From: gnosis@brahman.nullnet.fi (Gnosis)
Date: Sun, 12 Feb 95 10:08:22 EET
Newsgroups: alt.drugs
Subject: LSD Frequently Asked Questions [ FAQ ]
The Usenet alt.drugs LSD FAQ
Last updated 30 Dec 1994
Size 113 KB
Authors : dozens of people on the Net
Original editor: unknown
Previous editor: honig@buckaroo.ICS.UCI.EDU (David Honig)
Current editor: gnosis@brahman.nullnet.fi (Jani Poijarvi)
*****
NOTES:
[this is just the editor bitching about stuff, if you want to get down to
business skip to the next section]
The FAQ is currently suffering from 'virgins writing about sex' syndrome
since the current editor (me!) has never used LSD. I do have -some-
technical knowledge regarding the subject, and some of my friends have
used other psychedelics , but I do not
claim to be an expert, and I have merely tried to organize the previous
chaotic mess with little regard to finding out if the info within is actually
correct. Hence, if somebody more qualified than me wants the job, please
drop me note at the address above.
The primary change, aside from just cleaning up junk (spelling mistakes,
witty sig files, etc), has been the removal of over 100K of DMT info which,
while interesting, has no place in an LSD FAQ. Also, stuff that's "cute" but
really quite irrelevant (stories about people pitching no-hitters on acid and
crunchy PostScript graphics of the LSD molecule) has been omitted. It's all
available in separate files on hyperreal.com [now archived at erowid.org]
anyway. All told, the file shrank from nearly 290K to a more manageable 113K.
Lots of work still needs to be done. While the FAQ explains the background
and chemistry and all nicely, it does very little to prepare for the
user for the trip itself or the changes in mindset and attitude that
will most probably occur after the trip. I attempted to do something
about that by adding that little "Aftereffects" section at the end, but
that's not nearly enough. Input is very welcome.
*****
Synopsis / Table of Contents:
LSD (definition, introduction)
Delysid (medical fact sheet for pharmaceutical LSD, pharmacology)
Cautions, Real And Imagined:
Addiction Potential (none)
Adulterants (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 (caquired and lost quickly (3 days), no withdrawal)
Background:
Anthropology (and history)
Botany (sources in nature: mushrooms, ergot, morning glories,
hawaiian baby woodrose, tropical plants)
Chemistry (structure)
Mechanism of Action (uncertain)
Related Compounds (indoles: psilocybin, dimethyltryptamine (DMT) )
Manufacture (forget it)
Drug Testing (don't worry)
Legal Scheduling (sched. 1, no medical uses in US (despite past
effective use) )
Pragmatics:
Set and Setting (how to have a positive experience; LSD != beer)
Storage (keep in a cool dark dry place)
Combinations (cannabis is good, otherwise be careful)
Aftereffects (a user's viewpoint as to why it's a good thing)
References & Further Reading:
(Recommended)
_Psychedelic Encyclopedia_ by Peter Stafford
_LSD: My Problem Child_ by Albert Hofmann
_Licit & Illicit Drugs_ (Consumer Reports)
_Storming heaven : LSD and the American dream_ by Jay Stevens
*****
FORMATTING:
'*****' major division (usually a change of topic)
'.....' minor division (usually a change of author of text)
*****
LSD
Generic name for the hallucinogen lysergic acid
diethylamide-25. Discovered by Dr. Albert Hofmann in 1938, LSD is one
of the most potent mind-altering chemicals known. A white, odorless
powder usually taken orally, its effects are highly variable and begin
within one hour and generally last 8-12 hours, gradually tapering off.
It has been used experimentally in the treatment of alcoholics and
psychiatric patients. [Where it showed some success.] It
significantly alters perception, mood, and
psychological processes, and can impair motor coordination and skills.
During the 1950s and early 1960s, LSD experimentation was legally
conducted by psychiatrists and others in the health and mental health
professions. Sometimes dramatic, unpleasant psychological reactions
occur, including panic, great confusion, and anxiety. Strongly
affected by SET and SETTING. Classification: hallucinogens. Slang
names: acid, sugar. See also appendix B. (RIS 27:211-52 entries)
-- Research Issues 26, Guide to Drug Abuse Research Terminology,
available from NIDA or the GPO, page 54.
.....
Common Drug Slang Terms (NB: many of these refer to the carrier, ie, "Blotter"
or "Sugar Cubes". Often the local names will refer to patterns printed
on the blotter, eg, "Blue unicorn".):
Acid, 'Cid, Sid, Bart Simpsons, Barrels, Tabs, Blotter, Heavenly blue,
"L", Liquid, Liquid A, Lucy in the sky with diamonds, Microdots,
Mind detergent, Orange cubes, Orange micro, Owsley, Hits,
Paper acid, Sacrament, Sandoz, Sugar, Sugar lumps,
Sunshine, Tabs, Ticket, Twenty-five, Wedding bells, Windowpane,
etc.
.....
from the data sheet accompanying product:
(see also Physician's Desk Reference from mid-60's)
Delysid (LSD 25)
D-lysergic acid diethylamide tartrate
Sugar-coated tablets containing 0.025 mg. (25 ug.)
Ampoules of 1 ml. containing 0.1 mg. (100 ug.) for oral
administration.
The solution may also be injected s.c. or i.v. The
effect is identical with that of oral administration but
sets in more rapidly.
PROPERTIES
The administration of very small doses of Delysid
(1/2-2 ug./kg. body weight) results in transitory distur-
bances of affect, hallucinations, depersonalization, reliv-
ing of repressed memories, and mild neuro-vegetative symp-
toms. The effect sets in after 30 to 90 minutes and gen-
erally lasts 5 to 12 hours. However, intermittent distur-
bances of affect may occasionally persist for several days.
METHOD OF ADMINISTRATION
For oral administration the contents of 1 ampoule of
Delysid are diluted with distilled water, a 1% solution of
tartaric acid or halogen-free tap water.
The absorption of the solution is somewhat more rapid
and more constant that that of the tablets.
Ampoules which have not been opened, which have been
protected against light and stored in a cool place are
stable for an unlimited period. Ampoules which have been
opened or diluted solutions retain their effectiveness for 1
to 2 days, if stored in a refrigerator.
INDICATIONS AND DOSAGE
a) Analytical psychotherapy, to elicit release of
repressed material and provide mental relaxation, par-
ticularly in anxiety states and obsessional neuroses.
The initial dose is 25 ug. (1/4 of an ampoule or 1
tablet). This dose is increased at each treatment by
25 ug. until the optimum dose (usually between 50 and
200 ug.) is found. The individual treatments are best
given at intervals of one week.
b) Experimental studies on the nature of psychoses: By
taking Delysid himself, the psychiatrist is able to
gain an insight in the world of ideas and sensations of
mental patients. Delysid can also be used to induced
model psychoses of short duration in normal subjects,
this facilitating studies on the pathogenesis of mental
disease.
In normal subjects, doses of 25 to 75 ug. are generally
sufficient to produce a hallucinatory psychosis (on an
average 1 ug./kg. body weight). In certain forms of
psychosis and in chronic alcoholism, higher doses are
necessary (2 to 4 ug./kg. body weight).
PRECAUTIONS
Pathological mental conditions may be intensified by
Delysid. Particular caution is necessary in subjects with a
suicidal tendency and in those cases where a psychotic
development appears imminent. The psycho-affective lability
and the tendency to commit impulsive acts may occasionally
last for some days.
Delysid should only be administered under strict medi-
cal supervision. The supervision should not be discontinued
until the effects of the drug have completely worn off.
ANTIDOTE
The mental effects of Delysid can be rapidly reversed
by the i.m. administration of 50 mg. chlorpromazine.
[Erowid Note: Research by Aghajanian found that chlorpromazine
did not reverse LSD effects, but added its own new effects to
the LSD effects.
The book Chemical Warfare states:
"In a controlled study of its effects on scopolamine delirium,
however, George [Aghajanian] found not only that it didn't
work, but it made things worse. It deepened the stupor and
delayed recovery. Thorazine may have become popular, despite
a lack of true antidotal effectiveness, because it provided a
temporary respite to harried ER doctors." [Ketchum 2006, pg 121]
"[Aghajanian] George did find that it raised NF scores temporarily,
but did not shorten the overall duration of impairment. Surprisingly,
Thorazine sometimes even delayed the final return of performance
scores to baseline." [Ketchum 2006, pg 130]
There is no known way to "reverse" the effects of any psychedelic
although sedatives such as xanax or valium can help reduce some
of the uncomfortable related anxiety and are widely used in hospital
settings for 'bad trips'.]
SANDOZ LTD., BASLE, SWITZERLAND
9792*-Z1540 e.-sp./d.-fr.
Printed in Switzerland.
.....
~From: An Introduction to Pharmacology 3rd edition, JJ Lewis, 1964 (p 385)
Peripheral Actions
These include an oxytocic action and constriction of the blood vessels
of isolated vascular beds. In intact animals LSD causes a fall in
blood pressure, but its adrenergic blocking potency is low.
LSD causes mydriasis in man and other species. It also causes
hyperglycaemia and mydriasis, has a hyperthermic action and causes
piloerection. These effects are sympathetic in nature and are
abolished by ganglion blocking or adrenergic blocking agents.
Parasympathetic effects include salivation, lachyrmation, vomiting,
hypotension, and brachycardia. Low doses stimulate respiration but
larger doses depress it.
(NB: mydriasis = pupillary dilation)
.....
Hofmann thought the diethylamide version of the lysergic acid molecule
might be a respiratory stimulant... (see _Problem Child_ by Hofmann)
.....
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.
.....
"There is a great deal of superstition regarding purification of
psychedelics. Actually, any impurities which may be present as a
result of synthetic procedures will almost certainly be without any
effect on the trip. If there are 200 micrograms of LSD in a tablet,
there could only be 200 mics of impurities present even if the LSD was
originally only 50% pure (assuming nothing else has been added), and
few compounds will produce a significant effect until a hundred to a
thousand times this amount has been ingested. Even mescaline, which
has a rather specific psychedelic effect, requires about a thousand
thimes this amount."
.....
Note that: 1) on a piece of paper, vs. a tablet, you can't even add
significant amounts of adulterants 2) adulterants would cost, whereas
blank paper will rip someone off just as well.
LSD itself has some "body-kinks" on some people some times. Nausea is
one of them. its usually mild and transient. It also has speedlike
(ie, adrenergic stimulation) effects, etc.
(It is common for the uninformed to harbor fears (e.g., about adulterants)
instilled by ignorance and the current hysteria/propoganda. That's why this
FAQ exists.)
.....
[Referring to strychnine] 15 mg has been fatal, but a more typical fatal
dose is on the order of 50 mg. [Another post indicates 25 mg. as the LD50] 1
mg of strychnine orally probably has no observable pharmacological effects
in a typical adult. [1 mg being ten times the effective dose of LSD, by the
way.]
~From: Handbook of Poisoning, 10th ed, R.H. Dreisbach, M.D., PhD, Lange Med.
Pub. Co. Los Altos, Ca.: strychnine is lethal in 15-30 mg amounts to adult
humans. (Pure nicotine is fatal at 40 mg./person; cyanide salts are fatal
at about 100 mg./person) Strychnine causes death by respitory failure, via
increased spinal reflex excitability.
Actually, I think the fact that PharmChem analyzed something on the order of
2,000 LSD samples between 1972 and 1979 and never found one with strychnine
in it would be better. I'm going over all their data with a toothpick and
I'll get back to you on exactly what I find. It looks like the percent of
LSD with strychnine in it is, however, at least under .05%. More a little
later.
.....
According to Alexander Shulgin the definitive 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.
.....
Summary of Street Drug Results - 1973: "Of 189 samples of LSD quantitatively
analyzed, the average dose was 67.25 ug LSD. Of the 32 samples of alleged
mescaline actually containing mescaline, [...stuff about mescaline and
mushrooms deleted...] It is interesting to note the low incidence of
deception among the less sought after psychotomimetics LSD and PCP."
Most likely "good" acid is N-acetyl-LSD (ALD-52) [according to
_Psychedelic Encyclopedia_ it produces a smoother trip and is somewhat
commonly found in analysis -- references to the latter were provided]. while
"speedy" acid is LSD-25. You might want to inform her that those "speedy"
effects are also commonly reported side effects of legal drugs which
effect the 5-HT neurotransmitter system. And ditto on the potency issue --
you'd need mg quantities of strychnine to feel anything. And what you would
feel (according to descriptions I've read) does not match descriptions of
LSD "speed" effects. Most significantly because strychnine muscular effects
tend to fade in & out, while LSD "speed" effects are typically reported as
being consistent -- and there are other qualitative differences.
"actual experience"? ... no one here is likely to post descriptions of that
over the net, even in e-mail... I'm *quite* sure that some people could
though...
