoughts.  They usually decrease
quickly in number and intensity with time, and rarely occur more than
a few months after the original trip.

	A typical minor and pleasant flashback is the following:

--

	... Frequently afterward there is a momentary "opening"
("flash" would be too spastic a word) when for maybe a couple of
seconds an area one is looking at casually, and indeed unthinkingly,
suddenly takes on the intense vividness, composition, and significance
of things seen while in the psychedelic condition.  This "scene" is
nearly always a small field of vision -- sometimes a patch of grass, a
spray of twigs, even a piece of newspaper in the street or the remains
of a meal on a plate (Cohen 1970[1965], pp. 114-115)

--

	Here are two more troublesome examples:

--

	For about a week I couldn't walk through the lobby of A-entry
at the dorm without getting really scared, because of the goblin I saw
there when I was tripping. (Pope 1971, p. 93)

--

	A man in his late twenties came to the admitting office in a
state of panic.  Althought he had not taken any drug in approximately
2 moths he was beginning to re-experience some of the illusory
phenomena, perceptual distortions, and the feeling of union with the
things areound him that had previously occurred only under the
influence of LSD.  In addition, his wife had told him that he was
beginning to "talk crazy," and he had become frightened ... He was
concerned lest LSD have some permanent effect on him.  He wished
reassurance so that he could take it again.  His symptoms have
subsided but tend to reappear in anxiety-provoking situations.
(Frosch et al. 1965, p. 1237)

--

	Flashbacks are most likely to occur under emotional stress or
at a time of altered ego functioning; they are often induced by
conditions like fatigue, drunkenness, marihuana intoxication, and even
meditative states.  Falling asleep is one of those times of
consciousness change and diminished ego control; an increase in the
hypnagogic imagery common at the edge of sleep often follows
psychedelic drug use and can be regarded as a kind of flashback.
Dreams too may take on the vividness, intensity, and perceptual
peculiarities of drug trips; this spontaneous recurrence of
psychedelic experience in sleep (often very pleasant) has been called
the high dream (Tart 1972).  Marihuana smoking is probably the most
common single source of flashbacks.  Many people become more sensitive
to the psychedelic qualities of marihuana after using more powerful
drugs, and some have flashbacks only when smoking marihuana (Weil
1970).  In one study frequency of marihuana use was found to be the
only factor related to drugs that was correlated with number of
psychedelic flashbacks (Stanton et al. 1976).

	How common flashbacks are said to be depeds on how they are
defined.  By the broad definition we have been using, they occur very
often; probably a quarter or more of all psychedelic drug users have
experienced them.  A questionanaire survey of 2,256 soldiers (Stanton
and Bardoni 1972), leaving the definition to the respondents, revealed
that 23 percent of the men who used LSD had flashbacks.  In a 1972
survey of 235 LSD users, Murray P. Naditch and Sheridan Fenwick found
that 28 percent had flashbacks.  Eleven percent of this group (seven
men in all) called them very frightening, 32 percent called them
somewhat frightening, 36 percent called them pleasant, and 21 percent
called them very pleasant.  Sixty-four percent said that their
flashbacks did not disrupt their lives in any way; 16 percent (4
percent of the whole LSD-using group) had sought psychiatric help for
them (Naditch and Fenwick 1977).  In a study of 247 subjects who had
taken LSD in psychotherapy, William H. McGlothlin and David O. Arnold
found 36 cases of flashbacks, only one of which was seriously
disturbing (McGlothlin and Arnold 1971).  McGlothlin, defining
flashbacks narrowly for clinical purposes as "repeated intrusions of
frightening images in spite of volitional efforts to avoid them"
(McGlothlin 1974b, p. 291), estimates that 5 percent of habitual
psychedelic users have experienced them.

	There are few studies on the question of who is most
susceptible.  In 1974, R. E. Matefy and R. Krall compared psychedelic
drug users who had flashbacks with those who did not, and found no
significant differences in their biographies or on personality tests.
The main causes of flashbacks were stress and anxiety.  About 35
percent found them more or less pleasant, and the same proportion
thought they could control them.  Most accepted them as an inevitable
part of their lives as members of the psychedelic fraternity and did
not want help from psychiatry (Matefy and Krall 1974).  Naditch and
Fenwick found that the number of flashbacks, both pleasant and
unpleasant, was highly correlated with the number and intensity of bad
trips and the use of psychedelic drugs as self-prescribed
psychotherapy.  Those who enjoyed flashbacks and those who were
frightened by them did not differ significantly on tests of ego
functioning.

	A case seen in an outpatient setting in the late sixties
illustrates the kind of set and setting that may create flashback
problems.  PQ was a thirty-six-year-old single man who entered therapy
because of depression and anxiety.  He was a heavy drinker who was
passive, slovenly, and spent most of his time in bed.  Just before
taking to alcohol and his bed he had failed in an attempt to parlay a
gift from his wealthy father into a fortune on the stock market.
Despite a remarkable incapacity for insight, during a year in
psychotherapy he managed to give up alcohol and start a promising
business.  But his anxiety continued, and in order to allay it he had
to keep himself very busy wheeling and dealing.  Imitating his father,
a successful self-made man who had married a woman twenty years
younger than himself, PQ dated only women under the age of nineteen.
Being attractive to young women was so imporant to him that much of
his time was spent in the company of teenagers.  During business hours
he would wear a conservative three-piece suit and drive a new sedan,
but when he was with his young friends he would wear a leather jacket
and drive a motorcycle.  Anxiety and fears of inadequacy dominated
both of these lives.  Several months after therapy began, during a
weekend in a small resort town, his young friends decided to take LSD,
and he felt obliged to dissemble his fears and join them; it was his
first and only trip.  He felt a panic he had never known before; he
thought that he was losing his mind and going "out of control."  His
friends were so concerned thet they took him to a small hospital,
where he was given chlorpromazine and after six hours released in
their care.  The next day he had a flashback that lasted one or two
hours and was almost as frightening as the original experience.
Flashbacks continued for six months, their frequency, duration, and
severity eventually diminishing to the point where it was difficult
for him to determine whether they were related to the LSD trip or
merely an intensification of his usual anxiety.  In fact, the patient
described the flashbacks as being like very much enhanced anxiety
episodes.  Even several years after this experience, when he became
very anxious, he was reminded of the trip and these flashbacks.  He
denied that these experiences had any perceptual or cognitive aspect;
both during the LSD trip and later, the only symptom was panic.  There
is no question that the nature of his trip was influenced by the
unfortunate set and setting.  It is a matter of speculation what part
his underlying chronic anxiety played in the development and form of
the flashback phenomena.

	Several explanations for flashbacks have been proposed.  One
is that the drug has lowered the threshold for imagery and fantasy and
made them less subject to voluntary control; in another version of
this explanation, flashbacks are caused by a heightened attention to
certain aspects of immediate sensory experience suggested by drug
trips and reinforced by the community of drug users.  Something more
seems to be needed to account for repeated fearful relivings of
sequences from past drug trips, and these have been explained as
similar to traumatic neuroses precipitated by fright: disturbing
unconscious material has risen to consciousness during the drug trip
and can be neither accepted nor repressed.  For example, D. F. Saidel
and R. Babineau (1976) have reported a case of recurrent flashbacks --
three years of blurring images and auditory distortions, with some
anxiety and confusion -- which they regard as a neurosis founded on
the patient's problems with his career and his relationship to his
mother. (See also Horowitz 1969; Shick and Smith 1970; Heaton 1975.)
Another explanation treats the flashback as an example of recall
associated with a particular level of arousal. (Fischer 1971).  In
this conception the memory of an experience is best retrieved when the
rate of mental data-processing is the same as it was during the
original experience -- in other words, when the state of consciousness
in similar.  Therefore, psychedelic experiences are likely to be
recalled and relived when the ego's sorting and control of sensory
information is disturbed by drugs, stress, or the state of half-sleep.

	For a critique of flashback studies, see Stanton et al. 1976

	-	-	-	-	-	-	-








******************************

INSOMNIA:

Insomnia occurs frequently after the trip.  A mild, over-the-counter
sleeping aid can help, and these antihistamines do not produce adverse
interactions.  Also, some people like to consume a small amount of alcoholic
beverage to "smooth the jitteries".  The usual precautions about sleeping
aids if alcohol has been consumed apply of course.


******************************

TOLERANCE:

Aquired rapidly, within 3 days.  Tolerance dissipates equally rapidly,
without withdrawal, craving, or symptoms of addiction.

Cross-tolerance can and is developed between other indole hallucinogens, eg,
DMT, LSD and Psilocybin.

******************************

BOTANY:

Lysergic compounds appear in ergot, a fungal parasite of cereal grains;
morning glory and hawaiian baby wood rose seeds; psychedelic tryptamines
also occur in psilocybe mushrooms, in some south american trees and the
poison glands of the cane toad.  (Mescaline is not in this chemical family).

..............................



"Indole Alkaloids In Plant Hallucinogens"  Richard Evans Schultes, PhD.
Journal of Psychedelic Drugs Vol.8(No.1) Jan-Mar 1976

"The main constituent of the seeds of Rivea corymbosa is ergine or d-lysergic
acid amide. Minor alkaloids present are the related d-isolysergic acid amide
(isoergine), chanoclavine, elymoclavine and lysergol. The seeds of Ipomoea
violacea have a similar composition, but instead of lysergol, they have
ergometrine (ergonovine). Later, very minor amounts of two alkaloids
ergometrinine and penniclavine - were found in I. violacea by chromatography.
the total alkaloid content of the seeds of Ipomoea viloacea is approximately
five times as great as that of the seeds of Rivea corymbosa: 0.06% in the
former; 0.012% in the latter. This difference in the alkaloid content
explains why Indians employ smaller doses of seeds of the Ipomoea than of the
Rivea.

"Ethnopharmacology and Taxonomy of Mexican Psychodysleptic Plants"
 Jose Luis Diaz M.D.
 Journal of Psychedelic Drugs Vol. 11(1-2) Jan-Jun 1979

Seeds of various Morning Glories contain
 Ergolines:  ergine,isoergine,ergonovine
 Glucosides: turbicoryn [apparently in Rivea corymbosa only]

called Tlitlitzen (Aztec word for "The Divine Black One")
to the Aztecs, Black is a "hot" color,
a property of psychotropics associated with light

..............................

"The Botanical and Chemical Distribution of Hallucinogens"
Richard Evans Schultes, PhD.
Journal of Psychedelic Drugs Vol.9(No.3) Jul-Sep 1977

"I. violacea, often referred to by it's synonyms I. rubro-caerulea and
I. tricolor, is represented in horticulture by a number of "varieties,"
such as: Heavenly Blue, Pearly Gates, Flying Saucers, Wedding Bells,
Summer Skies, and Blue Stars - all of which contain the hallucinogenic
ergot alkaloids."

