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Entactogens that can be made by Aminizing your Kitchen's Spice Cabinet

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ShaggyFin

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If you have not read PIHKAL over and over and over in actual book form, then you may not have noticed this.
Sasha mentions the Magical Half Dozen, which is 2C-I, etc
He mentions the 10 Classic Ladies, which is Florence, Ganesha, etc.

But he also mentions that it may be possible to create Molecules using your own liver by turning different enzymes on and off. Then on one of the recipes he gives you a list of all the Phenethylmaines that can be found in your Kitchen's Spice Cabinet, and then throughout PIHKAL he gives you the recipes for each of those Phenethylamines. He says that they just need to be Aminized, either in your liver or in a lab, and they will become active. This theory has been proven by what is now called Oilahuasca. If you mix different things together you can get different effects from different Molecules, it is based on the idea of Pro-Drugs and CYP450 Enzymes (Similar to MAOs which are effected by MAOIs). Some people have reported Psychedelic effects from Mixing just Coffee, Almond, Cinnamon, Vanilla and Nutmeg.

koIVN4f.jpg


This is similar to how Saffrole, from Sassafras, can be used to make MDA or Ecstasy.

From the person who Discovered Oilahuasca

WraE8rK.gif


The benzene ring has 6 positions. In the graphical layout given below the following color guide is used:

position 1 = black (the important allyl side chain, required for conversion to an alkaloid)
position 2 = brown (a methoxy group here seems to cause LSD-like mental effects)
position 3 = red
position 4 = green (must be a methoxy or methylenedioxy group for psychedelic activity)
position 5 = blue (a methoxy or methylenedioxy group here seems to enhance visuals)
position 6 = purple (a methoxy group here probably adds speedy effects)

Position 1 has the allyl side chain hanging off of it. It's the same for all allylbenzenes. This is the part of the allylbenzene that reacts in the body to form a dimethylamine, piperidine, or pyrrolidine alkaloid, if digested properly. The details of this are discussed elsewhere.

In order to have psychedelic activity, position 4 must be a methoxy group. It can be tied to another methoxy group on position 5, as it is with myristicin and others. Two methoxy groups tied together are called a methylenedioxy group.

Position 4 cannot be a hydroxy group as it is in eugenol, hydroxychavicol, and chavicol. This can only lead to stimulant effects, not psychedelic effects.

At the bottom of the chart you can see eugenol, hydroxychavicol, and chavicol. These posses no psychedelic activity, even when properly metabolized. These are the only allylbenzenes in the chart that have a hydroxy group on the 4 position.

Above that we have methyl eugenol, chavibitol, and methyl chavicol. Methyl chavicol and methyl eugenol have psychedelic activity when properly metabolized. The effects of chavibitol are unknown, but are probably like a cross between methyl eugenol and methyl chavicol. The 5 position being a methoxy group seems to improve visual effects.

Above that we have croweacin, apiole, and safrole. Apiole and safrole are psychedelic when metabolized properly. Croweacin is a positional isomer of myristicin. It's activity is not known. It's very likely similar to myristicin, but probably more speedy like apiole. The 6 position being a methoxy group seems to add amphetamine style speedy effects.

Above that we have the ever so popular myristicin, and then dillapiole and the rare sarisan. Both myristicin and dillapiole are psychotic when properly metabolized. The activity of sarisan is unknown. It is a positional isomer of myristicin. It has a methoxy group on the 2 position instead of the 3 position. This probably gives it LSD-like mental effects which are attributed to dillapiole and gamma-asarone rather than myristicin.

Above that we have elemicin, 2,3,4,5-tetramethoxy-allylbenzene, and gamma-asarone. Elemicin is the only one of these that's known to have psychedelic activity when properly metabolized. When properly metabolized, it's effects are similar to myristicin, but more like mescaline. It has the same positional substitutions as myristicin, only the 4 and 5 positions are not tied together. Gamma-asarone is a positional isomer of elemicin and is probably the main active psychedelic compound in calamus oil from Nepal. The methoxy group on the 2 position is probably the reason calamus oil from Nepal has LSD-like mental effects shared by dillapiole and absent from most of the other allylbenzenes. I have no idea if 2,3,4,5-tetramethoxy-allylbenzene is active or not.