> Well, hypothetically speaking, I bought some from her friends, and I could
> probably surrender half a hit or a whole one, maybe, in the interest of
> science. Does anyone have facilities to perform a REAL (hypothetical)
> analysis of blotter to find out exactly what's in it?
Its been done....
> > Schnoll SH Vogel WH
> > Analysis of "street drugs".
> > N Engl J Med (1971 Apr 8) 284(14):791
This reference sucks.
> > Brown JK Shapazian L Griffin GD
> > A rapid screening procedure for some "street drugs" by thin-layer
> > chromatography.
> > J Chromatogr (1972 Jan 19) 64(1):129-33
Nope.
There's a LA County analysis of street drugs I've got (Clin Tox ~1984 I think)
that reports LSD as being >96% pure or blank (If I remember correctly) --
the rest most likely is substitutes, but it wasn't reported in the analysis.
.....
This is the PharmChem analysis of LSD from 1972 (vol 1, no 1) up to the time
that the DEA no longer allowed them to make quantitative measurements (1974-
vol 3, no 2 included). NOTE: NO STRYCHNINE! also note that PharmChem found
a sample of Shrooms contaminated with Strychnine in 1972 (vol 1, no 7), and
I would think it safe to assume that they also checked LSD for Strychnine.
*****
BAD TRIPS:
A person on LSD who becomes depressed, agitated, or confused may
experience these feelings in an overwhelming manner that grows on
itself. The best solution is to remove disturbing influences, get to
a safe, comforting environment, and reassure the tripper that things
are alright. It may comfort those who fear that they are losing their
minds to be reminded that it will end in several hours.
Authorities are fond of administering injections of anti-psychotic
drugs. Recovery in the presence of authorities, in hospitals or
police stations, is not pleasant. Sedatives or tranquilizers such as
Valium may help reduce panic and anxiety, but the best solution is
calm talking. Some claim that niacin (an over the counter vitamin
supplement) can abort a trip, but this may be due to a placebo effect
(niacin produces a flushing effect).
Remember that odd bodily sensations are normal and not harmful.
.....
"The distinction between psycholytic and psychedelic doses of LSD is used in
many scientific publications but seems to be ignored by popularizers who
either preach the "LSD utopia" or warn of the "decline of the West." A
psycholitic does, generally 75 or 100 - or at most 200 - micrograms, causes
a rush of thoughts, a lot of free association, some visualization
(hallucination) and abreaction (memories so vivid that one seems to relive
the experience). A psychedelic dose, around 500 micrograms, produces total
but temporary breakdown of usual ways of perceiving self and world and
(usually) some form of "peak experience" or mystic transcendence of ego.
"Bad trips" usually occur only on psychedelic doses."
.....
The best review of this question is Rick Strassman's "Adverse Reactions
to Psychedelic Drugs: a Review of the Literature" in _J. Nerv and Mental
Disease_ 172(10):577-595. He writes:
The most common adverse reaction is a temporary (less than 24 hours)
episode of panic --the "bad trip". Symptoms include frightening illusions/
hallucinations (usually visual and/or auditory); overwhelming anxiety
to the point of panic; aggression with possible violent acting-out behavior;
depression with suicidcal ideations, gestures, or attempts; confusion; and
fearfulness to the point of paranoid delusions.
Reactions that are prolonged (days to months) and/or require hospitalization
are often referred to as "LSD psychosis," and include a heterogenous
population and group of symptoms. Although there are no hard and
fast rules, some trends have been noted in these patients. There is a
tendency for people with poorer premorbid adjusment, a history of
psychiatric illness and/or treatment, a greater number of exposure to
psychedelic drugs (and correlatively, a great average total
cumulative dosage taken over time), drug-taking in an unsupervised
setting, a history of polydrug abuse, and self-therapeutic and/or
peer-pressure-submission motive for drug use, to suffer these consequences.
In spite of the impressive degree of prior problems noted in many of these
patients, there are occasional reports of severe and prolonged reactions
occuring in basically well adjusted individuals. In the same vein,
there are many instance of faily poorly adapted individuals who suffer
_no_ ill effects from repeated psychedelic drug use. In fact, it has been
hypothesized that some schizophrenics do not suffer adverse reactions
because of their familiarity with such acute altered states. Another
possibility is that there individuals may be "protected" by possible "down-
regulation" of the receptors for LSD, bu the (over-)production of some
endogenous compound. _Individual_ prediction of adverse reactions,
therefore, is quite difficult...
.....
Major "functional" psychosis vs. "LSD psychosis"
A diagnostic issue dealth with explicitly in only a few papers is that of
LSD-precipitated major functional illnesses, e.g. affective disorders
or schizophrenia. In other words, many of these so called LSD psychoses
could be other illnesses that were triggered by the stress of a traumatic
psychedelic drug experience. Some of the same methodological issues
described earlier affect these studies, but they are, on the averagem
better controlled, with more family and past psychiatric history available
for comparison.
Hensala et al. compared LSD-using and non-LSD-using psychiatric inpatients.
They found that this group of patients was generally of a younger age and
contained more characteristically disordered individuals than the non-
LSD-using group. Patients with specific diagnoses with or without LSD
histories were not compared. Based on their observations, they concluded
that LSD was basically just another drug of abuse in a population of
frequently hospitalized individuals in the San Francisco area, and that
it was unlikely that psychedelic use could be deemed etiological in the
development of their psychiatric disorders.
Roy, Breakey et al., and Vardy and Kay have attempted to relate LSD use to
the onset and revelopment of a schizophrenia-like syndrome. A few comments
regarding this conceptual framework seem in order, before their findings
are discussed. The major factor here is that of choosing schizophrenia,
or in the Vardy and Kay study, schizophreniform disorders, as the
comparison group. There is an implication here that LSD psychoses are
comparable, phenomenologically, to schizophrenia-like disorders, and that
LSD can "cause" the development of such disorders. The multiplicity of
symptoms and syndromes described in the "adverse reaction" literature
should make it clear that LSD can cause a number of reactions that can last
for any amount of time--from minutes to, possibly, years. I believe what
is being studied here is the question of the potential role of LSD in
accelerating or precipitating the onset of an illness that was "programmed"
to develop ultimately in a particular individual--in a manner comparable
to the major physical or emotional stress that often precipitates a bona
fide myocardial infarction in an individual with advanced coronary
atheresclerosis. The stress did not _cause_ the heart disease; it was
only the stimulus that accelerated the inexorable process to manifest
illness.
In looking at the relevant studies, Breakey et al. found that schizophrenics
who "used drugs" had an earlier onset of symptoms and hospitalization than
non-drug-using schizophrenics, and had possibly better premorbid personal-
ities than non-drug using patients (although Vardy and KAy have challenged
this analysis of Breakey's data).
Bowers compared 12 first-admission patients with psychosis related to LSD
use, requiring hospitalization and phenothiazines, to 26 patients hospital-
ized and treated with phenothiazines with no history of drug use. Six
of these controls had been previously hospitalized. Drug-induced psychotic
patients were found to have better premorbib histories and prognostic
indicators than the nondrug groups. There was no difference in rates of
family history of psychiatric illness. However, several issues flaw
this study. One is the poly-drug abusing nature of the "LSD-induced"
psychotic patients, compared to the controls. The role of LSD, therefore,
in causing or precipitating these symptomatic disorders, is open to dispute.
The other is the lack of an adequate comparison control group, i.e. the
controls were specified only as "psychotic," and did not necessarily
match the LSD group in either symptoms or diagnostic classification.
A follow-up study of the patients occured between 2 and 6 years later.
One half did well and one half did poorly, although the lack of a control
group for a follow-up in a similarly symptomatic control group makes
interpretation of the data difficult.
Roy, in a somewhat different design, compared chronic schizophrenic
patients (diagnosed according to DSM-III criteria) who had used LSD
within the week preceding hospitalization, and found no difference
in age of symptom onset or hospitalization compared to patients without
a history of illicit drug use.
Vardy and Kay, in an elegant study with a 3- and 5- year follow-up period,
demonstrated that patients hospitalized for a schizophrenic picture
that developed within two weeks of LSD use (patients with other diagnoses
were explicitly excluded form comparisons with non-drug-using
schizophrenics) were "fundamentally similar to schizophrenics in
geneology, phenomenology, and course of illness (165, p. 877). Pre-
morbid adjustment, age of onset of symptoms and hospitalization, family
history of psychosis or suicide, and most cognitive features were also
equal between groups. Family histories of alcohol abuse were markedly
great in the LSD group.
I believe these data, taken as a whole, limited as they are in terms of
comparing subgroups (i.e. LSD-using vs. non-LSD-using) of "schizophrenia-
like" disorders, point towar, at most, a possible precipitory role in
the development of these disorders, in a non specific and not
etiologically related manner.
*****
MYTHS:
LSD does not form "crystals" that reside in the body to be "dislodged"
later, causing flashbacks. LSD is a crystalline solid (though it is
unlikely that one would ever have enough to be visible to the naked
eye) but it is easily water soluble, thus cannot form bodily
deposits. Furthermore, it is metabolized and excreted in hours. The
bogus "loosened crystal" description in not necessary to explain
flashbacks, which are psychological phenomena (see FLASHBACKS).
LSD does not cause chromosome damage.
In Science 30 April 1972, Volume 172 Number 3982 p. 431-440 there was an
article by Norman I. Dishotsky, William D. Loughman, Robert E. Mogar and
Wendell R. Lipscomb titled "LSD and Genetic Damage - Is LSD chromosome
damaging, carcinogenic, mutagenic, or teratogenic?". They reviewed 68
studies and case reports published 1967-1972, concluding "From our own
work and from a review of literature, we believe that pure LSD ingested
in moderate doses does not damage chromosomes in vivo, does not cause
detectable genetic damage, and is not a teratogen or carcinogen in man."
Well, there's the study by Sidney Cohen which was cited here
recently, Journal of Nervous and Mental Disease, 130, 1960. The
following is from Jay Stevens' Storming Heaven: "Cohen surveyed a sample
of five thousand individuals who had taken LSD twenty-five thousand
times. He found and average of 1.8 psychotic episodes per thousand
ingestions, 1.2 attempted suicides, and 0.4 completed suicides.
'Considering the enormous scope of the psychic responses it induces,'
he concluded, 'LSD is an astonishingly safe drug.'"
Some urban legends: I've heard two "stories" about people blinding
themselves on "drugs". One was revealed as a hoax by the person who
perpetrated it (apparently it was intended to "illustrate" the dangers
of LSD), another is trotted out by anti-drug speakers at high schools:
1) Seven people on LSD stared at the sun and lost 90% of their reading
vision.
[Ed: See the file Erowid.org/chemicals/lsd/lsd_myth6.shtml
for more detailed information on the spread and mutation of the myth.]
2) A teenager arrested while on LSD plucked out his eyeballs in his
jail cell, and felt no pain.
While these are bogus, the drug has powerful effects on the mind
and the consumer should be aware of the hazards, and act appropriately.
.....
There is an occasionally circulated fake warning from some police department
about LSD-laced "tattoos" or stickers (the "blue star tattoo" story) being
given to children. This probably originated with some hick cop or ignorant
and panicky parent not understanding some children-cartoon (eg, mickey mouse
in sorcerer's garb) printed on a sheet of blotter.
.....
See also myths about testing in DRUG TESTING
*****
DANGERS:
Purely psychological hazards, not harmful to body. May release latent
psychosis or exacerbate depression, leading to irrational behavior. There
is also a danger of foolish or incautious behavior, e.g, misjudging
distances or thinking one can fly. Physical overdose is not a hazard,
though one may easily ingest more than one may be able to handle
psychologically.
.....
Because the "LSD psychosis" is not distinguishable from non-drug-
induced psychosis, we have reasonable evidence to conclude that LSD
was not the sole cause of psychosis. Instead, it would seem that the
drug brought on the problems in vulnerable individuals.
Interestingly, the rate of parental alcoholism was found to be much
higher in LSD patients than in other patients or in the general
population by one study (Vardy and Kay, Arch-Gen-Psych, 1983 40(8):
877-83).
.....
Lethal (toxic) doses of LSD are conservatively several tens of
thousands of times as much as a normal dose, making it (in the toxic
sense) one of the safest drugs known. See section on Pharmacology for
description of bodily side-effects.
The LD50 for psilocybin (active ingredient in mushrooms) is 275 mg/kg
i.v. in mice. Of course, it would take lots more p.o. to kill someone.
The reported LD50 values for LSD are 46, 16.5, 0.3 mg/kg I.V. for mice,
rats, and rabbits, respectively. Again, it's hard to accurately translate
these numbers to oral values.
Note that an average human dose is 0.001 mg/kg, ie, 1 microgram/kg, ie,
1 part per billion by weight.
.....
Never take any drugs while pregnant. Best to be prudent.
