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)
References & Further Reading:
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.
..=2E............................
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,
Sun****ne, Tabs, Ticket, Twenty-five, Wedding bells,
Windowpane,
etc.
..=2E............................
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.
..=2E............................
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 =3D pupillary dilation)
..=2E............................
Hoffman thought the diethylamide version of the lysergic acid
molecule
might be a respiratory stimulant... (see _Problem Child_ by Hoffman)
..=2E............................
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.
..=2E............................
>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."
..=2E............................
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.)
..=2E............................
[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.
..=2E............................
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.
..=2E............................
>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 re****ted 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
re****ted 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 re****ts LSD as being >96% pure or blank (If I remember
correctly)
--
the rest most likely is substitutes, but it wasn't re****ted in the
analysis.
..=2E............................
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 flu****ng effect).
Remember that odd bodily sensations are normal and not harmful.
******************************
>From page 8 of Robert Anton Wilson's *** 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 tem****ary 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 tem****ary (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
***ulative 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 re****ts 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...
..=2E.
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 ****d
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 re****ts 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 astoni****ngly 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.
..=2E............................
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.
..=2E............................
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.
..=2E............................
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).
..=2E............................
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=2Ev. in mice. Of course, it would take lots more p.o. to kill
someone.
The re****ted 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.
..=2E............................
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 Re****ts. 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."
..=2E............................
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 pro****tion
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 im****ant 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 dimini****ng 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 re****ted 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 relation****p to his
mother. (See also Horowitz 1969; ****ck 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).
..=2E............................
"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
..=2E............................
"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=2E 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 re****ted.
>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.
..=2E............................
"Burger's Medicinal Chemistry" Fourth Edition, Volume III
Chapter: "Hallucinogens" Alexander Shulgin
Composition, % of total alkaloids present
=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=
=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D
Compound R. corymbosa I. violacea
=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D
=3D=3D=3D=3D=3D=3D=3D=3D=3D=
=3D=3D=3D=3D=3D=3D=3D
=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=
=3D=3D=3D=3D=3D
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 sup****ting 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).
..=2E............................
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 re****ted 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
re****ted 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 re****ted
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 re****ted
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 rap****t
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 re****ted 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 sup****tive, therapeutic setting as re****ted 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 re****ted side effect, beginning about one half hour after
ingestion
and lasting a few minutes to several hours. Other re****ted side
effects not
commonly found with LSD were a drowsiness or tor**** (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).
..=2E............................
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 ****tion 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 re****ts 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.
..=2E............................
"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 im****tance 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 s*****onergic cell firing and seems to spare postsynaptic
s*****nergic
receptors. This preference is shared by other simillar hallucinogens
but in
a limited fa****on. Nonhallucinogenic analogs of LSD show no
preference.
These results suggest that there are two different steric
conformation
of
s*****onergic 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 s*****nergic 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.
..=2E............................
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.
..=2E............................
(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 s*****onin
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 sup****t 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=2ES. Snyder has tripped before =3D)
..=2E............................
>"If there's no do***entation, you can't tell bugs from features." ---C.P.
..=2E............................
>>Lysergic-acid diethylamide >> >>When ingested into the human body, LSD
act
as 5-HT (S*****onin) 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
im****tant 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 autorecet**** activity, but not necessarily directly.
>LSD also has effects on 5-HT1C receptors, and its not entirely sure what
t=
he
>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
halluci=
natory
>>effect. We are in effect dreaming while completely awake and aware.
>Actually, a better explanation is the increased firing of the locus
coerel=
eus
>by its disinhibition due to the neurons in the raphe slowing down (since
y=
ou
>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
a=
lso
>been associated with feelings of anxiety, and theorized that its invovled
>with depression. My guess is that the hallucinations and stimulatory
effe=
cts
>of LSD come from potentiating the l.c., while the effect on the 5-HT
neuro=
ns
>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 s*****onin, 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.
..=2E............................
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
re****ted 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: <221302Z24111...@[EMAIL PROTECTED]
>
Newsgroups: alt.drugs
From: an152...@[EMAIL PROTECTED]
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
h=2E..@[EMAIL PROTECTED]
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 re****t any problems, inappropriate use etc. to
a=2E..@[EMAIL PROTECTED]
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
..=2E............................
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.
..=2E............................
>From the Merck Medical Manual, 16th edition, page 2652:
"S*****onin (5-HT) is the neurotransmitter of many central neruons (eg
raphe
nucleus). ITs synthesis begins with the uptake of tryptophan into
s*****onergic neurons. Tryptophan is hydroxylated by the enzyme
tryptophan hydroxylase to 5-hydroxytryptophan and then decarboxylated
to s*****ontin (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.
..=2E............................
++++++++++++++++++++++++++++++
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
s*****onin, 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
re****ted 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: <221302Z24111...@[EMAIL PROTECTED]
>
Newsgroups: alt.drugs
From: an152...@[EMAIL PROTECTED]
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
h=2E..@[EMAIL PROTECTED]
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 re****t any problems, inappropriate use etc. to
a=2E..@[EMAIL PROTECTED]
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
..=2E............................
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 s*****onin 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
re****ted 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=2Em. 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.
/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/\/
\/\/=AD\
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=2E215).
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
trans****tation 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.
=2E.............................
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 do***ented
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 <1990Nov16.011656.2...@[EMAIL PROTECTED]
> m...@[EMAIL PROTECTED]
(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 re****ted 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
re****ted
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
Tryptoph=
an.
> ...
>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 do***ented 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.
--
smasc...@[EMAIL PROTECTED]
(root) [Sean] writes:
>Also, while I am asking...Simon & Schuster's guide to House Plants
enumera=
te
>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?
>=2E..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 re****t. 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 re****t of Arundo
being used as an hallucinogen, or even that such use is practical. ...
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