LSD FAQ

A very high quality document answering every question you could ever ask about lsd.


Author: David Honig (honig@ics.uci.edu)
Editor:
Last Update: 11 Aug 1991 [added BOTANY and ANTHROPOLOGY sections]
Subject: LSD

FORMATTING INFO:
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[This FAQ provided to reduce net bandwidth, as an
informational resource only.]

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CONTENTS: />
LSD (definition, introduction)
Delysid (PDR description of pharmaceutical LSD)
(pharmacology)

CAUTIONS, REAL AND IMAGINED
ADDICTION POTENTIAL (none)

ADULTERANTS (including the strychnine myth, manufacturing impurities, etc.)
BAD TRIPS (what
they are, how to avoid, what to do)
MYTHS (stamps for children, staring at the sun..)

DANGERS (LSD isn’t for morons…)
FLASHBACKS (what they are —post-traumatic stress
syndrome)
INSOMNIA (common, what to do)
TOLERANCE (aquired and lost quickly (3 days)
harmlessly, no withdrawl)

BACKROUND
ANTHROPOLOGY (and history)
BOTANY
(sources in nature)
CHEMISTRY (structure)
MECHANISM OF ACTION (uncertain)
RELATED
COMPOUNDS (psilocybin in mushrooms, ergot alkaloids in morning glories)

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 good time; lsd ain’t beer)

STORAGE (keep in a cool dark dry place)
SYNERGIES, BAD COMBINATIONS (cannabis is good,
otherwise be careful)

REFERENCES & FURTHER READING

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

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

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

…………………………

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 Physician’s Desk Reference:

Delysid (LSD 25)

D-lysergic acid diethylamide tartrate

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

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

The solution may also be injected s.c. or i.v. The

effect is identical with that of oral administration but
sets in more rapidly.

PROPERTIES

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

METHOD OF
ADMINISTRATION

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

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

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

INDICATIONS AND DOSAGE

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

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

In normal subjects, doses of 25 to 75 ug. are generally

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

PRECAUTIONS

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

last for some days.

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

ANTIDOTE

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

Literature
available on request.

SANDOZ LTD., BASLE, SWITZERLAND

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

…………………………

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

Peripheral
Actions

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

LSD causes mydriasis in man and other species. It
also causes
hyperglycaemia and mydriasis, has a hyperthermic action and causes

piloerection. These effects are sympathetic in nature and are
abolished by ganglion blocking
or adrenergic blocking agents.
Parasympathetic effects include salivation, lachyrmation,
vomiting,
hypotension, and brachycardia. Low doses stimulate respiration but
larger
doses depress it.

(nb: mydriasis = pupillary dilation)

…………………………

Hoffman thought the diethylamide version of the lysergic
acid molecule
might be a respiratory stimulant…

…………………………

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.
Rarely people use it to escape in a negative
way or as part of "polydrug abuse"
behavior or pattern of behavior.

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

ADULTERANTS:

Several problems are associated with street drugs: their unknown

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

…………………………

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

"There is a great
deal of superstition regarding purification of
psychedelics. Actually, any impurities which
may be present as a
result of synthetic procedures will almost certainly be without any

effect on the trip. If there are 200 micrograms oof 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.

…………………………

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

/> 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.

…………………………

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

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

deception among the less sought after psychotomimetics LSD and PCP."

…………………………

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 hostpitals 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).

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

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 soluable, 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.

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

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

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

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

…………………………

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

…………………………

See also myths about testing in DRUG TESTING />

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

DANGERS:

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

psychologically.

…………………………

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

877-83).

…………………………

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

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

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

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

…………………………

Never take any drugs
while pregnant.

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

FLASHBACKS:

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

A simple explanation of LSD
flashbacks, and of their changed character
after 1967, is available. According to this theory,
almost everybody
suffers flashbacks with or without LSD. Any intense emotional

experience–the death of a loved one, the moment of discovery that one is in
love, the moment
of an automobile smashup or of a narrow escape from a
smashup–may subsequently and
unexpectedly return vividly to consciousness
weeks or months later. Since the LSD trip is
often an intense emotional
experience, it is hardly surprising that it may similarly
"flash back."

<end quote>

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

INSOMNIA:

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

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

TOLERANCE:

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

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

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

BOTANY:

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

Wasson, an ethnomycological scholar and former banker (and the first

white to trip on shrooms with the mexican indians) proposed the
following explanation of the
Eleusian mysteries to Hoffman, an
ergot-alkaloid expert chemist, and Ruck, a greek scholar: />
The Secret of the ritual involved the personal visions induced by
drinking the grain
decoction administered to the inititiates. 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 backround on the use of
mushrooms and grains and their
role in the culture; Hoffman on the
psychoactivity of ergot strains; and Ruck on the
mythological and
cultural backround of the sect.

Evidence includes: Hoffman dosed
himself with large (ergot-derived)
doses of obstestric 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 suggeted (1957) that the word psychedelic
(meaning
mind-manifesting) be used as a generic term for this class of substances to

refer to their consciousness-expanding and psychotherapeutic function as
contrasted with the
hallucinogenic aspect. In 1960 Hoffman reported that he
had isolated d-lysergic acid amide
(LA) and d-isolysergic acid amide from the
seed of both Rivea corymbosa and Ipomoea violacea.
LA is very similar to LSD
in its psychological and physiological manifestations but is
reported to have
about one twentieth the psychological effectiveness of LSD (Cerletti & /> Doepfner, 1958).

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

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

Low
Dose, 20-50 Seeds (11 Subjects)

This dosage rarely produces any visual distortions,
although with eyes
closed there may be beginning imagery. Restlessness, evidenced by
alternating
periods of pacing about and lying down, may be present. There tends to be a

heightened awareness of objects and of nature, and enhanced rapport with
other persons. A
feeling of emotional clarity and of relaxation is likely to
persist for several hours after
other effects are no longer noticable.

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 cholorpromazine [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 commerically cultivated plants led us to
examine the ornamental
wood roses, Ipomoea tuberosa and Argyreia nervosa, both common Hawaiian
crops
that have assumed commerical importance as components of [the] dried tropical

flower industry." Comparing the seeds of these two plants with those of the
morning glory
varieties Pearly Gates and Heavenly Blue, they found the
following yield of alkaloids (mg of
alkaloid/g of seed material):

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

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

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

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

This is an excerpt from the article cited.