>In the Journal of Psychoactive Drugs, 1980, there is an article
>on an ergot derivative used in obstetrics which is an hallucinogen.
>Although the dose required is ten times the ED50 (.2 mg) no
>significant ill effects were reported.
>I believe the name of this drug is methyl ergovine(?)  The drug
>without the methyl group is supposed to be more effective.  It
>was (is?) a Sandoz drug, for those with a PDR.

Ergonovine and methylergonovine are both oxytocic agents: they increase
uterine tone and are used (rarely) to assist in delivery and (more
frequently) to stop post-partum uterine hemorrhage.  Less frequently,
they can be used to abort a migraine headache.  If they have any
hallucinogenic effects, it is certainly a well-kept secret.

I would be quite concerned about taking 10x the therapeutic dose
of a drug like ergonovine, since it can cause arterial spasm and
precordial distress even in healthy persons, and intense vaso-
constriction and gangrene can follow from an overdose.  These
are not drugs to fool around with.

Another related drug, 1-methyl-methylergonovine, or methysergide
(Sansert), is used in migraine prophylaxis, and is claimed to have
LSD-like actions when high doses are taken.  The methyl group on
the indole nitrogen reduces the drug's vasoconstrictive actions.
Chronic, uninterrupted use of the drug causes a fibrosis of the
heart valves and the lungs.


..............................

"Burger's Medicinal Chemistry" Fourth Edition, Volume III
Chapter: "Hallucinogens"  Alexander Shulgin

                  Composition, % of total alkaloids present
                  =========================================
Compound          R. corymbosa       I. violacea
===============   ================   ======================
Ergine (LA-111)   54, 48             58, 10-16, 5-10
Isoergine         17, 35             8, 18-26, 9-17
Ergometrine                          8
Elymoclavine      4                  4
Chanoclavine      4                  4
Lysergol          4

Total Alkaloids   .012, .04          .06, .04-.08, .02-.04
(% of dry weight
 of seeds)



******************************

ANTHROPOLOGY:


_The Road to Eleusius_ by Hoffman, Wasson, and Ruck.

Summary: A secret religion existed for 2,000 years in Greece (until
the christians displaced it around 400 AD).  The initiation was open
to anyone who spoke Greek and hadn't committed murder, once in their
life.  After 6 month long preparatory rituals, members walked to
Eleusius whereupon they underwent secret rituals.  The rituals
remained secret until the 1970's.

Wasson, an ethnomycological scholar and former banker (and the first
white to trip on shrooms with the mexican indians) proposed the
following explanation of the Eleusian mysteries to Hoffman, an
ergot-alkaloid expert chemist, and Ruck, a greek scholar:

The Secret of the ritual involved the personal visions induced by
drinking the grain decoction administered to the initiates.  The
domestication of grains permitted the development of greek
civilization; it also brought ergot fungus (of St. Anthony's fire
infamy).

The thin book contains their argument for the use of the ergot fungus
in Eleusian rites, Wasson providing some background on the use of
mushrooms and grains and their role in the culture; Hoffman on the
psychoactivity of ergot strains; and Ruck on the mythological and
cultural backround of the sect.

Evidence includes: Hoffman dosed himself with large (ergot-derived)
doses of obstetric compounds to assay their hallucinogenic potential,
and found them to possess such activity.  The Eleusian temple site still
remains, but there is no room to view theatric performances, just rows of
tripping initiates, further supporting their argument.

An interesting read, and its neat to think that the culture that
more or less lead to the western industrial one had psychedelic rites.
(Various greek prominant figures attended the rituals, including Plato).

..............................


IPOMOEA PURPUREA: A NATURALLY OCCURRING PSYCHEDELIC

Charles Savage, Willis W. Harman and James Fadiman

>From  "Altered States of Consciousness, A Book of Readings"
       edited by Charles Tart   BF311.T28

Of the naturally occurring plant alkaloids used in ancient and modern
religious rites and divination one of the least studied is ololiuqui. The
earliest known description of its use is by Hernandez, the King of Spain's
personal physician, who spent a number of years in Mexico studying the
medicinal plants of the Indians and "accurately illustrated ololiuqui as a
morning glory in his work which was not published until 1651" (Schultes,
1960). In his words, "When a person takes ololiuqui, in a short time he loses
clear reasoning because of the strength of the seed, and he believes he is in
communion with the devil" (Alacon, 1945). Schultes (1941) and Wasson (1961)
have reported in detail on the religious and divinatory use of two kinds of
morning-glory seeds, Rivea corymbosa and Ipomoea violacea, among the Mazatec
and Zapotec indians. The first of these is assumed to be the ololiuqui of the
ancient Aztecs.

In 1955 Osmond described personal experiments with Rivea corymbosa seeds and
reported that the effects were similar to those of d-lysergic acid
diethylamide (LSD-25). He suggested (1957) that the word psychedelic (meaning
mind-manifesting) be used as a generic term for this class of substances to
refer to their consciousness-expanding and psychotherapeutic function as
contrasted  with the hallucinogenic aspect. In 1960 Hoffman reported that he
had isolated d-lysergic acid amide (LA) and d-isolysergic acid amide from the
seed of both Rivea corymbosa and Ipomoea violacea. LA is very similar to LSD
in its psychological and physiological manifestations but is reported to have
about one twentieth the psychological effectiveness of LSD (Cerletti &
Doepfner, 1958).

The work of these investigators led us to a preliminary study of the
psychedelic properties of species of Ipomoea which are commonly found within
the continental United States. The seeds of Ipomoea purpurea, the common
climbing morning glory, resemble the seeds of Ipomoea violacea and have been
found to have similar psychedelic properties. Recent analysis by Taber et al.
(1963) has verified that LA is present in the varieties used and is probably
the primary active agent.

The effects of the seeds of Ipomoea purpurea (varieties Heavenly Blue and
Pearly Gates) in a total of 45 cases are summarized below. The subjects are
all normally functioning adults and the majority had previous experience with
LSD. The onset of effects is about half an hour after the seeds have been
chewed and swallowed and they last from five to eight hours.


               Low Dose, 20-50 Seeds (11 Subjects)

This dosage rarely produces any visual distortions, although with eyes
closed there may be beginning imagery. Restlessness, evidenced by alternating
periods of pacing about and lying down, may be present. There tends to be a
heightened awareness of objects and of nature, and enhanced rapport with
other persons. A feeling of emotional clarity and of relaxation is likely to
persist for several hours after other effects are no longer noticeable.

              Medium Dose, 100-150 Seeds (22 Subjects)

In this range the effects resemble those reported for medium-dose (75-150
micrograms) LSD experiences, including spatial distortions, visual and
auditory hallucinations, intense imagery with eyes closed, synaesthesia and
mood elevation. These effects, which occur mainly during the period of 1 to 4
hours after ingestion, are typically followed by a period of alert calmness
which may last until the subject goes to sleep.

              High Dose, 200-500 Seeds (12 Subjects)

In this range the first few hours may resemble the medium-dose effects
described above. However, there is usually a period during which the
subjective states are of a sort not describable in terms of images or
distortions, states characterized by loss of ego boundaries coupled with
feelings of euphoria and philosophical insight. These seem to parallel the
published descriptions of experiences with high doses (200-500 micrograms) of
LSD given in a supportive, therapeutic setting as reported by Sherwood et al.
(1962).

All the subjects who had previous experience with LSD claimed the effects of
the seeds were similar to those of LSD. Transient nausea was the most
commonly reported side effect, beginning about one half hour after ingestion
and lasting a few minutes to several hours. Other reported side effects not
commonly found with LSD were a drowsiness or torpor (possibly due to a
glucoside also present in the seeds) and a coldness in the extremities
suggesting that the ergine content of the seeds may be causing some vascular
constriction. (If this is the case, there may be some danger of ergot
poisoning resulting from excessive dosages of the seeds.) The only untoward
psychic effect was a prolonged (eight hours) disassociative reaction which
was terminate with chlorpromazine [Thorazine]. The possibility of prolonged
adverse reactions to the psychological effects of the seeds is essentially
the same as with LSD, and the same precautions should be observed (Cohen &
Ditman, 1963).

..............................

IPOMOEA.003   7-MAY-90

Additional Notes:
Ipomoea purpurea is sold as the "Heavenly Blue" variety of morning glory.
"Ipomoea tricolor" is the trade name used for that variety. It is identical
with the species of morning glory described above.

The seeds must be chewed or ground in order to be effective. Soaking the
ground seeds in water for several hours, filtering out the grounds,
and then drinking only the water portion of the mixture can reduce
some of the stomach-upset symptoms if such occur.

Unpleasant LSD and morning glory trips can be smoothed out or even
stopped by taking niacin (in the form of nicotinic acid, vitamin B-3 or
"niacin"). Vitamin C has been shown to reduce the incidence of paranoia and
prevent depletion of the vitamin from the adrenal glands during LSD trips.

There have been reports that commercially available packets of morning
glory seeds from some distributors are coated with fungicides or
other chemicals to increase shelf life or discourage the practice
of eating them. Seeds from plants grown in one's own garden will
be safe as long as you do not spray them with insecticides.

The last few notes about Niacin and Vitamin C are based on
a paperback edition of Hoffer & Osmonds "The Psychedelics"

It's pretty clear that the latin names of this plant are somewhat
confused (which is typical). Ipomoea purpurea, Ipomoea tricolor,
Ipomoea violacea and Ipomoea rubro-caerulea are all the same plant.

The other variety of morning glory, "Ololiuhqui" has at least two
Latin names as well: Rivea corymbosa, and Turbina corymbosa.

..............................

"Recreational use of Ergoline Alkaloids from Argyreia Nervosa"
William E. Shawcross
Journal of Psychedelic Drugs Vol. 15(4) Oct-Dec 1983

CHEMISTRY AND EFFECT OF THE SEEDS
The Hawaiian baby woodrose entered the drug scene in 1965 with the
publication of a paper in "Science" entitled "Ergoline Alkaloids in Tropical
Wood Roses" by Hylin and Watson. The wide circulation of this journal assured
thorough dissemination of the information they presented. They wrote, "The
possible health and legal problems associated with the presence of similar
compounds in commercially cultivated plants led us to examine the ornamental
wood roses, Ipomoea tuberosa and Argyreia nervosa, both common Hawaiian crops
that have assumed commerical importance as components of [the] dried tropical
flower industry." Comparing the seeds of these two plants with those of the
morning glory varieties Pearly Gates and Heavenly Blue, they found the
following yield of alkaloids (mg of alkaloid/g of seed material):

     Heavenly Blue        0.813
     Pearly Gates         0.423
     I. tuberosa          [None]
     A. nervosa           3.050

The seed of A. nervosa is the best plant source of ergoline alkaloids
discovered; it contains approximately 3 mg of alkaloidal material per gram of
seed. Approximately one-eighth of this is lysergamide.

