💾 Archived View for gemini.spam.works › mirrors › textfiles › drugs › faq-xtc.txt captured on 2023-01-29 at 06:51:30.
View Raw
More Information
⬅️ Previous capture (2020-10-31)
-=-=-=-=-=-=-
Subject: FAQ-Ecstasy
not yet organized, but maybe of interest to some.... contains Shulgin's
bibliography too
- *****************************
XTC FAQ
..............................
MDMA ;(extacy) (XTC); metheylenedimethoxymethamphetamine. Is an analog
of MDA (methylenedimethoxyamphetamine). MDA Was first synthesized in
1917 by Parke-Davis company as an appetite suppressant drug. The drug,
in addition to suppressing appetite, produced what is now termed as an
"entacto-effect" in the test subjects. Because of the adverse side
effects, Parke-Davis did not market the drug and let the patent expire.
The drug resurfaced in the 1960's along with the advent of many other
psychoactive substance. Known negative side effects are around a 40%
reduction of serotonergic synapses in the rat brain with a 5mg/kg dosage
(no data is available for neurotoxicity in humans). Cerebral spinal
fluid of admitted users has been shown to have a marked decrease in 5-HT
levels. More on the pharmacology later....
..............................
I can't find the strand, but this is intended to correct/clarify some
recent discussions of DOM (AKA STP).
When DOM (2,5-dimethoxy-4-methylphenylisopropylamine) first hit the
streets of San Francisco in the late sixties, it was distributed in
tablets of 10 or 20 mg. Threshold effects begin at 1 mg (you get
muscle tremors, facial flushing, and minor sensory amplification)
and the more you do, the longer and more intense the trip. Obviously,
if people took two or three tablets, they'd be in for a long trip.
So, the stories of DOM trips lasting for days are just the result
of people not knowing the ED. It is really a nice psychedlic at
5 mgs or so, no worse than LSD.
As for the stories of antipsychotics not helping or worsening a DOM trip,
such stories are nonsense from a pharmacological standpoint. There is
nothing really unusual about DOM as a psychedelic, if anything it is a
cleaner 5-HT2 agonist than LSD. This rumor was studied using 50-200 m
g chlorpromazine to counteract large DOM doses. While the effects of DOM w
eren't completely reversed, the chlorpromazine did calm the people down.
Check out Snyder et al (1968) in Amer. J. Psychiat. 125: 357-364 and
Hollister et al (1969) in Psychopharmacologia 14: 62-73 for studies on
humans with low and high doses respectively.
..............................
Subject: Re: Aminization of Nutmeg or Calamus
mcbeeb@jacobs.CS.ORST.EDU (Brian Mcbee) writes:
>So, if I had a batch of nutmeg or calamus, and I soaked it in an aqueous
>solution of ammonia... Hmm. Anyone have a recipe for making quick and
>dirty psychedelics from natural precursors? Something that doesn't involve
>expensive lab equipment or dangerous chemicals?
Try refluxing an Et2O extract of either in NH2CH3 with 200 mesh Al and
HgCl2 for a few hours. Try this and you will see God in short order.
Quick and dirty aminations are hard enough to do in your bath tub
with pure reagents.
..............................
alt.drugs by the one and only Tyrone Slothrop. Please edit
Asarone can be easily extracted from Acorus calamus roots by steam
distillation. This is a really nice process because it doesn't require
the use of any smelly, flammable and poisonous solvents. I've used it
to extract safrole from sasafrass roots. This will get rid of most of
the ``gunk'', but of course you will have a mix of aromatic oils.
Shulgin (1978) states: ``It is used as a medicine by the indians of
northern Canada (Hoffer and Osmond, 1967) where it is known by the name
of rat-root, and is claimed to have intoxicating properties similar to
those of LSD. The conversion of asarone to TMA-2 is easily realized...''
However, asarone is not the ``precursor to all the MDA analogs''.
It is the precursor to TMA-2. This is discussed in chapter 5 of
Strafford (1983). TMA-2 is 2,4,5-trimethoxyphenylisopropylamine.
Shulgin (1976) describes the effects as follows:
The first indications of intoxication usually noted are signs of physical
disturbance such as nausea, paraesthesia, and a modest reflexive mydriasis.
The central sensory changes appear in the second hour and are character-
ized by some exaggeration of visual input (especially in the appreciation of
colors and contrasts of lighting) and of empathy with irrational objects in
one's environment. These preludes lead to a plateau, form three to about
six hours following administration, which is an impressive altered state of
consciousness virtually free of the distortions and portentousness so com-
mon with LSD. The experience dissipates gradually, and is usually com-
pleted in 8-10 hours. A sharp dose-response curve exists for TMA-2 in that
several additional toxic symptoms have been reported at 25-30 mg levels.
There can be a pervasive mausea throughout the entire experimental
period, accompanied by actual vomiting, apparent fainting, and brief but
repeated periods of amnesia. Peripheral vision can be lost (this, apparently,
of hysterical origin) and the accompanying fear of being irrepaprably severed
from reality has led to situations that have proved difficult to manage.
Here was a world of simplicity and certainty no acidhead, no revolutionary
anarchist would ever find, a world based on the one and zero of life and
death. Minimal, beautiful. The patterns of lives and deaths....
...it would all be done with keys on alphanumeric keyboards that stood
for weightless, invisible chains of electronic presence or absence. If
patterns of ones and zeros were ``like'' patterns of human lives and
deaths, if everything about an individual could be represented in a
computer record by a long string of ones and zeros, then what kind of
creature would be represented by a long string of lives and deaths? It
would have to be up one level at least -- an angel, a minor god,
something in a UFO. It would take eight human lives and deaths just to
form one character in this being's name -- its complete dossier might
take up a considerable piece of the history of the world. We are digits
in God's computer... And the only thing we're good for, to be dead or
to be living, is the only thing He sees. What we cry, what we contend
for, in our world of toil and blood, it all lies beneath the notice of
the hacker we call God. -- Pynchon (1990)
- Tyrone Slothrop - from his scattering
Hoffer, A., and H. Osmond. 1967. The Hallucinogens, pp. 55-56. Academic
Press, New York.
Pynchon, Thomas. 1990. Vineland. Little, Brown and Co. Pp. 385.
Shulgin, A. T. 1976. Profiles of psychedelic drugs. 2. TMA-2.
J. Psychedelic Drugs 8: 169.
_____. 1978. Psychotomimetic drugs: structure-activity relationships.
In: Handbook of Psychopharmacology, Vol. 11: Stimulants. Iversen, Iversen
and Snyder [eds.]. Plenum Press, New York. Pp. 243-333.
Strafford, Peter. 1983. Psychedelics Encyclopedia. Houghton Mifflin.
Pp. 420.
-------end forwarded message--------
----------------begin forwarded message------------------
Subject: Re: Legal and better highs
>MDE - "Eve" An intellectual buzz, no emotional effects
>2-CB - (CBR) MDMA analog, visuals(sometimes frightening)
> Ultimate in telepathic communications
>
>2CT2 - Laboratory exotic - dark earthy visuals, like shrooms
>DIPT - Obscure compound - said only to effect perception of music
>DOET - "visual, pretty & pyschedlic, low dosages remove writing
> blocks
CBr a MDMA analog? CBr is 2,5-Dimethoxy-4-Bromophenethylamine. The
"sometimes frightening" part probably comes from taking more than the
full dose, and the literature suggests that with larger dosages come
disproportionately larger responses, unlike some other psychedelics
we all know and love. I've had very enlightening experiences with CBr,
and they grew better in quantum leap fashion.
+ wonderful and gently insightful (semi-wilderness, daytime, friends).
+ profoundly sexual with glimpses of bird-animal forms (indoors, nightime,
lover) minor telepathic imagery.
+ sexual and shamanic, native american imagery (indoors, day-night, alone).
+ profound native american imagery (indoors, night, after cannabis, friend)
actually slept a bit (too much cannabis) and awoke to the most wonderful
visuals (friend in other room - ditto).
+ full-blown spirit animals all night long (desert, night, friend, good THC
1/2 way thru trip) - mountain lion (very playful) and eagle most prominent
two deer (incredibly loving), a wolf (very brief), fantastic living plant
spirits, entities in mountain, mucho native american imagery, et. al.
very telepathic with friend. brief teleportation/desert-zoom experience.
understood the ancients' fascination with constellations. imparted with
sudden knowledge in extreme detail - confirmed later by ex-lover, scared
ex-lover shitless.
My last experience with CBr changed my life in many profound ways (for the
better). With THC and a little concentration I can get back to some of those
places. With no THC and a lot of concentration I can get back to some of
those places. Remember.
I believe CBr is recognized as an enthogen and an entactogen, and
unfortunately it's now Schedule 1. :-( Put this one on the top of
the list of drugs to be legalized.
DO NOT TAKE ANY DRUG YOU DO NOT UNDERSTAND. KNOW THE SOURCE.
>A friend of mine needs some information on a chemical called _SAPHROL_...
Safrole is 4-allyl-1,2-methylenedioxybenzene. Sassafras oil is about 75%
safrole. It has quite a pleasant and characteristic odor.
>The way he spoke about it makes me think that it is an illegal substance
>used in making some illicit substance.
The methylenedioxybenzene nucleus is found in MDA and MDMA. Amination at
the appropriate carbon of the olefinic side chain yields the former,
methylamination, the latter. I think this reaction is non-trivial due
to conjugation of the double bond with the aromatic ring; the syntheses
I have seen start with the ketone.
In article <eesnyder.676649391@beagle> eesnyder@boulder.Colorado.EDU (Eric E. Snyder) writes:
[regarding safrole]
>methylamination, the latter. I think this reaction is non-trivial due
>to conjugation of the double bond with the aromatic ring; the syntheses
^^^^^^^^^^^ ^^ ^^^ ^^^^^^ ^^^^
>I have seen start with the ketone.
