when tryptamine was injected into the PVN of rats pretreated with the monoamine oxidase inhibitor, pargyline, a strong anorectic effect was observed. The action of tryptamine in pargyline-treated rats was not affected by depletion of 5-HT levels in the PVN with PCPA. This indicates that the effect of tryptamine is not mediated by a release of endogenous 5-HT.
https://www.anoniem.org/...m.nih.gov/pubmed/2529575

DOSAGE : 250 mg, intravenously

DURATION : Very short

COMMENTS : (with up to 10 mg, intravenously) "There were no changes in blood pressure or self-rating scores."

(with 250 mg, intravenously) "Tryptamine was infused intravenously over a period of up to 7.5 minutes. Physical changes included an increases in blood pressure, in the amplitude of the patellar reflex, and in pupillary diameter. The subjective changes are not unlike those seen with small doses of LSD. A point-by-point comparison between the tryptamine and LSD syndromes reveals a close similarity which is consistent with the hypothesis that tryptamine and LSD have a common mode of action."

EXTENSIONS AND COMMENTARY : This quotation is from a paper by Martin and Sloan, published almost thirty years ago, that stands as our only measure of the human response to tryptamine. The first of the two reports in the comments took place 5 years earlier, with depressed patients and at very low levels of drug administration. It had already been established in rat and dog studies that tryptamine was known to enter the brain but, due to rapid metabolism, had only a short duration of central activity. Hence, the researchers in both these studies chose to employ an intravenous route of administration. There are a number of valuable points to be made in this latter report describing the 250 mg. study.

Clearly, the model drug in vogue at that time for central action was LSD, and all researcher felt that comparisons should be made to it, as sort of a gold standard. It was acknowledged that the setting in which an experiment took place could influence the outcome. Many studies with LSD were conducted in an environment that was quite different (in private living rooms, with good music and friendly faces) than these tryptamine experiments conducted in a clinical ward of the Lexington Addiction Center, with automatic patellar reflex hammer strokes and polygraphic pupillary diameter measurements, conducted in what was in fact a narcotics prison.

Most instructive was the statement that the tryptamine syndrome was similar to the LSD syndrome. This equation has been broadly quoted, but it is valuable to read, first hand, the explicit observations of central activity that supported this conclusion. These are quoted here:

"Shortly after the onset of the infusions, three of the patients became aware of the experimental setting and complained of a heaviness, tiredness or numbness of the limbs which subsequently became generalized to other parts of the body. With continued infusion, a variety of other visceral symptoms and signs emerged which have been previously described following administration of LSD and mescaline, including nausea, vomiting, dizziness, sweating, acute or dulled hearing, metallic taste, and a heaviness of body. Further, in 2 of the 4 subjects, there were visual changes (subsequently described as a heaviness behind the eyes, a clouding of vision, and lines or cobwebs)."

The tryptamine experience sounds pretty heavy, and it is almost as if every negative LSD or mescaline property was exhumed and displayed, to justify tryptamine as being similar to this widely accepted psychedelic drug.

Why is tryptamine of any interest at all? Just as the simple compound phenethylamine was the nucleus for all of the potential psychedelic compounds in PIHKAL, so tryptamine play a similar role as the nucleus of all drugs discussed in this volume. These are the structural basic-skeleton archetypes of these two corresponding classes of psychedelic drugs. Both are widely scattered throughout the plant Kingdom, and they are both normal components of the human animal. They both have amino acid origins, phenylalanine for phenethylamine and tryptophan for tryptamine, and these amino acids are extremely important factors in human biochemistry. And they, each in turn, can only provoke pharmacological effects when administered parenterally at very high levels.

Tryptophan, the metabolic precursor to tryptamine, is itself a centrally active amino acid. There is a complex, and little appreciated story associated with it as to its human psychopharmacology. Although tryptamine is only active parentally, tryptophan is active orally is directly converted to tryptamine, the two compounds must be considered in concert. What is the action of tryptophan, taken orally? Here are some quotations from the published literature, mostly with the voice of the giver, not the taker, with some copy taken from health-food store fliers of a decade ago.