There’s no record of Argyreia being used as an hallucinogen in
India, but it was used
externally as some kind of skin medicine.
There’s been speculation that Argyreia might have
been a component
of "Soma", but there’s no evidence for that, apparently.

Because there’s not a long history of human usage of Argyreia,
it may be that there are
glycosides not mentioned here that
take effect at higher doses or might cause stomach upset,
tachycardia
etc. The article mentioned intestinal complaints in one or two
cases at
higher experimental doses.


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

CHEMISTRY:

lysergic acid diethylamide _is_
lysergic acid diethylamide (or…
N,N-diethyl-D-lysergamide or…

9,10-Didehydo-N,N-diethyl-6-methylergoline-8B-carboxamide).

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

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

LSD-25 Lysergic acid

O CH2-CH3 O
|| / ||
|| / || /> -C–N C—OH
| \ |
| \ |
|___ CH2-CH3 |___
/ \ / \
/ \ / \

<< N—CH3 << N—CH3
\\ / \\ /
\\____/ \\____/
/ \ / \
/ \ /
\
< > < >
// \ / // \ /
// \_____/ // \_____/
| || || | || || /> | || || | || ||
| || || | || ||
\\ /\ / \\ /\ /
\\ / \ / \\ / \ /
N N /> H H

Ergot is a product of the fungus Claviceps purpurea. The bio-active

ingredients of ergot are all derivatives of lysergic acid. LSD is a
semisynthetic derivative
of lysergic acid. Thus LSD is an
"ergot"-like substance.

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

MECHANISM OF ACTION:

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

>From a chapter
titled Hallucinogens and Other Psychotomimetics: Biological
Mechanisms by S.J.Watson
/> "The current thesis of the effect of indole hallucinogens on
5-hydroxytrypamine might
be stated as follows: LSD acts to preferentially
inhibit serotonergic cell firing and seems to
spare postsynaptic serotnergic
receptors. This preference is shared by other simillar
hallucinogens but in
a limited fashion. Nonhallucinogenic analogs of LSD show no
preference.
These results suggest that there are two different steric conformation of

serotonergic receptors, one of which has higher affinity for LSD than the
other. In general,
5-ht is an inhibitory transmitter; thus, when its
activity is decreased, the next neuron in
the chain is freed from inhibition
and becomes more active. Since serotnergic systems appear
to be intimately
involved int eh control of sensation, sleep, attention, and mood, it may
be
possible to explain the actions of LSD and other hallucinogens by their
disinhibition
of these critical systems.

There is also evidence for interaction with dopaminergic
systems.

…………………………

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

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

…………………………

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

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

RELATED COMPOUNDS:

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

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

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

…………………………

1) DMT, DET, psylocin, psylocybin, : The mushroom
psylocybin cubensis
contains all four of these indole derivatives, as well as others. DMT
is
dimethyltryptamine, an indole derivative which has functionalized at the 3
position
with the dimethyl ethylamine group. It is a close relative to the
amino acid, tryptophan,
which until recently was available in bulk at
vitamin shops, until some jerk poisoned himself
by taking a wonga dose of
it. [Actually it may have been a single toxic batch mistakenly
produced in
Japan.] A prep came out in 1984 for LSD using l–tryptophan as the

precursor, so this may have facilitated the government’s pullin it from the
shelves. I can’t
find tryptophan anywhere, now, and I’ve tried, bud.
DMT, and it’s brother DET
(diethyltryptamine), have no oral activity,
so have to be smoked. They stink like fish oil
when lit, though. Both have
hallucinogenic effects within 2-3 minutes of toking, wand while
DMT lasts
for only a half hour, DET is a smoother, more euphoric high, lasting twice
as
long. DET has effects similar to psylocybin.
Psylocybin is DMT which has a functional group,
phosphoryloxy-, at the
4 position on the indole ring. This group is immediately converted
to
hydroxyl- as soon as the stuff hits your stomache to give the cousin,
psylocin. In
preparing the drug, then, it is not necessary to proceed beyond
the psylocin.
DMT and
DET are easily derived from many indole derivatives, the
easiest of which is indole-3-acetic
acid. I’ve done this reaction and it
stinks to high heaven of indole gunge, skatoles
(methylindoles), and
indenes. Bad news if you want to make it at home, because the stench
is
pervasive. Other derivatives, using phenyl or butyl groups have been
reported as
having oral activity, so it is not necessary to smoke the stuff.
Doses run at about a hundred
mgs for smoked drug, while psylocin is orally
active at about 5 mgs.
For a good
reference work on these compounds, their preps, and effects,
see Michael Valentine Smith’s
"Psychedelic Chemistry," publisher unknown.

Your Friendly Neighborhood
Chemical
Dude,
St. Theo

…………………………

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

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

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.

…………………………

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. />
I would suggest you read the article posted by Paul Hager paying particular

attention to the warning about water intoxication [12]:
In
<1991May7.141615.16477@news.cs.indiana.edu> hagerp@iuvax.cs.indiana.edu wrote
+
Recommended: "Dealing With Urine Tests on Short Notice"
+ by Dale Gieringer,
California NORML
+
+ Most folks recommend that people hydrate themselves — the idea /> + being that by drinking water and taking a diuretic that will
+ promote water loss, the
urine will be very dilute and THC metabolite
+ content from "tomatoe" consumption
will drop below the 100 ng/ml
+ threshold that defines a "positive".
+

+ Mr. Gieringer recommends that, the day before the test, the
+ person drink lots of water. I
would amend this to, drink your
+ normal "8 glasses" plus a few more. Don’t get
carried away with
+ drinking water — there is such a thing as "water
intoxication"
+ which can result in brain swelling and other nasties so don’t
+
chug-a-lug a gallon of water just before the test. After
+ hydrating, and a little before the
test, drink some more water
+ and use a diuretic (coffee is a weak diuretic). Urinate to

+ flush the bladder — the first urination of the day is the
+ one most charged with
metabolites. The pamphlet quotes from
+ a _High Times_ article, "How to Beat a Drug
Test":
+
+ Take an 80 mg dose of the prescription diuretic Lasix
+
(furosemide); take a hefty drink of water; piss two
+ or three times; then take the test. /> +
+ Some caution is to be exercised in taking diuretics. Consult
+ your
physician.
+
+ Mr. Gieringer also suggests that the clear, watery urine that
+
results from the above procedure is sometimes suspicious. He
+ recommends taking 50-100 mg of
vitamin B2 which will color
+ urine yellow for a couple of hours. Vitamin C does not
produce
+ this effect — contrary to rumor.
+
+ For more information, I’d suggest
contacting California NORML
+ directly at (415) 563-5858. They are located in San
Francisco.
+ It is also possible that Mr. Gieringer will respond directly
+ via his
canorml account.