For those of you that are unaware, MDMA is primarily manufactured from the safrole found in sassafras essential oil.

Many bioassays of sassafras and even pure safrole show little activity. Usually a slight sedative effect, and very mild MDMA-like effect might be felt if you’re lucky. Although a few people report almost full blown MDMA-like effects from sassafras as is, most people get no effects. This points in the direction of human metabolism altering the effects of safrole.

AFOAF once tried sassafras with a CYP1A2 inhibitor: German chamomile. This experiment produced stimulant effects unlike the effects had from just sassafras alone. There was mild euphoria, and some possible mild visuals effects.

Safrole is primarily inactivated by conversion into 1-hydroxysafrole by CYP2A6. German chamomile primarily inhibits CYP1A2, so AFOAF was using the wrong inhibitor, but it was somewhat effective.

Cinnamon bark oil is a potent CYP2A6 inhibitor. This should theoretically prevent CYP2A6 from turning safrole into 1-hydroxysafrole.

My theory is that about 2-5 grams of cinnamon, or 5-10 drops of cinnamon essential oil will contain enough cinnamaldehyde to inhibit CYP2A6 and allow MDMA-like effects to be experienced from sassafras or sassafras oil.

This is only a theory. As of yet AFOAF has not tried this. He will try this very soon. Incidentally, it is the 1-hydroxysafrole which is primarily formed by CYP2A6 which is considered weakly carcinogenic and not safrole itself. So by using cinnamon oil, the weak potential carcinogenicity of safrole should be greatly reduced.

For his test he plans on using German chamomile oil at 3 drops along with the cinnamon bark oil at 6 drops. He will use sassafras bark, freshly ground, extracted into milk with lecithin, just like how you make kava. This is the best way to extract the safrole without using a solvent. He will take the sassafras milk and the oils at the same time. Hopefully this produces an MDMA-like effect. We will see.



Here's a picture of what the CYP2A6 enzyme in humans does to safrole. Once converted to 1-hydroxysafrole by CYP2A6, it becomes much more polar (the XLogP drops from 3 way down to 1.9!), and so it's far more difficult for it to enter the brain, meaning it should be far less psychedelic (assuming that safrole is actually psychedelic before this conversion). For maximum entry into the brain, CYP2A6 should be inhibited to prevent this conversion. It’s possible that CYP1A2 might be able to perform this very same conversion (it does so with methyl chavicol and elemicin), so it too should be inhibited.

On the right you can see MDMA for comparison purposes. See how 1-hydroxysafrole is less like MDMA than safrole is? The XLogP3 of safrole is 3, MDMA is 2.2, and 1-hydroxysafrole is 1.9, being the most polar of the three. Safrole should more easily cross the blood brain barrier than MDMA, but once attacked by CYP2A6 enzymes, safrole turns into 1-hydroxysafrole, and that should help prevent it from entering the brain.

t4Rq3XF.gif


Later...
Well it was tried a few hours ago.

AFOAF used 5 grams of sassafras bark, 1 gram of lecithin, ground to powder, then mixed with 1 cup of steaming hot milk and 2 ml of vegetable oil. This was left to sit for 2 hours and was then filtered. It was super hard to filter. Decanting would be a better idea.

He then mixed 6 drops of cinnamon bark oil and 3 drops of German chamomile oil into it. The German chamomile would not mix into it and just floated to the top. He mixed it as good as he could and drank it down.

Its been about 3 hours and he feels NICE. There's very obvious euphoria. Sense of touch is enhanced. He feels good. There's no sedation felt at all. It’s mildly psychedelic.

This seemed to work. But he doesn’t know what MDMA really feels like so he can’t compare it to MDMA. It does feel like a phenethylamine though. It’s very different from taking sassafras on its own.

This is a light dose. I think 10-20 grams of bark would be much better.

I would love to hear what others more familiar with MDMA think about this combination. It seems to have worked to produce an MDMA-like effect, but until others more familiar with MDMA test this out, we should take that statement as simply a guess.


Procedure

Procedure, in plain English:

Pepper would be made into a tea. Solids filtered out.