COMMENTS : (with 2 g, orally) "I administered two grams to 7 normal subjects, and five of them became drowsy after 1-2 hours."

(with 2 g, orally) "The amino acid tryptophan is a safe, non-addictive sleeping aid which works because it is made into serotonin in the brain. Serotonin is the neurotransmitter which initiates sleep. Tryptophan is found in milk and bananas and can sometimes be purchased in pill form. Two grams of tryptophan just before bed is very helpful in getting to sleep. For best results take it on an empty stomach. Although milk contains tryptophan, the pure amino acid is more effective."

(with 5 g, orally) "I took five grams orally several times over a period of days (to study urinary metabolites) and I did not expect any psychological effects. Within an hour, there was a slight dizziness, a feeling of light-headedness and some euphoria which was comparable to whiskey."

(with 6 g, orally) "We gave six grams tryptophan orally to seven subjects. All became listless and yawned frequently, and five of them slept between the periods of testing. Three were unable to remain awake for more than a few minutes. All were easily aroused however, and then felt euphoric and were unusually voluble and overactive. One showed marked social disinhibition in his behavior. Two were clumsy in turning and tandem walking. One had a frontal headache and another was dizzy without vertigo."

(with 10 g, orally) "We gave our sixteen normal subjects 10 g d,l-tryptophan orally. All experienced symptoms such as changes in perception (lightheadedness and dizziness) and changes in mood, mainly euphoria. None of the thirty four chronic alcoholic subjects noted any symptoms at this dosage level."

(with 15 g, orally, with 150 mg iproniazid) "This was a daily treatment given to schizophrenic patients, tryptophan along with an antidepressant which is a monoamine oxidase inhibitor. Most showed marked changes such as an elevation in mood, an increased involvement with other people in their ward, and an increased extrovertism. A separate study of this combination with the addition of the amino acid l-methionine produced in about half of these patients a toxic or delirioid state."

CONTINUING COMMENTARY : Look at this fabulous story that unfolded some twenty years ago. It is completely coherent, and it is totally exciting. Let me try to distill the human information given above, into a logical flow. Tryptophan, a natural and nutritionally essential amino-acid, is a centrally active intoxicant and sleep-provider in man. It is converted metabolically to tryptamine which is a little bit psychedelic. When administered with methionine (another amino-acid known to methylate things) it produces methylated tryptamines, the two best studied being N-methyltryptamine (NMT) and N,N-dimethyltryptamine (DMT). The effects that result are hard to categorize, reflecting the diagnostic status of the patient. But something happens. In short, tryptophan, alone or in combination with MAO inhibitors or methyl donors, is a fabulous tool for exploring brain function. And it was an easily available research tool, openly explored by many private individuals. It was meeting a broad curiosity as to meeting a large number of human inadequacies.

Then, an incident occurred in 1989, at the Showa Denko company in Japan, where a change in the manufacturing procedure produced an impure product. The impurity led directly to a health problem, a condition with a flu-like syndrome called Eosinophilia-Myalgia Syndrome (EMS) which cause some 1500 incidents in the United States, including 38 deaths. The FDA quite rightly removed tryptophan from the market on the 17th of November, 1989 and banned its distribution. The source of the health problem was quite quickly identified, and the production operation was changed back to the original process, and the tryptophan product was again available free of any toxic impurity. This freedom from any impurity was acknowledged by the FDA, but they transferred the toxic aspect of the substance from the impurity contained within it (now no longer present) to the substance itself. The implied declaration was that tryptophan was intrinsically toxic.

The sale of tryptophan as dietary supplements for man is now illegal. Dietary supplements to animal stock feed is OK. Tryptophan is available to hospitals for use in critical situations. Tryptophan is available as a prescription drug. But it is not available in the health food stores and so cannot be explored by the lay researcher. The world of inquiring into the action on normals, schizophrenics, alcoholics, people who are overweight, people who are depressed, is denied both to the private individual and to the clinical researcher. There are commercially available drugs, all approved, that can play the same role. Within four days of the announced ban of tryptophan (after the problem had been resolved and corrected) a broad promotion of Prozac (an antidepressant similar in action to Tryptophan) appeared in Newsweek (March 26, 1990). Prozac is still widely promoted. Tryptophan is still not available to the private individual. Both can play the role of being an effective sedative.