That's isosafrole. The reaction isn't too difficult. One tries for
an anti-Markownikov addition in the presence of peroxide or other
source of free radicals. For the purposes mentioned, safrole undergoes
the appropriate addition very conveniently. Both safrole and isosafrole
do have a pleasant odor and have been used in flavorings, but perhaps
they can't be used anymore due to a possible cancer risk? Although I
think some "natural" root beers can contain some amount of "natural"
safrole, but none can be added. Regulations, regulations...
--
David J. Heisterberg djh@osc.edu We are NOT all
The Ohio Supercomputer Center djh@ohstpy.bitnet Keynesians now.
Columbus, Ohio 43212 ohstpy::djh
>Just for the record, mescaline is 3,4,5-trimethoxyphenylethylamine. It does not
>contain an indole ring, it is one of the hallucinogenic amphetamines, as is MDMA.
...just for the record, mescaline is *not* a so-called psychedelic amphetamine.
Amphetamine, aka phenylisopropylamine, has an alpha methyl group, and thus
possesses a chiral center. Phenylethylamines are achiral. This is important
because the alpha methyl group makes phenylisopropylamines poor substrates for
MAO. In contrast, phenylethylamines are excellent substrates for MAO. As a
result, mescaline is not a potent psychedelic (ED ca. 300 mg). However,
3,4,5-TMA, the phenylisopropylamine analog of mescaline is active at around
20 mg.
eesnyder@boulder.Colorado.EDU (Eric E. Snyder) writes:
>...just for the record, mescaline is *not* a so-called psychedelic amphetamine.
>Amphetamine, aka phenylisopropylamine, has an alpha methyl group, and thus
>possesses a chiral center. Phenylethylamines are achiral. This is important
>because the alpha methyl group makes phenylisopropylamines poor substrates for
>MAO. In contrast, phenylethylamines are excellent substrates for MAO. As a
>result, mescaline is not a potent psychedelic (ED ca. 300 mg). However,
>3,4,5-TMA, the phenylisopropylamine analog of mescaline is active at around
>20 mg.
Yeah, but does it get you off?
..............................
This is some information I recieved by email regarding a "new form"
of methamphetamine which has been reportedly appearing in Hawaii....
Here are some passages from an article titled "A Chemical and
Pharmacological Review of U4Euh/Intellex" by the "New Age Chemist"
in volume 4 of Psychedelic Monographs & Essays
(available from Rosetta, PO Pox 4611, Berkeley, CA 94704 ).
"Chemical names: 4-methyl aminorex, 4-methyl-5-phenyl-2-amino-oxazoline,
4,5-dihydro-4-methyl-5-phenyl-oxazolamine.
(note: oxazoline appears to be the ring formed by
-O-C(NH2)=N-CH(CH3)-CH-
1 2 3 4 5
"Common names: U4Euh, Euphoria, Intellex, Ice, Verbosamine
"History: 4-methyl aminorex was first synthesized and its anorexigenic
and stimulant properties discovered by the research group of George Poos
at McNeil labs in Ft. Washington, PA, in the early 60's. [see J. Med. Chem,
6:266, 1963]. ... Attention was primarily directed at the anorexegenic
properties and the central effects were regarded as unwanted side effects.
"When a high production lab was discovered in Gainesville, Florida in
1986, the DEA investigated and the material has subsequently been
consigned to Schedule I under the emergency scheduling provision of the
Controlled Substance Act for a one year period beginning Oct. 15, 1987.
(i don't know what the final disposition of the drug was but it's not
hard to guess...)
"Chemistry: 4-methyl aminorex is prepared through an addition and
spontaneous cyclizing reaction involving PPA.
(another paper in the the same volume says it is synthesized from PPA
and cyanogen bromide)
The simplicity of the synthesis, the ready availability of precursors,
high yields, and the interesting central effects suggest that this
material will be around for a long time to come.
"Pharmacological profile: ... Quantitatively, the experience is similar
to a long-lasting MDMA intoxication superimposed with methamphetamine,
with the added benefits of easy verbalization, free association, integration,
and elaboration of previous insights, making it a useful tool for
lecturers... Nothing is know about the pharmacokinetics or pharmacodynamics
of 4-methyl aminorex. The central effects (sympathomimetic) are believed
to be the result of increased release of catecholamines, and mimicking the
effects of these transmitters at receptor sites in the brainstem.
Subject: Ice, 4-methylaminorex (was Re: Mad About MDA...)
Message-ID: <1854@ursa-major.SPDCC.COM>
Date: 26 Feb 90 18:43:05 GMT
References: <11478@nigel.udel.EDU> <1990Feb23.043735.3160@spectre.ccsf.caltech.edu> <357@tau-ceti.isc-br.com>
Reply-To: dyer@ursa-major.spdcc.COM (Steve Dyer)
Distribution: alt
Organization: S.P. Dyer Computer Consulting, Cambridge MA
Lines: 17
Aminorex was withdrawn from the European market in the late 60's
after women who were given this drug as an appetite suppressant
developed chronic pulmonary hypertension, leading in most cases
to death and significant impairment in the rest. It was never
marketed in the U.S.
Since the mechanism of this deleterious effect is not known,
and knowing how similar 4-methyl aminorex is chemically and
pharmacologically to aminorex (it's related to aminorex in the
same way as methamphetamine is related to amphetamine or
phendimetrazine is to phenmetrazine), it seems imprudent
to recommend its recreational use.
..............................
In article <2160@sunset.MATH.UCLA.EDU> trainor@MATH.UCLA.EDU (Douglas J. Trainor) writes:
>Anyone got a list of common MAO inhibitors (i.e. food stuffs) that
>should not be consumed with MDMA? E.g., red wine, chicken liver,
>non-pasturized yogurt, ...
You've got it backwards. You're thinking of tyramine (a sympathomimetic
amine found in aged foods formed from the breakdown of tyrosine).
People taking MAO inhibitors avoid such foods because tyramine is
ordinarily quickly destroyed by MAO. In the presense of a MAO inhibitor,
tyramine is absorbed from the gut and produces symptoms of excessive
adrenergic activity: headache, raised blood pressure, etc. Severe cases
can cause a stroke.
I don't think there's any evidence that MDMA is a MAO inhibitor.
Yogurt probably isn't a big deal, though it's sometimes included on the list
of foods to avoid. Most cheeses other than cottage cheese are verboten.
Dried meats and sausages are out. Vegemite has loads of the stuff. Figures.
..............................
>No, those will do... "spinal drains" and "cheese toxins"... Cheese, I mean,
>sheesh.
Now that I've recovered from my sarcasm attack, let me tell you what I see
the risks are.
A real concern of mine is that you can't be sure with street drugs that what
you're taking is MDMA or not, how pure it is, or how much you're taking.
I suppose it depends on how trustworthy your source is.
Now, onto the drug itself. MDMA isn't much of a monoamine oxidase inhibitor,
so the bit about cheese is bogus. You'll hear other crap about not taking
any dairy products, but other rumor mongers will say that you need calcium
to keep you from grinding your teeth. All ridiculous. I'd eat whatever
you wanted in moderation (i.e., like always). Given a high enough dose of
MDMA, you're likely to demonstrate some teeth grinding; it's a simple
menifestation of the drug's dopaminergic actions and it comes with the
territory. Calcium isn't going to help.
MDMA has been shown to be toxic to serotonergic neurons in rats and primates
at doses only slightly higher than the typical recreational dose in humans
(on a mg/kg basis.) This should be tempered by the observation that there
have been no observable long-term behavioral effects in people who have
taken MDMA, but it is unfashionable to decapitate humans and examine their
brains' serotonergic neurons directly. Additionally, many drugs (meth-
amphetamine, fenfluramine) have similar effects in animal models, but they
are still used without any ill effects. I think the jury is still out, myself.
--
Steve Dyer
..............................
>
>MDMA has been shown to be toxic to serotonergic neurons in rats and primates
>at doses only slightly higher than the typical recreational dose in humans
>(on a mg/kg basis.) This should be tempered by the observation that there
>have been no observable long-term behavioral effects in people who have
>taken MDMA, but it is unfashionable to decapitate humans and examine their
>brains' serotonergic neurons directly. Additionally, many drugs (meth-
>amphetamine, fenfluramine) have similar effects in animal models, but they
>are still used without any ill effects. I think the jury is still out, myself.
>Steve Dyer
>dyer@ursa-major.spdcc.com aka {ima,harvard,rayssd,linus,m2c}!spdcc!dyer
>dyer@arktouros.mit.edu
>
I agree with that conclusion, but would also like to point to
a couple of related facts. First, people will show symptoms of
Parkinson's disease only after about 80 % of their dopaminergic
neurons are destroyed. Second, patients will notice a loss of memory
only after tests show their short term memory has been impaired by 85%
Which means that half your serotonergic receptors could be destroyed
and you would probably not notice any difference. The brain is a
wonderful organ with a lot of redundancy built in it! The problem is
that you might feel this loss of receptors later in life as some of
your brain cells die due to normal aging and there are not enough
"backup" receptors. Of course, no data exist on MDMA users who have been
using it for 50 years. Since MDMA has been shown to be toxic to some
animals, no research is likely to be done on humans for ethical
reasons. I have used MDMA (when it was legal) and enjoyed it, but now
I would be scared to do it even assuming it was still legal. This is of
course a personal opinion. Has there been some more recent info on
this serotonergic receptor stuff in the litterature?
Pierre St-Hilaire
MIT Media Laboratory
Subject: Re: long term dangers of MDMA
In article <90341.021142MASSOUD@auvm.auvm.edu> MASSOUD@auvm.auvm.edu (NADIM MASSOUD) writes:
>Hi, could any knowledgeble person tell me about the possible dangers
>of occasional MDMA use? I have read lots of articles on the subject,
>but no study offered convincing evidence as to the negative effects
>on humans.... All answers are greatly appreciated.. Thanks..
Well, that's because there ISN'T evidence of any observable deleterious
behavioral or neuropsychological effects in humans, but what is observed
in animal models (histological and neurochemical) probably should be
interpreted conservatively. Matt F. mentions that there are some upcoming
studies of HIAA levels in spinal fluid in MDMA users, a test which may be
a marker for evidence of neurotoxicity. On the other hand, Ricaurte's other
human studies have not been without criticism. We'll have to see.