*****
FLASHBACKS:
Quoted without permission from 'Licit and Illicit Drugs,' written by
Edward M. Brecher and the editors of Consumer Reports. ISBN: 0-316-15340-0
A simple explanation of LSD flashbacks, and of their changed character
after 1967, is available. According to this theory, almost everybody
suffers flashbacks with or without LSD. Any intense emotional
experience--the death of a loved one, the moment of discovery that one is in
love, the moment of an automobile smashup or of a narrow escape from a
smashup--may subsequently and unexpectedly return vividly to consciousness
weeks or months later. Since the LSD trip is often an intense emotional
experience, it is hardly surprising that it may similarly "flash back."
"Post-traumatic stress disorder has been commonly associated with war
veterans, but it also affects victims of disasters and violence... Experts
estimate that 1% of the population suffers from the disorder."
---LA Times, Feb 18 1992, p A3, "Journey For Better Life Hell For Some Women."
.....
Can smoking marijuana induce a flashback?
Also are you more likely to suffer flashbacks from having a bad trip?
Apparently yes and yes. The following is reproduced without
permission from Lester Grinspoon and James B. Bakalar, "Psychedelic
Drugs Reconsidered," Basic Books, Inc. New York, 1979. pp. 159-163.
I highly recommend this book, and if you find it please buy me one
too.
I typed this in a while ago and didn't type in the references at the
time (slap!). If you want them i'll see what i can do. Typos are
mine.
- - - - - - -
... Studies of flashbacks are hard to evaluate because the
term has been used so loosely and variably. On the broadest
definition, it means the transitory recurrence of emotions and
perceptions originally experienced while under the influence of a
psychedelic drug. It can last seconds or hours; it can mimic any of
the myriad aspects of a trip; and it can be blissful, interesting,
annoying, or frightening. Most flashbacks are episodes of visual
distortion, time distortion, physical symptoms, loss of ego
boundaries, or relived intense emotion lasting a few seconds to a few
minutes. Ordinarily they are only slightly disturbing, especially
since the drug user usually recognizes them for what they are; they
may even be regarded lightheartedly as "free trips." Occasionally
they last longer, and in a small minority of cases they turn into
repeated frightening images or thoughts. They usually decrease
quickly in number and intensity with time, and rarely occur more than
a few months after the original trip.
A typical minor and pleasant flashback is the following:
--
... Frequently afterward there is a momentary "opening"
("flash" would be too spastic a word) when for maybe a couple of
seconds an area one is looking at casually, and indeed unthinkingly,
suddenly takes on the intense vividness, composition, and significance
of things seen while in the psychedelic condition. This "scene" is
nearly always a small field of vision -- sometimes a patch of grass, a
spray of twigs, even a piece of newspaper in the street or the remains
of a meal on a plate (Cohen 1970[1965], pp. 114-115)
--
Here are two more troublesome examples:
--
For about a week I couldn't walk through the lobby of A-entry
at the dorm without getting really scared, because of the goblin I saw
there when I was tripping. (Pope 1971, p. 93)
--
A man in his late twenties came to the admitting office in a
state of panic. Althought he had not taken any drug in approximately
2 moths he was beginning to re-experience some of the illusory
phenomena, perceptual distortions, and the feeling of union with the
things areound him that had previously occurred only under the
influence of LSD. In addition, his wife had told him that he was
beginning to "talk crazy," and he had become frightened ... He was
concerned lest LSD have some permanent effect on him. He wished
reassurance so that he could take it again. His symptoms have
subsided but tend to reappear in anxiety-provoking situations.
(Frosch et al. 1965, p. 1237)
--
Flashbacks are most likely to occur under emotional stress or
at a time of altered ego functioning; they are often induced by
conditions like fatigue, drunkenness, marihuana intoxication, and even
meditative states. Falling asleep is one of those times of
consciousness change and diminished ego control; an increase in the
hypnagogic imagery common at the edge of sleep often follows
psychedelic drug use and can be regarded as a kind of flashback.
Dreams too may take on the vividness, intensity, and perceptual
peculiarities of drug trips; this spontaneous recurrence of
psychedelic experience in sleep (often very pleasant) has been called
the high dream (Tart 1972). Marihuana smoking is probably the most
common single source of flashbacks. Many people become more sensitive
to the psychedelic qualities of marihuana after using more powerful
drugs, and some have flashbacks only when smoking marihuana (Weil
1970). In one study frequency of marihuana use was found to be the
only factor related to drugs that was correlated with number of
psychedelic flashbacks (Stanton et al. 1976).
How common flashbacks are said to be depeds on how they are
defined. By the broad definition we have been using, they occur very
often; probably a quarter or more of all psychedelic drug users have
experienced them. A questionanaire survey of 2,256 soldiers (Stanton
and Bardoni 1972), leaving the definition to the respondents, revealed
that 23 percent of the men who used LSD had flashbacks. In a 1972
survey of 235 LSD users, Murray P. Naditch and Sheridan Fenwick found
that 28 percent had flashbacks. Eleven percent of this group (seven
men in all) called them very frightening, 32 percent called them
somewhat frightening, 36 percent called them pleasant, and 21 percent
called them very pleasant. Sixty-four percent said that their
flashbacks did not disrupt their lives in any way; 16 percent (4
percent of the whole LSD-using group) had sought psychiatric help for
them (Naditch and Fenwick 1977). In a study of 247 subjects who had
taken LSD in psychotherapy, William H. McGlothlin and David O. Arnold
found 36 cases of flashbacks, only one of which was seriously
disturbing (McGlothlin and Arnold 1971). McGlothlin, defining
flashbacks narrowly for clinical purposes as "repeated intrusions of
frightening images in spite of volitional efforts to avoid them"
(McGlothlin 1974b, p. 291), estimates that 5 percent of habitual
psychedelic users have experienced them.
There are few studies on the question of who is most
susceptible. In 1974, R. E. Matefy and R. Krall compared psychedelic
drug users who had flashbacks with those who did not, and found no
significant differences in their biographies or on personality tests.
The main causes of flashbacks were stress and anxiety. About 35
percent found them more or less pleasant, and the same proportion
thought they could control them. Most accepted them as an inevitable
part of their lives as members of the psychedelic fraternity and did
not want help from psychiatry (Matefy and Krall 1974). Naditch and
Fenwick found that the number of flashbacks, both pleasant and
unpleasant, was highly correlated with the number and intensity of bad
trips and the use of psychedelic drugs as self-prescribed
psychotherapy. Those who enjoyed flashbacks and those who were
frightened by them did not differ significantly on tests of ego
functioning.
A case seen in an outpatient setting in the late sixties
illustrates the kind of set and setting that may create flashback
problems. PQ was a thirty-six-year-old single man who entered therapy
because of depression and anxiety. He was a heavy drinker who was
passive, slovenly, and spent most of his time in bed. Just before
taking to alcohol and his bed he had failed in an attempt to parlay a
gift from his wealthy father into a fortune on the stock market.
Despite a remarkable incapacity for insight, during a year in
psychotherapy he managed to give up alcohol and start a promising
business. But his anxiety continued, and in order to allay it he had
to keep himself very busy wheeling and dealing. Imitating his father,
a successful self-made man who had married a woman twenty years
younger than himself, PQ dated only women under the age of nineteen.
Being attractive to young women was so imporant to him that much of
his time was spent in the company of teenagers. During business hours
he would wear a conservative three-piece suit and drive a new sedan,
but when he was with his young friends he would wear a leather jacket
and drive a motorcycle. Anxiety and fears of inadequacy dominated
both of these lives. Several months after therapy began, during a
weekend in a small resort town, his young friends decided to take LSD,
and he felt obliged to dissemble his fears and join them; it was his
first and only trip. He felt a panic he had never known before; he
thought that he was losing his mind and going "out of control." His
friends were so concerned thet they took him to a small hospital,
where he was given chlorpromazine and after six hours released in
their care. The next day he had a flashback that lasted one or two
hours and was almost as frightening as the original experience.
Flashbacks continued for six months, their frequency, duration, and
severity eventually diminishing to the point where it was difficult
for him to determine whether they were related to the LSD trip or
merely an intensification of his usual anxiety. In fact, the patient
described the flashbacks as being like very much enhanced anxiety
episodes. Even several years after this experience, when he became
very anxious, he was reminded of the trip and these flashbacks. He
denied that these experiences had any perceptual or cognitive aspect;
both during the LSD trip and later, the only symptom was panic. There
is no question that the nature of his trip was influenced by the
unfortunate set and setting. It is a matter of speculation what part
his underlying chronic anxiety played in the development and form of
the flashback phenomena.
Several explanations for flashbacks have been proposed. One
is that the drug has lowered the threshold for imagery and fantasy and
made them less subject to voluntary control; in another version of
this explanation, flashbacks are caused by a heightened attention to
certain aspects of immediate sensory experience suggested by drug
trips and reinforced by the community of drug users. Something more
seems to be needed to account for repeated fearful relivings of
sequences from past drug trips, and these have been explained as
similar to traumatic neuroses precipitated by fright: disturbing
unconscious material has risen to consciousness during the drug trip
and can be neither accepted nor repressed. For example, D. F. Saidel
and R. Babineau (1976) have reported a case of recurrent flashbacks --
three years of blurring images and auditory distortions, with some
anxiety and confusion -- which they regard as a neurosis founded on
the patient's problems with his career and his relationship to his
mother. (See also Horowitz 1969; Shick and Smith 1970; Heaton 1975.)
Another explanation treats the flashback as an example of recall
associated with a particular level of arousal. (Fischer 1971). In
this conception the memory of an experience is best retrieved when the
rate of mental data-processing is the same as it was during the
original experience -- in other words, when the state of consciousness
in similar. Therefore, psychedelic experiences are likely to be
recalled and relived when the ego's sorting and control of sensory
information is disturbed by drugs, stress, or the state of half-sleep.
For a critique of flashback studies, see Stanton et al. 1976
- - - - - - -
*****
INSOMNIA:
Insomnia occurs frequently after the trip. A mild, over-the-counter
sleeping aid can help, and these antihistamines do not produce adverse
interactions. Also, some people like to consume a small amount of alcoholic
beverage to "smooth the jitteries". The usual precautions about sleeping
aids if alcohol has been consumed apply of course.
*****
TOLERANCE:
Acquired 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).
LSD (lysergic acid diethylamide) itself is not found in plants, however
its close chemical cousin lysergic acid amide is.
.....
"Indole Alkaloids In Plant Hallucinogens" Richard Evans Schultes, PhD.
Journal of Psychedelic Drugs Vol.8(No.1) Jan-Mar 1976
"The main constituent of the seeds of Rivea corymbosa is ergine or d-lysergic
acid amide. Minor alkaloids present are the related d-isolysergic acid amide
(isoergine), chanoclavine, elymoclavine and lysergol. The seeds of Ipomoea
violacea have a similar composition, but instead of lysergol, they have
ergometrine (ergonovine). Later, very minor amounts of two alkaloids
ergometrinine and penniclavine - were found in I. violacea by chromatography.
the total alkaloid content of the seeds of Ipomoea viloacea is approximately
five times as great as that of the seeds of Rivea corymbosa: 0.06% in the
former; 0.012% in the latter. This difference in the alkaloid content
explains why Indians employ smaller doses of seeds of the Ipomoea than of the
Rivea.
"Ethnopharmacology and Taxonomy of Mexican Psychodysleptic Plants"
Jose Luis Diaz M.D.
Journal of Psychedelic Drugs Vol. 11(1-2) Jan-Jun 1979
Seeds of various Morning Glories contain
Ergolines: ergine,isoergine,ergonovine
Glucosides: turbicoryn [apparently in Rivea corymbosa only]
called Tlitlitzen (Aztec word for "The Divine Black One")
to the Aztecs, Black is a "hot" color,
a property of psychotropics associated with light
.....
"The Botanical and Chemical Distribution of Hallucinogens"
Richard Evans Schultes, PhD.
Journal of Psychedelic Drugs Vol.9(No.3) Jul-Sep 1977
"I. violacea, often referred to by it's synonyms I. rubro-caerulea and
I. tricolor, is represented in horticulture by a number of "varieties,"
such as: Heavenly Blue, Pearly Gates, Flying Saucers, Wedding Bells,
Summer Skies, and Blue Stars - all of which contain the hallucinogenic
ergot alkaloids."
.....
"Burger's Medicinal Chemistry" Fourth Edition, Volume III
Chapter: "Hallucinogens" Alexander Shulgin
Composition, % of total alkaloids present
=========================================
Compound R. corymbosa I. violacea
=============== ================ ======================
Ergine (LA-111) 54, 48 58, 10-16, 5-10
Isoergine 17, 35 8, 18-26, 9-17
Ergometrine 8
Elymoclavine 4 4
Chanoclavine 4 4
Lysergol 4
Total Alkaloids .012, .04 .06, .04-.08, .02-.04
(% of dry weight
of seeds)
*****
ANTHROPOLOGY:
_The Road to Eleusius_ by Hofmann, 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 Hofmann, 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; Hofmann on the
psychoactivity of ergot strains; and Ruck on the mythological and
cultural backround of the sect.
