LSD

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

	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
BEST: 	_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...

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

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 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.


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

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 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).

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

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.

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

FLASHBACKS:

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

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

   <end quote>

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


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

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:

"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 preparatory rituals, members walked to
Eleusius whereupon they underwent secret rituals.  The rituals
remained secret until the 1970's.

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

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

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

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

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

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


IPOMOEA PURPUREA: A NATURALLY OCCURRING PSYCHEDELIC

Charles Savage, Willis W. Harman and James Fadiman

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

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

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

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

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


               Low Dose, 20-50 Seeds (11 Subjects)

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

              Medium Dose, 100-150 Seeds (22 Subjects)

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

              High Dose, 200-500 Seeds (12 Subjects)

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

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

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

IPOMOEA.003   7-MAY-90

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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






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

CHEMISTRY:

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

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

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

	LSD-25				Lysergic acid

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

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

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


MECHANISM OF ACTION:

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

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

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

There is also evidence for interaction with dopaminergic systems.

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

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

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

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

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

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

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

P.S. Snyder has tripped before =)

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

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

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


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

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

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

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

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

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

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

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

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





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

RELATED COMPOUNDS:



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

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

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

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

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



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

MANUFACTURE:

Forget it.  Precursors (ergot alkaloids, used medicinally for migraines and
ob/gyn due to their vasoconstrictive effects) are closely watched.  (They
are obtained through commercially cultured ergot fungus; one could
theoretically extract lsyergic amides from morning glory or Hawaiian wood
rose seeds.)  (Though there are routes to synthesize lysergic acid from
"scratch", these are complicated also.)  Other typically needed chemicals
are very dangerous.  Serious experience in organic chemistry lab would be
necessary.  If you have to ask where to find the recipes, you don't know
enough about chemistry to try it.  (For the curious: the _Anarchists
Cookbook_ is a bad place to start.  _Psychedelic Chemistry_ is better, the
patent office or chem. lit. better.)  And you'll probably trip during
manufacture if you actually succeed.  Its easier and safer to buy it on the
black market.


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

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 electron impact mass spectrometry."
Journal of Analytical Toxicology.  v12n1, Jan-Feb 1988, p1-8.
[6]
Lim, H.K.; Andrenyak, D.; Francom, P.
"Quantification of LSD and N-demethyl-LSD in urine by gas chromatography/
resonance electron capture ionization mass spectrometry."
Analytical Chemistry.  v60, July 15 1988, p1420-25.
[7]
Papac, D.I.; Foltz, R.L.
"Measurement of lysergic acid dietylamide (LSD) in human plasma by gas
chromatography/negative ion chemical ionization mass spectrometry."
Journal of Analytical Toxicology.  v14n3, May-June 1990, p189-90.
[8]
Paul, B.D.; Mitchell J.M.; Burbage, R.; Moy, M; Sroka, R.
"Gas chromatographic-electron-impact mass fragmentometric determination
of lysergic acid diethylamide in urine."
Journal of Chromatography.  v529n1, July 13, 1990, p103-12.
[9]
Blum, L.M.; Carenzo, E.F.; Rieders, F.
"Determination of lysergic acid diethylamide (LSD) in urine by instrumental
high-performance thin-layer chromatography."
Journal of Analytical Toxicology.  v14n5, Sep-Oct 1990, p285-7.
[10]
Ratcliffe, W.A.; Fletcher, S.M.; Moffat, A.C.; et. al.
"Radioimmunoassay of Lysergic Acid Diethylamide (LSD) in serum and urine
by using antisera of different specificities."
Clinical Chemistry.  v23n2, Feb 1977, p169-74.
[11]
Cody, J.T.; Schwarzhoff, R.H.
"Impact of adulterants on RIA analysis of urine for drugs of abuse."
Journal of Analytical Toxicology.  v13n5, Sep-Oct 1989, p277-84.
[12]
Klonoff, D.C.
"Acute water intoxication as a complication of urine drug testing in the
workplace."
Journal of the American Medical Association.  v265n1, Jan 2 1991, p84-6.
[13]
Christie J.; White, M.W.; Wiles, J.M.
"A chromatographic method for the detection of LSD in biological liquids."
Journal of Chromatography.  v120n2, May 26, 1976, p496-501.
[14]
Twitchet, P.J.; Fletcher, S.M.; Sullivan, A.T.; Moffat, A.C.
"Analysis of LSD in human body fluids by high-performance liquid chromatography,
fluorescence spectroscopy and radioimmunoassay."
J. Chromatogr.  v150n1, March 11 1978, p73-84.