Then you would get some Anise Oil, B9 or Valerian Root (of Chinese Origin)

So that is your Pepperidine, and you activators. Now you need your Enzyme Inhibitors. You can add L-Lysine, but it is not necessary.

Vanilla and Cinnamon work, pick one or both. You also need the Aldehyde structure from one of these.

Next. German Chamomile, Cayenne Pepper Capsules or Tangerine Skin extract/capsules

Then
Almond extract, Anise Oil (if you already had it), Cinnamon, Lemon peel oil, Lime peel oil, or a cigarette or nicotine gum if you can't find anything else.

Then
CBD, Echinacea Purea, Pomegranate, Pummelo, or Calamus Oil.

Then
Clove oil, Catechin, Dill seed Oil or Goldenseal.

Then Kudzu or Glycerin or Caffeine

Not all of these things are neccisarry, but if you do 1 thing in each list, you should get very strong effects from whatever you take.

The best thing to take is Sweet Basil Extract, in it's pure form, it is known as Methyl Chavicol.

Take all that other stuff like 30 minutes to an hour before the Basil Extract, and redose the B9, Anise or Valerian root to keep the effects going without taking more.

Science

Graviola- 5-HT1a Agonist
Black Cohosh- 5-HT1A, 5-HT1D & 5-HT7 Binding
C. Foetida L.- 5-HT1A Agonist
Yokukansan- 5-HT1A Agonist
DMT hits all of these, and can be found in tons of plants.

Black Cohosh- 5-HT1D
maybe Rhodiola rosea, Albizia lebbeck & Albizia julibrissin.

5-HT1 Receptor Agonists:
Turmeric, Ginger, Ginko Bilboa, Lemon Essential Oil, Rauwolfia, Valerian, Yohimbe

Elmicin & Myristicin (in Nutmeg)- 5-HT2A Agonist
Estragole (in Sweet Basil)- 5-HT2A Agonist
Safrole (in Sassafras)- 5-HT2A Agonist

Cinnamon Bark- CYP2A6 & CYP2E1 Inhibitor (It will deplete your liver's Glutithione) Taken 1 Hour before Allybenzene,
Clove Leaf- CYP2C9, CYP3A4, CYP1A1 & CYP1B1 Inhibitor
German Chamomile- CYP1A2 Inhibitor (Caffeine may also do this)
GoldenSseal & Echinacea purpurea very effectively do the same thing.
Black seed oil, 50% EGCG, Valerian root oil, Pomegranate, Vitamin B9, 40% Ellagic extract, Rooibos 20% Gallic acid extract, Rutin, B3 & Kudzu

AllylBenzenes
Anethole, Apiol, Asarone, Carpacin, Chavibetol, Chavicol, Dillapiole, Eugenol, Isoeugenol, Isosafrole, Methyl Eugenol, Methyl Isoeugenol,

since Cinnamon is a Phenylpropanoid, and Phenylpropanoids are made from Phenelalamine, and people who took Phenelalamine claim to get better results. I decided to post a list of Phenylpropanoids also.
Caffeyl Alcohol, Cinnamaldehyde, Cinnamyl alcohol, alpha-Cyno-4-hydroxycinnamic acid, Ethyl Cinnamate, Lignin, 2,4-Methlenedioxypropiophenone, Neoflavonoids, Nordihydroguaiaretic acid, Phenylpropanoic acid, Phloretic acid, Rhododendrin & Suberin.

Star Anise Extract or B9 for CYP2C9 Induction

NMDA Receptor Plants:
Uncaria Rhynchophyllia
Psychotria Colorata
Huperzia Serrata

Most important things:
CYP2C9 Induction
Alcohol Dehydrogenase Induction
Aldehyde Dehydrogenase Inhibition
Piperidine and or Dimethylamine Supplementation
Methyl from foods
Exercise or compounds that produce effects like exercise

Less important, but still factors:
SSAO Inhibition (Caffeine, Phenethylamine, Phenelalamine, Tryptamine)
MAO-A Induction
MAO-B Induction
NDMA Antagonism
Prolactin Inhibition

Hungarian Parsley Seed is a better source of Myristicin than Nutmeg. The effects of it when activated properly are said to be like Mescaline and MDMA together. The P450 Enzymes CYP1A2 & CYP3A4 are what break this down and need to be inhibited. CYP2D6 could also play a big role.