I have no reason to beat the drum for MDMA, but the thing that makes me
somewhat suspicious and uneasy about the facileness of these studies
purporting to point to MDMA's neurotoxicity (and thus support the conclusion
that the drug should be banned), is that drugs which are far more neurotoxic
in the same models are used quite routinely without harm. Fenfluramine, a
serotonergic appetite suppressant is three times more potent than MDMA in
producing the same experimental lesions in animals. It has been marketed
and sold for more than 25 years, and millions of doses have been administered
to people, usually chronically, without any particular side effects which
would point to a lasting neurological lesion. In fact, one of its two isomers,
d-fenfluramine, is in the middle of clinical trials for FDA approval as an
appetite suppressant which lacks some of the side-effects of the racemic drug.
Methamphetamine also appears to be neurotoxic in the same models, but even
though it is a very abusable drug, no one would say that it produces obvious
neurological deficits when used in the treatment of narcolepsy or attention-
deficit disorder.
The lack of evidence of side effects in people who have used MDMA,
even in those who have used it more than a few times, taken together
with the evidence of the safe use of other drugs which would otherwise
be thought to be dangerous according to this model, suggests that
the neurotoxicity of MDMA in humans might very well have been exaggerated.
Now, you have to balance that rather cool assessment with the question
"Well, just what IS going on?" (especially if the studies in humans become
better refined.) Maybe there is a lot of redundancy in the areas where
MDMA (and other drugs) ostensibly exert their serotonergic neurotoxicity,
such that any deficit remains subclinical. What might it take to unmask
that damage in the future? Who knows?
It depends on how conservative you want to be.
--
Steve Dyer
dyer@ursa-major.spdcc.com aka {ima,harvard,rayssd,linus,m2c}!spdcc!dyer
dyer@arktouros.mit.edu, dyer@hstbme.mit.edu
Subject: Re: MDMA/Ecstasy
Summary: MDMA, MDA are neurotoxic to serotonergic neurons
In article <26C35239.2952@ics.uci.edu> honig@ics.uci.edu (David Honig) writes:
>I don't believe the neurotoxicity reports are relevent to human use; I know
>of people who've taken several times the usual dose with no adverse effects
>other than tiredness afterwards, and slight visuals during.
>David A. Honig
Yes, and I have a few friends who shoot MPTP and they haven't had any problems
either.
While I generally find your opinions to be thoughtful and well-informed, I
have a difficult time understanding your reasoning here, David. Are you
saying that, since you and people you know have noticed no obvious behavioral
(or introspective) correlates to MDMA's neurotoxicty, that neurotoxicity is
irrelevant? If so, this seems to be a very premature judgement to me. After
all, although we don't generally see any effects of dopamine depletion in
humans until they've lost 80 or more percent (at which point they develop
parkinson's syndrome), it isn't really advisable to shoot MPTP. Why weaken
the reliability of your system unless there are significant benefits to the
medication (as may be true in MDMA's use in psychotherapy)? Furthermore,
it may be that our tests just aren't sensitive enough to detect the behavioral
changes associated with the damage. There's been some recent success in
detecting damage to the dopaminergic system using reactions. While I don't
think this has yet been replicated in humans, researchers (Spirduso et all,
I think) have found that rats with dopamine losses of approx. 45% and more
have slightly impaired reaction times. Basically, it seems to me that
uncontrolled, anecdotal data shouldn't be relied on.
I realize that the serotonergic system is very different from the dopamine
one and that NO behavioral changes have been found for MDMA-induced seroton-
ergic depletion, still judging the neurotoxicity as "irrelevant" seems to
me to be very premature.
It seems to me that the benefits would have to be better than a good trip in
order to out weight the cost. Neurotoxic effects of MDMA have
been found at 3-4 times the effective dose (IP injected) in rats and monkeys
are even more susceptable. Admittedly, the "effective dose" is probably
on the high end (since one can't ask a rat if it feels good, but must give
enough to alter its behavior measurably), but even if we couldn't pick up
the neurotoxicity until 6-8 times the ED, that's still wouldn't be a very
safe window (given the variables and unknown doses involved and the likely-
hood of better tests revealing neurotoxicity at lower doses).
For those interested in reading primary sources on this subject, I recommend
the work by George Ricaurte, who's done a great deal of MDMA research
(including studies involving oral doses in squirrel monkeys). G. Battaglia's
also active in this field. I recall a paper in Pharmacol-Biochem-Behav.
(journal) in the Feb. 88 issue on the parameters of the neurotoxicity. In
any case, one would want to look up the latest articles by these two and read
the abstracts, intros, and discussions. People interested in the importance
of serotonin (5-hydroxytryptamine, 5-HT) should find the target article in
Behavioral and Brain Sciences (BBS, an excellent, readable journal with
important articles and extensive peer reviews). Serotonin is believed to
be related to aggression, sexual behavior, and sleep, to name a few things.
Oh, and it's also important in the activity of hallucinogens.
--Matt Funkchick.
den0@quads.uchicago.edu
Subject: Nutmeg & Psychedelic Amphetamines
In article <3894@ursa-major.SPDCC.COM>
dyer@ursa-major.spdcc.COM (Steve Dyer) writes:
>Huh? I believe that nutmeg contains several methoxy- and methylenedioxy-
>phenyl alkenes (essentially the deaminated forms of the psychedelic
>amphetamines.) I know of no evidence that they are biotransformed
>into the corresponding amphetamines.
As you may remember, we discussed this exact point some time ago. What
follows is a posting I made on the subject in October 1988. After posting
I tried 2 tablespoons of McCormick's (sp?) new from the store. I was
more moist and aromatic than I remembered, so maybe freshness makes a
difference. It left me slightly speedy and trippy. I've never taken
psychedelic amphetamines, but what I experienced was inline with what
I would have expect them.
Newsgroups: alt.drugs
Subject: Nutmeg
Date: 11 Oct 88 19:46:42 GMT
In article <451@husc6.harvard.edu> gallaghe@husc8.UUCP
(Paul Gallagher) writes (a nice article):
>Another household substance with psychedelic properties is nutmeg, which
>contains small amounts of the methoxylated amphetamine, myristicin.
In article <7388@bloom-beacon.MIT.EDU> dyer@arktouros.MIT.EDU
(Steve Dyer) writes:
>Myristicin is not a methoxylated amphetamine. It is in fact
>non-nitrogenous and only resembles the methoxylated amphetamines in their
>phenyl rings.
In article <1722@laidbak.UUCP> rayd@laidbak.UUCP (Ray Dueland) writes:
>The constituents of nutmeg don't contain psychedelic amphetamines, but
>do contain good MDMA, MDA, and DMA precursors. I'm not familiar with
I got curious enough about nutmeg to do some reading. Nutmeg contains
a variety of allylbenzenes (double bond between beta and gamma carbons),
all very similar to psychedelic amphetamines. I tried drawing the
compounds, but they're difficult in ASCII. The compounds all have the
allylbenzene in common, the differ in their substitutions at the 3,4,5
positions of the benzene ring. The compounds and their concentrations
from (1):
compound substitutions concentration
-------- ------------- -------------
myristicin 3-methoxy, 4,5-methylenedioxy 4.0%
safrole 3,4-methylenedioxy 0.6%
eugenol 3-methoxy, 4-hydroxyl 0.2%
elemicin 3,4,5-trimethoxy *
methyleugenol 3,4-dimethoxy *
----
- -mentioned in (4) and stated as being previously included with
the myristicin portion incorrectly.
Weil's (1) paper gives a broad history of nutmeg use as food and as
narcotic, and gives a summary of research into the pharmacological
effects of nutmeg. Some of the more interesting work cited is that by
Alexander Sulgin (3,4). Unfortunately some of the cited work is from an
unpublished paper, and the library didn't have the journal another
article was in (3) so I only saw excerpts.
The descriptions of the experience mentioned by Weil are consistent
with pyschedelic amphetamine experiences, although the initial phase
of an excitment and distorted perception is often followed by
narcosis, the effects sometimes reported as lasting days. There are a
wide variety of other toxic effects reported (infrequently, death) with
enough frequency to make it clear why this is not a widely abused
substance.
The psychedelic component is examined by Shulgin who concludes that
the hallucinogenic action is mainly from the myristicin and related
components. He notes that only know mechanism of metabolism of any of
the compounds is the detoxification of safrole to piperonylic acid.
This reaction show the capacity to oxidize an olefinic side chain.
He uses this fact to speculate on a possible pharmacologic mechanism
(quoted from Weil):
"Shulte suggests that, if this degradative process is `applicable to
myristicin, or especially to elemicin, a theoretical intermediate, a
vinyl alcohol, could undergo transamination producing the known
psychotomimetic drug, 3,4,5-trimethoxy amphetamine (TMA). The recent
description of the new, synthetic hallucinogen -
3-methoxy-4,5-methylenedioxy amphetamine (MMDA)-which might be
derived by an analogous process from myristicin, itself, is even more
suggestive of a psychotropic function for this component of nutmeg.'"
References
----------
1. Weil, Andrew (1965). Nutmeg as a Narcotic. 19(3), 194-217.
2. Truitt, Edward and others (1961). The Pharmacology of Myristicin; A
Contribution to the Psychoparmacology of Nutmeg. 2(4), 205.
3. Shulgin, Alexander T. (1963). Concerning the pharmacology of nutmeg.
Mind 299-303.
4. Shulgin, Alexander T. (1964). Composition of the myristicin fraction
from oil of nutmeg. Nature, 197:4865, p.379.
--
Ray Dueland
raydu@ico.isc.com
...uunet!ico!raydu
Subject: Shulgin
More on Shulgin from Email sent to me -
--
I sent away to shulgin for his book on the controlled substances act.