Hylin and Watson found the major alkaloidal constituents in A. nervosa seeds to
be ergine (780 mcg/g of fresh seed) and isoergine and penniclavine (555 mcg).

[Note: Argyreia nervosa has NO history of shamanic use as a hallucinogen]

This is an excerpt from the article cited.
There's no record of Argyreia being used as an hallucinogen in
India, but it was used externally as some kind of skin medicine.
There's been speculation that Argyreia might have been a component
of "Soma", but there's no evidence for that, apparently.
Because there's not a long history of human usage of Argyreia,
it may be that there are glycosides not mentioned here that
take effect at higher doses or might cause stomach upset, tachycardia
etc. The article mentioned intestinal complaints in one or two
cases at higher experimental doses.






******************************

CHEMISTRY:

lysergic acid diethylamide _is_ lysergic acid diethylamide (or...
N,N-diethyl-D-lysergamide or...
9,10-Didehydo-N,N-diethyl-6-methylergoline-8B-carboxamide).

Only one stereoisomer (the d-) is psychoactive.  Thus, racemic (l/d 50-50 mix)
lsd shows half the potency of the dextro form.  In synthesis it is possible
to recover the l-form for the lysergic acid.

Lysergic Acid Diethylamide is LSD rather than LAD because the German word
for acid is saeure (sp).

	LSD-25				Lysergic acid

        O      CH2-CH3                  O
       ||     /                        ||
       ||    /                         ||
        -C--N                           C---OH
        |    \                          |
        |     \                         |
        |___   CH2-CH3                  |___
       /    \                          /    \
      /      \                        /      \
    <<        N---CH3               <<        N---CH3
     \\      /                       \\      /
      \\____/                         \\____/
      /     \                         /     \
     /       \                       /       \
    <         >                     <         >
  // \       /                    // \       /
 //   \_____/                    //   \_____/
 |    ||   ||                    |    ||   ||
 |    ||   ||                    |    ||   ||
 |    ||   ||                    |    ||   ||
 \\   /\   /                     \\   /\   /
  \\ /  \ /                       \\ /  \ /
         N                               N
         H                               H

Ergot is a product of the fungus Claviceps purpurea.  The bio-active
ingredients of ergot are all derivatives of lysergic acid.  LSD is a
semisynthetic derivative of lysergic acid.  Thus LSD is an
"ergot"-like substance.

******************************


MECHANISM OF ACTION:

(Note: the mechanism of action of LSD and other psychedelics is uncertain.)

From a chapter titled Hallucinogens and Other Psychotomimetics: Biological
Mechanisms by S.J.Watson

"The current thesis of the effect of indole hallucinogens on
5-hydroxytrypamine might be stated as follows: LSD acts to preferentially
inhibit serotonergic cell firing and seems to spare postsynaptic serotnergic
receptors.  This preference is shared by other simillar hallucinogens but in
a limited fashion.  Nonhallucinogenic analogs of LSD show no preference.
These results suggest that there are two different steric conformation of
serotonergic receptors, one of which has higher affinity for LSD than the
other.  In general, 5-ht is an inhibitory transmitter; thus, when its
activity is decreased, the next neuron in the chain is freed from inhibition
and becomes more active.  Since serotnergic systems appear to be intimately
involved int eh control of sensation, sleep, attention, and mood, it may be
possible to explain the actions of LSD and other hallucinogens by their
disinhibition of these critical systems.

There is also evidence for interaction with dopaminergic systems.

..............................

LSD acts as a 5HT autoreceptor agonist in the raphe nucleus.  These
autoreceptors are typically considered to be 5HT1As.  It also acts as a 5HT2
agonist, which is thought to be the main site of hallucinogenic activity.
It's probably best called a a mixed 5HT2/5HT1 receptor partial agonist.

I don't know of its effects on dopamine.  Wouldn't be surprised if it has
'em; the systems aren't really functionally separable.  The DA effects
wouldn't be necessary for hallucinogenic activity, I'd bet.

..............................

(From Snyder, "Drugs and the Brain", 1986, Sci Am Books Inc., Reprinted w/o
permission, blah, blah, blah... )

  In more recent studies, Aghajanian has focuses not on the serotonin neu-
rons of the raphe nuclei but on the norepinephrine neurons of the locus
coeruleus. As we saw in Chapter 6, the locus coeruleus cell bodies give rise to
axons that ramify all over the brain and provide the majority of the norepi-
nephrine neuronal input in most brain regions. Amphetamine releases norepi-
nephrine from these nerve terminals by diplacing the norepinephrine from the
neurotransmitter storage vesicles. Presumably, the overall influence of amphet-
amine on brain function is therefore somewhat different than what occurs
when the locus coeruleus fires rapidly.  The amphetamine-induced seepage of
norepinephrine out of nerve terminals probably elicts a milder type of activa-
tion than does the repetitive and presumably more robust ejection of norepi-
nephrine that occurs with rapid firing of the locus coeruleus. Drug-induced
changes in animal behavior support this conceptual model.  Amphetamine elic-
its behavioral activation, represented by the rats or mice running about the
cage. In contrast, electrical stimulation of the locus coeruleus produces a more
dramatic startle response. It is difficult to observe a rat and make inferences
about what the animal is feeling, but rats in whom the locus coeruleus has been
stimulated seem to go into a state of panic. They stare about, hyper-responsive
to all stimuli in the enviornment, whether visual, auditory, or tactile.
  Rats show the same hyper-responsiveness to environmental-stimuli--
jumping abruptly at the sound of fingers snapping or in response to a puff of
air in the face--when they have been treated with a psychedelic drug.  And as
you will recall, hyper-responsiveness to sensory stimuli of all modalities is
just what one observes in humans under the influence of psychedelic drugs.  At-
tracted by the similarity between the behavior of rats on LSD and their reac-
tion to stimulation of the locus coeruleus, Aghajanian embarked in 1980 upon
a series of studies to evaluate how psychedelic drugs affect the locus
coeruleus. He showed that any kind of sensory stimulation--sight, sound, smell,
taste, or tactile sensation--speeds up the firing of locus coeruleus neurons in
rats, and that the accelerated firing is greatly enhanced by treating the
animals with LSD or mescaline.  In contrast, nonpsychedelic drugs, such as
amphetamines and antidepressants, fail to exert this effect.  Moreover, the LSD
analogue methysergide, which has no psychedelic effects in humans, is
correspondingly ineffective in enhancing the reactivity of locus coeruleus
neurons to sensory stimulation.
  Although psychedelic drugs increase the response of locus coeruleus cells to
sensory stimulation, they do not cause the neurons to fire spontaneously in the
absence of such stimulation.  Moreover, directly applying LSD or mescaline to
locus coeruleus neurons does not enhance the neurons' reponse to sensory
stimulation. We must therefore conclude that the effect of psychedelic drugs on
sensory stimulation is indirect--the drugs presumably interact with a different
set of neurons that in turn make direct contact with the locus coeruleus.
  What is particularly fascinating about Aghajanian's findings is how nicely
they correspond to what we know about the effects of psychedelic drugs in
humans, and how readily they explain the way psychedelic drugs accentuate all
our sensory perceptions. The locus coeruleus is a funneling mechanism that
integrates all sensory input. Viewed in this way, the observations of
Aghajanian can explain synesthesia. If the locus coeruleus lumps all types of
sensory messages--from sights, sounds, tactile pressures, smells, tastes--into
a generalized excitation system within the brain, one can readily appreciate
that stimulation of the locus coeruleus will cause the drug user to feel that
sensations are crossing the boundaries between different modalities.
  Aghajanian's research may also illuminate how LSD influences the user's
sence of self. The greatly accelerated firing of the locus coeruleus presumably
provokes a powerful, patterned release of norepinephrine from nerve terminals
throughout the brain. As we discussed earlier, the consequent alerting action
would be much more pronounced than what occurs with the far more gradual
leaking out of norepinephrine produced when amphetamine displaces the
transmitter from the storage vesicles. This extremely enhanced level of alert-
ness might possibly account for the "transendent" mental state produced by
psychedelic drugs. In other words, in a state of such heightened awareness, the
drug user may become conscious of an "inner self" to which he or she is
normally oblivious.

Did that answer any of your questions?  Probably not, but I thought it was
interesting.

P.S. Snyder has tripped before =)

..............................

>"If there's no documentation, you can't tell bugs from features." ---C.P.

..............................


>>Lysergic-acid diethylamide >> >>When ingested into the human body, LSD act
as 5-HT (Serotonin) autoreceptor >>inhibitor, thus it is a 5-HT agonist.
LSD increases the level of active 5-HT >>molecules by disaffecting their
autoreceptors (a safeguard type feature in the >>brain which reduces levels
of certain neurotransmitter and the like).

That "thus" in the first sentence should be an "and."  I'm not certain
what "disaffecting" should be (autoreceptors' only true loyalty is
to the laws of chemistry & physics) for the second sentence to be
true.

The autoreceptors in question are 5-HT1As.  5-HT2s, which are not
autoreceptors and which hallucinogens agonize, seem to be the more
important ones for hallucinogenic activity. Hallucinogens need not
affect 1As directly (some definitely don't).  However, 5-HT2 receptor
activation seems to facilitate presynaptic 1A function (such that,
for example, hallucinogen use produces rapid 5-HT2 downregulation
which, in turn, decreases 5-HT1A function).  So hallucinogens would
inhibit autorecetpor activity, but not necessarily directly.

>LSD also has effects on 5-HT1C receptors, and its not entirely sure what the
>specific receptor mechanism is -- there's also the question of why the
>psychological effects seem to last much longer than the presence of the LSD
>molecule.  One thing that is fairly sure is that LSD shuts down the firing of
>the seratonin neurons in the raphe, though.

It is difficult to separate 1Cs from 2s because of their great similarity.
However, hallucinogens seem to be all 2 & 1C agonists.  Molecules which (like
LSD) are partial 2 agonists, and which (unlike LSD) are 1c antagonists
are not hallucinogenic.

I believe that the effects of DOI (and probably LSD) on firing in the
raphe nucleus are not blocked by 5-HT2 antagonists (like ketanserin),
implying that these effects are not mediated by 5-HT2 receptors.
Oddly enough, ritanserin (which antagonizes 2 and 1C) doesn't block
'em either.  That's kind of mysterious to me.

>  5-HT has been implicated in
>>certain behaviors, notably dreaming and sleep, which explains the hallucinatory
>>effect.  We are in effect dreaming while completely awake and aware.

>Actually, a better explanation is the increased firing of the locus coereleus
>by its disinhibition due to the neurons in the raphe slowing down (since you
>are inhibiting an inhibitory neuron the result is excitation...).  The l.c.
>has been associated with being a "sensory highway" in the brain, and has also
>been associated with feelings of anxiety, and theorized that its invovled
>with depression.  My guess is that the hallucinations and stimulatory effects
>of LSD come from potentiating the l.c., while the effect on the 5-HT neurons
>in the raphe is responsible for its entheogenic effect on the mind.