Elmicin is something you either need Chromotography type knowledge to get, or you have to buy it in small quantities. When activated properly it is like Mescaline, when activated wrong it is like Melatonin (sleepy). CYP1A1, CYP1B1, CYP1A2, CYP2A6, CYP2C9, CYP2A6, CYP2C9 & CYP2E1 are what are needed to be inhibited to activate this. CYP2D6 could also play an important role.

Safrole is like MDMA when activated properly and like Melatonin when not. CYP2A6, CYP2C9, and CYP2E1 are most important for this. CYP2D6 could also be important.

Methyl Chavicol when activated properly is like a light speedy LSD, when activated wrong it is said to be almost like Marijuana. CYP1A2 and CYP2A6 inhibit it, and CYP2D6 could also be important.

If the CYP2D6 Enzyme is inhibited with all the others, these are possibly visually hallucinogenic Oilahuascas. And the Methyl Chavicol doesn't build a tolerance (the others do) it actually gets stronger for you every time you use it, or you can use less.

Several allylbenzenes have been proven to form up to 3 alkaloid metabolites after ingestion by several animals.[2][3] They do not form amphetamines in vivo as has been speculated in the past. The alkaloids detected in animal urine are tertiary aminopropiophenones of 3 possible subtypes: dimethylamines, piperidines, and pyrrolidines.[1][2][3][4]

The allylbenzene elemicin has been proven to form all 3 different alkaloid metabolites after ingestion in animals by analyzing urine using gas-liquid chromatography and chemical ionization mass spectrometry.[1]

Safrole is also proven to form all three alkaloid metabolites after ingestion.[2]

Myristicin appears to only form piperidines and pyrrolidines. Dimethylamines of myristicin have not been detected.[3]

Allylbenzene, from which all allylbenzenes are derived, forms piperidine and dimethylamine alkaloids.[4]

Propenylbenzene and its derivatives (asarone, anethole, etc.) do not form alkaloid metabolites.[4]

Here is how it works

CYP Enzymes (Drug Metabolism, etc)


Induction and Inhibition (Anti-Oxidants, etc)


All inhibitors of oxidative 17bHSD2 will prevent activation of allylbenzenes. This enzyme must be induced, not inhibited. It's the single most important enzyme to induce. If oxidative 17bHSD2 is not functioning, allylbenzenes cannot produce psychedelic activity. Naringenin also potently inhibits 17bHSD2. Grapefruit contains large amounts of naringenin, and also prevents the psychedelic action of allylbenzenes if taken before allylbenzenes. Inhibition lasts approximately 4-8 hours.

Oilahuasca Diet

Here's a list of all known 17bHSD2 inhibitors that should be avoided 4-8 hours prior to using allylbenzenes:
•Quercetin and all food or supplements containing large amounts of it.
•Apples (0.0263% quercetin)[6]
•Cabbage (0.01% quercetin)[6]
•Cranberry (0.025% quercetin)[6]
•Evening-Primrose (20% quercetin)[6]
•Galangin and all food or supplements containing large amounts of it.
•Garlic (0.02% quercetin)[6]
•Grapefruit (contains naringenin, kaempferol, galangin, and quercetin)
•Himalayan Mayapple (1.2% quercetin)[6]
•Kaempferide and all food or supplements containing large amounts of it.
•kaempferol and all foods that contain large amounts it.
•Mayapple (5% quercetin)[6]
•Naringenin and all food or supplements containing large amounts of it.
•Neem (0.1% Quercetin)[6]
•Oats (0.031% Quercetin)[6]
•Onions (4.81% quercetin).[6]
•Orange (4.58% naringenin)[6]
•Tea (10-25 mg/L quercetin, 6.3-17 mg/L kaempferol [7]).[6]
•Tomato (contains kaempferol, naringenin)
•Yuzu (contains naringenin)

Tasting

Sasha used to invent brand new Molecules that had never been recorded before, and then he would taste them to discover their effects.

Here is how tasting works.