> I am asking for …[a description]… of each thing that LSD
leaves behind
> that can be detected, and of each method used to beat each test.
/> 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 electon 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.)

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

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
refridgeration, 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 ???

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

SYNTHESIS:

Don’t try it, too difficult and
risky both physically and
legally. Precursor medical drugs (ob/gyn and migraine ergot

alkaloids) are watched.

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

/> REFERENCES & FURTHER READING:

Historical:
Ceremonical Chemistry
[Szasz] (excellent)
Storming Heaven
Acid Dreams
Drugs and the Brain

Psychedelics Reconsidered
Electric Koolaid Acid Test
LSD: My Problem Child [Hofmann] /> Leary’s autobiography (_Flashbacks_)
The Great Drug War
Dealing With Drugs
/> Use-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
/> 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 Addictvie 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.Hoffman
charles C Thomas Publisher

Springfield Ill 1980

The Behavioral Efffects 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
abnormalitie
in offspring of rats; LSD: no teratogenicity in rats congentital

malformation s induced bhy 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"

…………………………

(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)

******************************END OF
FAQ******************************



Add A Comment

The following large (200K) file is the updated LSD FAQ incorporating

various posts that I’ve collected since this faq first came out.

There is a “Changes” section near the top. This also contains

info on other tryptamine psychedelics, viz. DMT and psilocybin.

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

The Usenet alt.drugs LSD FAQ

Last Update: 9 Aug 94

Subject: LSD

Size: Now 200K, 80K gzip’d

Formatting Info:

topic break: ******************************

within-topic break: …………………………

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

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

Caveat:

[NB: This FAQ provided to reduce the Net's bandwidth / confusion /

misinformation, as an informational resource ONLY. There are some

very informed, and some very clueless people on the Net. This

FAQ tries to shift the balance. The truth shall set you free,

as they say.]

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

Changes since Previous Version

- added synthesis notes, MAPS

- merged misc. files and references, organizations, the baseball

story, recipes I’m not competent to judge

- added scholarly section on creativity

- include more info on related active tryptamine derivatives

- traded off half-a-decibel of signal-to-noise for wider scope

- added mycological horticultural note

- added postscript stereoimage of structure

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

Synopsis / Table of Contents:

LSD (definition, introduction)

Delysid (medical fact sheet for pharmaceutical LSD) (pharmacology)

Cautions, Real And Imagined:

Addiction Potential (none)

Adulterants (including the strychnine myth, manufacturing impurities, etc.)

Bad Trips (what they are, how to avoid, what to do)

Myths (stamps for children, staring at the sun..)

Dangers (LSD isn’t for morons…)

Flashbacks (what they are —post-traumatic stress syndrome)

Insomnia (common, what to do)

Tolerance (aquired and lost quickly (3 days) harmlessly, no withdrawal)

Backround:

Anthropology (and history)

Botany (sources in nature: mushrooms, ergot, morning glories,

hawaiian baby woodrose, tropical plants)

Chemistry (structure)

Mechanism of Action (uncertain)

Related Compounds (indoles: psilocybin, DiMethylTryptamine (DMT) )

Manufacture (forget it)

Drug Testing (don’t worry)

Legal Scheduling (sched. 1, no medical uses in US (despite past effective use))

Pragmatics:

Set and Setting (how to have a positive experience; lsd != beer)

Storage (keep in a cool dark dry place)

Synergies, Bad Combinations (cannabis is good, otherwise be careful)

References & Further Reading:

(Recommended)

_Psychedelic Encyclopedia_ by Peter Stafford

_LSD: My Problem Child_ by Albert Hofmann

_Licit & Illicit Drugs_ (Consumer Reports)

_Storming heaven : LSD and the American dream_ by Jay Stevens

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

LSD

Generic name for the hallucinogen lysergic acid

diethylamide-25. Discovered by Dr. Albert Hofmann in 1938, LSD is one

of the most potent mind-altering chemicals known. A white, odorless

powder usually taken orally, its effects are highly variable and begin

within one hour and generally last 8-12 hours, gradually tapering off.

It has been used experimentally in the treatment of alcoholics and

psychiatric patients. [Where it showed some success.] It

significantly alters perception, mood, and

psychological processes, and can impair motor coordination and skills.

During the 1950s and early 1960s, LSD experimentation was legally

conducted by psychiatrists and others in the health and mental health

professions. Sometimes dramatic, unpleasant psychological reactions

occur, including panic, great confusion, and anxiety. Strongly

affected by SET and SETTING. Classification: hallucinogens. Slang

names: acid, sugar. See also appendix B. (RIS 27:211-52 entries)

– Research Issues 26, Guide to Drug Abuse Research Terminology,

available from NIDA or the GPO, page 54.

…………………………

Common Drug Slang Terms (NB: many of these refer to the carrier, ie, “Blotter”

or “Sugar Cubes”. Often the local names will refer to patterns printed

on the blotter, eg, “Blue unicorn”.):

Acid, ‘Cid, Sid, Bart Simpsons, Barrels, Tabs, Blotter, Heavenly blue,

“L”, Liquid, Liquid A, Lucy in the sky with diamonds, Microdots,

Mind detergent, Orange cubes, Orange micro, Owsley, Hits,

Paper acid, Sacrament, Sandoz, Sugar, Sugar lumps,

Sunshine, Tabs, Ticket, Twenty-five, Wedding bells, Windowpane,

etc.

…………………………

from the data sheet accompanying product:

(see also Physician’s Desk Reference from mid-60’s)

Delysid (LSD 25)

D-lysergic acid diethylamide tartrate

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

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

administration.

The solution may also be injected s.c. or i.v. The

effect is identical with that of oral administration but

sets in more rapidly.

PROPERTIES

The administration of very small doses of Delysid

(1/2-2 ug./kg. body weight) results in transitory distur-

bances of affect, hallucinations, depersonalization, reliv-

ing of repressed memories, and mild neuro-vegetative symp-

toms. The effect sets in after 30 to 90 minutes and gen-

erally lasts 5 to 12 hours. However, intermittent distur-

bances of affect may occasionally persist for several days.