This isn't the full story since this decrease in firing (in the raphe) is still
produced by hallucinogens even after chronic treatment with hallucinogens.
Since tolerance does develop to hallucinogens, we would have
expected to see it in the firing.  Of course, rate of firing and amount
of 5-HT released _are_ two different things.  Besides, tolerance may
occur via another route.





******************************

RELATED COMPOUNDS:



Related compounds are the indole hallucinogens including DMT
(dimethyl-tryptamine), DET (diethyl-), etc.; psilocybin; lysergic acid.  DMT
is very fast acting, lasting less than an hour.  Psilocybin, found in
hallucinogenic (aka magic or mexican) mushrooms, has effects similar to LSD
but they work for approximately half the duration.  These are all indole
derivatives like the neurotransmitter serotonin, 5-hydroxy-tryptamine.
"Indole" is the name of the 6-carbon ring attached to the 5-ring containing
a nitrogen. The lysergic acid molecule contains an indole structure plus
additional rings.

LSD's two ethyl groups hanging off the amine may be replaced with
other carbon chains for compounds with different durations, potencies,
and effects.

While LSD is semi-synthetic, DMT and psilocybin are found in nature.
See the sections on BOTANY and ANTHROPOLOGY for info on related
natural (plant) compounds and their uses.

..............................

   1) DMT, DET, psylocin, psylocybin, : The mushroom psylocybin cubensis
contains all four of these indole derivatives, as well as others. DMT is
dimethyltryptamine, an indole derivative which has functionalized at the 3
position with the dimethyl ethylamine group.  It is a close relative to the
amino acid, tryptophan, which until recently was available in bulk at
vitamin shops, until some jerk poisoned himself by taking a wonga dose of
it. [Actually it may have been a single toxic batch mistakenly produced in
Japan.] A prep came out in 1984 for LSD using l--tryptophan as the
precursor, so this may have facilitated the government's pullin it from the
shelves. I can't find tryptophan anywhere, now, and I've tried, bud.
     DMT, and it's brother DET (diethyltryptamine), have no oral activity,
so have to be smoked. They stink like fish oil when lit, though. Both have
hallucinogenic effects within 2-3 minutes of toking, wand while DMT lasts
for only a half hour, DET is a smoother, more euphoric high, lasting twice
as long. DET has effects similar to psylocybin.
     Psylocybin is DMT which has a functional group, phosphoryloxy-, at the
4 position on the indole ring. This group is immediately converted to
hydroxyl- as soon as the stuff hits your stomach to give the cousin,
psylocin. In preparing the drug, then, it is not necessary to proceed beyond
the psylocin.
     DMT and DET are easily derived from many indole derivatives, the
easiest of which is indole-3-acetic acid. I've done this reaction and it
stinks to high heaven of indole gunge, skatoles (methylindoles), and
indenes. Bad news if you want to make it at home, because the stench is
pervasive. Other derivatives, using phenyl or butyl groups have been
reported as having oral activity, so it is not necessary to smoke the stuff.
Doses run at about a hundred mgs for smoked drug, while psylocin is orally
active at about 5 mgs.

[this warning was recently posted to alt.drugs -cak]

Message-ID: <221302Z24111994@anon.penet.fi>
Newsgroups: alt.drugs
From: an152823@anon.penet.fi
Date: Thu, 24 Nov 1994 22:11:17 UTC
Subject: !! DMT WARNING !!

DMT WARNING!!

Under the heading "related compunds" in the LSD.FAQ, where it refers to the
tryptamines, specifically smoked DMT, it says, "Doses run at about a hundred
mgs for smoked drug," Smoking 100mg of DMT is a very bad idea. Realistically
20-30mg is a low-end average dose and 50-60mg gets pretty hairy.

The faq needs fixin big time.

-------------------------------------------------------------------------
To find out more about the anon service, send mail to help@anon.penet.fi.
Due to the double-blind, any mail replies to this message will be anonymized,
and an anonymous id will be allocated automatically. You have been warned.
Please report any problems, inappropriate use etc. to admin@anon.penet.fi.

[back to the regularly scheduled FAQ -cak]

     For a good reference work on these compounds, their preps, and effects,
see Michael Valentine Smith's "Psychedelic Chemistry," publisher unknown.


                                   Your Friendly Neighborhood Chemical
                                                Dude,
                                   St. Theo


..............................

             DMT
                                CH
                              /   3
        // \\---  --- CH CH N
        || ||   ||      2  2  \
        \\ //\ /                CH
              N                   3
              H



 When DMT is smoked or injected, effects begin in seconds, reach a peak in
five to twenty minutes and end after a half hour or so. This has earned it the
name "businessman's trip." The brevity of the experience make its intensity
bearable, and, for some, desirable.

 At least two synthetic drugs in which the methyl group of DMT is replaced by
a higher radical are psychedelic:

              /\       (CH2)2-N(C2H5)2     /\      (CH2)2-N(CH2CH2CH2)2
             // \ ____/                   // \ ____/
            |   ||   ||                  |   ||   ||
            |   ||   ||                  |   ||   ||
             \\ /\   /                    \\ /\   /
              \/  \N/                      \/  \N/
                   H                            H

        N,N-diethyltryptamine          N,N-dipropyltryptamine

 The drug DET is active at the same dose as DMT and the effects last slightly
longer, about one and a half to two hours. DPT is longer-acting still and has
fewer autonomic side effects. In therapeutic experiments its action continues
for one and a half to two hours at the lowest effective dose, 15 to 30mg, and
for four to six hours at doses in the range of 60 to 150mg. Both DET and DPT
are milder than DMT. The drug 6-FDET (6-fluorodiethyltryptamine) resembles DET
in its effects. All these drugs, like DMT, are inactive orally and must be
smoked or injected. Dibutyltryptamine (DBT) and higher substitutions are
inert, but other synthetic drugs related to DMT may be psychoactive.


..............................



From the Merck Medical Manual, 16th edition, page 2652:

"Serotonin (5-HT) is the neurotransmitter of many central neruons (eg raphe
nucleus).  ITs synthesis begins with the uptake of tryptophan into
serotonergic neurons.  Tryptophan is hydroxylated by the enzyme
tryptophan hydroxylase to 5-hydroxytryptophan and then decarboxylated
to serotontin (5-hydroxytryptamine) by the enzyme aromatic L-amino
acid decarboxylase.  Levels of 5-HT are controlled by the uptake
of tryptophan and intraneuronal MAO.  Metabolism occurs mainly via
MAO to 5-hydroxyindoleacetic acid."

The Merck also states that tyrosine is the precursor of norepinephrine,
acetylcholine's precursor is choline, tyrosine is the precursor of
dopamine, GABA is made from glutamic acid.


..............................



++++++++++++++++++++++++++++++


DMT FAQ (Draft, inserted into LSD FAQ)
8 Aug 94



DMT, DiMethylTryptamine, or 3-(2-(dimethylamino)ethyl)-indole is a chemical
in the same class of drugs as Psilocybin and LSD.  Structurally related to
serotonin, their effects on the body are similar and cross-tolerance can and
is developed between DMT, LSD and Psilocybin.

DMT is not absorbed into the blood stream when taken orally and therefore is
usually inhaled as a powder or smoked.






 A little drivel from your neighborhood chemist regarding some
questions recently asked. If I'm erroneous in anything I spout,
let me know. Thanks.
   1) DMT, DET, psylocin, psylocybin, : The mushroom psylocybin
cubensis contains all four of these indole derivatives, as well as
others. DMT is dimethyltryptamine, an indole derivative which has
functionalized at the 3 position with the dimethyl ethylamine group.
It is a close relative to the amino acid, tryptophan, which until
recently was available in bulk at vitamin shops, until some jerk
poisoned himself by taking a wonga dose of it. A prep came out in
1984 for LSD using l--tryptophan as the precursor, so this may have
facilitated the government's pullin it from the shelves. I can't find
tryptophan anywhere, now, and I've tried, bud.
     DMT, and it's brother DET (diethyltryptamine), have no oral
activity, so have to be smoked. They stink like fish oil when
lit, though. Both have hallucinogenic effects within 2-3 minutes of
toking, wand while DMT lasts for only a half hour, DET is a smoother,
more euphoric high, lasting twice as long. DET has effects similar
to psylocybin.
     Psylocybin is DMT which has a functional group, phosphoryloxy-,
at the 4 position on the indole ring. This group is immediately converted
to hydroxyl- as soon as the stuff hits your stomache to give the
cousin, psylocin. In preparing the drug, then, it is not necessary
to proceed beyond the psylocin.
     DMT and DET are easily derived from many indole derivatives, the
easiest of which is indole-3-acetic acid. I've done this reaction and it
stinks to high heaven of indole gunge, skatoles (methylindoles), and
indenes. Bad news if you want to make it at home, because the stench is
pervasive. Other derivatives, using phenyl or butyl groups have been
reported as having oral activity, so it is not necessary to smoke the
stuff. Doses run at about a hundred mgs for smoked drug, while psylocin
is orally active at about 5 mgs.

[this warning was recently posted to alt.drugs -cak]

Message-ID: <221302Z24111994@anon.penet.fi>
Newsgroups: alt.drugs
From: an152823@anon.penet.fi
Date: Thu, 24 Nov 1994 22:11:17 UTC
Subject: !! DMT WARNING !!

DMT WARNING!!

Under the heading "related compunds" in the LSD.FAQ, where it refers to the
tryptamines, specifically smoked DMT, it says, "Doses run at about a hundred
mgs for smoked drug," Smoking 100mg of DMT is a very bad idea. Realistically
20-30mg is a low-end average dose and 50-60mg gets pretty hairy.

The faq needs fixin big time.

-------------------------------------------------------------------------
To find out more about the anon service, send mail to help@anon.penet.fi.
Due to the double-blind, any mail replies to this message will be anonymized,
and an anonymous id will be allocated automatically. You have been warned.
Please report any problems, inappropriate use etc. to admin@anon.penet.fi.

[back to the regularly scheduled FAQ -cak]

     For a good reference work on these compounds, their preps, and
effects, see Michael Valentine Smith's "Psychedelic Chemistry," publisher
unknown.

                                   Your Friendly Neighborhood Chemical
                                                Dude,
                                   St. Theo


..............................


existing literature on each drug (some would have hundreds of references and
some perhaps two), the facts that are known concerning history, human
pharmacology and human psychopharmacology will be amalgamated into a
"profile." The drugs to be presented will be chosen randomly, rather than with
preference given to popularity, unusual potency, or current availability.
Botanical mixtures will not be considered as such, but as their known active
compnents. As there are upwards of a hundred psychedelic drugs currently
known, it is expected that these "profiles" will eventually form an extensive
reference atlas of compactly prsented drug information.