A quotation from the FDA Dietary Supplement Task Force Report, page 2, June 15, 1993, deserves careful reading.

"The [FDA] Task Force considered various issues in its deliberations, including ... what steps are necessary to ensure that the existence of dietary supplements on the market does not act as a disincentive for drug development."
What are dietary supplements? How might they get in the way of pharmaceutical industry creations? Where is the line to be drawn between nature and big business? What plants are there that might serve as health adjuncts? I truly think that we are being had by the powers that be, who are authorized to control our access to medicines. Today we cannot eat ABC because it contains an outlawed drug. Tomorrow we cannot eat DEF because it is suspected of containing an outlawed drug. The day after tomorrow, we cannot eat GHI because it has not been shown to be free of outlawed drugs. And yet, everything in the drug store had its origins somewhere in a botanist's observation or in a chemist's mistake. Where does this oppression stop? When do we say, hold, enough?

We must be free to eat this plant, and smell that flower, as we choose to. To deny us this right, is to deny us a simple, and basic freedom that is our Constitutional identity. If I want to continue to eat bananas and drink milk, I will do so, and get off of my back. If I want to consume tryptophan because I feel it brings me closer to God and Jesus, or makes me sleep better, I will consume tryptophan. You, the empowered authority, will not tell me not to. As was so eloquently expressed in Leonard Bernstein's West Side Story, when the hero group of heroes came up against the authority group of authorities, they said, "Hey, Officer Cronsky, fuck you."

There are a pile of pharmacological details that should be collected and disposed of. For example, l-tryptophan is the natural and normal amino acid and yet it is more toxic than the unnatural d-isomer. The rat data would suggest that it might be a problem at a something over a 100 gram dose, although I know no one who has nibbled that high. In fact, l-tryptophan is the most toxic (in rats at least) of all the natural dietary amino acids. Interesting. So what? And there is a botanical side to all of this. Gramine is a synthetic precursor of tryptamine, and yet it has been reported here and there as a natural plant component. The same is true for indole-3-ethanol. Yet, both of these can serve you in the laboratory for the synthesis of tryptamine and, of course, of DMT. The plant world seems to be fully aware of these same processes.

A final comment to connect man and plant. The primary animal metabolite of both tryptamine and of DMT is the corresponding indoleacetic acid which is itself a potent plant hormone. This just happens to be one of the most thoroughly studied plant growth hormones, and has been isolated from a number of natural sources. Less well studied is the reduction product of the intermediate aldehyde, by the action of monoamine oxidase, to the corresponding alcohol, indole-3-ethanol or tryptophol. This rather rare plant stimulant has recently been found in cucumber seedlings, but has also been shown to be present in trace amounts (along with the hormone indoleacetic acid, MMT and DMT) in at least one Ayahuasca component, the Illinois Bundleflower legume, Desmanthus illinoesis. Another circle has closed upon itself in an interesting way.
-shulgin TIHKAL

Sorry for posting the whole entry, but it would have been difficult to divide into short sections for brevity, as all the information is interrelated.

If I'm misunderstanding the question, just tell me to STFU.

I think a lot of what you are looking for is in the name. MAOI or mono-amine oxidase inhibitor drugs deactivate the enzyme mono-amine oxidase. This enzyme serves two purposes. Primarily it regulates levels of nuero-receptors. Without it, things like serotonin-syndrome would happen from the build up of serotonin. We would constantly be in an intoxicated and unstable state of mind and the gut would be pretty much fucked. It's also responsible for breaking down mono-amine toxins.

By taking a weak MAOI such as harmine or harmaline, one allows in chemicals like DMT that would otherwise be recognized as toxic and broken down. Other chemicals like psilocybin or LSD which have a low affinity for MAO, but still some affinity, are potentiated.

