Text File

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

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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

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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.

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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.

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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.

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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...

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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.

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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.

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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.

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>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."

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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.

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[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.

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>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."

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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.

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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).

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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.

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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.

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See also myths about testing in DRUG TESTING

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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.

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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).

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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.

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Never take any drugs while pregnant.

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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>

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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.

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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.

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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

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"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."

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"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)

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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).

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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).

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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.

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"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.

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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.

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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.

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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.

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

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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.

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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

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

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DRUG TESTING:

No risk. Its not looked for, hard to find, and transient.

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"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.

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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.

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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.

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> 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

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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

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LEGAL SCHEDULING:

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

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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.

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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.

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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 ???

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SYNTHESIS:

Don't try it, too difficult and risky both physically and legally. Precursor medical drugs (ob/gyn and migraine ergot alkaloids) are watched.

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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

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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)

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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"

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(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)

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