He sent me back a letter which included the following:
"I am presently struggling through my book on the entire phenylethylamine
area, and with the smiles of the almighty, it will be done soon. This is
a novel, PIHKAL, that embodies all I have uncovered in my research over the
last forty years, some published but mostly unpublished. It will have the
world's longest footnote, with the recipes and dosages and duration and
descriptions of experiences and related comments on all the phenylethylamines
I have ever made or looked at. Some 250 of them. (!) ... And, as I had
said, all published as fiction. PIHKAL is the acronym for "Phenylethylamines
I Have Known and Loved"
The book should be done by the end of the year.
DRUG QUIZ
(answers follow posting)
(1) What is the present Schedule, within the CSA, for each of the
following drugs:
(a) the hallucinogen Tiletamine?
(b) the stimulant U-4-E-uh (Methylaminorex)?
(c) the narcotic Benzylfentanyl?
(2) Was MDMA (Ecstasy) a Scheduled drug on March 1, 1988?
(3) What material is listed as #8254 in the DEA computer?
(4) What drug is Scheduled but has yet to be synthesized?
THE CONTROLLED SUBSTANCES ACT
This is a 383 page manual containing all details of the Federal Drug
Law, including names, schedules, definitions, DEA code numbers,
structures, regulatory authority, history, drug formulae, plant
sources, synonyms, CAS registries, chemical names, and more.
$34.95, plus $4.00 s/h ____ Bill me ____ Check enclosed
SHIP TO: ORDER FROM:
Name ___________________ Alexander T. Shulgin
Address ___________________ 1483 Shulgin Road
City, Zip ___________________ Lafayette, CA 94549
Answers:
(1) a: not scheduled
b: Schedule I
c: not scheduled
(2) No.
(3) Tapioca starch
(4) MMDA-4
..............................
Just in case you were having trouble getting the Shulgin bibliography
to come out right, I have received the following.
--------begin forwarded message---------------
Mr. Berryhill:
In article <10567@nigel.udel.EDU> you give a bibliography of
Dr. Alexander T. Shulgin's work:
>. . . I have the references in troff format. For those not
>familiar with this format, I include a list of the format commands.
Now, I consider myself a neutral in the so-called "War" on drugs,
because I have strong feelings on both sides of the issue, but
out of sheer hacker curiosity, I tried yesterday to troff your
bibliography. Here are a few suggestions, based on what works
at my site and what doesn't:
Tyrone Slothrop wishes to add the following remarks to the recent
posting of the re-formatted bibliography of Shulgin's publications...
------begin forwarded message-------------
I haven't read alt.drugs in ages. But looking in today I am glad to see
that my efforts to make the Shulgin bibliography available were not wasted.
Some persons have even endeavored to make the troff formatting nicer. Thank
you. I noticed that somehow, some pieces of the file have gotten lost.
There was a deletion of a second author in one 1976 reference. These were
present in the original, so I am making it available again. The guess by
Rich Thomson (5739) and others on this reference was not correct.
While I am glad that the bibliography is being passed around, I am
disappointed that the Pynchon quote was stripped off. I add these quotes
for their literary merit, to turn people on to Pynchon, to raise the
collective conscious level, and your indulgence is a small price I ask in
exchange for the information I provide.
- Tyrone Slothrop -- from his scattering
Subject: The End of Psychedelic Exploration - from Slothrop
Homage To: Shulgin's Psychedelic Publications
Alexander Shulgin is the worlds foremost developer and explorer of
psychedelic drugs. He has been, and remains, a prolific writer. His
publications provide a great introduction to the diverse world of
psychedelics, and provide and inspiration for psychedelic exploration.
However, Shulgin has informed me that the publishing of any
human data on new compounds had to stop abruptly with the enactment
of the Analogue Drug Bill in 1986. This particular bit of obscenity
makes the generation, or even the attempted generation, of any altered
state of consciousness a felonious act. The continuing publication of
experimental results in the medical and scientific literature is now
totally impossible. For this reason I think it is worthwhile to
provide a complete list of his psychedelic publications. They are
well referenced, and can lead to much other psychedelic literature.
Shulgin crossed the diamond with the pearl and gave birth to all forms of
light: "It is early morning now. Slothrop's breath is white on the air.
He is just up from a dream. Part I of a poem, with woodcuts accompanying
the text - a woman is attending a dog show which is also, in some way, a
stud service. She has brought her Pekingese, a female with a sickeningly
cute name, Mimsy or Goo-Goo or something, here to be serviced. She is
passing the time in a garden setting, with some other middle-class ladies
like herself, when from some enclosure nearby she hears the sound of
her bitch, coming. The sound goes on and on for much longer than
seems appropriate, and she suddenly realizes that the sound is her own
voice, this interminable cry of dog-pleasure. The others, politely, are
pretending not to notice. She feels shame, but is helpless, driven now by
a need to go out and find other animal species to fuck. She sucks the
penis of a multicolored mongrel who has tried to mount her in the
street. Out in a barren field near a barbed-wire fence, winter fires across
the clouds, a tall horse compels her to kneel, passively, and kiss his
hooves. Cats and minks, hyenas and rabbits, fuck her inside automo-
biles, lost at night in the forests, out beside a waterhole in the desert.
"As Part II begins, she has discovered she's pregnant. Her husband, a
dumb, easygoing screen door salesman, makes an agreement with her:
her own promise is never stated, but in return, nine months from now,
he will take her where she wants to go. So it is that close to the end of
her term he is out on the river, and American river, in a rowboat, hauling
on the oars, carrying her on a journey. The key color in this section is
violet.
"Part III finds her at the bottom of the river. She has drowned. But all
forms of life fill her womb. 'Using her as mermaid' (line 7), they trans-
port her down through these green river-depths. 'It was down, and out
again./ Old Squalidozzi, ploughman of the deep,/ At the end of his
day's sowing/ Sees her verdigris belly among the weeds' (lines 10-13),
and brings her back up. He is a classically-bearded Neptune figure with
an old serene face. From out of her body streams a flood now of dif-
ferent creatures, octopuses, reindeer, kangaroos, 'Who can say all the
life/ That left her womb that day?' Squalidozzi can only catch a
glimpse of the amazing spill as he bears her back toward the surface.
Above, it is a mild and sunlit green lake or pond, grassy at the banks,
shaded by willows. Insects whine and hover. The key color now is
green. 'And there as it broke to sun/ Her corpse found sleep in the
water/ And in the summer depths/ The creatures took their way/ Each
to its proper love/ In the height of afternoon/ As the peaceful river
went....'" Pynchon (1973, p. 446-447)
For reprints of Shulgin's publications, write to:
Alexander T. Shulgin
1483 Shulgin Road
Lafayette, CA 94549
Be merciful. He is out of many of the older papers, and probably doesn't
have reprints of the longer review articles. Don't request reprints of
articles that you can get at the library. After each article I have
included a number. These are the numbers that Shulgin uses to reference
his papers. If you include these it will make it easier for him to
locate them. I have the references in troff format. For those not
familiar with this format, I include a list of the format commands.
\fI start italics
\fG start greek
\fR end italics or greek
\u shift up half line, begin superscript or end subscript
\d shift down half line, begin subscript or end superscript
\s+2 increase point size by two
\s-2 decrease point size by two
\*' accent on preceding letter
\*: umlaut on preceding letter
.XP
Pynchon, Thomas. 1973. Gravity's Rainbow. The Viking Press, N.Y. Pp. 760.
.XP
Shulgin, A. T., S. Bunnell, and T. Sargent. 1961. The psychotomimetic
properties of 3,4,5-trimethoxyamphetamine. Nature 189: 10011-1012. 12
.XP
_____. 1963. Psychotomimetic agents related to mescaline. Experientia
19: 127. 19
.XP
_____. 1963. Composition of the myristicin fraction from oil of nutmeg.
Nature 197: 379. 20
.XP
_____. 1963. Concerning the pharmacology of nutmeg. Mind 1: 299-302. 23
.XP
_____. 1964. 3-methoxy-4,5-methylenedioxy amphetamine, a new
psychotomimetic agent. Nature 201: 1120-1121. 29
.XP
_____. 1964. Psychotomimetic amphetamines: methoxy 3,4-dialkoxyamphetamines
Experientia 20: 366. 30
.XP
_____, and H. O. Kerlinger. 1964. Isolation of methoxyeugenol and trans-
isoelemicin from oil of nutmeg. Naturwissenschaften 15: 360-361. 31
.XP
_____. 1965. Synthesis of the trimethoxyphenylpropenes. Can. J. Chem.
43: 3437-3440. 43
.XP
_____. 1966. Possible implication of myristicin as a psychotropic substance
Nature 210: 380-384. 45
.XP
_____. 1966. The six trimethoxyphenylisopropylamines
(trimethoxyamphetamines). J. Med. Chem. 9: 445-446. 46
.XP
_____, T. Sargent, and C. Naranjo. 1966. Role of 3,4-dimethoxyphenethylamin
in schizophrenia. Nature 212: 1606-1607. 48
.XP
_____, T. Sargent, and C. Naranjo. 1967. The chemistry and psychopharmacolo
of nutmeg and of several related phenylisopropylamines. \fIIn\fR D. H.
Efron [ed.]: Ethnopharmacologic search for psychoactive drugs. U. S. Dept.
of H. E. W., Public Health Service Publication No. 1645. Pp. 202-214.
Discussion: ibid. pp. 223-229. 49
.XP
_____, and T. Sargent. 1967. Psychotropic phenylisopropylamines derived
from apiole and dillapiole. Nature 215: 1494-1495. 50
.XP
Sargent, T. W., D. M. Israelstam, A. T. Shulgin, S. A. Landaw, and N. N.
Finley. 1967. A note concerning the fate of the 4-methoxyl group in
3,4-dimethoxyphenethylamine (DMPEA). Biochem. Biophys. Res. Commun.
29: 126-130. 52
.XP
Naranjo, C., A. T. Shulgin, and T. Sargent. 1967. Evaluation of
3,4-methylenedioxyamphetamine (MDA) as an adjunct to psychotherapy.