Simply taking an MAOI by itself allows endogenous nuerochemicals to build up. Yohimbe for example works as a weak MAOI and raises blood pressure which is why it is a functional aphrodisiac. Not only does it promote genital sensitivity via blood pressure, but it allows nuerochemicals responsible for the mental side of sexual stimulation to build up as MAO is inhibited.

Not at all syberdelic, you're right on the money

What you said about taking a MAOI and this increasing endogenous neurotransmitters, many of which are monoamines, is very intriguing and I think it is something that needs to be researched further.

I wonder what effects a diet high in MAOIs would have in comparison to a low-MAOI diet.

syberdelic - diet isn't an issue with Harmalas, Tyramine has no negative interaction with Harmalas/reversible MAO-A inhibition. Also, i've been taking super strong dosages of Rue daily for 8 months or so now, haven't noticed any dietary reactions or any negative side-effects from regular consumption, in fact, the more the Rue is taken, the more the Harmala's reverse tolerance builds up, which not only makes the Rue dose stronger each time so you can back the dosage down bit by bit as you go along to stay within a somewhat consistent dosage range, but the side-effects like nausea, vomiting, body load, and motor function impairment of stronger dosages go away allowing you to handle stronger dosages more easily and it feels a lot cleaner with the reverse tolerance than without it.

Maybe I have received some bad information.

So, if I'm taking pharmahuasca with harmine or harmaline, I can forget about the diet??
Go ahead and eat that pepperoni pizza for breakfast and then dose in the evening?

But even so, I'd be weary of taking the stuff over a long period of time.

ShamensStamen, I would like to know what effects you've personally experienced with dosing harmalas regularly, as far as increased endogenous neurotransmitters go. I'm very curious about this, so give me all the details!

ShamenStamen, I totally agree with your advice for people to first explore the harmalas before using them as a means to orally activating DMT. There is so much more to the harmalas than just a DMT enabler.

Personal metabolic and enzymatic differences cannot be disregarded. Everyone should discover for themselves how they respond. Some have no problems with tyramine, some have no problems with the nausea. People differ.

Finally, it should be worth mentioning that harmalas are traditionally employed by indigenous Amazonian healers to sensitize themselves to various substances found in the flora of their native ecosystem. It pays to bear this in mind while ingesting the various substance found in our modern ecosystem.

Well, now that it feels basically like a clean and stable medication/anti-depressant even at very strong dosages for me, i'd say it basically feels like an anti-depressant of sorts, i can feel the previous nights Rue dose for the next day or so, i have a noticeably clearer and more stable headspace/mind, i can feel the extra neurotransmitters a good bit, but it's not as noticeable unless i smoke some Cannabis which really brings things out more for me. It's also helped some with weight loss, it's helped me clean up my diet a bit and get me wanting to eat healthier, it's helped me quit smoking Tobacco, and over all the Rue just feels quite healthy for me. Once the Harmala-related side-effects go away it's a lot easier to work with.

Well, now that it feels basically like a clean and stable medication/anti-depressant even at very strong dosages for me, i'd say it basically feels like an anti-depressant of sorts, i can feel the previous nights Rue dose for the next day or so, i have a noticeably clearer and more stable headspace/mind, i can feel the extra neurotransmitters a good bit, but it's not as noticeable unless i smoke some Cannabis which really brings things out more for me. It's also helped some with weight loss, it's helped me clean up my diet a bit and get me wanting to eat healthier, it's helped me quit smoking Tobacco, and over all the Rue just feels quite healthy for me. Once the Harmala-related side-effects go away it's a lot easier to work with.

pitubo, those PDFs you shared don't open on my phone. Maybe it's a problem on my end but you might wanna look into that.

In another thread, dreamer042 made some very relevant comments about the difference between daytime and nighttime dosing of harmalas. He speculates that daytime dosing causes enhancement of stimulatory neurohormones, while nighttime dosing enhances the relaxing and revitalizing process.

I just checked and they download and display fine for me.