Evidence includes: Hofmann dosed himself with large (ergot-derived)
doses of obstetric compounds to assay their hallucinogenic potential,
and found them to possess such activity. The Eleusian temple site still
remains, but there is no room to view theatric performances, just rows of
tripping initiates, further supporting their argument.
An interesting read, and its neat to think that the culture that
more or less lead to the western industrial one had psychedelic rites.
(Various greek prominant figures attended the rituals, including Plato).
.....
IPOMOEA PURPUREA: A NATURALLY OCCURRING PSYCHEDELIC
Charles Savage, Willis W. Harman and James Fadiman
>From "Altered States of Consciousness, A Book of Readings"
edited by Charles Tart BF311.T28
Of the naturally occurring plant alkaloids used in ancient and modern
religious rites and divination one of the least studied is ololiuqui. The
earliest known description of its use is by Hernandez, the King of Spain's
personal physician, who spent a number of years in Mexico studying the
medicinal plants of the Indians and "accurately illustrated ololiuqui as a
morning glory in his work which was not published until 1651" (Schultes,
1960). In his words, "When a person takes ololiuqui, in a short time he loses
clear reasoning because of the strength of the seed, and he believes he is in
communion with the devil" (Alacon, 1945). Schultes (1941) and Wasson (1961)
have reported in detail on the religious and divinatory use of two kinds of
morning-glory seeds, Rivea corymbosa and Ipomoea violacea, among the Mazatec
and Zapotec indians. The first of these is assumed to be the ololiuqui of the
ancient Aztecs.
In 1955 Osmond described personal experiments with Rivea corymbosa seeds and
reported that the effects were similar to those of d-lysergic acid
diethylamide (LSD-25). He suggested (1957) that the word psychedelic (meaning
mind-manifesting) be used as a generic term for this class of substances to
refer to their consciousness-expanding and psychotherapeutic function as
contrasted with the hallucinogenic aspect. In 1960 Hofmann reported that he
had isolated d-lysergic acid amide (LA) and d-isolysergic acid amide from the
seed of both Rivea corymbosa and Ipomoea violacea. LA is very similar to LSD
in its psychological and physiological manifestations but is reported to have
about one twentieth the psychological effectiveness of LSD (Cerletti &
Doepfner, 1958).
The work of these investigators led us to a preliminary study of the
psychedelic properties of species of Ipomoea which are commonly found within
the continental United States. The seeds of Ipomoea purpurea, the common
climbing morning glory, resemble the seeds of Ipomoea violacea and have been
found to have similar psychedelic properties. Recent analysis by Taber et al.
(1963) has verified that LA is present in the varieties used and is probably
the primary active agent.
The effects of the seeds of Ipomoea purpurea (varieties Heavenly Blue and
Pearly Gates) in a total of 45 cases are summarized below. The subjects are
all normally functioning adults and the majority had previous experience with
LSD. The onset of effects is about half an hour after the seeds have been
chewed and swallowed and they last from five to eight hours.
Low Dose, 20-50 Seeds (11 Subjects)
This dosage rarely produces any visual distortions, although with eyes
closed there may be beginning imagery. Restlessness, evidenced by alternating
periods of pacing about and lying down, may be present. There tends to be a
heightened awareness of objects and of nature, and enhanced rapport with
other persons. A feeling of emotional clarity and of relaxation is likely to
persist for several hours after other effects are no longer noticeable.
Medium Dose, 100-150 Seeds (22 Subjects)
In this range the effects resemble those reported for medium-dose (75-150
micrograms) LSD experiences, including spatial distortions, visual and
auditory hallucinations, intense imagery with eyes closed, synaesthesia and
mood elevation. These effects, which occur mainly during the period of 1 to 4
hours after ingestion, are typically followed by a period of alert calmness
which may last until the subject goes to sleep.
High Dose, 200-500 Seeds (12 Subjects)
In this range the first few hours may resemble the medium-dose effects
described above. However, there is usually a period during which the
subjective states are of a sort not describable in terms of images or
distortions, states characterized by loss of ego boundaries coupled with
feelings of euphoria and philosophical insight. These seem to parallel the
published descriptions of experiences with high doses (200-500 micrograms) of
LSD given in a supportive, therapeutic setting as reported by Sherwood et al.
(1962).
All the subjects who had previous experience with LSD claimed the effects of
the seeds were similar to those of LSD. Transient nausea was the most
commonly reported side effect, beginning about one half hour after ingestion
and lasting a few minutes to several hours. Other reported side effects not
commonly found with LSD were a drowsiness or torpor (possibly due to a
glucoside also present in the seeds) and a coldness in the extremities
suggesting that the ergine content of the seeds may be causing some vascular
constriction. (If this is the case, there may be some danger of ergot
poisoning resulting from excessive dosages of the seeds.) The only untoward
psychic effect was a prolonged (eight hours) disassociative reaction which
was terminate with chlorpromazine [Thorazine]. The possibility of prolonged
adverse reactions to the psychological effects of the seeds is essentially
the same as with LSD, and the same precautions should be observed (Cohen &
Ditman, 1963).
.....
IPOMOEA.003 7-MAY-90
Additional Notes:
Ipomoea purpurea is sold as the "Heavenly Blue" variety of morning glory.
"Ipomoea tricolor" is the trade name used for that variety. It is identical
with the species of morning glory described above.
The seeds must be chewed or ground in order to be effective. Soaking the
ground seeds in water for several hours, filtering out the grounds,
and then drinking only the water portion of the mixture can reduce
some of the stomach-upset symptoms if such occur.
Unpleasant LSD and morning glory trips can be smoothed out or even
stopped by taking niacin (in the form of nicotinic acid, vitamin B-3 or
"niacin"). Vitamin C has been shown to reduce the incidence of paranoia and
prevent depletion of the vitamin from the adrenal glands during LSD trips.
There have been reports that commercially available packets of morning
glory seeds from some distributors are coated with fungicides or
other chemicals to increase shelf life or discourage the practice
of eating them. Seeds from plants grown in one's own garden will
be safe as long as you do not spray them with insecticides.
The last few notes about Niacin and Vitamin C are based on
a paperback edition of Hoffer & Osmonds "The Psychedelics"
It's pretty clear that the latin names of this plant are somewhat
confused (which is typical). Ipomoea purpurea, Ipomoea tricolor,
Ipomoea violacea and Ipomoea rubro-caerulea are all the same plant.
The other variety of morning glory, "Ololiuhqui" has at least two
Latin names as well: Rivea corymbosa, and Turbina corymbosa.
.....
"Recreational use of Ergoline Alkaloids from Argyreia Nervosa"
William E. Shawcross
Journal of Psychedelic Drugs Vol. 15(4) Oct-Dec 1983
CHEMISTRY AND EFFECT OF THE SEEDS
The Hawaiian baby woodrose entered the drug scene in 1965 with the
publication of a paper in "Science" entitled "Ergoline Alkaloids in Tropical
Wood Roses" by Hylin and Watson. The wide circulation of this journal assured
thorough dissemination of the information they presented. They wrote, "The
possible health and legal problems associated with the presence of similar
compounds in commercially cultivated plants led us to examine the ornamental
wood roses, Ipomoea tuberosa and Argyreia nervosa, both common Hawaiian crops
that have assumed commerical importance as components of [the] dried tropical
flower industry." Comparing the seeds of these two plants with those of the
morning glory varieties Pearly Gates and Heavenly Blue, they found the
following yield of alkaloids (mg of alkaloid/g of seed material):
Heavenly Blue 0.813
Pearly Gates 0.423
I. tuberosa [None]
A. nervosa 3.050
The seed of A. nervosa is the best plant source of ergoline alkaloids
discovered; it contains approximately 3 mg of alkaloidal material per gram of
seed. Approximately one-eighth of this is lysergamide.
Hylin and Watson found the major alkaloidal constituents in A. nervosa seeds to
be ergine (780 mcg/g of fresh seed) and isoergine and penniclavine (555 mcg).
[Note: Argyreia nervosa has NO history of shamanic use as a hallucinogen]
This is an excerpt from the article cited.
There's no record of Argyreia being used as an hallucinogen in
India, but it was used externally as some kind of skin medicine.
There's been speculation that Argyreia might have been a component
of "Soma", but there's no evidence for that, apparently.
Because there's not a long history of human usage of Argyreia,
it may be that there are glycosides not mentioned here that
take effect at higher doses or might cause stomach upset, tachycardia
etc. The article mentioned intestinal complaints in one or two
cases at higher experimental doses.
*****
CHEMISTRY:
lysergic acid diethylamide _is_ lysergic acid diethylamide (or...
N,N-diethyl-D-lysergamide or...
9,10-Didehydo-N,N-diethyl-6-methylergoline-8B-carboxamide).
Only one stereoisomer (the d-) is psychoactive. Thus, racemic (l/d 50-50 mix)
lsd shows half the potency of the dextro form. In synthesis it is possible
to recover the l-form for the lysergic acid.
Lysergic Acid Diethylamide is LSD rather than LAD because the German word
for acid is saeure (sp).
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.
From the Merck Index:
5505. Lysergamide. 9,10-Didehydro-6-methylergoline-
8beta-carboxamide; lysergic acid amide; ergine. C16H17N3O;
mol wt 267.32. C 71.88%, H 6.41%, N 15.72%, O 5.99%.
Isoln from _Rivea_corymbosa_(L.) and from _Ipomoea_tricolor_
Cav., _Convolvulaceae_: Hofmann, Tscherter, _Experientia_ 16,
414 (1964). Prepn from lysergic acid hydrazide: Ainsworth,
U.S. pat. 2,756,235 (1956 to Lilly); from lysergic acid and
phosgene-dimethylformamide complex: Patelli, Bernardi,
U.S. pat. 3,141,887 (1964 to Farmitalia). Microbiological
production: Rutschmann, Kobel, U.S. pat. 3,219,545 (1965
to Sandoz).
H. CONH2
'. /
/ \
/ \
|| |
|| N
/\\ /\ / \
/ \\ / \ / CH3
|| | | \
|| | | H
\ // \ /
\// \/
| ||
| ||
HN-------
Prisms from methanol. dec 242deg. [alpha](5461)(20) + 15% (c = 0.5 in
pyridine).
Methanesulfonate, C7H21N3O4S, prisms from methanol +
acetone, dec 232deg.
Note: This is a controlled substance (depressant) listed in
the U.S. code of Federal Regulations, Title 21 Part 1308.13
(1987).
5506. Lysergic Acid. 9,10-Didehydro-6-methylergoline-
8-carboxylic acid. C16H16N2O2; mol wt 268.32. C 71.62%,
H 6.01%, N 10.44%, O 11.93%. Lysergic acid and isolyser-
gic acid are the main cleavage products formed on alkaline
hydrolysis of the alkaloids which are characteristic of ergot.
Jacobs, Craig et al., _J._Biol._Chem._ 104, 547 (1934); 125, 289
(1938); 130, 399 (1939); 145, 487 (1942); _J._Org._Chem._ 10,
76 (1945). High-yield production by _Claviceps_paspali_:
Arcamone et al., _Proc._Roy._Soc._ (London), _Ser._B_, 155, 26
(1961). total synthesis: Kornfeld et al., _J._Am._Chem._Soc._
76, 5256 (1954); 78, 3087 (1956); M. Julia et al., _Tetrahedron_
_letters_ 1969, 1569; V.W. Armstrong et al., ibid. 1976, 4311;
W. Oppolzer et al., _Helv._Chem._Acta_ 64, 478 (1981); R.
Ramage et al., _Tetrahedron_ 37, Suppl. 9, 157 (1981); J.
Rebek, D.F. Tai, _Tetrahedron_Letters_ 24, 859 (1983). Ste-
reochemistry: Stoll et al., _Helv._Chem._Acta 37, 2039 (1954);
Stenlake, _J._Chem._Soc._ 1955, 1626; Leeman, Fabbri, _Helv._
_Chim._Acta_ 42, 2696 (1959). Absolute configuration: Stad-
ler, Hofmann, ibid. 45, 2005 (1962).
H. COOH
'. /
/ \
/ \
|| |
|| N
/\\ /\ / \
/ \\ / \ / CH3
|| | | \
|| | | H
\ // \ /
\// \/
| ||
| ||
HN-------
Haxagonal scales, plates with one or two moles H20 from
water, mp 240deg (dec). [alpha](D)(20) + 40deg (c = 0.5 in pyridine).
Behaves as an acid and base, pKa 3.44, pKb 7.68. Moder-
ately sol in pyridine. Sparingly sol in water and in neutral
organic solvents; sol in NaOH, NH4OH, Na2CO3, and HCL
solns. Slighly sol in dil H2SO4.