Med. Pharmacol. Exp. 17: 359-364. 53
.XP
Shulgin, A. T. 1968. The ethyl homologs of 2,4,5-trimethoxyphenylisopropyl-
amine. J. Med. Chem. 11: 186-187. 54
.XP
_____, T. Sargent, and C. Naranjo. 1969. Structure activity relationships
of one-ring psychotomimetics. Nature 221: 537-541. 57
.XP
_____. 1969. Recent developments in cannabis chemistry. J. Psyched. Drugs
2: 15-29. 58
.XP
_____. 1969. Psychotomimetic agents related to the catecholamines.
J. Psyched. Drugs 2(2): 12-26. 59
.XP
_____. 1970. Chemistry and structure-activity relationships of the
psychotomimetics. \fIIn\fR: D. H. Efron [ed.]. Psychotomimetic Drugs.
Raven Press, New York. Pp. 21-41. 60
.XP
_____. 1970. The mode of action of psychotomimetic drugs; some qualitative
properties of the psychotomimetics. Neur. Res. Prog. Bull. 8: 72-78. 61
.XP
_____. 1970. 4-alkyl-dialkoxy-\fGa\fR-methyl-phenethylamines and their
pharmacologically-acceptable salts. U. S. Patent 3,547,999, issued Dec. 15,
1970. 63
.XP
_____, T. Sargent, and C. Naranjo. 1971. 4-bromo-2,5-dimethoxyphenyliso-
propylamine, a new centrally active amphetamine analog. Pharmacology
5: 103-107. 64
.XP
_____. 1971. Chemistry and sources. \fIIn\fR: S. S. Epstein [ed].
Drugs of abuse: their genetic and other chronic nonpsychiatric hazards.
The MIT Press, Cambridge, Mass. Pp 3-26. 65
.XP
_____. 1971. Preliminary studies of the synthesis of nitrogen analogs
of \fGD\fR\u\s-21\s+2\d-THC. Acta Pharm. Suec. 8: 680-681. 66
.XP
_____. 1972. Hallucinogens, CNS stimulants, and cannabis. \fIIn\fR:
S. J. Mule/*' and H. Brill [eds.]: Chemical and biological aspects of
drug dependence. CRC Press, Cleveland, Ohio. Pp. 163-175. 67
.XP
_____. 1973. Stereospecific requirements for hallucinogenesis.
J. Pharm. Pharmac. 25: 271-272. 68
.XP
_____. 1973. Mescaline: the chemistry and pharmacology of its analogs.
Lloydia 36: 46-58. 69
.XP
_____. 1973. The narcotic pepper - the chemistry and pharmacology of
\fIPiper methysticum\fR and related species. Bull. Narc. 25: 59-74.
Le poivre stupe\*'fiant - chemie et pharmacologie du \fIPiper methysticum\fR
et des espe\*'ces apparente\*'es. Bull. Stupe\*'fiants 25: 61-77. 70
.XP
_____, T. Sargent, and C. Naranjo. 1973. Animal pharmacology and human
psychopharmacology of 3-methoxy-4,5-methylenedioxyphenylisopropylamine
(MMDA). Pharmacology 10: 12-18. 71
.XP
_____. Drugs of abuse in the future. Drug abuse in America Vol. 1.
pp. 209-236. U.S.G.P.O. 5266-00004. Reprinted: Clin. Tox. 8: 405-456. 72
.XP
Kalbhen, D. A., T. Sargent, A. T. Shulgin, G. Braun, H. Stauffer, N. Kusubov,
and M. L. Nohr. 1974. Human pharmacodynamics of the psychodysleptic
4-bromo-2,5-dimethoxyphenylisopropylamine labelled with \u82\dBr.
IRCS (Int. Res. Comm. Sys.) 2: 1091. 73
.XP
Sargent, T., D. A. Kalbhen, A. T. Shulgin, H. Stauffer, and N. Kusubov. 1975
A potential new brain-scanning agent: 4-\u77\dBr-2,5-dimethoxyphenyliso-
propylamine (4-Br-DPIA). J. Nucl. Med. 16: 243-245. 74
.XP
Shulgin, A. T., and M. F. Carter. 1975. Centrally active phenethylamines.
Psychopharm. Commun. 1: 93-98. 75
.XP
Sargent, T., D. A. Kalbhen, A. T. Shulgin, G. Braun, H. Stauffer, and
N. Kusubov. 1975. \fIIn vivo\fR human pharmacodynamics of the
psychodysleptic 4-Br-2,5-dimethoxyphenylisopropylamine labelled with
\u82\dBr or \u77\dBr. Neuropharmacology 14: 165-174. 76
.XP
_____. 1975. The chemical catalysis of altered states of consciousness.
Altered states of consciousness, current views and research problems.
The drug abuse council, Washington, D. C. Pp. 123-134. 77
.XP
_____. 1975. Drug use and anti-drug legislation. The PharmChem
Newsletter 4 (#8). 79
.XP
_____, and D. C. Dyer. 1975. Psychotomimetic phenylisopropylamines. 5.
4-alkyl-2,5-dimethoxyphenylisopropylamines. J. Med. Chem. 18: 1201-1204. 80
.XP
_____, and C. Helisten. 1975. Differentiation of PCP, TCP, and a
contaminating precursor PCC, by thin layer chromatography. Microgram 8:
171-172. 81
.XP
Helisten, C., and A. T. Shulgin. The detection of 1-piperidinodydlohexane-
carbonitrile contamination in illicit preparations of 1-(1-phenylcyclohexyl)
piperidine and 1-(1-(2-thienyl)cyclohexyl)piperidine. J. Chrom. 117:
232-235. 82
.XP
Shulgin, A. T. 1976. Psychotomimetic agents. \fIIn\fR: M. Gordon [ed.]
Psychopharmacological agents, Vol. 4. Academic Press, New York.
Pp. 59-146. 83
.XP
_____. 1976. Abuse of the term "amphetamines". Clin. Tox. 9: 351-352. 84
.XP
_____. 1976. Profiles of psychedelic drugs. 1. DMT. J. Psychedelic
Drugs 8: 167-168. 85
.XP
_____. 1976. Profiles of psychedelic drugs. 2. TMA-2. J. Psychedelic
Drugs 8: 169. 86
.XP
_____, and D. E. MacLean. 1976. Illicit synthesis of phencyclidine (PCP)
and several of its analogs. Clin. Tox. 9: 553-560. 87
.XP
Nichols, D. E., and A. T. Shulgin. 1976. Sulfur analogs of psychotomimetic
amines. J. Pharm. Sci. 65: 1554-1556. 89
.XP
Sargent, T., A. T. Shulgin, and N. Kusubov. 1976. Quantitative
measurement of demethylation of \u14\dC-methoxyl labeled DMPEA and TMA-2
in rats. Psychopharm. Commun. 2: 199-206. 90
.XP
Standridge, R. T., H. G. Howell, J. A. Gylys, R. A. Partyka, and A. T.
Shulgin. 1976. Phenylalkylamines with potential psychotherapeutic utility.
1. 2-amino-1-(2,5,-dimethoxy-4-methylphenyl)butane. J. Med. Chem.
19: 1400-1404. 91
.XP
_____. 1976. Profiles of psychedelic drugs. 3. MMDA. J. Psychedelic
Drugs 8: 331. 92
.XP
_____. 1977. Profiles of psychedelic drugs. 4. Harmaline. J. Psychedelic
Drugs 9: 79-80. 93
.XP
_____. 1977. Profiles of psychedelic drugs. 5. STP. J. Psychedelic Drugs
9: 171-172. 94
.XP
Nichols, D. E., A. T. Shulgin, and D. C. Dyer. 1977. Directional lipophilic
character in a series of psychotomimetic phenethylamine derivatives. Life
Sciences 21: 569-576. 95
.XP
Jacob, P. III, G. Anderson III, C. K. Meshul, A. T. Shulgin, and N.
Castagnoli Jr. 1977. Mononethylthio analogues of 1-(2,4,5-trimethoxyphenyl)
2-aminopropane. J. Med. Chem. 20: 1235-1239. 96
.XP
White, T. J., D. Goodman, A. T. Shulgin, N. Castagnoli Jr., R. Lee, and
N. L. Petrakis. 1977. Mutagenic activity of some centrally active aromatic
amines in \fISalmonella typhimurium\fR. Mutation Research 56: 199-202. 97
.XP
Braun, U., A. T. Shulgin, G. Braun, and T. Sargent III. 1977. Synthesis
and body distribution of several iodine-131 labeled centrally acting
drugs. J. Med. Chem. 20: 1543-1546. 98
.XP
Sargent, T. III, T. F. Budinger, G. Braun, A. T. Shulgin, and U. Braun.
1978. An iodated catecholamine congener for brain imaging and metabolic
studies. J. Nucl. Med. 19: 71-76. 99
.XP
Shulgin, A. T. 1978. Psychotomimetic drugs: structure-activity
relationships. \fIIn\fR: L. L. Iversen, S. D. Iversen, and S. H. Snyder
[eds.], Handbook of psychopharmacology, Vol. 11. Plenum Press, New
York. Pp. 243-333.
.XP
Sargent, T. III, G. Braun, U. Braun, T. F. Budinger, and A. T. Shulgin.
1978. Brain and retina uptake of a radio-iodine labeled psychotomimetic
in dog and monkey. Commun. Psychopharm. 2: 1-10. 101
.XP
Braun, G., A. T. Shulgin, and T. Sargent III. 1978. Synthesis of
\u123\dI-labelled 4-iodo-2,5-dimethoxyphenylisopropylamine. J. Labelled
Comp. and Radiopharm. 14: 767-773. 102
.XP
Murdock, J. E., J. R. Patty, and A. T. Shulgin. 1978. A novel illicit
amphetamine laboratory. Microgram 11: 98-101. 103
.XP
Anderson, G. M. III, G. Braun, U. Braun, D. E. Nichols, and A. T. Shulgin.
1978. Absolute configuration and psychotomimetic activity. \fIIn\fR:
G. Barnett, M. Trsic, and R. Willette [eds.], QuaSAR Research Monograph 22.
N.I.D.A. Washington, D.C. Pp. 8-15. 104
.XP
Braun, U., G. Braun, P. Jacob III, D. E. Nichols, and A. T. Shulgin.