                               1. DMT

Description and properties:

 DMT, N,N-diemethyltryptamine, Nigerine, desoxybufotenine,
3-(2-dimethylaminoethyl)-indole is a white, pungent-smelling, crystalline
solid with a melting point of 49-50 degrees Celsius, hydrochloride salt
hygroscopic, picrate m.p. 171-172 degrees Celsius and methiodide m.p. 215-216
degrees Celsius. It is insoluble in water, but soluble in organic solvents and
aqueous acids.

History:

 DMT was first synthesized  in 1931, and demonstrated to be hallucinogenic in
1956. It has been shown to be present in many plant genera (Acacia,
Anandenanthera, Mimosa, Piptadenia, Virola) and is a major component of
several hallucinogenic snuffs (cohoba, parica, yopo). It is also present in
the intoxicating beverage "ayahuasca" made from Banisteriopsis caapi, and it
may have oral effectiveness due to the presence of several naturally occuring
inhibitors of catabolic deamination.

Human Biochemistry and Pharmacology:

 Both the parent compound tryptamine and the N-methyltransferase system which
is capable of converting it to DMT, occur in humans, but there is as yet no
evidence that DMT is formed "in vivo". DMT has nonetheless been identified in
trace amounts in the blood and urine of both normals and of schizophrenic
patients, but its origins and functions are unknown. Following intramuscular
administration, maximum blood levels of about 100 ng/ml are observed in 10
minutes, coincident with the maximum changes in electroencephalographic
responses. The plasma clearance t-1/2 [half-life] is about 15 minutes.
Elevated blood levels of indoleacetic acid (IAA) are seen during the time of
peak effects, implying its role as a metabolite. Urine levels of IAA are also
elevated and account for about 30% of the administered drug. An increase in
5-hydroxy-IAA excretion suggests the involvement of serotonin in DMT action.
Unchanged DMT is not excreted.

Human Psychopharmacology:

 DMT is inactive orally at dosages of over 1000mg. With intramuscular
injection, there is an abrupt threshold of activity shown with 30mg, and a
complete psychedelic experience results from the administration of 50-70mg
(75mg subcutaneously, 30mg by inhalation). An unusual feature of the induced
intoxication is the speed of onset and short duration. Within 5 minutes of
administration there is mydriasis [dilated pupils], tachycardia [rapid heart
beat], a measurable increase in blood pressure, and related vegetative
disturbances which usually persist througout the drug experience. In 10-15
minutes, the full intoxication is realized, generally characterized by
hallucinations with the eyes either open or closed, and extensive movement
within the visual field. There is difficulty in the expression of one's
thoughts, and in concentration on a given subject. There is usually a mood
change to the euphoric with unmotivated laughter, but instances have been
reported in which paranoid ideation has promoted anxieties and feelings of
forboding into a state of panic. The subject is largely symptom-free at 60
minutes, although some residual effects have been seen in the second hour.
With the inhalation route of administration the time scale is contracted, with
onset of effects noted in 10 seconds, a short period of full intoxication at
2-3 minute, and a complete freedom from any residual effects within 10
minutes. At higher drug levels, there are increased vegetative symptoms, and
these effectively overwhelm the psychedelic experience at dosages of 150mg
i.m.  Interactions with other drugs are rarely seen; a sensitivity has been
observed with pretreatment with methlysergide, but there is no cross-tolerance
with LSD. Repeated usage does not appear to lead to either physical or
psychological dependency.

Legal Status:

 DMT is explicitly named as a Schedule I drug in the Federal Controlled
Substances Act; registry number 7435.
/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\

                                 DMT

         [Excerpt from a pharmacology textbook published in 1988]

Chemical structure and source:

 This is the prototype member of the tryptamine subclass of indole
derivatives. The structural formula is:

                         /\       (CH2)2-N(CH3)2
                        // \ ____/
                       |   ||   ||
                       |   ||   ||
                        \\ /\   /
                         \/  \N/
                              H

                   N,N-dimethyltryptamine


The drug is a constituent of many of the same South American snuffs and drinks
that contain other psychedelic indole deriviatives, it is often found in the
same plants as 5-MeO-DMT, and Indians add a substance containing it to drinks
containing harmala alkaloids. DMT is the major constituent of the bark of
Virola calophylla, mentioned above; it is also found in the seeds of
Anadenanthera peregina; in the seeds of the vine Mimosa hostilis, used in
easter Brazil to make a drink called "ajuca" or "jurema"; in the leaves of
Banisteriopsis rusbyana, which are added to the harmaline drinks derived from
other plants of the Banisteriopsis genus to make "oco-yage"; and in the leaves
of Psychotria viridis, also added to the Banisteriopsis drinks. Like
5-MeO-DMT, DMT must be combined with monoamine oxydase inhibitors to become
active orally.

Dose:

 First strong effects are felt at about 50mg, whether it is smoked or
injected. Tolerance develops only after extremely frequent use - injections
every two hours for three weeks in rats; at that dose frequency, but not
otherwise, there is also a cross-tolerance between DMT and LSD (Rosenberg et.
al. 1964; Kovacic and Domino, 1976).

Physiological effects:

 Resembles LSD, but sympathomimetic symptoms like dilated pupils, heightened
blood pressure, and increased pulse rate are more common and more intense.

Psychological Effects:

 Like LSD but often more intense. Since it is not taken by mouth, the effects
come on suddenly and can be overwhelming. The term "mind blowing" might have
been invented for this drug. The experience was described by Alan Watts as
like "being fired out of the nozzle of an atomic cannon" (Leary 1968a p.215).
Thoughts and visions crowd in at great speed; a sense of leaving or
transcending time and a feeling that objects have lost all form and dissolved
into a play of vibrations are characteristic. The effect can be like instant
transportation to another universe for a timeless sojourn.

Duration of action:

 When DMT is smoked or injected, effects begin in seconds, reach a peak in
five to twenty minutes and end after a half hour or so. This has earned it the
name "businessman's trip." The brevity of the experience make its intensity
bearable, and, for some, desirable.

 At least two synthetic drugs in which the methyl group of DMT is replaced by
a higher radical are psychedelic:

              /\       (CH2)2-N(C2H5)2     /\      (CH2)2-N(CH2CH2CH2)2
             // \ ____/                   // \ ____/
            |   ||   ||                  |   ||   ||
            |   ||   ||                  |   ||   ||
             \\ /\   /                    \\ /\   /
              \/  \N/                      \/  \N/
                   H                            H

        N,N-diethyltryptamine          N,N-dipropyltryptamine

 The drug DET is active at the same dose as DMT and the effects last slightly
longer, about one and a half to two hours. DPT is longer-acting still and has
fewer autonomic side effects. In therapeutic experiments its action continues
for one and a half to two hours at the lowest effective dose, 15 to 30mg, and
for four to six hours at doses in the range of 60 to 150mg. Both DET and DPT
are milder than DMT. The drug 6-FDET (6-fluorodiethyltryptamine) resembles DET
in its effects. All these drugs, like DMT, are inactive orally and must be
smoked or injected. Dibutyltryptamine (DBT) and higher substitutions are
inert, but other synthetic drugs related to DMT may be psychoactive.
 ..............................

        Remember the L-Tryptophan scare a little while ago?  Well I have
been thinking about it and have come up with a conspiracy theory.  It
may be off base but it was fun to come up with it.

        Ever since the War on Drugs the government has become increasingly
protective of precursors for drug manufacture.  Some friends of mine and
I were talking about Tryptophan, and it came up that it could be used as
the base for several drugs.

        So maby the government generated the Trypto scare so people would
be scared to buy/use it and stores would take it off their shelves.  Has
anyone on the net known anyone who got sick from L-Tryptophan?

        The following is a simple reaction to synthesize DMT from Tryptophan.
using no hard to get or controlled chemicals save L-Tryptophan.
WARNING...
WARNING...
WARNING... This is something I just came up with and may work but I am no
chemist, j!ust a Software Engineering type, so research it yourself or lets
have some net/chem/god help us out.  These two reactions can be found
and read about in any good library.

        The first reaction is using Trypto and Sodium HydroChlorite (AKA
Chlorox) in a 1:1 reaction to produce Indole Acetaldehype(IAA).  This
reaction was use by some company to produce IAA to use to stimulate plant
growth.  The yield should be 70-80%.

        The second reaction is the IAA and Dimethyl Formamide in a 1:4
reaction to produce DMT.  Dimethyl-F is supposedly a very common organic
solvent easy to get and not controlled.  This reaction is documented in a
paper called the 'Leukart Reaction'.  This paper should also have the
instructions on cleaning the DMT from the other byproducts of these
reactions.

Remember this is just to strengthen my conspiracy theory.  It is not
guaranteed correct.


             Tryptophan

                       NH
                       | 2
                       |
        // \\---  --- CH -- CO H
        || ||   ||            2
        \\ //\ /
              N
              H

              |
              |         + 1 Molar Equiv
              |
             \|/          Sodium Hydrochlorite (chlorox)


        Indole Acetaldehyde
              (IAA)

        // \\---  --- CH CHO
        || ||   ||      2
        \\ //\ /
              N
              H
                               CH
              |              /   3    Di-Methyl Amine
              |    <------ NH
              |              \
              |                CH
              |                  3
              |
              |                 Leukart Reaction
              |                     4 Equivs
              |                        Dimethyl Formamide
              |                     1 Equivs
              |                        IAA
             \|/

             DMT
                                CH
                              /   3
        // \\---  --- CH CH N
        || ||   ||      2  2  \
        \\ //\ /                CH
              N                   3
              H


Disclamer :
                The above may not be even remotely correct.  I myself
                Don't do drugs, Legal or not.  I don't advocate makings
                using or selling drugs.   But I do think they should all
                be Legal and everyone should educated on there effects.
                The choice should be ours.... Mycal

(C) 1990 Mycal Johnson All Rights Reserved.  Distribute this post in anyway
        for non commercial use.

In article <1990Nov16.011656.2696@everexn.com> mycal@everexn.com (Mike Johnson) writes:
>        Remember the L-Tryptophan scare a little while ago?  Well I have
>been thinking about it and have come up with a conspiracy theory.  It
>may be off base but it was fun to come up with it.

I'm pretty sure the ~5000 reported cases of EMS (eosinophilia-myalgia
syndrome) and 27 deaths, and their connection to a batch of Showa Denko
tryptophan is real.  But, I do like a good conspiracy...

>        Ever since the War on Drugs the government has become increasingly
>protective of precursors for drug manufacture.

Not too many years ago any old Joe could buy isosafrole (precursor to MDA)
or phenylacetone (precursor to amphetamine) and all necessary apparatus
and ancilliary chemicals with no more than a money order, [fake] signature,
and the address of, say, a vacant house or apartment.  Nowadays it seems
even MEK (methylethylketone) is difficult to obtain.

>        So maby the government generated the Trypto scare so people would
>be scared to buy/use it and stores would take it off their shelves.  Has
>anyone on the net known anyone who got sick from L-Tryptophan?