METHOD OF ADMINISTRATION

For oral administration the contents of 1 ampoule of

Delysid are diluted with distilled water, a 1% solution of

tartaric acid or halogen-free tap water.

The absorption of the solution is somewhat more rapid

and more constant that that of the tablets.

Ampoules which have not been opened, which have been

protected against light and stored in a cool place are

stable for an unlimited period. Ampoules which have been

opened or diluted solutions retain their effectiveness for 1

to 2 days, if stored in a refrigerator.

INDICATIONS AND DOSAGE

a) Analytical psychotherapy, to elicit release of

repressed material and provide mental relaxation, par-

ticularly in anxiety states and obsessional neuroses.

The initial dose is 25 ug. (1/4 of an ampoule or 1

tablet). This dose is increased at each treatment by

25 ug. until the optimum dose (usually between 50 and

200 ug.) is found. The individual treatments are best

given at intervals of one week.

b) Experimental studies on the nature of psychoses: By

taking Delysid himself, the psychiatrist is able to

gain an insight in the world of ideas and sensations of

mental patients. Delysid can also be used to induced

model psychoses of short duration in normal subjects,

this facilitating studies on the pathogenesis of mental

disease.

In normal subjects, doses of 25 to 75 ug. are generally

sufficient to produce a hallucinatory psychosis (on an

average 1 ug./kg. body weight). In certain forms of

psychosis and in chronic alcoholism, higher doses are

necessary (2 to 4 ug./kg. body weight).

PRECAUTIONS

Pathological mental conditions may be intensified by

Delysid. Particular caution is necessary in subjects with a

suicidal tendency and in those cases where a psychotic

development appears imminent. The psycho-affective lability

and the tendency to commit impulsive acts may occasionally

last for some days.

Delysid should only be administered under strict medi-

cal supervision. The supervision should not be discontinued

until the effects of the drug have completely worn off.

ANTIDOTE

The mental effects of Delysid can be rapidly reversed

by the i.m. administration of 50 mg. chlorpromazine.

Literature available on request.

SANDOZ LTD., BASLE, SWITZERLAND

9792*-Z1540 e.-sp./d.-fr.

Printed in Switzerland.

…………………………

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

Peripheral Actions

These include an oxytocic action and constriction of the blood vessels

of isolated vascular beds. In intact animals LSD causes a fall in

blood pressure, but its adrenergic blocking potency is low.

LSD causes mydriasis in man and other species. It also causes

hyperglycaemia and mydriasis, has a hyperthermic action and causes

piloerection. These effects are sympathetic in nature and are

abolished by ganglion blocking or adrenergic blocking agents.

Parasympathetic effects include salivation, lachyrmation, vomiting,

hypotension, and brachycardia. Low doses stimulate respiration but

larger doses depress it.

(nb: mydriasis = pupillary dilation)

…………………………

Hoffman thought the diethylamide version of the lysergic acid molecule

might be a respiratory stimulant… (see _Problem Child_ by Hoffman)

…………………………

The “speedy” quality of unadulterated LSD is due to the pharmacological

actions of LSD itself, and not necessarily due to decomposition or impurities.

LSD typically causes early adrenergic effects such as sweating, nervousness,

jaw grinding and insomnia which are easily confused with the side effects

of amphetamine.

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

ADDICTION POTENTIAL:

Zero physical addiction potential. Not something that makes you want to

do it again immediately.

Essentially zero psychological addiction potential.

Rarely people use it to escape in a negative way or as part of “polydrug

abuse” behavior or pattern of behavior. Usually in this case other

drugs are causing more harm, and the fundamental problem is a personal

difficulty; the escapism/distraction is a symptom.

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

ADULTERANTS:

Several problems are associated with street drugs: their unknown

purity and their unknown strength. Because of its extreme cheapness

and potency, the purity of LSD in blotter form is not an issue: either

it’s lsd or untreated paper. The purity of powders, pills, and liquids

cannot be assumed as safe. With regards to uncertain strength, the

strength of hits these days is low, 100 micrograms or so. One should

be careful and assume that the smallest square in a tiling of a sheet

is a dose, even if a printed pattern covers several. An experienced

person could judge the strength of a dose, and if it is assumed all

doses on a sheet have been processed equivalently, those doses would

be calibrated for others, much like anything else.

…………………………

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

“There is a great deal of superstition regarding purification of

psychedelics. Actually, any impurities which may be present as a

result of synthetic procedures will almost certainly be without any

effect on the trip. If there are 200 micrograms of LSD in a tablet,

there could only be 200 mics of impurities present even if the LSD was

originally only 50% pure (assuming nothing else has been added), and

few compounds will produce a significant effect until a hundred to a

thousand times this amount has been ingested. Even mescaline, which

has a rather specific psychedelic effect, requires about a thousand

thimes this amount.”

…………………………

Note that: 1) on a piece of paper, vs. a tablet, you can’t even add

significant amounts of adulterants 2) adulterants would cost, whereas

blank paper will rip someone off just as well.

LSD itself has some “body-kinks” on some people some times. Nausea is

one of them. its usually mild and transient. It also has speedlike

(ie, adrenergic stimulation) effects, etc.

(It is common for the uninformed to harbor fears (e.g., about adulterants)

instilled by ignorance and the current hysteria/propoganda. That’s why this

FAQ exists.)

…………………………

[Referring to strychnine] 15 mg has been fatal, but a more typical fatal

dose is on the order of 50mg. [Another post indicates 25 mg. as the LD50] 1

mg of strychnine orally probably has no observable pharmacological effects

in a typical adult. [1 mg being ten times the effective dose of LSD, by the

way.]

From: Handbook of Poisoning, 10th ed, R.H. Dreisbach, M.D., PhD, Lange Med.

Pub. Co. Los Altos, Ca.: strychnine is lethal in 15-30 mg amounts to adult

humans. (Pure nicotine is fatal at 40 mg./person; cyanide salts are fatal

at about 100 mg./person) Strychnine causes death by respitory failure, via

increased spinal reflex excitability.

Actually, I think the fact that PharmChem analyzed something on the order of

2,000 LSD samples between 1972 and 1979 and never found one with strychnine

in it would be better. I’m going over all their data with a toothpick and

I’ll get back to you on exactly what I find. It looks like the percent of

LSD with strychnine in it is, however, at least under .05%. More a little

later.