Methyl ester, thin leaflets from benzene, mp 168deg.
Note: This is a controlled substance (depressant) listed in
the U.S. code of Federal Regulations, title 21 Part 1308.13
(1987).
5507. Lysergide. 9,10-Didehydro-N,N-diethyl-6-meth-
ylergoline-8beta-carboxamide; N,N-diethyl-D-lysergamide; D-
lysergic acid diethylamide; LSD; LSD-25; Lysergsaure Di-
ethylamid. C20H25N3O; mol wt 323.42. C 74.27%, H 7.79%,
N 12.99%, O 4.95%. Microbal formation by _Claviceps_pas-
pali_ over the hydroxyethylamide; Arcamone et al., _Proc._
Roy._Soc._(London) 155B, 26 (1961). Partial synthesis: Stoll,
Hofmann, _Helv._Chim._Acta_ 26, 944 (1943); 38, 421 (1955).
Industrial prepn: Pioch; Garbrecht, U.S. pats. 2,736,728;
2,774,763 (both 1956 to Lilly); Patelli, Bernardi, U.S. pat.
3,141,887 (1964 to Farmitalia). Isotope-labeled LSD: Stoll
et al., _Helv._Chim._Acta_ 37, 820 (1954). Toxicity data: E.
Rothlin, _Ann._N.Y._Acad._Sci._ 66, 668 (1957). Review: Hof-
fer, _Clin._Pharmacol._Ther._ 6, 183 (1965). Book: _The_Use_of_
LSD_in_Psychotherapy_and_Alcoholism_, H.A. Abramson, Ed.
(Bobbs-Merrill, Indianapolis, 1967) 697 pp.
/ C2H5
H. CON
'. / \ C2H5
/ \
/ \
|| |
|| N
/\\ /\ / \
/ \\ / \ / CH3
|| | | \
|| | | H
\ // \ /
\// \/
| ||
| ||
HN-------
Pointed prisms from benzene, mp 80-85 degs. [alpha](D)(20) + 17deg (c =
0.5 in pyridine). uv max (ethanol): 311 nm (E(1 cm)(1%) 257).
LD50 in mice, rats, rabbits (mg/kg): 46, 16.5, 0.3 i.v.
(Rothlin).
D-Tartrate, C46H64N6O10, solvated, elongated prisoms from
methanol, mp 198-200deg. [alpha](D)(20) + 30 deg. Soluble in water.
Caution: This is a controlled substance (hallucinogen)
listed in the U.S. Code of Federal Regulations, Title 21 Part
1308.11 (1987).
USE: In biochemical research as an antagonist to serotonin.
Has been used experimentally as adjunct in study and treat-
ment of mental disorders.
NOTES: Not guaranteed to be free from typos.
Underlines are supposed to be italic (ie book/journal titles, etc)
Alpha, beta, and deg are the greek letters and the degree symbol
[alpha](D)(20) means a greek letter in [] followed by a subscript
and then a superscript (I don't know *WHAT* this actually is)
The chemical structures are almost exactly what the Merck manual has
drawn. Almost nothing was lost in the conversion to ASCII.
*****
MECHANISM OF ACTION:
(Note: the mechanism of action of LSD and other psychedelics is uncertain.)
From a chapter titled Hallucinogens and Other Psychotomimetics: Biological
Mechanisms by S.J.Watson
"The current thesis of the effect of indole hallucinogens on
5-hydroxytrypamine might be stated as follows: LSD acts to preferentially
inhibit serotonergic cell firing and seems to spare postsynaptic serotnergic
receptors. This preference is shared by other simillar hallucinogens but in
a limited fashion. Nonhallucinogenic analogs of LSD show no preference.
These results suggest that there are two different steric conformation of
serotonergic receptors, one of which has higher affinity for LSD than the
other. In general, 5-ht is an inhibitory transmitter; thus, when its
activity is decreased, the next neuron in the chain is freed from inhibition
and becomes more active. Since serotnergic systems appear to be intimately
involved int eh control of sensation, sleep, attention, and mood, it may be
possible to explain the actions of LSD and other hallucinogens by their
disinhibition of these critical systems.
There is also evidence for interaction with dopaminergic systems.
.....
LSD acts as a 5HT autoreceptor agonist in the raphe nucleus. These
autoreceptors are typically considered to be 5HT1As. It also acts as a 5HT2
agonist, which is thought to be the main site of hallucinogenic activity.
It's probably best called a a mixed 5HT2/5HT1 receptor partial agonist.
I don't know of its effects on dopamine. Wouldn't be surprised if it has
'em; the systems aren't really functionally separable. The DA effects
wouldn't be necessary for hallucinogenic activity, I'd bet.
.....
(From Snyder, "Drugs and the Brain", 1986, Sci Am Books Inc., Reprinted w/o
permission, blah, blah, blah... )
In more recent studies, Aghajanian has focuses not on the serotonin neu-
rons of the raphe nuclei but on the norepinephrine neurons of the locus
coeruleus. As we saw in Chapter 6, the locus coeruleus cell bodies give rise to
axons that ramify all over the brain and provide the majority of the norepi-
nephrine neuronal input in most brain regions. Amphetamine releases norepi-
nephrine from these nerve terminals by diplacing the norepinephrine from the
neurotransmitter storage vesicles. Presumably, the overall influence of amphet-
amine on brain function is therefore somewhat different than what occurs
when the locus coeruleus fires rapidly. The amphetamine-induced seepage of
norepinephrine out of nerve terminals probably elicts a milder type of activa-
tion than does the repetitive and presumably more robust ejection of norepi-
nephrine that occurs with rapid firing of the locus coeruleus. Drug-induced
changes in animal behavior support this conceptual model. Amphetamine elic-
its behavioral activation, represented by the rats or mice running about the
cage. In contrast, electrical stimulation of the locus coeruleus produces a more
dramatic startle response. It is difficult to observe a rat and make inferences
about what the animal is feeling, but rats in whom the locus coeruleus has been
stimulated seem to go into a state of panic. They stare about, hyper-responsive
to all stimuli in the enviornment, whether visual, auditory, or tactile.
Rats show the same hyper-responsiveness to environmental-stimuli--
jumping abruptly at the sound of fingers snapping or in response to a puff of
air in the face--when they have been treated with a psychedelic drug. And as
you will recall, hyper-responsiveness to sensory stimuli of all modalities is
just what one observes in humans under the influence of psychedelic drugs. At-
tracted by the similarity between the behavior of rats on LSD and their reac-
tion to stimulation of the locus coeruleus, Aghajanian embarked in 1980 upon
a series of studies to evaluate how psychedelic drugs affect the locus
coeruleus. He showed that any kind of sensory stimulation--sight, sound, smell,
taste, or tactile sensation--speeds up the firing of locus coeruleus neurons in
rats, and that the accelerated firing is greatly enhanced by treating the
animals with LSD or mescaline. In contrast, nonpsychedelic drugs, such as
amphetamines and antidepressants, fail to exert this effect. Moreover, the LSD
analogue methysergide, which has no psychedelic effects in humans, is
correspondingly ineffective in enhancing the reactivity of locus coeruleus
neurons to sensory stimulation.
Although psychedelic drugs increase the response of locus coeruleus cells to
sensory stimulation, they do not cause the neurons to fire spontaneously in the
absence of such stimulation. Moreover, directly applying LSD or mescaline to
locus coeruleus neurons does not enhance the neurons' reponse to sensory
stimulation. We must therefore conclude that the effect of psychedelic drugs on
sensory stimulation is indirect--the drugs presumably interact with a different
set of neurons that in turn make direct contact with the locus coeruleus.
What is particularly fascinating about Aghajanian's findings is how nicely
they correspond to what we know about the effects of psychedelic drugs in
humans, and how readily they explain the way psychedelic drugs accentuate all
our sensory perceptions. The locus coeruleus is a funneling mechanism that
integrates all sensory input. Viewed in this way, the observations of
Aghajanian can explain synesthesia. If the locus coeruleus lumps all types of
sensory messages--from sights, sounds, tactile pressures, smells, tastes--into
a generalized excitation system within the brain, one can readily appreciate
that stimulation of the locus coeruleus will cause the drug user to feel that
sensations are crossing the boundaries between different modalities.
Aghajanian's research may also illuminate how LSD influences the user's
sence of self. The greatly accelerated firing of the locus coeruleus presumably
provokes a powerful, patterned release of norepinephrine from nerve terminals
throughout the brain. As we discussed earlier, the consequent alerting action
would be much more pronounced than what occurs with the far more gradual
leaking out of norepinephrine produced when amphetamine displaces the
transmitter from the storage vesicles. This extremely enhanced level of alert-
ness might possibly account for the "transendent" mental state produced by
psychedelic drugs. In other words, in a state of such heightened awareness, the
drug user may become conscious of an "inner self" to which he or she is
normally oblivious.
Did that answer any of your questions? Probably not, but I thought it was
interesting.
P.S. Snyder has tripped before =)
.....
>>Lysergic-acid diethylamide
>>
>>When ingested into the human body, LSD act as 5-HT (Serotonin) autoreceptor
>>inhibitor, thus it is a 5-HT agonist. LSD increases the level of active
>>5-HT molecules by disaffecting their autoreceptors (a safeguard type feature
>>in the brain which reduces levels of certain neurotransmitter and the like).
That "thus" in the first sentence should be an "and." I'm not certain
what "disaffecting" should be (autoreceptors' only true loyalty is
to the laws of chemistry & physics) for the second sentence to be
true.
The autoreceptors in question are 5-HT1As. 5-HT2s, which are not
autoreceptors and which hallucinogens agonize, seem to be the more
important ones for hallucinogenic activity. Hallucinogens need not
affect 1As directly (some definitely don't). However, 5-HT2 receptor
activation seems to facilitate presynaptic 1A function (such that,
for example, hallucinogen use produces rapid 5-HT2 downregulation
which, in turn, decreases 5-HT1A function). So hallucinogens would
inhibit autorecetpor activity, but not necessarily directly.
>LSD also has effects on 5-HT1C receptors, and its not entirely sure what the
>specific receptor mechanism is -- there's also the question of why the
>psychological effects seem to last much longer than the presence of the LSD
>molecule. One thing that is fairly sure is that LSD shuts down the firing of
>the seratonin neurons in the raphe, though.
It is difficult to separate 1Cs from 2s because of their great similarity.
However, hallucinogens seem to be all 2 & 1C agonists. Molecules which (like
LSD) are partial 2 agonists, and which (unlike LSD) are 1c antagonists
are not hallucinogenic.
I believe that the effects of DOI (and probably LSD) on firing in the
raphe nucleus are not blocked by 5-HT2 antagonists (like ketanserin),
implying that these effects are not mediated by 5-HT2 receptors.
Oddly enough, ritanserin (which antagonizes 2 and 1C) doesn't block
'em either. That's kind of mysterious to me.
> 5-HT has been implicated in
>>certain behaviors, notably dreaming and sleep, which explains the hallucinatory
>>effect. We are in effect dreaming while completely awake and aware.
>Actually, a better explanation is the increased firing of the locus coereleus
>by its disinhibition due to the neurons in the raphe slowing down (since you
>are inhibiting an inhibitory neuron the result is excitation...). The l.c.
>has been associated with being a "sensory highway" in the brain, and has also
>been associated with feelings of anxiety, and theorized that its invovled
>with depression. My guess is that the hallucinations and stimulatory effects
>of LSD come from potentiating the l.c., while the effect on the 5-HT neurons
>in the raphe is responsible for its entheogenic effect on the mind.
This isn't the full story since this decrease in firing (in the raphe) is still
produced by hallucinogens even after chronic treatment with hallucinogens.
Since tolerance does develop to hallucinogens, we would have
expected to see it in the firing. Of course, rate of firing and amount
of 5-HT released _are_ two different things. Besides, tolerance may
occur via another route.
*****
RELATED COMPOUNDS:
Related compounds are the indole hallucinogens including DMT
(dimethyl-tryptamine), DET (diethyl-), etc.; psilocybin; lysergic acid. DMT
is very fast acting, lasting less than an hour. Psilocybin, found in
hallucinogenic (aka magic or mexican) mushrooms, has effects similar to LSD
but they work for approximately half the duration. These are all indole
derivatives like the neurotransmitter serotonin, 5-hydroxy-tryptamine.
"Indole" is the name of the 6-carbon ring attached to the 5-ring containing
a nitrogen. The lysergic acid molecule contains an indole structure plus
additional rings.
LSD's two ethyl groups hanging off the amine may be replaced with
other carbon chains for compounds with different durations, potencies,
and effects.
While LSD is semi-synthetic, DMT and psilocybin are found in nature.
See the sections on BOTANY and ANTHROPOLOGY for info on related
natural (plant) compounds and their uses. Also see the Psilocybe
Mushroom and DMT FAQs for more information on these compounds.