Considering the numbers above, it's not surprising that noone has reported
any first-hand experience with tryptophan-related EMS.

If we believe the EMS problem is real, and government-generated, this
would make for an intriguing conspiracy.  Let us also add that many are
eagerly pointing the finger at genetic engineering as the root cause of
the problem.  Showa Denko used a bacillus genetically engineered to produce
higher yields of tryptophan.  Now, can someone postulate a role for
Lyndon LaRouche?

>        The following is a simple reaction to synthesize DMT from Tryptophan.
> ...
>WARNING... This is something I just came up with and may work but I am no
                              ^^^^^^^^^^^^^^^^^^^
Admit it, you did research!  Well, conspiracies do need some grounding in
fact.

>        The first reaction is using Trypto and Sodium HydroChlorite (AKA
>Chlorox)                                             [hypochlorite]

You are perhaps refering to

    R. A. Gray [Pineapple Research Institute of Hawaii]
    Preparation and Properties of 3-Indoleacetaldehyde [IAc]
    Arch. Biochem. Biophysics 81, 480-8 (1959)

Not merely "AKA Chlorox [sic]", but Clorox was the actual reagent!

Aldehydes can be difficult to prepare (contrast to ketones) as they are
easily oxidized to acids.  Special care was taken by Gray to prevent this,
and IAc was actually obtained as the bisulfite addition product, "which
was stable for many years."

>        The second reaction is the IAA and Dimethyl Formamide in a 1:4
>reaction to produce DMT.

Dimethylamine is really the reagent of interest here (which you did
indicate in your drawings).

>solvent easy to get and not controlled.  This reaction is documented in a
>paper called the 'Leukart Reaction'.  This paper should also have the

The Leukart-Wallach reaction is well-known.  The original publications are

    Leukart
    Chem. Ber. 18, 2341 (1885) {Ger.}

    Wallach
    Ann. Chem. 272, 100 (1892) {Ger.}

Formic acid or a formamide is used as a reducing agent. DMF
(dimethylformamide) is probably to be prefered as IAc is not stable in
acidic solution.

>Disclamer :
>                The above may not be even remotely correct.  I myself

As an outline it was pretty darn good.  You've shown there's no reason
people outside a particular field can't learn some factual information
about current topics.  Although I'm sure it's not necessary, I will add
that a list of reagents does not a synthesis make!

So, yes, it's not difficult to make DMT from tryptophan.  But it's also
not difficult to make DMT from many other starting materials.  Indole
itself is readily 3-substituted (but note that indole has a horrible,
intense fecal odor!) and there are also many well known reactions to
produce directly 3-substituted indoles from simpler precursors.

Now, do more than a handful of people actually know about DMT?  I guess
it must have had some use in the '60s, but I don't recall ever hearing
it mentioned in the press as a drug of abuse.  Perhaps it has made come-
back?  If people will lick toads for bufotenine, well, there's just no
telling...

It may be the case that peoples' desire for drugs is matched by their
ingenuity to discover and re-discover many substances.  If so, the WoD
officials have a lesson to learn.  Granted the analogue drug bill
effectively makes many known and unknown chemicals illegal, it may yet
become a burden simply to keep the testing and analysis procedures up to
date.
--

smaschue@ucsd.edu (root) [Sean] writes:
>Also, while I am asking...Simon & Schuster's guide to House Plants enumerate
>many plants that are rumored to have narcotic properties as common house
>plants or curio plants.  Datura for one and mimosa pudica (sensitva) I have
>heard contain DMT?  Are there sources for these plants and publications on
>their properties?
>...doesn't this seem very interesting?

Sure does. Where'd you hear about Mimosa pudica containing DMT?
There are two species of Mimosa that have been used in the Amazon
that certainly contain DMT: Mimosa hostilis and Mimosa verrucosa.
A hallucinogenic drink called Jurema was made from the roots of
Mimosa hostilis.

A taped interview with Dennis McKenna from 1985 makes mention of several
other members of the pea family (Leguminosae) that contain DMT:
Acacia flabiphylla, which I haven't been able to find any reference
to anywhere else, and Desmodeum (only the genus was mentioned, the common
name for these are "Tick Trefoil"). An tree in this same group is
Anadenanthera peregrina, seeds of which are used for psychedelic snuffs in
the Amazon, and which also grows in the West Indies, including Puerto Rico.

(This tape, "Dennis McKenna/2 (1985)", is available from:
 Something's Happening Productions, Box 8381, Universal City, CA 91608)

In another tape Dennis' brother, Terence, made passing mention of
a plant, Desmanthus illinoensis, that was recently discovered to contain
DMT as 6% of it's dry weight, according to his report. Desmanthus is
closely related to Mimosa, and grows in the midwestern prairies of
the continental US.

If you run across a specimen of this in a University's botanical collection,
or in the field, I'd like to know about it.  Preserved or living specimens
in herbarium collections almost always include the date and place they
were collected.

Desmanthus illinoensis is listed in
_Petersen's Field Guide to Eastern/Central Medicinal Plants_
but the drawing is misleading. (It shows the pinnae of the compound
leaves as alternating instead of opposite). The best illustration I've
run across is in
 _An Illustrated Flora of the Northeastern United States and Canada_ Vol.II
where it's listed as Acuan illinoensis. Unfortunately the measurements
for various features of the plant are in error there.
Decent descriptions are found in the
_New York Botanical Garden Illustrated Encyclopedia of Horticulture_ and
the _Standard Encyclopedia of Horticulture_ Vol 2.


Two other plants reputed to contain DMT are Desfontainia spinosa, a
holly-like ornamental plant available at some nurseries, and
Arundo donax, the Giant River Reed, (used for clarinet reeds among other
things) which grows all over the place along rivers and in urban
environments where it's used for landscaping. The rootstocks of Arundo donax
are supposedly DMT-bearing, but there's never been a report of Arundo
being used as an hallucinogen, or even that such use is practical.
---------------------------------------------------------------------------

As far as Datura and other plants in the nightshade family (Solanaceae)
are concerned, they contain anticholinergic alkaloids like hyoscyamine,
atropine or scopolamine, none of which are considered psychedelic, but
which do cause delirium and hallucinations and are quite toxic and risky.





--------------------------------------------------


Here is the second in a series of "Gracie and Zarkov" articles.

-- Chris

============================================

DMT - HOW AND WHY TO GET OFF
. . . a note from underground
by "Gracie and Zarkov"

Copyright December 1984 by Gracie and Zarkov Productions. We believe that
in a truly free society the price of packaged information would be driven
down to the cost of reproduction and transmission.  We, therefore, give
blanket permission and encourage photocopy, quotation, reprint or entry
into a database of all or part of our articles provided that the copier
or quoter does not take credit for our statements.
Revised August 1985.

Number 3.

DMT, (N,N-dimethyltryptamine is not orally active (by itself), and must
be smoked to experience its effects.  Tolerance for the drug builds
almost immediately.  If you don't get enough in the first 30 seconds,
smoking more will not put you into the far out visionary DMT state, but
will only result in a more "ordinary" hallucinogenic state. If on an
attempt, you don't get enough, you must wait at least one hour before
trying again (smoking multiple doses within the hour can result in you
seeing the patterns but it is almost impossible to break through to the
extreme states described below).  Furthermore, the actual mechanics of
smoking DMT can be quite tricky.  In our experience, without careful
attention to technique, about half the DMT shots misfire.  Therefore, it
is essential to use effective technique in order not to waste the drug.
In this paper we offer three different tested techniques in an easy to
follow step-by-step format;  We have also included our description
(however inadequate) of what a DMT trip is like.

We are well aware of how scarce a substance DMT is.  We had to undertake
a long, intensive search to secure a supply of this marvelous drug in the
smokeable, freebase form.  The search was well worth it!  One of the
reasons for writing this paper is, hopefully, to increase the demand for
DMT.  If this paper intrigues you, we suggest that the you seek out a
supply of your own.  Laok for DMT in the smokeable freebase, not
hydrochloride form.  You will not be disappointed.

Getting Ready1.  We recommend a uniformly, though not brightly, lit room.  Unlike with
mushrooms, in total darkness the DMT visions are rather drab.  In full
sunlight the colors are unbelievably intense with red and gold
predominating but we feel that bright sunlight tends to obscure some of
the intricate detail so characteristic of DMT visions.  We usually do it
during the day in a room that is brightly lit with indirect light.

2.  Get comfortably seated where you can lie back and rest your head
during the trance.  If you smoke DMT standing up, you will almost
certainly fall on your ass if you get a good hit!

3.  We recommend a dosage of about 40-50 mg.  The dosage should be
weighed out and not eyeballed.  Dosages below 25 mg yield only physical
and threshold psychedelic effects.  Dosages between 25 mg and 40 mg are
usually not enough to display the full range of the unique DMT effects
described below.  Dosages in excess of 55 mg, particularly if you are
successful in holding all of the vapor in your lungs, can be VERY heavy
and are not recommended for f irst time users.

Method One:  The "Freebase" Method

4a.  Obtain a "freebase" airpipe such as the one illustrated below.  Use
with the largest funnel type bowl you can find.  Insert the largest fine
mesh stainless steel screen that will fit into the bowl.  Then sprinkle
the DMT uniformly over the center of the mesh screen.  Make sure to keep
thE DMT away from the edges of the screen so that when it melts it does not
run over the edge of the screen.

     \  /
\\  __||__            _==_        ________________
 \\/  ||  \          |    |____  / _______________
  \   ||  |          |     ___ \/ /
   |  ||  |          |    |   \  /
   |      |          |    |    \/
   \______/           \__/

FREE BASE AIR PIPE   CLASSIC DMT PIPE

5a.  Hold a match or torch above the screen and inhale deeply and slowly.
Do not let the flame touch the DMT as this will destroy much of the drug.
DMT melts and vaporizes easily so the point is to let the hot air rushing
by the flame into the pipe vaporize the DMT.  It is quite easy to
vaporize the DMT and end up with the airchamber full of white DMT vapor.

Method Two:  The Classic Psychedelic Ranger Method

4b.  If you hanq out around a good glass blower or long time "head" you
might be able to obtain a classic DMT pipe such as the one illustrated.
Load the DMT into the glass reaction chamber and heat the outside bottom
of the chamber with a flame.

5b.  When the white vapor appears, breathe in deeply and slowly.  If you
inhale too soon or too quickly, the powdered DMT will be blown down your
throat.  It is not active that way.  Make sure that all of the DMT is
vaporized.  In the absence of a classic DMT pipe, some people use a
regular "hash oil" pipe heated from the outside.  We find this too tricky
to be reliable.  You are just as likely to end up with boiling liquid DMT
in your mouth.  (That's why the classic pipe has a "V" shaped stem.)  We
personally use the "freebase" method.

In either case...