…………………………

According to Alexander Shulgin the difinitive answer is that strychnine is

neither used in the synthesis, produced by the synthesis, or a possible

contaminant of the synthesis. But just look at the structures of strychnine

vs Lysergic acid/LSD/etc and you should be able to understand that readily.

…………………………

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

Summary of Street Drug Results - 1973: “Of 189 samples of LSD quantitatively

analyzed, the average dose was 67.25ug LSD. Of the 32 samples of alleged

mescaline actually containing mescaline, [...stuff about mescaline and

mushrooms deleted...] It is interesting to note the low incidence of

deception among the less sought after psychotomimetics LSD and PCP.”

Most likely “good” acid is N-acetyl-LSD (ALD-52) [according to

_Psychedelic Encyclopedia_ it produces a smoother trip and is somewhat

commonly found in analysis -- references to the latter were provided]. while

“speedy” acid is LSD-25. You might want to inform her that those “speedy”

effects are also commonly reported side effects of legal drugs which

effect the 5-HT neurotransmitter system. And ditto on the potency issue –

you’d need mg quantities of strychnine to feel anything. And what you would

feel (according to descriptions I’ve read) does not match descriptions of

LSD “speed” effects. Most significantly because strychnine muscular effects

tend to fade in & out, while LSD “speed” effects are typically reported as

being consistent — and there are other qualitative differences.

“actual experience”? … no one here is likely to post descriptions of that

over the net, even in e-mail… I’m *quite* sure that some people could

though…

> Well, hypothetically speaking, I bought some from her friends, and I could

> probably surrender half a hit or a whole one, maybe, in the interest of

> science. Does anyone have facilities to perform a REAL (hypothetical)

> analysis of blotter to find out exactly what’s in it?

Its been done….

> > Schnoll SH Vogel WH

> > Analysis of “street drugs”.

> > N Engl J Med (1971 Apr 8) 284(14):791

This reference sucks.

> > Brown JK Shapazian L Griffin GD

> > A rapid screening procedure for some “street drugs” by thin-layer

> > chromatography.

> > J Chromatogr (1972 Jan 19) 64(1):129-33

Nope.

There’s a LA County analysis of street drugs I’ve got (Clin Tox ~1984 I think)

that reports LSD as being >96% pure or blank (If I remember correctly) –

the rest most likely is substitutes, but it wasn’t reported in the analysis.

…………………………

This is the PharmChem analysis of LSD from 1972 (vol 1, no 1) up to the time

that the DEA no longer allowed them to make quantitative measurements (1974-

vol 3, no 2 included). NOTE: NO STRYCHNINE! also note that PharmChem found

a sample of Shrooms contaminated with Strychnine in 1972 (vol 1, no 7), and

I would think it safe to assume that they also checked LSD for Strychnine.

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

BAD TRIPS:

A person on LSD who becomes depressed, agitated, or confused may

experience these feelings in an overwhelming manner that grows on

itself. The best solution is to remove disturbing influences, get to

a safe, comforting environment, and reassure the tripper that things

are alright. It may comfort those who fear that they are losing their

minds to be reminded that it will end in several hours.

Authorities are fond of administering injections of anti-psychotic

drugs. Recovery in the presence of authorities, in hospitals or

police stations, is not pleasant. Sedatives or tranquilizers such as

Valium may help reduce panic and anxiety, but the best solution is

calm talking. Some claim that niacin (an over the counter vitamin

supplement) can abort a trip, but this may be due to a placebo effect

(niacin produces a flushing effect).

Remember that odd bodily sensations are normal and not harmful.

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

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

“The distinction between psycholytic and psychedelic doses of LSD is used in

many scientific publications but seems to be ignored by popularizers who

either preach the “LSD utopia” or warn of the “decline of the West.” A

psycholitic does, generally 75 or 100 - or at most 200 - micrograms, causes

a rush of thoughts, a lot of free association, some visualization

(hallucination) and abreaction (memories so vivid that one seems to relive

the experience). A psychedelic dose, around 500 micrograms, produces total

but temporary breakdown of usual ways of perceiving self and world and

(usually) some form of “peak experience” or mystic transcendence of ego.

“Bad trips” usually occur only on psychedelic doses.”

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

The best review of this question is Rick Strassman’s “Adverse Reactions

to Psychedelic Drugs: a Review of the Literature” in _J. Nerv and Mental

Disease_ 172(10):577-595. He writes:

The most common adverse reaction is a temporary (less than 24 hours)

episode of panic –the “bad trip”. Symptoms include frightening illusions/

hallucinations (usually visual and/or auditory); overwhelming anxiety

to the point of panic; aggression with possible violent acting-out behavior;

depression with suicidcal ideations, gestures, or attempts; confusion; and

fearfulness to the point of paranoid delusions.

Reactions that are prolonged (days to months) and/or require hospitalization

are often referred to as “LSD psychosis,” and include a heterogenous

population and group of symptoms. Although there are no hard and

fast rules, some trends have been noted in these patients. There is a

tendency for people with poorer premorbid adjusment, a history of

psychiatric illness and/or treatment, a greater number of exposure to

psychedelic drugs (and correlatively, a great average total

cumulative dosage taken over time), drug-taking in an unsupervised

setting, a history of polydrug abuse, and self-therapeutic and/or

peer-pressure-submission motive for drug use, to suffer these consequences.

In spite of the impressive degree of prior problems noted in many of these

patients, there are occasional reports of severe and prolonged reactions

occuring in basically well adjusted individuals. In the same vein,

there are many instance of faily poorly adapted individuals who suffer

_no_ ill effects from repeated psychedelic drug use. In fact, it has been

hypothesized that some schizophrenics do not suffer adverse reactions

because of their familiarity with such acute altered states. Another

possibility is that there individuals may be “protected” by possible “down-

regulation” of the receptors for LSD, bu the (over-)production of some

endogenous compound. _Individual_ prediction of adverse reactions,

therefore, is quite difficult…

Major “functional” psychosis vs. “LSD psychosis”

———————————————–

A diagnostic issue dealth with explicitly in only a few papers is that of

LSD-precipitated major functional illnesses, e.g. affective disorders

or schizophrenia. In other words, many of these so called LSD psychoses

could be other illnesses that were triggered by the stress of a traumatic

psychedelic drug experience. Some of the same methodological issues

described earlier affect these studies, but they are, on the averagem

better controlled, with more family and past psychiatric history available

for comparison.