Mescaline analogs: substitutions at the 4-position. \fIIn\fR:
G. Barnett, M. Trsic, and R. Willette [eds.], QuaSAR Research Monograph 22.
N.I.D.A. Washington, D.C. Pp. 27-37. 105
.XP
Partyka, R. A., R. T. Standridge, H. G. Howell, and A. T. Shulgin. 1978.
2-amino-1-(2,5-dimethoxyphenyl)butanes. U.S. Patent 4,105,695, issued
Aug. 8, 1978. 106
.XP
Shulgin, A. T., and D. E. Nichols. 1978. Characterization of three new
psychotomimetics. \fIIn\fR: R. C. Stillman and R. E. Willette [eds.],
The psychopharmacology of hallucinogens. Pergamon Press, New York.
Pp. 74-83. 107
.XP
Glennon, R. A., L. B. Kier, and A. T. Shulgin. 1979. Molecular
connectivity analysis of hallucinogenic mescaline analogs. J. Pharm.
Sci. 68: 906-907. 108
.XP
Shulgin, A. T. 1979. Chemistry of phenethylamines related to mescaline.
J. Psychedelic Drugs 11: 41-52. 109
.XP
_____. 1979. Profiles of psychedelic drugs. 6. \fGa\fR,O-DMS.
J. Psychedelic Drugs 11: 247. 110
.XP
_____. 1979. Profiles of psychedelic drugs. 7. Mescaline. J.
Psychedelic Drugs 11: 355. 111
.XP
Standridge, R. T., H. G. Howell, H. A. Tilson, J. H. Chamberlain, H. M.
Holava, J. A. Gylys, R. A. Partyka, and A. T. Shulgin. 1980.
Phenylalkylamines with potential psychotherapeutic utility. 2. Nuclear
substituted 2-amino-1-phenylbutanes. J. Med. Chem. 23: 154-162. 112
.XP
Braun, U., A. T. Shulgin, and G. Braun. 1980. Centrally active
N-substituted analogs of 3,4-methylenedioxyphenylisopropylamine
(3,4-methylenedioxyamphetamine). J. Pharm. Sci. 69: 192-195. 113
.XP
Kantor, R. E., S. D. Dudlettes, and A. T. Shulgin. 1980. 5-methoxy-
\fGa\fR-methyltryptamine (\fGa\fR,O-dimethylserotonine) a hallucinogenic
homolog of serotonin. Biol. Psychiat. 15: 349-352. 114
.XP
Shulgin, A. T. 1980. Profiles of psychedelic drugs. 8. psilocybin.
J. Psychedelic Drugs 12: 79. 115
.XP
Braun, U., A. T. Shulgin, and G. Braun. 1980. Pru\*:fung auf
Aktivita\*:t und Analgesia von N-substituierten Analogen des Amphetamin-
Derivates 3,4-Methylendioxyphenylisopropylamin. Arzneim. Forsch.
30: 825-830. 116
.XP
Shulgin, A. T. 1980. Profiles of psychedelic drugs. 9. LSD.
J. Psychedelic Drugs 12: 173-174. 117
.XP
_____. 1981. Hallucinogens. \fIIn\fR: M. E. Wolff [ed.], Burger's
medicinal chemistry. Wiley & Co. Pp. 1109-1137.
.XP
_____. 1981. Profiles of psychedelic drugs. 10. DOB. J. Psychoactive
Drugs 13: 99. 119
.XP
_____, and M. F. Carter. 1981. N,N-diisopropyltryptamine (DIPT) and
5-methoxy-N,N-diisopropyltryptamine (5-MeO-DIPT). Two orally active
tryptamine analogs with CNS activity. Commun. Psychopharmacol.
4: 363-369. 120
.XP
Jacob, P., and A. T. Shulgin. 1981. Sulfur analogues of psychotomimetic
agents. Monothio analogues of mescaline and isomescaline. J. Med. Chem.
24: 1348. 121
.XP
Domelsmith, L. N., T. A. Eaton, K. N. Houk, G. M. Anderson, R. A. Glennon,
A. T. Shulgin, N. Castagnoli, and P. A. Kollman. 1981. Photoelectron
spectra of psychotropic drugs. 6. Relationships between physical
properties and pharmacological actions of amphetamine analogues.
J. Med. Chem. 24: 1414. 122
.XP
Shulgin, A. T. 1981. Chemistry of psychotomimetics. \fIIn\fR:
F. Hoffmeister and G. Stille [eds.], Handbook of experimental pharmacology,
Vol. 55/III. Springer-Verlag, Berlin Heidelberg. Pp. 3-29.
.XP
_____. 1981. Profiles of psychedelic drugs. 11. Bufotenine.
J. Psychoactive Drugs 13: 389. 124
.XP
_____, and P. Jacob. 1982. Potential misrepresentation of 3,4-methylene-
dioxyamphetamine (MDA). A toxicological warning. J. Anal. Tox. 6: 71. 127
.XP
_____, and P. Jacob. 1982. 1-(3,4-methylenedioxyphenyl)-3-aminobutane:
a potential toxicological problem. J. Toxicol. - Clin. Toxicol. 19: 109. 12
.XP
Jacob, P., and A. T. Shulgin. 1983. Sulfur analogues of psychotomimetic
agents. 2. Analogues of (2,5-dimethoxy-4-methylphenyl)- and (2,5-
dimethoxy-4-ethylphenyl)-isopropylamine. J. Med. Chem. 26: 746. 130
.XP
Shulgin, A. T. 1983. Twenty years on an ever-changing quest. \fIIn\fR:
L. Grinspoon and J. B. Bakalar [eds.], Psychedelic Reflections. Human
Sciences Press, New York. 131
.XP
Sargent, T., A. T. Shulgin, and C. A. Mathis. 1982. New iodinated
amphetamines by rapid synthesis for use as brain blood flow indicators.
J. Lab. Cmpds. and Radiopharm. 19: 1307. 132
.XP
Jacob, P., and A. T. Shulgin. 1984. Sulfur analogues of psychotomimetic
agents. 3. The ethyl homologues of mescaline and their monothio analogues.
J. Med. Chem. 27: 881-888. 133
.XP
Sargent, T., A. T. Shulgin, and C. A. Mathis. 1984. Radiohalogen-labeled
imaging agents. 3. Compounds for measurement of brain blood flow by
emission tomography. J. Med. Chem. 27: 1071-1077. 135
.XP
Repke, D. B., D. B. Grotjahn, and A. T. Shulgin. 1985. Psychotomimetic
N-methyl-N-isopropyltryptamines. Effects of variation of aromatic
oxygen substituents. J. Med. Chem. 28: 892. 136
.XP
Shulgin, A. T. 1985. What is MDMA? PharmChem Newsletter 14: 3
(May-June, #3). 137
.XP
Lemaire, D., P. Jacob, and A. T. Shulgin. 1985. Ring substituted
beta-methoxyphenethylamines: a new class of psychotomimetic agents active
in man. J. Pharm. Pharmacol. 37: 575. 138
.XP
Mathis, C. A., T. Sargent, and A. T. Shulgin. 1985. Iodine-122 labeled
amphetamine derivatives with potential for PET brain blood-flow studies.
J. Nucl. Med. 26: 1295. 139
.XP
_____, _____, and _____. 1986. Synthesis of 122-I and 125-I-labeled-
\fImeta\fR-dimethoxy-N,N-dimethyliodophenylisopropylamines. J. Labelled
Comp. Radiopharm. 23: 115. 140
.XP
Shulgin, A. T., L. A. Shulgin, and P. Jacob. 1986. A protocol for the
evaluation of new psychoactive drugs. Methods and Findings in
Experimental and Clinical Pharmacology 8: 313. 141
.XP
Nichols, D. E., A. J. Hoffman, R. A. Oberlender, P. Jacob, and A. T.
Shulgin. 1986. Derivatives of 1-(1,3-benzodioxol-5-yl)-2-butanamine:
representatives of a novel therapeutic class. J. Med. Chem. 29: 2009. 143
.XP
Mathis, C. A., A. T. Shulgin, Y. Yano, and T. Sargent. 1986. \u18\dF-
labelled N,N-dimethylamphetamine analogues for brain imaging studies.
Appl. Radiat. Isot. 37: 865. 144
.XP
Shulgin, A. T. 1986. The background and chemistry of MDMA. J. Psychoactive
Drugs 18: 291-304. 145
.XP
Sargent, T. W., A. T. Shulgin, and C. A. Mathis. 1987. Rapid brain
scanning pharmaceutical. U. S. Patent 4,647,446. 146
.XP
McKenna, D. J., C. A. Mathis, A. T. Shulgin, T. Sargent, and J. M. Saavedra.
1987. Autoradiographic localization of binding sites for \u125\dI-DOI,
a new psychotomimetic radioligand, in the rat brain. Eur. J. Pharmacol.
137: 289-290. 147
.XP
Shulgin, A. T. 1987. The 'social-chemistry' of pharmacological discovery.
Social Pharmacology 1: 279-290. 148
.XP
_____. 1987. Reference information on MDMA. Analog 9: #4 (page 10). 149
.XP
_____. 1988. DIPT: the distortion of music. Reality Hackers #6 (Winter
1988) p. 27. 152.
.XP
_____. 1988. THE CONTROLLED SUBSTANCES ACT: A resource manual of the
current status of the federal drug laws. 383 pp., published in Lafayette,
California 94549 April 1988. 154
.XP
_____. In press. History of MDMA. \fIIn\fR: S. Peroutka [ed.], MDMA:
"Ecstasy" and human neurotoxin? Kluwer Academic Publishers, Norwell, MA,
02061.
------end forwarded message----------
--
Subject: mdma neurotoxocity
Yesterday, I posted info on MDMA, working from memory. Today, I brought
the June '91 High Times article on the Bridge Conference, held at
Stanford (!) February 2-3. Here are some excerpts from the article
regarding MDMA:
... Bruce Eisner eloquently characterized MDMA ("ecstasy") as a
substance which reveals "the inner nature of human beings, that
we all have a core of love and beauty that we can tap into".
