Date: Tue, 9 Dec 1997 05:23:42 EST
From: Chris Jenks <email@example.com>
To: Multiple recipients of list <firstname.lastname@example.org>
Subject: Harmaline/Syrian Rue
At 01:05 PM 12/2/97 EST, DH <email@example.com> wrote:
> BTW, please enlighten me about Harmaline, what pray tell is it?
>is that what we find in DMT? (forgive my ignorance)
At 05:09 PM 12/8/97 EST, Siriuself <Siriuself@aol.com> wrote:
>where can syrian rue seeds be purchased?
The following quotes are from Dr. Sasha Shulgin's new book TIHKAL
(Tryptamines I Have Known And Loved), the sequel to PIHKAL (Phenethylamines
I Have Known And Loved), which are available from Mind Books, and I highly
recommend them to anyone interested in the chemistry or pharmacology of
tryptamine or phenethylamine psychedelics. Although harmine and harmaline
are carbolines, not tryptamines, there is a section in TIHKAL about them
because of their use in ayahuasca, which also contains DMT, which IS a
"[...] The role of the B. caapi component of hoasca is being taken over,
at least in the United States, almost exclusively by the plant Peganum
harmala [a.k.a. Syrian Rue], although there are a number of alternate
beta-carboline sources such as the seeds of Tribulis terristris which have
been used in man. P. harmala is a rich source of both harmaline and of
harmine and is readily available from a number of domestic sources. If the
local Indian/Arab retail store does not recognize this binomial, try
another name for this product: "esfand." You may be surprised to find that
they sell this incense in one pound packages, even in five pound packages.
Since this seed contains most of the same alkaloids that are found in the
B. caapi component of hoasca, the choice of this plant as a substitute has
a certain authenticity." - pp. 294-295.
"One must keep in mind that there is also harmaline as well as harmine
present in sizable amounts in these seeds [P. harmala], as compared to the
largely harmine contribution of B. caapi to native ayahuasca. In the one
assay I have run, they are present in pretty much equal quantities. Both
are effective inhibitors of the amine oxidase enzyme system of the body,
which is nature's own way of protecting us from poisons such as DMT." - p. 298
"How much of these several beta-carbolines does a given weight of P.
harmala seeds represent? The alkaloid content has been reported to cover
quite a wide range (from as low as two and as high as six percent), so a
gram of seeds has potentially twenty to sixty milligrams of the desired
alkaloids. But here, suddenly, there is a new and treacherous variable.
There is a difference between weights and volumes; grams are weights and
the kitchen containers are volumes. From one individual seed, to a level
teaspoonful of seeds, to a one-shot saki tumbler full of seeds, one will
have a dry gross weight of from two and a half milligrams to three
milligrams, to maybe three grams, to a half ounce (almost fifteen grams).
The alkaloidal content will be in the ballpark range of a tenth of a
milligram, to something over a hundred milligrams, to something over a half
gram for each of these measuring units. So, a typical individual dosage of
P. harmala seeds for an ayahuasca experiment would be a level teaspoonful,
or three grams, or something over a thousand seeds if you have tweezers and
patience rather than a kitchen." - p. 301
For Exhibit B, let me present the latest Patent by Howard Lotsof:
Lotsof, Howard S. "Method of treating chemical dependency using
beta-carboline alkaloids, derivatives and salts thereof.", United States
patent, (January 7, 1997), 5,591,738.
Within this exciting document appears the following interesting studies:
A twenty-three year old, 140 pound male human subject using one to three
grams of cocaine daily via nasal administration was provided a single dose
of 500 mg of harmaline HCl per os. Subject immediately discontinued cocaine
use. Subject's cocaine use was interrupted for a period of four months.
Subject had been previously treated with 500 mg of a total alkaloid extract
of T. iboga with no significant effect on drug use. Conversely, it should
be noted, however, that three persons successfully treated with ibogaine
had no response to the administration of harmaline in interrupting their
A thirty-six year old, 136 pound male human subject using twenty dollars
worth of heroin a day (approximately 40 mg/day) via IV route. The subject
interspersed his use of heroin with 15 mg and 30 mg injections of morphine
and unknown quantities of pantopon. The subject was given an IV injection
of 100 mg of harmaline HCl. A second 100 mg IV injection of harmaline HCl
was given six hours later. Subject discontinued heroin use for a period of
three weeks after which contact with the subject was lost. Subject's
cigarette consumption which had been between one and two packs a day
immediately ceased. This continued for ten days after which subject began
smoking at a reduced rate. It should be noted that IV administration of
harmala alkaloids are significantly more toxic than oral administrations
and it is advised that they not be used in medical practice.
Male subject, twenty-four years of age, weighing 153 pounds was using 20
mg of heroin and 250 mg of cocaine per day both via IV route and was
drinking twelve to sixteen cups of coffee per day. Subject was administered
750 mg of harmaline base in a split dose of 500 mg followed by 250 mg
twenty minutes later. Subject's use of heroin and cocaine ceased
immediately. Coffee consumption initially dropped to one half to one cup
per day but, was increased to three to four cups per day within two weeks.
Cocaine use ceased for a period of two months at which time subject began
nasal use of approximately 50 mg/day. Within three months subject was using
cocaine and amphetamine IV and barbiturates per os. Subject has not
returned to heroin use at this time but, contact with the subject was lost
and no further information was available.
Male subject, age twenty-two, estimated weight 120 pounds, using two
grams of amphetamine and/or desoxyephederine per day via IV route was
administered 500 mg of harmaline base. Subject immediately ceased stimulant
use. Contact was lost two weeks later when subject left city in which
treatment was administered for location unknown.
The present invention, thus, affords an effective means of treating a
chemical dependency disorder, an abuse syndrome or a combination thereof.
The effectiveness thereof is evidenced by either a reduced or interrupted
intake of substances tending to cause the disorder or syndrome. Thus, as
described hereinabove, the treatment of the present invention leads to
either a reduced or interrupted intake of such substances by the subject
mammal. Further, this result may be obtained without generating a
subsequent chemical dependency disorder or abuse syndrome based upon the