*****
MANUFACTURE:
Forget it. Precursors (ergot alkaloids, used medicinally for migraines and
ob/gyn due to their vasoconstrictive effects) are closely watched. (They
are obtained through commercially cultured ergot fungus; one could
theoretically extract lsyergic amides from morning glory or Hawaiian wood
rose seeds.) (Though there are routes to synthesize lysergic acid from
"scratch", these are complicated also.) Other typically needed chemicals
are very dangerous. Serious experience in organic chemistry lab would be
necessary. If you have to ask where to find the recipes, you don't know
enough about chemistry to try it. (For the curious: the _Anarchists
Cookbook_ is a bad place to start. _Psychedelic Chemistry_ is better, the
patent office or chem. lit. better.) And you'll probably trip during
manufacture if you actually succeed. Its easier and safer to buy it on the
black market.
.....
>In the Journal of Psychoactive Drugs, 1980, there is an article
>on an ergot derivative used in obstetrics which is an hallucinogen.
>Although the dose required is ten times the ED50 (.2 mg) no
>significant ill effects were reported.
>I believe the name of this drug is methyl ergovine(?) The drug
>without the methyl group is supposed to be more effective. It
>was (is?) a Sandoz drug, for those with a PDR.
Ergonovine and methylergonovine are both oxytocic agents: they increase
uterine tone and are used (rarely) to assist in delivery and (more
frequently) to stop post-partum uterine hemorrhage. Less frequently,
they can be used to abort a migraine headache. If they have any
hallucinogenic effects, it is certainly a well-kept secret.
I would be quite concerned about taking 10x the therapeutic dose
of a drug like ergonovine, since it can cause arterial spasm and
precordial distress even in healthy persons, and intense vaso-
constriction and gangrene can follow from an overdose. These
are not drugs to fool around with.
Another related drug, 1-methyl-methylergonovine, or methysergide
(Sansert), is used in migraine prophylaxis, and is claimed to have
LSD-like actions when high doses are taken. The methyl group on
the indole nitrogen reduces the drug's vasoconstrictive actions.
Chronic, uninterrupted use of the drug causes a fibrosis of the
heart valves and the lungs.
.....
>You mean to tell me that the people who make LSD have a GC/MS in their
>basement and know how to use it properly.
No, but they probably run the GC/MS where they work and can sneak samples
in -- or else know someone in a chem department somewhere that can do it
for them.
>I had no idea that the field was
>so high tech.
LSD is not particularly easy to synthesize. It certainly takes a little bit
more than 2nd year O-Chem to do it. There are various synthetic methods
floating around the net, along with methods published in _psychedelic
chemistry_ but i gather that they're all more difficult than some relatively
recent methods...
.....
When I saw the subjects relating to the synthesis of LSD, I knew the
information would be outdated. It's humourous to see people who think
they're in the know giving out information that was outdated even in the 70's.
Lysergic acid amides are commonly made by a simple and efficient procedure
using POCl3 and the desired amine in CHCl3 solution. I doubt that this
procedure is used by the majority of clandestine chemists, but since I
don't know any, I wouldn't know. By the description of the procedure,
it's simple and uses relatively safe reagents. (I have a reference, but
not handy...) And you won't find it in any obvious places even in the
most recent Merck because LSD is not the product of focus in the article.
This is why I doubt that unsavvy clandestine chemists would be using this
procedure. But according to the article, the method has a broad scope
and has been used by Nichols and Oberlender for some other lysergic acid
amides. (The article in question regards 9,10 saturated derivatives
tested for emetic properties.) It's time to stop turning to those stupid
"how to make your very own drug" guides and learn how to read real chemsitry
literature. If you can't, don't bother...
Even the synthesis of lysergic acid is outdated. Rebek has described
an extremely elegant synthesis of methyl lysergate from L-tryptophan
which gives only the natural isomer of lysergic acid. It's still a
several step procedure, but most of the reagents are fairly common and the
yields are greatly improved over past syntheses.
This brings me to an interesting side-note. Several years ago, analogues
of LSD that were 2 and 3 times as potent as LSD were synthesized. These
went largely unnoticed and would most likely prove of little interest
to clandestine chemists because LSD was the precursor used and the loss
in synthesis outweighed the gain in potency. But using Rebek's synthesis,
one could simply alter the procedure slightly and intorduce the groups
that make the compounds more potent. When the 6N-methyl group is replaced
by ethyl or allyl, it becomes 2 and 3 times as potent respectively.
I am posting this for general information. I may post references if I
decide it would be prudent. Requests will be ignored and I ask you not to
send e-mail requesting references. But if you just want to chat about them
and maybe speculate on subjective effects or other avenues of substitution...
I don't know if I'll ever see the day that research in this area is open
and legal, but I'd love to...
*****
DRUG TESTING:
No risk. Its not looked for, hard to find, and transient.
.....
"A maximum concentration of 2-8 ng/ml [Plasma concentration of LSD]
was reached 1.0-1.25 h after an oral dose of 160 ug.
...[A] value of 2.9 h for the elimination half-life of LSD from
plasma [was reached].
[Upshall, D.G., Wailling, D.G.: The determination of LSD in
human plasma following oral administration.
Clinica Chimica Acta 36, 67-73 (1972)]
Second of all, LSD and its metabolites are detectable in the urine
for much longer than one hour.
"LSD and its metabolites were still detectable in human urine for
as long as 4 days after the ingestion of 0.2 mg of the drug.
[Faed, E.M., McLeod, W.R.: A urine screening test of lysergide.
Journal of Chromatographic Science. 11, 4-6 (1973)]
Note that standard, cheap initial drug screening does not use
chromatography or mass-spectrometry, and does not look for LSD.
.....
There were rumors going around that LSD could be detected
by drug tests fo thirty days. I think this reference and
abstract makes it clear that it is probably 4 days, max.
(see the end of the abstract)
IDNUM 03319915
TYPE Journal paper
DATE 880715
AUTHOR Heng Keang Lim; Andrenyak, D.; Francom, P.; Foltz, R.L.; Jones, R.T.
Center for Human Toxicology, Utah Univ., Salt Lake City, UT, USA
TITLE Quantification of LSD and N-demethyl-LSD in urine by gas
chromatography/resonance electron capture ionization mass
spectrometry
SOURCE Analytical Chemistry; vol.60, no.14; 15 July 1988; pp. 1420-5
SUBJECT chromatography; electron capture; mass spectroscopic chemical
analysis; organic compounds; quantification; gas chromatography;
resonance electron capture ionisation mass spectrometry; LSD;
N-demethyl-LSD; urine; lysergic acid diethylamide; human; in vitro;
in vivo; aromatic hydroxylation; drug; metabolite;
N-tri-fluoroacetyl derivatives; calibration curves; urinary
concentrations; adult volunteer; excretion; elimination half-lives;
4 to 6 hrs; 8 to 10 hrs
Numerical data: time 1.4E+04 to 2.2E+04 s; time 2.9E+04 to 3.6E+04 s
Class codes: A8280M; A8280B; A3470
CODEN ANCHAM
ABSTRACT Demethylation of lysergic acid diethylamide (LSD) in the human has
been demonstrated, both in vitro and in vivo, and aromatic
hydroxylation at positions 13 and 14 has been tentatively
identified. A gas chromatography/resonance electron capture
ionization mass spectrometry (GC/MS) assay for LSD and
N-demethyl-LSD in urine has been developed, in which the drug and
its metabolite are converted to their N-tri-fluoroacetyl derivatives
prior to GC/MS analysis. Linear and reproducible calibration curves
have been obtained for LSD concentrations from 0.05 to 5.0 ng/mL,
and for N-demethyl-LSD concentrations from 0.03 to 5.0 ng/mL. The
assay was used to determine the urinary concentrations of LSD and
N-demethyl-LSD following administration of a single oral dose of the
drug (1 mu g/kg) to an adult volunteer. The rates of excretion of
LSD and N-demethyl-LSD reached maxima in urine collected at time
intervals of 4-6 and 8-10 h after administration, respectively. The
elimination half-lives for LSD and N-demethyl-LSD were 3.6 and 10.0
h, respectively
MISCELLANEOUS
Treatment: experimental
Anal. Chem. (USA)
Abstract number(s): A89037987
ISSN: 0003-2700
Refs: 15
.....
If you smoke only occasionally (once or twice a month) you are likely
to pass a urine test within no more than 3-5 days. If you smoke several
times a week, you should allow at least 3-4 weeks, and if you smoke
several time daily, you may need 6 weeks or more (84 days is the record).
However, there are ways that can help you pass a urine test on shorter
notice. For info, contact California NORML, 2215-R Market St. #278,
San Francisco CA 94114; (415) 563-5858.
What they are most likely to detect about a diluted sample is incorrect
temperature. More and more labs are checking to see that the specimen is
within the range 92-100 degrees F. To my knowledge, no one looks at cholrine
or fluorine. Howver, there has been some talk of testing creatanin levels,
which can tell if urine has been diluted.
Actually, your friend took an unnecessary risk in diluting his sample
in the first place. The fact is that occasional marijuana use (say, on the
order of once a month or two weeks) is typically detectable only 2-5 days.
A lot of occasional users get really paranoid because they hear of marijuana]
staying around 4-6 weeks, but this is true only for regular users who smoke
every day. For info about urine testing, send to Cal. NORML, 2215-R Market
St. #278, San Francisco CA 94114 (415) 563-5858.
.....
Spinal taps are not particularly useful (cerebro-spinal fluid doesn't
concentrate LSD or metabolites) and are never done under any
circumstances: they are painful and dangerous.
.....
You might want to mention that Abbie Hoffman's _Steal This Urine Test_
has a table which claims lsd is detectable for 40 days. I'm almost sure
this was a typo.
.....
> 1] How long can LSD be detected in the body?
This varies by the test being used, the detection limit placed on the test,
the point of collection and type of the sample fluid, the amount of LSD that
was taken, and the individual in question.
Assuming the testers are using an RIA screening test with the cutoff set at
0.1 ng/ml and assuming that the user has recently emptied their bladder,
then the detection limit for one hit (100 ug) is normally around 30 hours.
Each doubling of the initial amount will add about 5 hours. Thus taking 8
hits will leave a user vulnerable for approximately 2 days. (NOTE: This is
based on the data in [7])
> 2] What exact form of test can be used to detect LSD in the body? There
are a number of tests which can be used to detect LSD in the body.
Abuscreen, a product of Roche Diagnostic Systems, is a series of
RadioImmunoAssay (RIA) tests, one of which is used to detect LSD and its
metabolites in whole blood, serum (blood), urine and stomach contents [1].
RIA can in theory be used to detect quantities as small as 0.020 nanograms
(ng) per milliliter (ml) of sample [2]. Laboratory tests have shown that
RIA results are accurate down to at least 0.1 ng/ml [3]. The manufacturer
recommends limiting the cutoff to 0.5 ng/ml.
EMIT, a product of Syva Corporation, is another series of tests, one of
which can be used to detect LSD and its metabolites in serum and urine.
EMIT stands for Enzyme Multiplied Immunoassay Technique.
Both EMIT and Abuscreen are "positive/negative" response tests (much like
pregnancy tests) which require periodic equipment calibration and consume
chemicals for each test performed. A basic battery of tests costs approx.
$15-$25 per person [4]. The basic tests (recommended by NIDA) include
marijuana, cocaine, amphetamines, opiates, and phencyclidine (PCP).
Normally, unless an (employer) specifically requests the test, an LSD assay
is not run.
Both Roche and Syva recommend confirmation of positive results by using a
different test. The usual method of confirming positive results is some
form of chromatography. These include High Performance Thin Layer
Chromatography (HPTLC)[3], and different forms of Gas Chromatography/Mass
Spectrometry (GC/MS)[5][6][7][8][9]. HPTLC and GC/MS can be used to give
quantitative results as opposed to the Boolean results from EMIT or
Abuscreen. Laboratory tests have shown that GC/MS test for LSD in urine[6]
and blood[7] can be accurate down to 0.1 ng/ml. The cost for confirmation
of a positive screening test is approximately $50-60.
Positive results to either EMIT and RIA are held to be "probable cause" by
U.S. courts. GC/MS results are held to be "proof" by U.S. courts.
> I am asking for an actual text message containing a short, precise >
description of each test,
Immunoassays chemicals are created by injecting animals (rabbits, sheep,
donkey, etc) with the drug to be tested for and an albumin which force the
animal to produce antibodies. The antibodies are then removed from the
animal, purified and bottled. In RIA tests, the antibodies are then added
to the fluid sample with a radioactively labeled chemical. Any of the drug
(or similar chemicals) found in a sample that is being tested will react
with this glop and by measuring the radioactivity, the amount of drugs can
be determined [2][10].
> 3] How can such a test be beaten?
While there is some literature on adulterating urine samples to produce
false negative results [11], there has been little written that applies
specifically to the LSD screening tests.