Sorry this was so long but I thought it deserved it :-)
Enjoy a "referenced" article.
Tim Basher

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

There were rumors going around that LSD could be detected
by drug tests fo thirty days.  I think this reference and
abstract makes it clear that it is probably 4 days, max.
(see the end of the abstract)

 IDNUM     03319915
 TYPE      Journal paper
 DATE      880715
 AUTHOR    Heng Keang Lim; Andrenyak, D.; Francom, P.; Foltz, R.L.; Jones, R.T.
           Center for Human Toxicology, Utah Univ., Salt Lake City, UT, USA
 TITLE     Quantification of LSD and N-demethyl-LSD in urine by gas
           chromatography/resonance electron capture ionization mass
           spectrometry
 SOURCE    Analytical Chemistry; vol.60, no.14; 15 July 1988; pp. 1420-5
 SUBJECT   chromatography; electron capture; mass spectroscopic chemical
           analysis; organic compounds; quantification; gas chromatography;
           resonance electron capture ionisation mass spectrometry; LSD;
           N-demethyl-LSD; urine; lysergic acid diethylamide; human; in vitro;
           in vivo; aromatic hydroxylation; drug; metabolite;
           N-tri-fluoroacetyl derivatives; calibration curves; urinary
           concentrations; adult volunteer; excretion; elimination half-lives;
           4 to 6 hrs; 8 to 10 hrs
           Numerical data: time 1.4E+04 to 2.2E+04 s; time 2.9E+04 to 3.6E+04 s
           Class codes: A8280M; A8280B; A3470
 CODEN     ANCHAM
 ABSTRACT  Demethylation of lysergic acid diethylamide (LSD) in the human has
           been demonstrated, both in vitro and in vivo, and aromatic
           hydroxylation at positions 13 and 14 has been tentatively
           identified. A gas chromatography/resonance electron capture
           ionization mass spectrometry (GC/MS) assay for LSD and
           N-demethyl-LSD in urine has been developed, in which the drug and
           its metabolite are converted to their N-tri-fluoroacetyl derivatives
           prior to GC/MS analysis. Linear and reproducible calibration curves
           have been obtained for LSD concentrations from 0.05 to 5.0 ng/mL,
           and for N-demethyl-LSD concentrations from 0.03 to 5.0 ng/mL. The
           assay was used to determine the urinary concentrations of LSD and
           N-demethyl-LSD following administration of a single oral dose of the
           drug (1 mu g/kg) to an adult volunteer. The rates of excretion of
           LSD and N-demethyl-LSD reached maxima in urine collected at time
           intervals of 4-6 and 8-10 h after administration, respectively. The
           elimination half-lives for LSD and N-demethyl-LSD were 3.6 and 10.0
           h, respectively
 MISCELLANEOUS
           Treatment: experimental
           Anal. Chem. (USA)
           Abstract number(s):  A89037987
           ISSN: 0003-2700
           Refs: 15

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

LEGAL SCHEDULING:

Class I, "no medical use" --- mostly for political reasons, as it was
and is used in psychotherapy.  (Current use is in Switzerland.)


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

SET and SETTING:

"SET" is the expectations a person brings with them.  "Setting" is the
environment that a person is in.  Set includes expectations about the
drug's actions and how the person will react.  Setting includes the
social and physical conditions.  For LSD and the hallucinogen-type
drug more than other psychoactives, set and setting are very important
in determining the nature of the experience.  These factors make the
difference between, e.g., the experiences of someone taking the drug
for enhancement at a concert, for psychotherapy in an doctor's office,
in a religious context, or in the outdoors for an aesthetic
experience.  For best results, one should take LSD only with people
one trusts in safe, comfortable surroundings, free of everyday
intrusions.  Tripping alone is a very risky thing to do, that
inexperienced people should avoid.

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

STORAGE:

First, note that LSD is a fairly stable organic molecule, no more or
less fragile than other molecules with comparable structures.

The main factors to be concerned with are moisture (due to leaching
and facilitated chemical reactions in the presense of moisture),
oxygen, light, and temperature.  Reaction rates typically depend upon
temperature exponentially.  These factors basically apply to all
organic compounds.