He would invent a new Molecule, similar in structure to an existing molecule. And he would use different tests to see what the Molecule looked like, for example he had a machine that could tell him a few things, and if you put bromide on a molecule and it turns to blood colored or white you can tell it has different things attached to it.

Then, he would take this new Molecule, measure out 1µg and eat it.

Then over 3-4 days he would record the effects, if any, using a scale of +, ++, +++ or ++++
And the 3rd or 4th day he would take 5µg

Then 3-4 days later 10µg

Then 3-4 days later 15µg

Until he found the threshold dosage. At which point he would invite others to try it so he could see how it effected different people. Then they would compare the effects to other things they had taken and determine the Structure Activity Relationship (SAR).

The Shulgin Scale
+, ++, +++, ++++ or +1, +2, +3, +4
+1= Tipsy
+2= High/Drunk, etc. But you could still go to the store
+3= If you went in public, people would say "I think that person is on something"
+4= Seeing God

And now people say "Threshold/Weak", "Medium", "Strong" in terms of that moments mental effects or the effects of a dosage, but Shulgin had things like "Museum Doses" where he would take like 10mg of 2C-I so that the Museum would come alive.
 
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I found this page that gives dosages, for activators at least
http://herbpedia.wikidot.com/oilahuasca-activators

Also, Anti-Oxidants have been used like MAOIs in some of these mixtures.

Myristicin Extract, which is made from Nutmeg, can also be used in place of Methyl Chavicol from Basil.

The effects can range from Ecstasy like to Mescaline like, depending if you do it kind of right or all right.

Also, I have not tried this. There is a structure very similar to Propofol in Thyme called Thymol, but it is broken down in the stomach. So it may be possible to use Thyme extract and digest it like Propofol.

And according to Wikipedia
Thymol has been shown to act as a positive allosteric modulator of GABAa in vitro.

For more information look up Oilahuasca, and share any new info or experiences here. This is probably the most through guide about what plants can be used.
 
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And doctors are hardly even aware of these effects. The only time a doctor will talk about anything even close to this is when they tell people taking Liver medication not to drink Grapefruit juice because it might kill them. And the reason is because some liver medications break down too well and must be taken in massive doses 8g+ but if you drink Grapefruit juice your body will not break it down as well and you may end up getting the whole 8g+
 
Also, for anyone who is worried about depleting your Glutithione levels in your liver. Just have some Tumeric handy and take it when you are done, the levels will go back to normal.

And this stuff all seems kind of extreme when you are reading it not in plain English, but these are Herbs that everyone eats every day, and these effects happen to them every day. They just don't add an allylbenzene to get the psychoactive effects.
 
If you have ever specifically drank or ate something because it was an Anti-Oxidant, then you have already been doing this on purpose, and you didn't even know.
 
The most simple mixture that anyone has ever posted with reported effects, and they said that they did this on accident, was Coffee, Almond, Cinnamon, Vanilla and Nutmeg.

Everyone should at least try that.
 
The first person to actually get in to this stuff, after Sasha theorized it, said that he got interested when he noticed that Elimicin and Mystricin are inactive when taken alone, but when taken together in Nutmeg they produce the drunk nauseous feeling with the slight psychedelic effects, which is what happens when you take nutmeg alone in large doses. So he started trying to figure out what Elimicin and Mystricin were, and then found out about CYP450 Enzymes, so read about them on PubMed. Made a short guide, and then people started trying it and found different things that worked the best. And eventually got the effects to the strength of Mescaline.
 
And I found out about it when I was making a list of plants that hit different Serotonin/5-HT receptors, so I added what I was doing to what they were doing.

Graviola- 5-HT1a Agonist
Black Cohosh- 5-HT1A, 5-HT1D & 5-HT7 Binding
C. Foetida L.- 5-HT1A Agonist
Yokukansan- 5-HT1A Agonist
DMT hits all of these, and can be found in tons of plants.

Black Cohosh- 5-HT1D
maybe Rhodiola rosea, Albizia lebbeck & Albizia julibrissin.