The immunsoassay tests vary in their specificity. Some display a relatively
low cross-reactivity[13], others a high cross-reactivity[14]. The exact
metabolites of LSD in humans have not been fully determined yet, though
animal studies have been done. The only verified human metabolite I could
find in the literature was N-demethyl-LSD[6] but I did not check all the
references.
FOOTNOTES:
[1]
Altunkaya, D; Smith R.N.
"Evaluation of a commercial radioimmunoassay kit for the detection of
lysergide (LSD) in serum, whole blood, urine, and stomach contents"
Forensic Science International. v47n2, September 1990, p113-21.
[2]
Taunton-Rigby, A.; Sher, S.E.; Kelley, P.R.
"Lysergic Acid Diethylamide: Radioimmunoassay"
Science. v181, July 13 1973, p165-6.
[3]
McCarron, M.M.; Walberg, C.B.; Baselt, R.C.
"Confirmation of LSD intoxication by analysis of serum and urine."
Journal of Analytical Toxicology. v14n3, May-June 1990, p165-7.
[4]
Berg, E.
"Drug-testing methods: what you should know."
Safety & Health. v142n6, Dec 1990, p52-6.
[5]
Lim, H.K.; Andrenyak, D.; Francom, P.; Bridges, R.R.; Foltz, R.L.
"Determination of LSD in urine by capillary column gas chromatography
and electron impact mass spectrometry."
Journal of Analytical Toxicology. v12n1, Jan-Feb 1988, p1-8.
[6]
Lim, H.K.; Andrenyak, D.; Francom, P.
"Quantification of LSD and N-demethyl-LSD in urine by gas chromatography/
resonance electron capture ionization mass spectrometry."
Analytical Chemistry. v60, July 15 1988, p1420-25.
[7]
Papac, D.I.; Foltz, R.L.
"Measurement of lysergic acid dietylamide (LSD) in human plasma by gas
chromatography/negative ion chemical ionization mass spectrometry."
Journal of Analytical Toxicology. v14n3, May-June 1990, p189-90.
[8]
Paul, B.D.; Mitchell J.M.; Burbage, R.; Moy, M; Sroka, R.
"Gas chromatographic-electron-impact mass fragmentometric determination
of lysergic acid diethylamide in urine."
Journal of Chromatography. v529n1, July 13, 1990, p103-12.
[9]
Blum, L.M.; Carenzo, E.F.; Rieders, F.
"Determination of lysergic acid diethylamide (LSD) in urine by instrumental
high-performance thin-layer chromatography."
Journal of Analytical Toxicology. v14n5, Sep-Oct 1990, p285-7.
[10]
Ratcliffe, W.A.; Fletcher, S.M.; Moffat, A.C.; et. al.
"Radioimmunoassay of Lysergic Acid Diethylamide (LSD) in serum and urine
by using antisera of different specificities."
Clinical Chemistry. v23n2, Feb 1977, p169-74.
[11]
Cody, J.T.; Schwarzhoff, R.H.
"Impact of adulterants on RIA analysis of urine for drugs of abuse."
Journal of Analytical Toxicology. v13n5, Sep-Oct 1989, p277-84.
[12]
Klonoff, D.C.
"Acute water intoxication as a complication of urine drug testing in the
workplace."
Journal of the American Medical Association. v265n1, Jan 2 1991, p84-6.
[13]
Christie J.; White, M.W.; Wiles, J.M.
"A chromatographic method for the detection of LSD in biological liquids."
Journal of Chromatography. v120n2, May 26, 1976, p496-501.
[14]
Twitchet, P.J.; Fletcher, S.M.; Sullivan, A.T.; Moffat, A.C.
"Analysis of LSD in human body fluids by high-performance liquid chromatography,
fluorescence spectroscopy and radioimmunoassay."
J. Chromatogr. v150n1, March 11 1978, p73-84.
Sorry this was so long but I thought it deserved it :-)
Enjoy a "referenced" article.
Tim Basher
.....
There were rumors going around that LSD could be detected
by drug tests fo thirty days. I think this reference and
abstract makes it clear that it is probably 4 days, max.
(see the end of the abstract)
IDNUM 03319915
TYPE Journal paper
DATE 880715
AUTHOR Heng Keang Lim; Andrenyak, D.; Francom, P.; Foltz, R.L.; Jones, R.T.
Center for Human Toxicology, Utah Univ., Salt Lake City, UT, USA
TITLE Quantification of LSD and N-demethyl-LSD in urine by gas
chromatography/resonance electron capture ionization mass
spectrometry
SOURCE Analytical Chemistry; vol.60, no.14; 15 July 1988; pp. 1420-5
SUBJECT chromatography; electron capture; mass spectroscopic chemical
analysis; organic compounds; quantification; gas chromatography;
resonance electron capture ionisation mass spectrometry; LSD;
N-demethyl-LSD; urine; lysergic acid diethylamide; human; in vitro;
in vivo; aromatic hydroxylation; drug; metabolite;
N-tri-fluoroacetyl derivatives; calibration curves; urinary
concentrations; adult volunteer; excretion; elimination half-lives;
4 to 6 hrs; 8 to 10 hrs
Numerical data: time 1.4E+04 to 2.2E+04 s; time 2.9E+04 to 3.6E+04 s
Class codes: A8280M; A8280B; A3470
CODEN ANCHAM
ABSTRACT Demethylation of lysergic acid diethylamide (LSD) in the human has
been demonstrated, both in vitro and in vivo, and aromatic
hydroxylation at positions 13 and 14 has been tentatively
identified. A gas chromatography/resonance electron capture
ionization mass spectrometry (GC/MS) assay for LSD and
N-demethyl-LSD in urine has been developed, in which the drug and
its metabolite are converted to their N-tri-fluoroacetyl derivatives
prior to GC/MS analysis. Linear and reproducible calibration curves
have been obtained for LSD concentrations from 0.05 to 5.0 ng/mL,
and for N-demethyl-LSD concentrations from 0.03 to 5.0 ng/mL. The
assay was used to determine the urinary concentrations of LSD and
N-demethyl-LSD following administration of a single oral dose of the
drug (1 mu g/kg) to an adult volunteer. The rates of excretion of
LSD and N-demethyl-LSD reached maxima in urine collected at time
intervals of 4-6 and 8-10 h after administration, respectively. The
elimination half-lives for LSD and N-demethyl-LSD were 3.6 and 10.0
h, respectively
MISCELLANEOUS
Treatment: experimental
Anal. Chem. (USA)
Abstract number(s): A89037987
ISSN: 0003-2700
Refs: 15
*****
LEGAL SCHEDULING:
Class I, "no medical use" --- mostly for political reasons, as it was
and is used in psychotherapy. (Current use is in Switzerland.)
Though LSD has very different subjective qualities than MDMA, Dutch psy
chiatrist Dr. Hans Bastiaans' use of LSD for decades in the treatment of
concentration camp survivors is an inspiring example of the beneficial use of
psychedelics in the treatment of people with severe trauma.
*****
SET and SETTING:
"SET" is the expectations a person brings with them. "Setting" is the
environment that a person is in. Set includes expectations about the
drug's actions and how the person will react. Setting includes the
social and physical conditions. For LSD and the hallucinogen-type
drug more than other psychoactives, set and setting are very important
in determining the nature of the experience. These factors make the
difference between, e.g., the experiences of someone taking the drug
for enhancement at a concert, for psychotherapy in an doctor's office,
in a religious context, or in the outdoors for an aesthetic
experience. For best results, one should take LSD only with people
one trusts in safe, comfortable surroundings, free of everyday
intrusions. Tripping alone is a very risky thing to do, that
inexperienced people should avoid.
*****
STORAGE:
First, note that LSD is a fairly stable organic molecule, no more or
less fragile than other molecules with comparable structures.
The main factors to be concerned with are moisture (due to leaching
and facilitated chemical reactions in the presense of moisture),
oxygen, light, and temperature. Reaction rates typically depend upon
temperature exponentially. These factors basically apply to all
organic compounds.
Sealing in AL foil in a cool dark place is fine. Some recommend
refrigeration, but be careful about nosy guests, condensation, and frost.
Multiple, redundant seals are suggested, eg., paper in metal foil in
plastic in a metal candy tin which has been taped shut. Should last
at least a presidential term.
Wallets are contraindicated as storage locations due to sweat.
*****
SYNERGIES, BAD COMBINATIONS:
Smoking cannabis products considerably increases the effects,
increasing the visuals and also possibly increasing the cognitive and
linguistic disorders. As the effects of LSD wear off, marijuana may
bring them back, and also ease the jitteriness some dislike. Nitrous
oxide goes well with LSD, though one should be extra careful (not to
suffocate or fall down) with the nitrous because of the effects of the
LSD. MDA & cousins can go well, but people on these drugs should not
take LSD unless they are familiar with the latter's effects.
Alcohol's effects are largely overwhelmed by LSD, and they act in opposite
ways: alcohol being a depressant and LSD being a (hyper)stimulant.
Generally mixing stimulants and sedatives is counterproductive.
MAO inhibitors ???
Amphetamines and cocaine ???
*****
AFTEREFFECTS:
The psychedelic experience is not something that should be undertaken
lightly. While you will be physically OK after the trip, and odds are
you'll still have all the bolts in your head screwed in right afterward,
the trip is very likely to cause lasting mental changes. All the following
effects are strongest in the days or weeks after the trip, but they
may well continue in some form for the rest of your life. You may see mild
hallucinations in dark rooms or with your eyes closed. Objects may seem to
vibrate. After prolonged use tracers and open-eye hallucinations may
appear. Especially immediately after the trip, you may experience odd mood
swings and irrational impulses (harmless ones, but people may still think
you're nuts if you fulfill the impulse of "Gee, I really want to jump up on
that rock and bounce on it because life is so wonderful"). Your perception
of objects is very likely indeed to change. You may become captivated by
sights such as snow falling on a dark winter night or the shadows caused by
a candle flame.
Insights acquired during the trip may also have lasting effects. There
are many cases of people discovering a hidden aspect of themselves, ie.
that they are homosexual or that the philosophy/religion they have adhered
to their life is wrong. While the insight itself may be beneficial, the
process of adjusting to it is often painful.
Very few LSD users regret taking the drug, but before taking it one should
still be aware of what may happen. LSD is not an ticket to nirvana or the
cure to all the problems of humanity.
.....
It seems to me that among the many positive benefits from drug use, especially
acid and to a lesser degree other hallucinogens is an enhanced appreciation of
beauty. That is finding aesthetically pleasing images that other people tend to
ignore or not appreciate. Things like enjoying the pattern of frost that forms
on a glass, or the lights of a city, or just the paterns formed on the inside of
our eyelids. This is not just limited to the periods when one is actually under
the effects of the substance. For example while driving into a city at night
with a mixed group of people, one of the persons in the car who occaisionally
uses acid was very taken with the image and described it in very poetic
picturesque words, without exception those who also used drugs were able to
sympathize and understand what the person was talking about. The rest of the
car just looked at them strangely. Or another instant that comes to mind is
the time someone came in from outside very excited and told about how pretty
the lights shining off the frost on the cars in the parking lot looked, the
only people who went back out to look at this were those that had at some point
partaken of these psychoactives. Annother example is a time early in the
morning after a long night of talking and general togetherness, everyone was
sitting back with thier eyes closed and talking about the images that were
coming to thier mind, talking about what they could see in thier mind's eye,
and sharing it with the others there, going from one person to annother
around the room, the people who did drugs had visions that were remarkably more
detailed, vivid, and unusual. Further they could seem to relate to what the
otehr people were describing better.
Let me emphasize that in none of these instances was anyone under the
influence of anything, this was merely their normal mindset. It is not that the
non-users couldn't see the beauty, it is just that they were not excited or
empassioned about it, it did not touch them as deeply.
*****
REFERENCES & FURTHER READING:
HISTORICAL:
LSD: My Problem Child [A. Hofmann, PhD] (excellent)
Storming heaven : LSD and the American dream [Jay Stevens]. (excellent)
Ceremonical Chemistry [T. Szasz, M.D.] (excellent)
Acid Dreams
Drugs and the Brain
Psychedelics Reconsidered
Electric Koolaid Acid Test
Flashbacks (Leary's autobiography)
The Great Drug War
Dealing With Drugs
USAGE/INFORMATIONAL:
Psychedelic Encyclopedia [Stafford] (excellent)
Psychedelic Chemistry [M.V.Smith]
Biochemical Basis of Neuropharmacology (technical)
Consumer Reports: Licit & Illicit Drugs
Recreational Drugs
REFERENCE:
Merck Handbook
Physician's Desk Reference
The Botany And Chemistry Of Hallucinogens, Shultes & Hofmann
JOURNALS:
Journal of Psychoactive (formerly Psychedelic) Drugs
.....
AUTHOR: Cohen, Sidney
AUTHOR AFFILIATION:
U California School of Medicine, Neuropsychiatric
Inst, Los Angeles
TITLE: LSD: The varieties of psychotic experience.