Sealing in AL foil in a cool dark place is fine.  Some recommend
refrigeration, but be careful about nosy guests, condensation, and frost.
Multiple, redundant seals are suggested, eg., paper in metal foil in
plastic in a metal candy tin which has been taped shut.  Should last
at least a presidential term.

Wallets are contraindicated as storage locations due to sweat.

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

SYNERGIES, BAD COMBINATIONS:

Smoking cannabis products considerably increases the effects,
increasing the visuals and also possibly increasing the cognitive and
linguistic disorders.  As the effects of LSD wear off, marijuana may
bring them back, and also ease the jitteriness some dislike.  Nitrous
oxide goes well with LSD, though one should be extra careful (not to
suffocate or fall down) with the nitrous because of the effects of the
LSD.  MDA & cousins can go well, but people on these drugs should not
take LSD unless they are familiar with the latter's effects.

Alcohol's effects are largely overwhelmed by LSD, and they act in opposite
ways: alcohol being a depressant and LSD being a (hyper)stimulant.
Generally mixing stimulants and sedatives is counterproductive.

MAO inhibitors ???
Amphetamines and cocaine ???

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

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:
LSD: My Problem Child [A. Hofmann, PhD] (excellent)
Storming heaven : LSD and the American dream  [Jay Stevens]. (excellent)
Ceremonical Chemistry [T. Szasz, M.D.]	(excellent)
Acid Dreams
Drugs and the Brain
Psychedelics Reconsidered
Electric Koolaid Acid Test
Flashbacks (Leary's autobiography)
The Great Drug War
Dealing With Drugs

	USAGE/INFORMATIONAL:
Psychedelic Encyclopedia [Stafford] (excellent)
Psychedelic Chemistry [M.V.Smith]
Biochemical Basis of Neuropharmacology (technical)
Consumer Reports: Licit & Illicit Drugs
Recreational Drugs

	REFERENCE:
Merck Handbook
Physician's Desk Reference
The Botany And Chemistry Of Hallucinogens, Shultes & Hofmann

	JOURNALS:
Journal of Psychoactive (formerly Psychedelic) Drugs



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

 AUTHOR:    Cohen, Sidney
 AUTHOR AFFILIATION:
            U California School of Medicine, Neuropsychiatric
            Inst, Los Angeles
 TITLE:     LSD: The varieties of psychotic experience.
 SOURCE:    Journal of Psychoactive Drugs  1985 Oct-Dec Vol 17(4)
              291-296
 ABSTRACT:  Discusses the contributing factors (e.g., preexisting
            character structure, insecurity, negative experience,
            current mood and stress level) and prevention and
            treatment of acute and prolonged psychotic reactions
            to LSD. (10 ref)

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


Additional (detailed) References (in random order):

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

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

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

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


J. Psychoactive Drugs Vol 21 (1) Jan-Mar 1989

The 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 Effects Of Drugs
(Ch 4 Hallucinogens: Complications of LSD: A Review of the Literature;
Dimensions of the LSD, Methlphenidate, and Chlordiazepoxide
Experiences; LSD: Injection Early in Pregnancy Produces Abnormality
in Offspring of Rats; LSD: No Teratogenicity in Rats;  Congenital
Malformation Induced by Mescaline, LSD, and Bromolysergic Acid in
the Hamster;  Drug Motivated-Behavior: The Effect of Morning Glory Seeds
On Motor Activity In Chicks) (Also Includes Weil'S Study Of "Clinical and
Psychological Effects Of Marijuana In Man")
D.W. Matheson M.A. Davidson Holt Rinehart
Winston Inc 1972


any textbook titled "Physiological Psychology"

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

(about  visual disturbances: )
Migraine: the evolution of a common disorder
O. Sacks
U CAl press 1970

Brain Damage, Behavior, And The Mind
M. Williams
John Wiley & Sons 1979
ch 5 Disorders of visual perception

Mescal And Mechanisms Of Hallucinations
Heinrich Kluver
U. Chicago Press 1930

Drugs And The Brain
Perry Black MD, Ed
Johns Hopkins Press 1969
behavioral effects of LSD in subhuman primates


Hallucinations
Sci Am
R.K.Siegal
(see also article on phosphenes in amateur scientist column in another issue)


Luria's _The Shattered Mind_



******************************END OF FAQ******************************
[FYI only, consult your shamans & attorneys etc., you are self-responsible.]