The question on everyone else's minds seemed to be whether
this miraculous chemical also causes brain damage in humans.
In several presentations, audience questions about this issue
were addressed by Debby Harlow and Jerome Beck, authors of a
sociological study of MDMA funded by the National Institute
on Drug Abuse; Dennis McKenna, who has been associated with
some of the major MDMA neurotoxicity researchers; and David
Nichols, whose 20 years of research on the effects of psychedelics
on rats at the Pharmacology Department of Purdue University has
also been funded by the NIDA. They did their best to dispel
several myths about MDMA toxicity, and to set the record straight
on what is known about MDMA neurotoxicity in humans.
The first myth put to rest was that MDMA causes Parkinson's
disease or a Parkinson's-like syndrome. This rumor was
apparently caused by confusion of MDMA with MPTP, an impurity
present in a designer analog of heroin, long-term use of which
has caused at least one case of this kind of effect. The second
misapprehension concerned the fact that MDMA causes some sort of
drainage of spinal fluid. This misconception somehow resulted
from a misunderstanding of research into the effects of MDMA on
levels of the neurotransmitter serotonin, which are accessed
through spinal taps. It's the spinal taps that drain the fluid,
NOT the MDMA.
Research into possible MDMA-caused damage to serotonin neurons
has spawned a great deal of anxiety and misinterpretation. (Some
of the problem results from the fact that MDMA research has been
frequently confused with MDA research). Huge, repeated doses of
MDMA administered to rats DO cause selective damage to serotonin-
receptor sites. (Mice are apparently less sensitive). A similar
effect has been observed in primates at dosages above, but
approximating, human levels. Recovery from this damage seems to
occur in about four months, followed mysteriously by a reappearance
of deterioration.
David Nichols offered the most detailed and cogent explanation of
what happens in this process. The temporary decrease in serotonin
levels following an MDMA trip, which initiates a massive release
of serotonin, causes the absorption into serotonin neurons of
another neurotransmitter, dopamine, in place of serotonin.
Dopamine does not belong in these serotonin-receptor sites, and
it is likely that a toxic metabolite created by the enzyme-induced
breakdown of dopamine causes the observed damage. This
deterioration is "axodentritic", which means that it occurs in the
terminals of the nerve cell, not in its main body.
A number of other relevant facts were noted. Nichols pointed out
that for over 20 years, large doses of fenfluoramine -- an FDA-
approved, MDMA-related chemical prescribed as an appetite
suppressant -- have been taken by one and a half to two million
people in the US. This drug is twice as toxic as MDMA and is
ingested on a daily basis. However, no aberrations have been
observed.
Furthermore, Harlow remarked that there are no "behavioral
correlates" to MDMA neurotoxicity in any mammals, including
humans. This means that no cognitive, emotional, or physiological
dysfunctions have been observed to occur as a result of this
nerve damage. Harlow asked how, without such correlates, "can
we know that this is a negative thing ? What the neurotoxicity
researchers are calling brain DAMAGE is really brain CHANGE".
Dennis McKenna agreed: "There is no rational reason to assume
that this is negative, given the well-known plasticity of the
brain".
One psychopharmacologist, who has asked not to be quoted by name,
takes this issue even further. "Who knows ? Maybe the trimming
back of serotonin receptors has the effect of pruning the psyche!"
For those still concerned about brain damage from MDMA, Nichols
referred to a study involving MDMA and the popular antidepressant
Prozac. The latter drug blocks the "reuptake" or reabsorption of
serotonin into serotonin nerve cells, and has been shown to
counteract as well the absorption of the culprit neurotransmitter
dopamine into these same cells after administration of MDMA in
rats. The conclusion is that a single therapeutic dose of Prozac
taken three hours after MDMA would block any possible neuro-
toxicity in humans, and one dose three-to-six-hours after MDMA
should significantly decrease such damage.
In spite of all the controversy, there is still no positive
indication that the animal studies have any bearing on humans.
Nichols flatly summed up the situation: "There is no evidence
of MDMA neurotoxicity in humans".
In article <1083@tau-ceti.isc-br.com> geraldb@tau-ceti.isc-br.com (Gerald
Bryan (Denver)) writes:
>Here's what I've read about MDMA's effects:
>
> o In the average person, given the right set and setting, there are no
> long lasting psychological effects that would generally be considered
> deleterious.
>
> o One of the arguments used by the DEA to schedule MDMA was that tests
> done with MDA (note, not the same as MDMA) on rats showed some damage
> at nerve cell receptor sites.
> o After being scheduled, similar tests were done with MDMA, also showing
> similar "neurotoxocity", though not as bad as that with MDA.
> o Further tests revealed that the nerve cell receptor site damage goes
> away after a period of abstinence (I believe the period of time was
> 1 month). Also, the amounts of MDMA needed to produce the neurotoxicity
> were significantly higher than human dosages (I think based on body
> weight).
You get the quote unquote neurotoxic effect in squirrel monkeys at about
2-3 times the human ED orally (based on body weight).
> o There is at least one commonly prescribed drug, called something like
> Fleurotin (help me on this one, netters), that fails the neurotoxicity
> test worse than MDMA, yet no one seems concerned about it when
> prescribing the drug.
Fenfluramine. Used for weight loss.One difference between MDMA and Fenfluramine
is that MDMA is used recreationally. The comparison is a good one given
that Fenfluramine has been prescribed for many years with no noticable
problems. My inclination would be to hold off on it for a few years. It's
good for weight loss but there are other drugs.
Given MDMA's very probable efficacy in therapy (as Lester Grinspoon has
argued), there is no way that it should be Schedule I. At worst, it
should be categorized with its cousins, amp and MA, in Schedule II where
researchers can get to it more easily.
As has been previously posted here (by, I think, Tim Basher) there is a
good chance that the neurotoxic effects of MDMA can be prevented, without
effecting its psychactive effects. The neurotoxic effects of MDMA happen
AFTER the psychoactive ones. A 5-HT reuptake blocker administered at
this point can prevent the 5-HT neurotoxicty. I've all but seen it done
in real time with microdialysis (with fenfluramine and fluoxetine) in
rats.
> o The neuro-toxicity has never been observed in humans (but, I've
> always wondered, how would they know ?)
5-HIAA levels in the spinal fluid have been found to be lowered in human users,
suggesting that the neurotoxicity exists as well.
> o There is some disagreement about what the perceived (and temporary)
> neuro-toxicity means, if anything. It's more than just a
> disagreement -- I don't think anyone has ventured to guess what it
> implies. Not saying that I agree with this, but I once heard
> Andrew Weil venture that the supposed neurotoxicity might even be
> beneficial brain pruning, much like that that occurs normally
> in infants.
The only successful experiments I've seen were with dopamine neurotoxicity
from MA. This was a poster at Neuroscience which found that DA loss of
about 50% was correlated with the number of times a rat slipped when
walking across a thin beam. Weil's 'beneficial brain pruning' seems
intuitively implausible to me, but that's just my inclination.
> o According to Dr. David Nichols (within the last several months),
> MDMA has not been proven to cause any damage (he may have qualified
> this with the word "permanent" -- see the HT article mentioned below).
> Dr. David Nichols, by the way, is probably the number 2 psychedelic
> chemist in the world today, right after Alexander Shulgin.
Dr. Nichols is correct. And Gerald is correct that Nichols knows what he's
talking about.
>Sources: "Ecstasy: The MDMA Story" by Bruce Eisner.
> This month's High Times coverage of the psychedelics conference
> held in Santa Cruz, San Francisco, or some place like that.
>--
>gerald Bryan | "I don't like myself sober," confided Alan Watts to a
> | friend of mine, "so I spend much of my time drunk."
> | -- Robert S. deRopp
From: Chemical & Engineering News. September 9, 1985.
"3,4-methylenedioxymethamphetamine (MDMA)....
H H To a number of psychiatrists scattered across
\ / the country, MDMA is a useful therapeutic tool.
C Those psychiatrists have been using MDMA quietly
/ \ since the mid-1970's in counseling sessions as
O O an adjunct to psychotherapy. They report that,
\ / when used under controlled conditions, MDMA has
----- few negative side effects and can act to ease
// \\ psychic trauma and break down barriers to
'< >` communication.
\ /
===== The National Institute on Drug Abuse (NIDA)
\ maintains that MDMA is a 'nationwide problem
/ as well as a serious health threat.' According
H C--< to a NIDA publication, MDMA users experience problems
3 \ similar to those associated with use of amphetamines
NHCH and cocaine. The publication cites specifically
3 'psychological difficulties, including confusion,
depression, sleep problems, drug craving, severe
anxiety, and paranoia - during and sometimes weeks
after taking MDMA.'
MDMA was first synthesized and patented by E. Merck & Co., Germany,
in 1914 as an appetite suppressant. The compound was never marketed,
however, and the patent on it has long since expired.
It is currently accepted CHEMICAL ABSTRACTS designation is
N, alpha-dimethyl-1,3-benzodioxole-5-ethanamine. On the street,
it is sold as MDMA, MDM, Adam, Ecstasy, or XTC.
Chemically, MDMA is related both to methamphetamine and
3,4-methylenedioxyamphetamine (MDA). According to a number of
research workers, however, it bears little pharmacological relationsh\
ip
to those drugs. 'It stands out as unique in its constellation of
properties,' says one.
Unlike MDA, MDMA appears to have almost no hallucinogenic properties.
Nor is its effects primarily that of a stimulant such as
methamphetamine. Instead, MDMA seems to break down barriers to
communication between people, ease psychic trauma, and allow
individuals access to repressed psychological information.
George Greer, a psychiatrist in private practice in Santa Fe, N.M.,
...concluded that 'the single best use of MDMA is to facilitate
more direct communication between people involved in a significant
emotional relationship....'
The psychiatrists who have used MDMA in therapy also believe that
it has relatively low abuse potential because its beneficial or
pleasant side effects diminish rapidly with regular use.
...DEA proposed in July, 1984 that MDMA be classified as a Schedule I
controlled substance.