6.  The smoke is very harsh.  It tastes like burning plastic.  It isn't
particularly hot, but you will have a tendency to cough.  On each toke
try to hold your breath for as long as possible.  Exhale and immediately
take a second toke.  The physical effects, a buzzing or vibration
throughout your whole body, come on first.  The intensity of these
effects is not a reliable guide to the dosage of DMT that you have
consumed.  Keep taking lungfuls and holding them until all of the
premeasured DMT is consumed.  Gracie suggests that the best way to smoke
DMT is to try to smoke as much as you can before you inevitablly fall
into a trance.  While not recommended for beginners, it does capture the
approach you should take towards smoking your premeasured dose.

One advantage of the "freebase" method is that the 50 mg of DMT can be
divided into three toke sized piles.  The smaller amount can be easily
vaporized and inhaled in one breath with the screen being reloaded with
DMT after each toke.

7.  Just as you feel yourself "going over the top", exhale.  Breathe
normally, close your eyes and enjoy the visions.

Your companions should be instructed to take the pipe from you when you
close your eyes because you will have poor motor control. Since you will
be in a trance for 4-8 minutes, you should also have told them not to
disturb you.  To them you will look like you are asleep.  This is not a
social drug or one to be taken casually; you will be entranced.

8.  When you come our of the trance, remain seated for about 10 more
minutes as you will still have only shaky control of your limbs.

9.  In 30 minutes from the time you started you will be pretty much down,
but still euphoric.  You will be completely down after a total of about
one hour.

1O.  We do not recommend that DMT be combined with other drugs.  It
should be done on a clean head.  Marijuana fogs the effects.  It is not a
party drug:  the effects are most entertaining experienced in a quiet
room.  When DMT is smoked at the peak of a mushroom or LSD trip, the
effects are spectacular, but only recsmmended for the experienced, most
brave (or some might say, most foolhardy) of investigators.  The effects
used at the peak of another psychedelic can last for several hours.

NOTES ON THE VISUAL STAGES OF A DMT TRIP:

0 - 20 seconds - a scratchiness in the lungs

20 - 30 seconds - a buzzing starts in the ears, rising in tone and volume
to an incredible intensity. Its like cellophane being ripped apart (or
the fabric of the universe being torn asunder). Your body will vibrate in
sympathy with this sound, and you will notice a sharp blood pressure
rise.  You may feel like you are deeply under water.  Wearing a unitard
or leotard and tights helps to minimize this sensation.  Your visual
field will also vibrate in resonance to the sound and will finally be
completely obscured by the visions.

30 seconds - 1 minute - You break through into DMT hyperspace.  Often at
this point, users believe that their hearts or breathing have stopped.
This is not true.  To an outside observer, you are breathing normally and
your pulse, while elevated, is strong.  We believe that this subjective
effect is due to your "internal clock" being slowed so greatly that the
subjective time interval between breaths or heartbeats seems like an
eternity.  Synthetic DMT has been extensively tested by medical
authorities here and in Europe.  It is perfectly safe with no lasting
physical effects at these doses.  However, since smoked DMT causes an
abrupt blood pressure increase, it is probably not good for people with
abnormally high blood pressure.

1 minute - 2 - 5 minutes - depending on dosage:  DMT hyperspace.  For all
practical purposes, you will no longer be embodied.  You will be part of
tne intergalactic information network.  You may experience any of the
following:

o  Sense of transcending time or space
o  Strange plants or plantlike forms
o  The universe of formless vibration
o  Strange machines
o  Alien music
o  Alien languages, understandable or not
o  Intelligent entities in a variety of forms

Do not be amazed and do not try to actively direct your observations but
merely pay attention.  The beings can show you amazing things, but if you
try to impose vour personal trip on the DMT you will find that you cannot
and may become frightened.

At the end of the "flash" of the visions you will have an after-vision of
circular interlocking patterns in exquisite colors. It has been described
as looking at a vaulted ceiling or dome.  If you did not "breakthrough"
to the levels described above, this "chrysanthemum" pattern, as we call
it, is all you will see.  It is worth the trip, too.

You may begin to wonder how you will ever find your way back to your
body.  If you have taken enough DMT to fully "breakthrough", by the time
you can even wonder about it, you are almost back.  Trust in your own
wetware; your psyche and your body will be reunited. Worrying will only
prolong the process.

5 - 12 minutes - The visions have subsided. There are still patterns when
you close your eyes, but with eyes open the world is back. At this point
a flood of information may rush through your mind. The phase is fleeting.
In order to preserve your DMT ideation, we recommend that you begin
talking as soon as you come out of the visionary state.  Don't try for
complete sentences but get as many ideas out as you can while you can.
Have a tape recorder running during the trip and you can review your
thoughts at a later time.

15 - 30 minutes - The ideation flood subsides leaving you euphoric.  You
may still have a trace of the vibrations in your body.

30 - 60 minutes - The euphoria subsides.

60+ minutes - You are completely down.

Note:  While we recommend above not to combine DMT with other
hallucinogens, we have had excellent results using DMT as a "pre-dose"
for LSD, MDM, MDA, or mushrooms.  The technique is to take the second
hallucinogen orally just as you come out of the vision state.  The
resulting trip will be more profound and will help you to understand the
strange and alien vistas which you were shown while on the DMT. (For more
details, see our Note from underground no. 4.)

Method Three:  The Tryptamine Giggles

If the description of the DMT effects sound too heavy for you, (we
certainly don't deny that DMT can be a heavy trip) 25 mg of DMT can be
mixed with some dope in a joint or in a pipe and smoked in a liesurely
fashion.  The giggley mood lift is quite pleasant.  The occasional
breaking through of abstract hallucinatory patterns can liven up an
otherwise quite ordinary stoned-again evening.  However, we would
recommend that before you burn up all your DMT in this fashion that you
at least try one high dose trip as described.

Finally, while there is no such thing as a "typical" DMT experience, we
have attached a note of ours (reprinted from High Frontiers, issue 2) to
this paper which describes one of our DMT trips.  The most accessible
information on DMT is Peter Stafford's Psychedelics Encyclopedia.
Terence McKenna, who offers, in our opinion, the most sophisticated
analysis of the DMT experience, has two excellent cassette tapes which
discuss the DMT state:  Mind, Molecules &Maqic. June 1984; and Tryptamine
Hallucinogens and Consciousness,  December 1982.  They are available from
Dolphin Tapes, P.O. Box 71, Big Sur, CA  93920 for $9.00 plus tax and
$2.00 postage.

=============================================================================

a hit of dmt 10/9/84 - zarkov

i loaded about 40-50 milligrams of dmt into a glass pipe on top of a
small amount of damiana.  even though i had been warned, i was still
shocked at how harsh the first toke was.  it tasted and smelled like
burning plastic.  i involuntarily exhaled.  i immediately took a second
toke.  the heavy white smoke rushed up the pipe as harsh as before, but i
was somewhat better prepared for the terrible taste and i was able to
hold the smoke for a few seconds.  i exhaled, took a third toke, and was
able to hold this last lungful.  suddenly i began to hear a loud,
moderately high-pitched carrier wave.  immediately, the room started
vibrating in sympathy.  the pattern on the wall hangings oscillated madly
in time to the buzzing that overlaid the carrier waves fundamental tone.
simultaneously, a heavy, trembling feeling swept over my entire body as
if i were being propelled at multiple g acceleration by some giant rocket
engine.  my visual field dissolved in the most amazing colors.  i could
not see the room over the intensity of the visual effects.  the events of
the preceding paragraph occurred in the space of a few short seconds.

closing my eyes, i got a glimpse of several entities moving in front of a
giant complex control panel.  the visions were not crystal clear and
seemed as if i were viewing it through a scrim.  the creatures were
bipedal and of about human size.  it was impossible to say more other
than they did not move like the giant insect creatures i have seen
clearly under the influence of stropharia mushrooms.  there was a direct
awareness of an overwhelmingly powerful and knowledgable *presence*!  it
was neither frightening, nor encouraging.  it was just mentally there.  a
thought came, unbidden, into my head.  i realized that i was viewing god
central.  the central panel i saw was the control panel for the entire
universe.the vision was fleeting and dissolved into a vision of much greater
clarity.  a gaggle of elf-like creatures in standard issue irish elf
costumes, complete with hats, looking like they had stepped out of a
hallmark cards happy saint patricks day display, were doing strange
things with strange objects that seemed to be a weird hybrid between
crystals and machines.

this vision was also fleeting, and it dissolved into a visual pattern
unlike that experienced by me on any other psychedelic or combination of
psychedelics.  the visuals were interlocking sinusoidal patterns arranged
in a japanese chrysanthemum pattern that filled my entire visual field.
the pattern was ever-changing and the colors of the individual patterns
changed independently of the underlyng pattern.  the colors were intense
and came in a magnificent variety of colors: metallics, monochromes,
pastels, each flickering in and out of existence as if obeying some
undetected ordering principle.

an idea came into my head that i was seeing the true universe or
universe as it really exists.  that is to say, i was seeing *directly*
the vibrations of every particles in the universe that i was somehow in
contact with.  i was directly seeing the universe withough ordering
it into an arbitrary reality tunnel -- i.e., perceived solid, objective
reality.  the visual pattern seemed to be a sort of m-dimensional
lissajous curve formed by the intersection of i with the shock wave of
space-time causality.

the carrier wave remained strong throughout the experience.  while
definitely the same type of phenomena as the carrier wave heard under the
influence of psilocybin mushrooms, the dmt carrier wave was *much* louder
than even the loud carrier wave heard under the influence of ten grams of
very potent, dried stropharia mushrooms.  also, by comparison to the
mushroom experience, the carrier wave sounded as a purer tone -- i.e.,
the sinusoidal component dominated the buzzng component.  my throat was
too sore from the harsh smoke and the control of my breathing was
hindered by the intensity of the expereince, so i was unable to sing or
even generate a solid tone, to attempt audio driving of the visuals.

the overwhelming sense of a *presence* did not disappear when the vision
changed to visual patterns, but remained an almost palpable entity as lon
as the visuals remained intense.  i never felt the foreboding -- let
alone the direct challenges -- i have felt under the influence of
stropharia mushrooms whenever the feeling of contact with the presence
has been strong.  the presence was just there and *very* powerful.  i
felt that i had glimpsed whiteheads god.

the period of intense visuals lasted about eight minutes.  the side
effects remained unpleasant, but easily ignorable.  the dmt left me
euphoric and very bemused for about an hour.

definitely far out and very impressive!



--------------------------------------------------

>
>
> 	After reading the 'Time and Mind' article kindly typed in by Bob
> 	I am intrigued to hear more about DMT, I was always under
> 	the impression that LSD-25 was the strongest hallucinogen available
> 	but even under the influence (of some pure liquid) it has always been
> 	the real world around me that was distorted in some way and not some
> 	fantasy land (although you could imagine it to be a fantasy land, the
> 	very fact that you are conciously imagining it to be real is constantly
> 	reminding you that its not.)
>
> 	So is DMT that superior an hallucinogenic?