Hensala et al. compared LSD-using and non-LSD-using psychiatric inpatients.

They found that this group of patients was generally of a younger age and

contained more characteristically disordered individuals than the non-

LSD-using group. Patients with specific diagnoses with or without LSD

histories were not compared. Based on their observations, they concluded

that LSD was basically just another drug of abuse in a population of

frequently hospitalized individuals in the San Francisco area, and that

it was unlikely that psychedelic use could be deemed etiological in the

development of their psychiatric disorders.

Roy, Breakey et al., and Vardy and Kay have attempted to relate LSD use to

the onset and revelopment of a schizophrenia-like syndrome. A few comments

regarding this conceptual framework seem in order, before their findings

are discussed. The major factor here is that of choosing schizophrenia,

or in the Vardy and Kay study, schizophreniform disorders, as the

comparison group. There is an implication here that LSD psychoses are

comparable, phenomenologically, to schizophrenia-like disorders, and that

LSD can “cause” the development of such disorders. The multiplicity of

symptoms and syndromes described in the “adverse reaction” literature

should make it clear that LSD can cause a number of reactions that can last

for any amount of time–from minutes to, possibly, years. I believe what

is being studied here is the question of the potential role of LSD in

accelerating or precipitating the onset of an illness that was “programmed”

to develop ultimately in a particular individual–in a manner comparable

to the major physical or emotional stress that often precipitates a bona

fide myocardial infarction in an individual with advanced coronary

atheresclerosis. The stress did not _cause_ the heart disease; it was

only the stimulus that accelerated the inexorable process to manifest

illness.

In looking at the relevant studies, Breakey et al. found that schizophrenics

who “used drugs” had an earlier onset of symptoms and hospitalization than

non-drug-using schizophrenics, and had possibly better premorbid personal-

ities than non-drug using patients (although Vardy and KAy have challenged

this analysis of Breakey’s data).

Bowers compared 12 first-admission patients with psychosis related to LSD

use, requiring hospitalization and phenothiazines, to 26 patients hospital-

ized and treated with phenothiazines with no history of drug use. Six

of these controls had been previously hospitalized. Drug-induced psychotic

patients were found to have better premorbib histories and prognostic

indicators than the nondrug groups. There was no difference in rates of

family history of psychiatric illness. However, several issues flaw

this study. One is the poly-drug abusing nature of the “LSD-induced”

psychotic patients, compared to the controls. The role of LSD, therefore,

in causing or precipitating these symptomatic disorders, is open to dispute.

The other is the lack of an adequate comparison control group, i.e. the

controls were specified only as “psychotic,” and did not necessarily

match the LSD group in either symptoms or diagnostic classification.

A follow-up study of the patients occured between 2 and 6 years later.

One half did well and one half did poorly, although the lack of a control

group for a follow-up in a similarly symptomatic control group makes

interpretation of the data difficult.

Roy, in a somewhat different design, compared chronic schizophrenic

patients (diagnosed according to DSM-III criteria) who had used LSD

within the week preceding hospitalization, and found no difference

in age of symptom onset or hospitalization compared to patients without

a history of illicit drug use.

Vardy and Kay, in an elegant study with a 3- and 5- year follow-up period,

demonstrated that patients hospitalized for a schizophrenic picture

that developed within two weeks of LSD use (patients with other diagnoses

were explicitly excluded form comparisons with non-drug-using

schizophrenics) were “fundamentally similar to schizophrenics in

geneology, phenomenology, and course of illness (165, p. 877). Pre-

morbid adjustment, age of onset of symptoms and hospitalization, family

history of psychosis or suicide, and most cognitive features were also

equal between groups. Family histories of alcohol abuse were markedly

great in the LSD group.

I believe these data, taken as a whole, limited as they are in terms of

comparing subgroups (i.e. LSD-using vs. non-LSD-using) of “schizophrenia-

like” disorders, point towar, at most, a possible precipitory role in

the development of these disorders, in a non specific and not

etiologically related manner.

MYTHS:

LSD does not form “crystals” that reside in the body to be “dislodged”

later, causing flashbacks. LSD is a crystalline solid (though it is

unlikely that one would ever have enough to be visible to the naked

eye) but it is easily water soluble, thus cannot form bodily

deposits. Furthermore, it is metabolized and excreted in hours. The

bogus “loosened crystal” description in not necessary to explain

flashbacks, which are psychological phenomena (see FLASHBACKS).

LSD does not cause chromosome damage.

In Science 30 April 1972, Volume 172 Number 3982 p. 431-440 there was an

article by Norman I. Dishotsky, William D. Loughman, Robert E. Mogar and

Wendell R. Lipscomb titled “LSD and Genetic Damage - Is LSD chromosome

damaging, carcinogenic, mutagenic, or teratogenic?”. They reviewed 68

studies and case reports published 1967-1972, concluding “From our own

work and from a review of literature, we believe that pure LSD ingested

in moderate doses does not damage chromosomes in vivo, does not cause

detectable genetic damage, and is not a teratogen or carcinogen in man.”

Well, there’s the study by Sidney Cohen which was cited here

recently, Journal of Nervous and Mental Disease, 130, 1960. The

following is from Jay Stevens’ Storming Heaven: “Cohen surveyed a sample

of five thousand individuals who had taken LSD twenty-five thousand

times. He found and average of 1.8 psychotic episodes per thousand

ingestions, 1.2 attempted suicides, and 0.4 completed suicides.

‘Considering the enormous scope of the psychic responses it induces,’

he concluded, ‘LSD is an astonishingly safe drug.’”

Some urban legends: I’ve heard two “stories” about people blinding

themselves on “drugs”. One was revealed as a hoax by the person who

perpetrated it (apparently it was intended to “illustrate” the dangers

of LSD), another is trotted out by anti-drug speakers at high schools:

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

vision.

2) A teenager arrested while on LSD plucked out his eyeballs in his

jail cell, and felt no pain.

While these are bogus, the drug has powerful effects on the mind

and the consumer should be aware of the hazards, and act appropriately.

…………………………

There is an occasionally circulated fake warning from some police department

about LSD-laced “tattoos” or stickers (the “blue star tattoo” story) being

given to children. This probably originated with some hick cop or ignorant

and panicky parent not understanding some children-cartoon (eg, mickey mouse

in sorcerer’s garb) printed on a sheet of blotter.