...DEA's Frank Sapienza...defends DEA's action on the grounds that
research conducted at the University of Chicago demonstrated that
MDA is selectively neurotoxic to seratonergic neurons in the brain.
Although MDMA's mechanism of action remains unknown, research has
shown that its action involves seratonergic neurons. By extrapolatio\
n,
MDMA also might be neurotoxic to such neurons.
Such a classification, however, creates a catch-22 situation for
the proponents of MDMA as a useful therapeutic drug. The laws
applying to Schedule I controlled substances make it quite difficult
to obtain approval to conduct clinical trials of a drug. Because
it is impossible to obtain patent protection on MDMA, it is unlikely
that a pharmaceutical firm will undertake the costly effort to
obtain FDA approval for its use. "
If anyone is interested I would be willing to find out if there has been
any further research on MDMA and report any results of the research.
A few people have written to me, asking for more information on the
possible neurotoxic effects of MDMA. So off I went, once more, to the
library in search of...
"The Journal of Phamacology and Experimental Therapeutics", 1987, 240(1), 1-7.
_Neurotoxicity of the Psychedelic Amphetamine, Methylenedioxymethamphetamine_
by Christopher Joseph Schmidt
[Ed. note - All emphasis mine]
"The neurochemical effects of the unique psychedelic agent,
methylenedioxymethamphetamine (MDMA), inidicate it may be a
seratonergic neurotoxin related to agents such as p-chloro-
amphetamine (PCA)."
"The results clearly demonstrate that MDMA has two distinct
influences on the serotonergic system of the rat brain, both
of which are manifested by a significant decrease in the
concentration of 5-HT (serotonin). Whereas the first effect
of MDMA appears to produce a REVERSIBLE depletion of 5-HT,
the second is due to a NEUROTOXIC effect of the drug on
serotonergic neurons or nerve terminals."
"As demonstrated by the results of the experiments...these
two effects can be separated temporally into an early and a
later phase."
"This early phase of depletion was REVERSIBLE because cortical
serotonin concentrations had recovered to control levels by
24 hours."
"The depletion observed at 3 hr is due almost completely
to the acute effect of the drug inasmuch as it is reversed
completely by 24 hr...."
"However, transmitter concentrations were reduced significantly
1 week later, indicating a second phase of depletion. The
latter phase of depletion was associated with a decrease in
synaptosomal serotonin uptake due to a loss in the number of
uptake sites with no change in the affinity of the carrier
for serotonin."
"The similarities between the neurochemical effects of
MDMA and those reported for PCA led us to suggest that
the long-term depletions of 5-HT produced by MDMA and PCA
occurred though similar mechanisms, i.e., a selective
degeneration of seratonergic neurons or nerve terminals."
"... The results from the uptake studies here present [the
confirming] biochemical evidence of TERMINAL DAMAGE."
Okay, folks. That is the bottom line. Ecstasy does have a neurotoxic effect.
I will quote some more on the author's views on what this means to humans.
"Although it is difficult to extrapolate from animal studies
to the human situation, some comment about the risk to human
MDMA users seems appropriate ...."
"It is first important to point out that the parenteral doses
used in this study are approximately 4 to 8 times the human
oral dose. There is also evidence to suggest that drugs such
as MDMA and MDA may be subject to significant first pass
metabolism .... This would mean that the does used in this
study may be even further from those to which a user taking
the drug p.o. is normally exposed. However, all effects
described in this study were produced with a SINGLE ADMINISTRATION
of MDMA; consequently, the possible cumulative effects of
multiple MDMA exposures remain to be evaluated. Finally ...
the possibility that humans might ... be more sensitive
to MDMA-induced neurotoxicity must not be overlooked."
Well that's the bad news. The good news is ...
"Coadministration of the selective seratonin uptake inhibitor,
fluoxetine, completely blocked the reduction in cortical
serotonin concentrations 1 week after MDMA. Administration
of fluoxetine at various times after MDMA revealed that the
long-term effects of the drug developed independently of the
acute depletion of serotonin."
"...[The] inhibition of the uptake system by 3 hr postMDMA can
still completely protect the serotonergic neurons from the later
effects of MDMA."
But the good news gets worse ...
"At 6 hr after MDMA the irreversible effects of the drug have
progress to the extent that the administration of the fluoxetine
at this point blocks only an approximate 50% of the depletion."
"By 12 hr the steps required for the drug's irreversible effects
... have been completed."
However, more good news is ...
"The two phases of 5-HT depletion are also differentiated by
their stereoselectivity ... The long term or persistent
effect of MDMA on serotonergic neurons is ... a property of
[only] the (+)-stereoisomer."
The bad news is ...
According to Christopher (in a telephone conversation), it
is this (+)-stereoisomer which is PROBABLY responsible for
most of MDMA's interesting effects (this info is from other
peoples' behaviorial studies). And also that by blocking the
acute effect you PROBABLY block its interesting effects also.
He said it was not his area of expertise but that this was
his impression from his reading.
This article is very well written. It includes methodology, results,
and a nice bibliography. You should be able to find the journal in a good
hospital or medical school library. If you cannot locate it, reprints
can be requested by writing:
Christopher J. Schmidt
Merrill Dow Research Institute
2110 E. Galbraith Road
Cincinnati, OH 45215
Please, do not say I sent you :-) I already called him once.
Once again I will offer to find out more, if there is something you need
to know. If you want to try to locate info yourself here is the data
you might need. Try Chemical Abstracts. Look under C H NO .
11 15 2
Then look under 1,3-Benzodioxole-5-ethanamine
-alpha,alpha-dimethyl
Thanx, Tim, for your research & that highly informative article.
Here's the latest on it's legality. It's previous classification as a
Schedule 1 drug has been struck down. I don't understand where that leaves
it now; I'm sure it's still controlled, but this may open the way for
further research, as well as legal progress.
Here's the text from High Times, January 1988:
COURT VOIDS "ECSTASY" PROHIBITION
In a landmark ruling, a U.S. Court of Appeals judge struck down the
classification of MDMA ("Ecstasy") as a Schedule 1 drug under the Controlled
Substances Act in a decree issued this past September.
There are five classifications for drugs under the CSA. A substance may be
classified as Schedule 1 if it is found to have: a high potential for abuse;
no accepted medical use; no way to safely supervise its medical use.
Marijuana and heroin are currently classified as Schedule 1 substances, for
which the CSA mandates the most severe controls and penalties.
The Drug Enforcement Agency had initially classified MDMA as a Schedule 1
substance in 1984. The ruling was challenged but the scheduling was
subsequently upheld in a 1985 decision. However, the ruling was challenged
again, this time by Dr. Lester Grinspoon, an associate professor of psychiatry
at Harvard Medical School. Dr. Grinspoon contended that his research on the
therapeutic uses of MDMA would be eliminated by its Schedule 1 classification.
He cited four reasons for the classification to be voided, challenging the
DEA's assertion that the drug has a high potential for abuse and contending
that the ruling was based "upon incomplete and arbitrary recommendations from
the Secretary of Health and Human Services."
Dr. Grinspoon further contended that the DEA had applied the wrong legal
standards in making its assessment and in classifying MDMA as a Schedule 1
substance. Grinspoon's arguments were eventually upheld and the ruling was
vacated and remanded back to the administrator of the DEA "for further
proceedings consistent with this opinion." The DEA may decide to reclassify,
or sharpen its legal argument and continue to press for Schedule 1
classification. So stay tuned: a battle has been won, but the war continues.
In article <1235@laidbak.UUCP>, shawn@laidbak.UUCP (Shawn McKay) writes:
> I know I spelled that wrong, but I don't remember seeing a proper name for
> it, if memory serves, this was recently made illegal in CA, anyone ever have
> any experience with it? Know what its effect is/was or where it comes from?
>
> Thanks.
> -- Shawn
XTC is one of the more common names for a drug named MDMA. MDMA is one of
many metamphetamines like MDA, Crystal Meth, and others. MDMA is one of the
least toxic of these, although it still does some damage to your liver. But
then, alcohol in reasonable quantities does a lot more damage to your liver.
MDA is the worst. The effects of MDMA as I experienced an unspecified time
ago last about half as long as those of MDA, only 4 to 6 hours. It is taken
in crystal form, in caplets or just solved in water. The effects are quite
pleasant (trust me). The stuff does something to your nerves. Feeling and
touching things becomes the most awesome experience. Soft objects (especially
cats!) feel very different. It is hard to describe. Other people are also
a nice ecxperience. You feel like hugging them all the time (this is the
reason people call it XTC/ecstacy or just the love drug.
I'm not a chemist, so I can't tell what it actually does, but I know that
it drains water from your spine or something like that. That's why drinking
liquids like water or juices is absolutely necessary when on MDMA. The
chemists here might even be able to explain to me why it is very harmful to
drink alcoholic beverages, to eat/drink dairy products or to eat chocolate.
Prices for MDMA are not really high, but since availbility varies, it is
hard for me to jut give a price. I paid around $5 per hit. I expect that most
prices are somewhere between $4 and $10.
..............................
Not completely on subject, but I would like to comment on the ingestion of MDMA
analogs.Not long ago I would have warned everyone off it and its analogs becauseshortly after the appearance of "X" and its rapid growth as a psuedo-
legal drug, scientific reports started to surface stating that permanent damage
was caused to dopamine receptors in certain parts of the brain. Now 2 and 3
years after those reports very similar tests have been done by various groups
and they show that the results of the government sponsored original trials are
not reproducable. Clearly these too are to some extent goverment sponsored, but
seem to lack the bias the previous experiments had(I'm trusting a biologist on
this, I don't claim to be able to analyze neurobiological techniqe). In any caseeveryone should be aware that the effective doses for MDA and its analogs are
quite close to the LD50. And finaly,does anyone know anything about the effects
of "euphoria", its chemical structure or relation to other newly developed
psychedelics. Maybe my feeling of outrage is silly after watching the responce
so far of the war on drugs, but asking scientists to fake reports sets a really
bad precident. May be this should have just been posted to alt.conspiricy.
If you would like the references to the papers above please send e-mail they
should be available in full at your local large sized clollage library.