There are three issues here which are a little confused:
1) strength in the sense of effective dose,
2) strength in terms of subjective intensity,
3) being a superior hallucinogen in some subjective sense.

Comparing DMT and LSD, the first is easy.
The effective dose of LSD is around 100 ug, of DMT is around 60 mg,
so in this sense, LSD is a much stronger hallucinogen.

In terms of intensity, they are difficult to compare. Part of the intensity
of DMT stems from the fact that the onset is virtually instantaneous;
one is taken from feeling normal to the peak of the trip in the space
of a few seconds, and this can be totally disorienting and frightening.
DMT does not have the euphoria of LSD, in fact it can be quite
uncomfortable. Also, the smoking of DMT is quite unpleasant compared
with eating some small object. The types of hallucinations experienced
within the peak of the DMT trip differ markedly from those in the peak
of the LSD trip. This difference is very hard to describe, although
one might contrast the dripping flowing colourful experience of LSD
with the DMT visuals in which everything becomes super sharp to the
point of being ripped into fragments, like placing a photo in a blender.
There is some colour enhancement, but it is more like lightning-bolts
of colour rather than flowing ripples of colour, and colours may
be actually entirely changed and several multiple images seen at once.
The 20-30 minute come-down of DMT is similar in experience and intensity
to a small dose of LSD, however one is likely to be too shattered by
the initial peak to worry about this much. The account Bob posted is
highly subjective and metaphorical (as is this one, I suppose) and I
doubt that many people would experience DMT in the way described there.
However, extending the duration of DMT by the use of monoamineoxidase
inhibitors (Ayahuasca,Yage,etc.) is supposed to be a very intense
experience and could give one time to become more involved in it.
It is possible to lose all contact with the senses and the world
briefly while on DMT, as it is, e.g. from a combination of nitrous
oxide and LSD. Also, psiloc(yb)in seems to have some similarity to
DMT whilst retaining similarity to LSD, in that during the psilocin
experience one can be transported into a different reality, although
one which is still definitely based sensually on this one, and
not be able to remember or understand everday reality.
Other hallucinogenic experiences, e.g. the delerium caused by
anti-cholinergics, might be still more intense than DMT in terms
of being completely removed from traditional reality, but I don't
think anyone would recommend experimenting with these dangerous
substances.

In terms of which is the superior hallucinogen, it depends on your
taste. DMT is very interesting and extremely intense, but not
necessarily pleasant. LSD has more potential for pure recreation.
Most people would probably prefer LSD as a recreational hallucinogen,
and it would be ill-advised for someone who was not very familiar
with coping with the intensity of LSD to be thrust into the
intensity of DMT. On the other hand, if you don't like DMT, you only
have to hang on for a few minutes, whereas if you don't like LSD
you have to hang on for several hours.

This is, of course, apart from the dosage, all subjective.

..............................

> Does anyone know if 4-MeO-DMT is pharmacologically active?
> This would be the methyl analog of psilocin, 4-OH-DMT of
> mushroom fame.
>
> Shulgin, among others, has made a number of tryptamine analogs.
> This one seems like a logical target but I have never seen it
> in the literature.  Does anyone have any information on this
> compound?

Here is the best I can do to answer this:
Extract from Hallucinogens: Neurochemical, Behavioral, & Clinical
Perspectives, edited by B.L. Jacobs, Raven Press, New York (c) 1984

Medicinal Chemistry and Structure-Activity relationships of Hallucinogens
- David E. Nichols & Richard A. Glennon
p. 124

"
4-methoxy-N,N-dimethyl tryptamine (4-OMeDMT) has been examined only in
animal studies and has shown behavioral activity roughly comparable to
that of DMT (65,236,238). It has also produced discriminative stimulus
effects similar to those of 5-OMeDMT with a potency somewhat less than
that of DMT but greater than that of either 6-OMeDMT or 7-MeODMT (93).
In drug discrimination studies using DOM as the training drug, 4-OMeDMT
was more active than DMT but less active than DET (91).

References:
(65)
Gressner, P.K., Godse D.D., Krull,A.H.,& Mc Mullen, J.M. (1968)
Structure-activity relationships among 5-MeODMT, 4-HODMT (psilocin)
and other substituted tryptamines. (life Sci., 7:267-277)

(91)
Glennon, R.A., Young, R., Jacyno, J.M., Slusher, R., and Rosecrans,J.A.
(1983)
DOM stimulus generation to LSD and other hallucinogenic indolealkamines.
Eur.J.Pharmacol.,86:453-459

(93)
Glennon,R.A.,Young,R.,Rosecrans,J.A.,& Kallman,M.J (1980): Hallucinogenic
agents as discriminative stimuli: Correlation with serotonin receptor
affinities. Psychopharmacology, 68:155-158.

(236) Ulyeno, E.T. (1969): Alteration of a learned response of the
squirrel monkey by hallucinogens. Int.J.Neuropharmacol. 8:245-253.

(238) Ulyeno, E.T. (1971): relative potency of amphetamine derrivatives.
Psychopharmacologia 19:381-387



..............................


Check out these. Looks like you already have the articles about
Acacias from the Australian Journal of Chemistry.


-----------------------------------------------
J. Agriculture and Food Chemistry 35:361-365
(1987) Thompson, A. C., Nicollier, G. F. and Pope, D. F.
"Indolealkylamines of Desmanthus illinoensis and their growth
inhibition activity."
-----------------------------------------------
Smith, T. A. (1977) "Tryptamine and related compounds in plants."
Phytochemistry 16:171-175.
An excellent short guide to the literature for many
tryptamine-containing plants.
-----------------------------------------------


I'm having trouble uploading to this Usenet node, otherwise I'd send
you excerpts from several related articles.


------------------------------
marsthom@qed.cts.com (Mark Thompson)  or  qed!marsthom
The QED BBS -- (310)420-9327


..............................

>Can anyone tell me about this drug (IT-290)?  Especially if it really exists.

IT-290 is alfa-methyltryptamine. It's an orally active psychedelic
tryptamine, dosage about 30 mg.
..............................

Article 38451 of alt.drugs:
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From: mtymp15@staff.tc.umn.edu (David Hutton)
Subject: New posting: DMT FAQ
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                         How To Make DMT

DMT stands for N,N-dimethyltryptamine. It is a semisynthetic
compound similar to psilocin(the hallucinogenic substance in
psilocybin) ins structure. The most common method of ingestion is
smoking. Soaked parsley leaves are the usual method of ingestion
although persons have dipped marijuana in it and said the
experience was fantastic. The following recipe can be performed in
the kitchen.

Recipe for DMT:

Mix thoroughly and dissolve 25 grams of indole with a pound of
dry ethyl ether in a 2000 ml flask(2 quart jar.)

2. Take an ice tray and fill with chipped or shaved ice. Cool
solution for about 35 minutes until it reaches 0 degrees C. At the
same time cool 50 ml dry oxalychloride to about 5 degrees below 0
C. in the same ice tray.

3. VERY slowly add the oxalychloride solution to the indole
solution. These two chemicals are highly reactive. Avoid boiling
over, contact with skin, and fumes.

4. Wait until all the bubbling has died down, then add a few
handfuls of table salt to the ice tray, to cool the solution
further. Label the solution "solution 1" and put it in the
freezer.

5. Cool 100 ml. of dry ethyl ether in a 500 ml. flask to 0 degrees
C. in a salted ice tray. At the same time cool an unopened bottle
of dimethylamine to 0 degrees C. in the same ice bath.

6. Open the seal of the dimethylamine bottle and slowly pour a
steady stream into the ether. Label "solution 2."

7. Very slowly and carefully add solution "1" and "2" together.

8. Now take the mixed solutions from the ice tray and bring up to
room temperature stirring the solution all the time. You should be
left with a solution that is almost clear. If it is still murky,
continue stirring until it becomes as clear as possible.

9. Now filter the solution to seperate the precipitate by suction.

                       <---Solution and Precipitate
        ------------
        \          /<---Funnel  /    / <-- Rubber hose to
         \        /     and    /    /      Vacuum source
          \      /      Filter/____/
     \*****\    /*************{   }*****/ <--- Two hole
      \****{    }*************{   }****/       rubber stopper
       \   {    }             {   } <-/--- Glass Tube
        \  {    }             {   }  /
         | {    }             {   } |
         |                          |
         |                          |
         |                          |
         |                          |
         |__________________________|
                  Figure A.

10. Refilter with suction after pouring technical ether over the
precipitate.

11. Repeat filtering once more with ether, then twice with water.

12. Let this substance dry on a plastic or china plate.(do not use
metal) After drying, a solid material will be formed. Take
particles and place them in an 800 ml beaker.

13. Mix 100 ml. benzene with 100 ml. methyl alcohol. After this
mixture has been stirred, cover solid particles from step 12 with
about 1/2 inch of the solution and heat the beaker in water until
all solid material had dissolved. Add more solvent if
necessary.(Note: Do not place beaker in water bath directly over
the flame.)

14. After all solid material has dissolved, remove beaker from the
heat, and allow to cool. As it cools, small needle-shaped crystals
will appear. When this happens, try to pour off as much solvent as
possible without disturbing the crystals.

15. Place crystals in a 1000 ml flask and dissolve in
tetrahydrofurane.(Use only as much as absolutely necessary.) Label
this solution "A".

16. Slowly mix 200 ml. tetrahydrofurane and 20 grams lithium
aluminum hydride in a 500 ml flask, and label it solution "B".
(By the way, lithuim aluminum hydride ignites on contact with
moisture. Protect eyes and hands.)

17. Mix solutions "A" and "B" slowly, stirring constantly.

18. Prepare a water bath and heat solution for three hours,
stirring for four minutes every half hour. When not stirring, make
sure to use aspirator tube.
                             /  / <--- Rubber Tubing
                             ---
                         \**{   }**/<---- One hole rubber stopper
                         /**{   }**\      and glass tubing
                        /   {   }   \
                       /    {   }    \
                       :             :
                       :             :
                       :             :
      \ ~~~~~~~~~~~~~~~:_____________:~/
       \______________________________/

           Heat source

           Figure B.

Place Figure B. flask at a higher level than Figure A. flask. Run
tube from Figure B. flask down to left side of figure A. flask,
replacing funnel with glass tubing. Disconnect right side tube
from vacuum source. This will be used as the aspirator tube.

19. When this is completed, allow the flask to remain at room
temperature for about 20 minutes. Then place in salted ice bath,
and cool to 0 degrees C. Add a small amount of chilled methanol,
stirring gently until solution appears murky.

20. Filter this murky solution through a paper filter in a funnel,
and collect the filtered liquid in a flask.

21. Add 100 ml. of tetrahydrofuran through the filter and collect
in the same flask. Now heat the solution in a water bath until
most of the tetrahydrofuran is evaporated and a gooey substance
remains.

22. Place