SOURCE: Journal of Psychoactive Drugs 1985 Oct-Dec Vol 17(4)
291-296
ABSTRACT: Discusses the contributing factors (e.g., preexisting
character structure, insecurity, negative experience,
current mood and stress level) and prevention and
treatment of acute and prolonged psychotic reactions
to LSD. (10 ref)
.....
Additional (detailed) References (in random order):
"Indole Alkaloids In Plant Hallucinogens" Richard Evans Schultes, PhD.
Journal of Psychedelic Drugs Vol.8(No.1) Jan-Mar 1976
"Ethnopharmacology and Taxonomy of Mexican Psychodysleptic Plants"
Jose Luis Diaz M.D.
Journal of Psychedelic Drugs Vol. 11(1-2) Jan-Jun 1979
"The Botanical and Chemical Distribution of Hallucinogens"
Richard Evans Schultes, PhD.
Journal of Psychedelic Drugs Vol.9(No.3) Jul-Sep 1977
"Burger's Medicinal Chemistry" Fourth Edition, Volume III
Chapter: "Hallucinogens" Alexander Shulgin
J. Psychoactive Drugs Vol 21 (1) Jan-Mar 1989
The Addictive Behaviors: treatment of alcoholism, drug use, smoking, and
obesity
W.R. Miller, Ed
(small amount of info on use of psychedelics in psychotherapy)
Pergammon press 1986
Biological Basis Of Behavior
N.Chalmers R. Crawley S.P.R.Rose Eds
Open Univ Press Harper & Row1971
Recreational Drugs
Young Klein Beyer
Collier Books, div of Macmillan pub co 1977
The Biochemical Basis Of Neuropharmacology
J.R.Cooper F.E.Bloom R.H.Roth
Oxford Univ Press 1982 (4th ed)
Craving For Ecstasy: Consciousness And Chemistry Of Escape
H.Milkman S.Sunderwirth
Lexington Books, DC Heath and co 1987
A Primer of Drug Action
R.M.Julian
W.H.Freeman & Co.1978
LSD & Creativity
O.Janiger, M.D.de Rios
J. Psychoactive Drugs Vol 21 (1) Jan-Mar 1989
An Introduction To Pharmacology
J.J.Lewis
Williams and wilkins Co, Baltimore 1964 (3rd edition)
Metabolism Of Drugs Of Abuse
Spectrum Publications 1976
Dist by Halstead Press of John Wiley Press
L. Lemberger
Medicinal Chemistry: a series of monographs
G.deStevens Ed
Vol 4: Psychopharmaceutical agents
M. Gordon (ed)
Vol I, ch 13: psychomimetic compounds D.F.Downing
Vol II, ch 4: psychomimetic agents by A.T.Shulgin
Academic press 1976
The Road To Eleusis
Unveiling the secret of the mysteries
R.G.Wasson, A.Hoffman, C.A.P.Ruck
harcourt brace jovanovich inc. 1978
Lsd Man And Society
R.C.Debold, R.C.Leaf Eds
Wesleyan U press
Middletown Conn 1967
Hallucinogenic Plants (A Golden Guide) New York: Golden Press
1976
Shultes, R.E., Smith E.W.
The Sun And The Moon
A.Weil, MD
The Natural Mind
A.Weil, MD 1986
Houghton-mifflin pub co.
Sacred Narcotic Plants Of The New World Indians
H. Schleiffer ed.
Hafner press 1973
Div of mcmillan pub co
Moksha: Writings On Psychedlics And The Visionary Experience
A.C.huxley
stonehill pub co., NY
M.Horowitz, C. palmer Eds 1977
Psychedelic Chemistry
m.v.smith
2nd edition 1973
rip off press
Psychotropic Methoxyamphetamines: Structure And Activity In Man
S.H.Snyder, E.Richelson, H.Weingartner, LA.Faillace
Ethnopharmacological Search For Psychoactive Drugs
Proc of a symposium in SF, Ca Jan 28-30 1967
D.H.Efron, B.Holmstedt, N.S.Kline eds
US Dept of HEW
The Botany And Chemistry Of Hallucinogens
R.E.Schultes, A.Hofmann
charles C Thomas Publisher
Springfield Ill 1980
The Behavioral Effects Of Drugs
(Ch 4 Hallucinogens: Complications of LSD: A Review of the Literature;
Dimensions of the LSD, Methlphenidate, and Chlordiazepoxide
Experiences; LSD: Injection Early in Pregnancy Produces Abnormality
in Offspring of Rats; LSD: No Teratogenicity in Rats; Congenital
Malformation Induced by Mescaline, LSD, and Bromolysergic Acid in
the Hamster; Drug Motivated-Behavior: The Effect of Morning Glory Seeds
On Motor Activity In Chicks) (Also Includes Weil'S Study Of "Clinical and
Psychological Effects Of Marijuana In Man")
D.W. Matheson M.A. Davidson Holt Rinehart
Winston Inc 1972
any textbook titled "Physiological Psychology"
.....
*BOOKS*
(For a complete listing of books that we have in the No More
Drug War Foundation Research Library, e-mail or write your
address to me:
Gerald Bryan, Secretary
The No More Drug War Foundation
2045 Kearney St.
Denver, CO 80207-3919
303/388-5495 days
303/394-3930 evenings)
BREAKING THE IMPASSE IN THE WAR ON DRUGS, by Steven Wisotsky,
1986, 279 pages, $35.00, Greenwood Press. Sympathetic to the
idea of legalization. Can be ordered from publisher at 88
Post Road West, Box 5007
PSYCHEDELIC DRUGS RECONSIDERED, by Lester Grinspoon & James B.
Bakalar, 1979, 1981, Basic Books, Inc. Good book that covers
all aspects of psychedelic drugs, written by Harvard professors.
You can probably order this from anywhere.
ECSTASY: THE MDMA STORY, by Bruce Eisner, mid-1980s. Covers
all aspects of this drug, good book, available anywhere.
PSYCHEDELICS ENCYCLOPEDIA, by Peter Stafford, Revised Edition,
1983, J.P. Tarcher, Inc. Great resource book, you can probably
order this from anywhere (huge bookstore in Denver had it in
stock)
*ORGANIZATIONS*
The Drug Policy Foundation The grand-father of all the
4801 Massachusetts Ave., N.W. legalization groups, this one
Suite 400 appeals to educated mainstream
Washington, D.C. 20016-2087 folk. Holds annual conference,
202/895-1634 has respectability. This is a
MUST-JOIN !!
Multidisciplinary Assoc. for Educational group seeking to
Psychedelic Studies (MAPS) give drug study legitimization
23A Shaler Lane through normal public policy
Cambridge, MA 02138 channels. Supports drug
617/547-7271 research projects worldwide.
The Albert Hofmann Foundation Educational group seeking to
132 West Channel Road build a library to house
Suite 324 vast amount of research work
Santa Monica, CA 90402 done on consciousness, including
extensive LSD studies.
Coalition for 100% Drug Reform Political, grass-roots activist
9 Bleecker Street group seeking an end to zero-
New York, NY 10012 tolerance policies and promoting
212/995-1245 safe drug use education. They
have a drug reform conference
scheduled for Dec 1-3.
The No More Drug War Foundation Activist group seeking to bring
Box 18780 an end to the drug war through
Denver, CO 80218 grass-roots political action &
303/320-1910 education.
N.O.R.M.L. Still around, still holding pot
2001 'S' Street, N.W. rallies. Good for people who
Suite 640 want MJ legalized but don't care
Washington, D.C. 20009 about other drugs.
202/483-5500
Ed Hassle's Freedom Fighters Activist group associated with
Trans-High Corp High Times. Similar agenda to
211 East 43rd St. NORML.
NY, NY 10017
PRIDE Yes, this is an anti-drug,
50 Hurt Plaza pro-drug-war group, but they
Suite 210 publish a good newsletter
Atlanta, Georgia 30303 that informs well on what the
404/577-4500 opposition is doing.
800/241-7946
.....
(about visual disturbances: )
Migraine: the evolution of a common disorder
O. Sacks
U CAl press 1970
Brain Damage, Behavior, And The Mind
M. Williams
John Wiley & Sons 1979
ch 5 Disorders of visual perception
Mescal And Mechanisms Of Hallucinations
Heinrich Kluver
U. Chicago Press 1930
Drugs And The Brain
Perry Black MD, Ed
Johns Hopkins Press 1969
behavioral effects of LSD in subhuman primates
Hallucinations
Sci Am
R.K.Siegal
(see also article on phosphenes in amateur scientist column in another issue)
Luria's _The Shattered Mind_
Multidisciplinary Association for Psychedelic Studies (MAPS) -
Your Psychedelic Pharmaceutical Company
by Rick Doblin, MAPS President
MAPS, 1801 Tippah Avenue, Charlotte, NC. 28205 Phone (704) 3
58-9830, FAX (704) 358-1650, e-mail RICKMAPS@aol.com
Becoming a member of the Multidisciplinary Association for Psychedelic
Studies, Inc. (MAPS) and receiving the MAPS newsletter is an excellent way to
stay abreast of the latest developments in psychedelic research around the
world. In addition, your membership donation will be used to support
research into the medical uses of MDMA, LSD, marijuana,
and a cornucopia of other fascinating compounds.
MAPS is an IRS-approved non-profit corporation supported by tax-deductible
contributions from a membership of about five hundred people and growing.
MAPS works to develop the medical potential of MDMA and other psychedelics
by assisting researchers around the world to design, obtain governmental
approval for, fund, conduct and report on psychedelic research. MAPS is
also involved in research exploring the medical use of marijuana. MAPS'
primary goals are to help researchers conduct the studies necessary to
transform MDMA and marijuana into FDA-approved prescription medicines. For
MDMA, this is an estimated ten-year, $10 million project; for mar
ijuana, a two-year, $500,000 task.
MAPS offers its members a quarterly newsletter reporting on MAPS-sponsored
and other psychedelic research in progress both in the US and abroad,
political developments that affect psychedelic research and use, and
conferences, books and articles of interest. In addition, MAPS offers for
sale various unique publications (for example the protocol submitted to the
FDA for the investigation of the use of MDMA in the treatment of pain and
distress in terminal cancer patients), videotapes (of a MAPS benefit held in
Berkeley in 1990 that featured Jerry Beck, Ram Dass, Bruce Eisner, Rick
Doblin, Laura Huxley, Emerson Jackson, Mark Kleiman, Timothy Leary, Dennis
McKenna, Terence McKenna, Ralph Metzner, Andrew Weil, and Robert Zanger), and
audiotapes (of a MAPS seminar held in Prague in 1992 featuring Ram Dass, Ken
Ring and Richard Yensen discussing working with the terminally
ill with psychedelics).
Since its inception in 1986, MAPS has invested about $75,000, donated by
its members, into preliminary FDA-required 28-day MDMA toxicity studies in
the dog and rat. These studies were submitted to the FDA in order to open
MAPS' FDA Drug Master File for MDMA. These toxicity studies were a
prerequisite for all FDA-approved studies involving the administration of
MDMA to human volunteers. When UC Irvine psychiatrist Dr. Charles Grob
applied to the FDA to conduct human research with MDMA, MAPS provided him
with written permission to cross-reference its MDMA Drug Master File. This
document saved Dr. Grob from having to reproduce the toxicity data, a hurdle
that he would have foun
d prohibitively expensive.
MAPS has also invested an additional $125,000 on pilot studies into the
effect of MDMA on the serotonin levels of humans, on MDMA neurotoxicity
studies in the primate, and on protocol design for Phase 1 and Phase 2 human
studies with MDMA. In addition to MAPS' preliminary toxicity research and its
subsequent efforts on protocol design, MAPS successfully assisted Dr.
Charles Grob in obtaining FDA permission to study the effects of MDMA on
human volunteers. Dr. Grob's study is the first that the FDA has ever
permitted involving the administration of MDMA to human volunteers. The
study is designed to gather information for a subsequent study by Dr. Grob
which will investigate the use of MDMA in the treatment of pain and distress
in end-stage pancreatic cancer patients. MAPS intends to raise funds for Dr.
Grob's studies and provide him with whatever scientific and profess
ional support he may need to conduct his experiments. One function of
MAPS is to conduct MDMA research as if MAPS were a pharmaceutical company
interested in making MDMA into a prescription medicine. The critical
difference is that MAPS makes its data available for free to responsible
researchers to help advance the field of MDMA research rather than keep the
data as proprietary information. In this way, duplication of expensive
required studies is eliminated and researchers can focus on research
rather than profit considerations.
*****
This file is in the public domain. Distribute freely.
-- __
Jani "Gnosis" Poijärvi On the neverending quest /(o\ BRAHMAN
gnosis@brahman.nullnet.fi for knowledge by identity. \o)/ +358-0-498797