5-HT1 Receptor Agonists:
Turmeric, Ginger, Ginko Bilboa, Lemon Essential Oil, Rauwolfia, Valerian, Yohimbe

Elmicin & Myristicin (in Nutmeg)- 5-HT2A Agonist
Estragole (in Sweet Basil)- 5-HT2A Agonist
Safrole (in Sassafras)- 5-HT2A Agonist

Cinnamon Bark- CYP2A6 & CYP2E1 Inhibitor (It will deplete your liver's Glutithione) Taken 1 Hour before Allybenzene,
Clove Leaf- CYP2C9, CYP3A4, CYP1A1 & CYP1B1 Inhibitor
German Chamomile- CYP1A2 Inhibitor (Caffeine may also do this)
GoldenSseal & Echinacea purpurea very effectively do the same thing.
Black seed oil, 50% EGCG, Valerian root oil, Pomegranate, Vitamin B9, 40% Ellagic extract, Rooibos 20% Gallic acid extract, Rutin, B3 & Kudzu

AllylBenzenes
Anethole, Apiol, Asarone, Carpacin, Chavibetol, Chavicol, Dillapiole, Eugenol, Isoeugenol, Isosafrole, Methyl Eugenol, Methyl Isoeugenol,

since Cinnamon is a Phenylpropanoid, and Phenylpropanoids are made from Phenelalamine, and people who took Phenelalamine claim to get better results. I decided to post a list of Phenylpropanoids also.
Caffeyl Alcohol, Cinnamaldehyde, Cinnamyl alcohol, alpha-Cyno-4-hydroxycinnamic acid, Ethyl Cinnamate, Lignin, 2,4-Methlenedioxypropiophenone, Neoflavonoids, Nordihydroguaiaretic acid, Phenylpropanoic acid, Phloretic acid, Rhododendrin & Suberin.

Star Anise Extract or B9 for CYP2C9 Induction

Most important things:
CYP2C9 Induction
Alcohol Dehydrogenase Induction
Aldehyde Dehydrogenase Inhibition
Piperidine and or Dimethylamine Supplementation
Methyl from foods
Exercise or compounds that produce effects like exercise

Less important, but still factors:
SSAO Inhibition (Caffeine, Phenethylamine, Phenelalamine, Tryptamine)
MAO-A Induction
MAO-B Induction
NDMA Antagonism
Prolactin Inhibition
 
Sasha's Words on this

One of the banes of the archivist is having to choose one pattern of organization over another. The book store owned by a language scholar will have the German poets and playwrights and novelists here, and the French ones over there. Next door, the book store is run by a letters scholar, and the poetry of the world is here, and the plays of the world are there, regardless of the language of origin. The same obtains with spices, and essential oils, and amphetamines. The spice cabinet is a rich source of chemical treasures, each source plant containing a host of com-pounds, some of which are true essential oils. And the next spice from the next plant has some of the same components and some new ones. Does one organize by plant (spice or herb) or by essential oil (amphetamine)? Let's do it by the ring substitution pattern of the amphetamine, and gather the spices and oils as a secondary collection.

(1) The 4-methoxy pattern. The pivotal essential oil is 4-allylanisole, or methyl chavicol, or estragole (called esdragol in the old literature). This allyl compound is found in turpentine, anise, fennel, bay, tarragon, and basil. Its smell is light, and reminiscent of fennel. The propenyl analogue is called anethole, or anise camphor, and it is found in both anise and camphor. It is a waxy solid, and has a very intense smell of anise or fennel. At low concentrations, it is sweet, as in magnolia blossoms, where it is also found. The drinks that turn cloudy with water dilution (Pernod-like liqueurs, and ouzo and roki), are heavy with it, since it was the natural flavoring in the original absinthe. That drink was very popular in the last century, as an intoxicant which produced an altered state of consciousness beyond that which could be ascribed to alcohol alone. It contained wormwood, which proved to be neurologically damaging. The flavorings, such as anethole, are still big things in synthetic liqueurs such as vermouth. Old anethole, when exposed to air and light, gets thick and sticky and yellowish, and becomes quite disagreeable to taste. Maybe it is polymerizing, or maybe oxidizing to stuff that dimerizes. Whatever. These changes are why old spices in the cabinet are best discarded. And adding ammonia to any of these natural product oils produces, in principle, 4-methoxyamphetamine, 4-MA.