…………………………

See also myths about testing in DRUG TESTING

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

DANGERS:

Purely psychological hazards, not harmful to body. May release latent

psychosis or exacerbate depression, leading to irrational behavior. There

is also a danger of foolish or incautious behavior, e.g, misjudging

distances or thinking one can fly. Physical overdose is not a hazard,

though one may easily ingest more than one may be able to handle

psychologically.

…………………………

Because the “LSD psychosis” is not distinguishable from non-drug-

induced psychosis, we have reasonable evidence to conclude that LSD

was not the sole cause of psychosis. Instead, it would seem that the

drug brought on the problems in vulnerable individuals.

Interestingly, the rate of parental alcoholism was found to be much

higher in LSD patients than in other patients or in the general

population by one study (Vardy and Kay, Arch-Gen-Psych, 1983 40(8):

877-83).

…………………………

Lethal (toxic) doses of LSD are conservatively several tens of

thousands of times as much as a normal dose, making it (in the toxic

sense) one of the safest drugs known. See section on Pharmacology for

description of bodily side-effects.

The LD50 for psilocybin (active ingredient in mushrooms) is 275 mg/kg

i.v. in mice. Of course, it would take lots more p.o. to kill someone.

The reported LD50 values for LSD are 46, 16.5, 0.3 mg/kg I.V. for mice,

rats, and rabbits, respectively. Again, it’s hard to accurately translate

these numbers to oral values.

Note that an average human dose is 0.001 mg/kg, ie, 1 microgram/kg, ie,

1 part per billion by weight.

…………………………

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

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

FLASHBACKS:

Quoted without permission from ‘Licit and Illicit Drugs,’ written by

Edward M. Brecher and the editors of Consumer Reports. ISBN: 0-316-15340-0

A simple explanation of LSD flashbacks, and of their changed character

after 1967, is available. According to this theory, almost everybody

suffers flashbacks with or without LSD. Any intense emotional

experience–the death of a loved one, the moment of discovery that one is in

love, the moment of an automobile smashup or of a narrow escape from a

smashup–may subsequently and unexpectedly return vividly to consciousness

weeks or months later. Since the LSD trip is often an intense emotional

experience, it is hardly surprising that it may similarly “flash back.”

“Post-traumatic stress disorder has been commonly associated with war

veterans, but it also affects victims of disasters and violence… Experts

estimate that 1% of the population suffers from the disorder.”

—LA Times, Feb 18 1992, p A3, “Journey For Better Life Hell For Some Women.”

…………………………

Can smoking marijuana induce a flashback?

Also are you more likely to suffer flashbacks from having a bad trip?

Apparently yes and yes. The following is reproduced without

permission from Lester Grinspoon and James B. Bakalar, “Psychedelic

Drugs Reconsidered,” Basic Books, Inc. New York, 1979. pp. 159-163.

I highly recommend this book, and if you find it please buy me one

too.

I typed this in a while ago and didn’t type in the references at the

time (slap!). If you want them i’ll see what i can do. Typos are

mine.

- - - - - - -

… Studies of flashbacks are hard to evaluate because the

term has been used so loosely and variably. On the broadest

definition, it means the transitory recurrence of emotions and

perceptions originally experienced while under the influence of a

psychedelic drug. It can last seconds or hours; it can mimic any of

the myriad aspects of a trip; and it can be blissful, interesting,

annoying, or frightening. Most flashbacks are episodes of visual

distortion, time distortion, physical symptoms, loss of ego

boundaries, or relived intense emotion lasting a few seconds to a few

minutes. Ordinarily they are only slightly disturbing, especially

since the drug user usually recognizes them for what they are; they

may even be regarded lightheartedly as “free trips.” Occasionally

they last longer, and in a small minority of cases they turn into

repeated frightening images or thoughts. They usually decrease

quickly in number and intensity with time, and rarely occur more than

a few months after the original trip.

A typical minor and pleasant flashback is the following:

… Frequently afterward there is a momentary “opening”

(”flash” would be too spastic a word) when for maybe a couple of

seconds an area one is looking at casually, and indeed unthinkingly,

suddenly takes on the intense vividness, composition, and significance

of things seen while in the psychedelic condition. This “scene” is

nearly always a small field of vision — sometimes a patch of grass, a

spray of twigs, even a piece of newspaper in the street or the remains

of a meal on a plate (Cohen 1970[1965], pp. 114-115)

Here are two more troublesome examples:

For about a week I couldn’t walk through the lobby of A-entry

at the dorm without getting really scared, because of the goblin I saw

there when I was tripping. (Pope 1971, p. 93)

A man in his late twenties came to the admitting office in a

state of panic. Althought he had not taken any drug in approximately

2 moths he was beginning to re-experience some of the illusory

phenomena, perceptual distortions, and the feeling of union with the

things areound him that had previously occurred only under the

influence of LSD. In addition, his wife had told him that he was

beginning to “talk crazy,” and he had become frightened … He was

concerned lest LSD have some permanent effect on him. He wished

reassurance so that he could take it again. His symptoms have

subsided but tend to reappear in anxiety-provoking situations.

(Frosch et al. 1965, p. 1237)

Flashbacks are most likely to occur under emotional stress or

at a time of altered ego functioning; they are often induced by

conditions like fatigue, drunkenness, marihuana intoxication, and even

meditative states. Falling asleep is one of those times of

consciousness change and diminished ego control; an increase in the

hypnagogic imagery common at the edge of sleep often follows

psychedelic drug use and can be regarded as a kind of flashback.

Dreams too may take on the vividness, intensity, and perceptual

peculiarities of drug trips; this spontaneous recurrence of

psychedelic experience in sleep (often very pleasant) has been called

the high dream (Tart 1972). Marihuana smoking is probably the most

common single source of flashbacks. Many people become more sensitive

to the psychedelic qualities of marihuana after using more powerful

drugs, and some have flashbacks only when smoking marihuana (Weil

1970). In one study frequency of marihuana use was found to be the

only factor related to drugs that was correlated with number of

psychedelic flashbacks (Stanton et al. 1976).

How common flashbacks are said to be depeds on how they are

defined. By the broad definition we have been using, they occur very

often; probably a quarter or more of all psychedelic drug users have

experienced them. A questionanaire survey of 2,256 soldiers (Stanton

and Bardoni 1972), leaving the definition to the respondents, revealed

that 23 percent of the men who used LSD had flashbacks. In a 1972

survey of 235 LSD users, Murray P. Naditch and Sheridan Fenwick found

that 28 percent had flashbacks. Eleven percent of this group (seven

men in all) called them very frightening, 32 percent called them

somewhat frightening, 36 percent called them pleasant, and 21 percent

called them very pleasant. Sixty-four percent said that their

flashbacks did not disrupt their lives in any way; 16 percent (4

percent of the whole LSD-using group) had sought psychiatric help for

them (Naditch and Fenwick 1977). In a study of 247 subjects who had

taken LSD in psychotherapy, William H. McGlothlin and David O. Arnold

found 36 cases of flashbacks, only one of which was seriously

disturbing (McGlothlin and Arnold 1971). McGlothlin, defining

flashbacks narrowly for clinical purposes as “repeated intrusions of

frightening images in spite of volitional efforts to avoid them”

(McGlothlin 1974b, p. 291), estimates that 5 percent of habitual

psychedelic users have experienced them.

There are few studies on the question of who is most

susceptible. In 1974, R. E. Matefy and R. Krall compared psychedelic

drug users who had flashbacks with those who did not, and found no

significant differences in their biographies or on personality tests.

The main causes of flashbacks were stress and anxiety. About 35

percent found them more or less pleasant, and the same proportion

thought they could control them. Most accepted them as an inevitable

part of their lives as members of the psychedelic fraternity and did

not want help from psychiatry (Matefy and Krall 1974). Naditch and

Fenwick found that the number of flashbacks, both pleasant and

unpleasant, was highly correlated with the number and intensity of bad

trips and the use of psychedelic drugs as self-prescribed

psychotherapy. Those who enjoyed flashbacks and those who were

frightened by them did not differ significantly on tests of ego

functioning.

A case seen in an outpatient setting in the late sixties

illustrates the kind of set and setting that may create flashback

problems. PQ was a thirty-six-year-old single man who entered therapy

because of depression and anxiety. He was a heavy drinker who was

passive, slovenly, and spent most of his time in bed. Just before

taking to alcohol and his bed he had failed in an attempt to parlay a

gift from his wealthy father into a fortune on the stock market.

Despite a remarkable incapacity for insight, during a year in

psychotherapy he managed to give up alcohol and start a promising

business. But his anxiety continued, and in order to allay it he had

to keep himself very busy wheeling and dealing. Imitating his father,

a successful self-made man who had married a woman twenty years

younger than himself, PQ dated only women under the age of nineteen.

Being attractive to young women was so imporant to him that much of

his time was spent in the company of teenagers. During business hours

he would wear a conservative three-piece suit and drive a new sedan,

but when he was with his young friends he would wear a leather jacket

and drive a motorcycle. Anxiety and fears of inadequacy dominated

both of these lives. Several months after therapy began, during a

weekend in a small resort town, his young friends decided to take LSD,

and he felt obliged to dissemble his fears and join them; it was his

first and only trip. He felt a panic he had never known before; he

thought that he was losing his mind and going “out of control.” His

friends were so concerned thet they took him to a small hospital,

where he was given chlorpromazine and after six hours released in

their care. The next day he had a flashback that lasted one or two

hours and was almost as frightening as the original experience.

Flashbacks continued for six months, their frequency, duration, and

severity eventually diminishing to the point where it was difficult

for him to determine whether they were related to the LSD trip or

merely an intensification of his usual anxiety. In fact, the patient

described the flashbacks as being like very much enhanced anxiety

episodes. Even several years after this experience, when he became

very anxious, he was reminded of the trip and these flashbacks. He

denied that these experiences had any perceptual or cognitive aspect;

both during the LSD trip and later, the only symptom was panic. There

is no question that the nature of his trip was influenced by the

unfortunate set and setting. It is a matter of speculation what part

his underlying chronic anxiety played in the development and form of

the flashback phenomena.

Several explanations for flashbacks have been proposed. One

is that the drug has lowered the threshold for imagery and fantasy and

made them less subject to voluntary control; in another version of

this explanation, flashbacks are caused by a heightened attention to

certain aspects of immediate sensory experience suggested by drug

trips and reinforced by the community of drug users. Something more

seems to be needed to account for repeated fearful relivings of

sequences from past drug trips, and these have been explained as

similar to traumatic neuroses precipitated by fright: disturbing

unconscious material has risen to consciousness during the drug trip

and can be neither accepted nor repressed. For example, D. F. Saidel

and R. Babineau (1976) have reported a case of recurrent flashbacks –

three years of blurring images and auditory distortions, with some

anxiety and confusion — which they regard as a neurosis founded on

the patient’s problems with his career and his relationship to his

mother. (See also Horowitz 1969; Shick and Smith 1970; Heaton 1975.)

Another explanation treats the flashback as an example of recall

associated with a particular level of arousal. (Fischer 1971). In

this conception the memory of an experience is best retrieved when the

rate of mental data-processing is the same as it was during the

original experience — in other words, when the state of consciousness

in similar. Therefore, psychedelic experiences are likely to be

recalled and relived when the ego’s sorting and control of sensory

information is disturbed by drugs, stress, or the state of half-sleep.

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

- - - - - - -

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

INSOMNIA:

Insomnia occurs frequently after the trip. A mild, over-the-counter

sleeping aid can help, and these antihistamines do not produce adverse

interactions. Also, some people like to consume a small amount of alcoholic

beverage to “smooth the jitteries”. The usual precautions about sleeping

aids if alcohol has been consumed apply of course.

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

TOLERANCE:

Aquired rapidly, within 3 days. Tolerance dissipates equally rapidly,

without withdrawal, craving, or symptoms of addiction.

Cross-tolerance can and is developed between other indole hallucinogens, eg,

DMT, LSD and Psilocybin.

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

BOTANY:

Lysergic compounds appear in ergot, a fungal parasite of cereal grains;

morning glory and hawaiian baby wood rose seeds; psychedelic tryptamines

also occur in psilocybe mushrooms, in some south american trees and the

poison glands of the cane toad. (Mescaline is not in this chemical family).

…………………………

“Indole Alkaloids In Plant Hallucinogens” Richard Evans Schultes, PhD.

Journal of Psychedelic Drugs Vol.8(No