(2) The 3,4-dimethoxy pattern. The main actor here is methyleugenol, or 4-allyl-1,2-dimethoxybenzene. This is located in almost every item in the spice cabinet. It is in citronella, bay (which is laurel, which is myrtle), pimiento, allspice, pepper, tree-tea oil, and on and on. It has a faint smell of cloves, and when dilute is immediately mistaken for carnations. The propenyl analogue is, not unreasonably, methylisoeugenol, a bit more scarce, and seems to always be that little minor peak in any essential oil analysis. The compounds missing that methyl group on the 4-oxygen are famous. The allyl material is eugenol, 4-allylguaiacol, and it is in cinnamon, nutmeg, cloves, sassafras and myrrh. You taste it and it burns. You smell it and think immediately of cloves. And its property as an anesthetic, in the form of a clove, is well known in the folk-treatment of toothaches. Actually, flowers of clove (the gillyflower, like the carnation) are the small, pointy things that decorate baked hams and, when stuck into apples, make pomander balls. This anesthetic property has recently led to a drug abuse fad, called clove cigarettes. Very strong, very flavorful, and very corrosive things from Southeast Asia. The eugenol that is present numbs the throat, and allows many strong cigarettes to be smoked without pain. The propenyl analogue is isoeugenol, with a smell that is subtle but very long lasting, used more in soaps and perfumes than in foods. The amine addition to the methyleugenol world produces 3,4-dimethoxyamphetamine, or 3,4-DMA. The isomer with the other methyl group missing is chavibetol (3-hydroxy-4-methoxyallylbenzene) and is found in the pepper leaf that is used with betel nut. A couple of positional rearrangement isomers of methyleugenol are known in the plant world. The 2,4-isomer is called osmorrhizole, and the conjugated form is isoosmorrhizole or nothosmyrnol; both are found in carrot-like vegetables. They, with ammonia, would give 2,4-DMA. And the 3,5-dimethoxyallylbenzene isomer from artemisia (a pungent herb commonly called mugwort) and from sage, would give rise to 3,5-DMA. This is an unexplored isomer which would be both an antidote for opium as well as a stimulant, if the classical reputation of mugwort is transferred to the amphetamine.

(3) The 3,4-methylenedioxy pattern. One of the most famous essential oils is safrole, or 4-allyl-1,2-methylenedioxybenzene. This is the mainstay of sassafras oil, and it and its conjugated isomer isosafrole have a smell that is immediately familiar: root beer! These are among the most widely distributed essential oils, being present in most of the spices, including the heavies such as cinnamon and nutmeg. I am not aware of the 2,3-isomer ever having been found in nature. Adding ammonia to either would give MDA.

(4) The 3-methoxy-4,5-methylenedioxy pattern. The parent compound is myristicin, 5-allyl-1-methoxy-2,3-methylenedioxybenzene, and the source of this is nutmeg (or the botanically parallel material, mace). The nutmeg is the seed of the tree Myristica fragrans and mace is the fibrous covering of the seed. The two spices are virtually identical as to their chemical composition. Myristicin and the conjugated isomer isomyristicin are also found in parsley oil, and in dill. This was the oil that was actually shown to be converted to MMDA by the addition of ammonia by passage through an in vitro liver preparation. So here is the major justification for the equation between the essential oils and the Essential Amphetamines. Care must be taken to make an exact distinction between myristicin (this essential oil) and myristin (the fat) which is really trimyristin or glyceryl trimyristate from nutmeg and coconut. This is the fat from myristic acid, the C-14 fatty acid, and these two similar names are often interchanged even in the scientific literature.

(5) The 2-methoxy-3,4-methylenedioxy pattern. This is the second of the three natural methoxy methylenedioxy orientations. Croweacin is 2-methoxy-3,4-methylenedioxyallylbenzene, and it takes its name from the binomial for the plant Eriostemon crowei from the worlds of rue and the citrus plants. It corresponds to the essential amphetamine MMDA-3a. This oil is found in plants of the Family Rutaceae. My memories of this area of botany are of Ruta graveolens, the common rue, whose small leaves smelled to me, for all the world, like cat urine. This plant has always fascinated me because of a most remarkable recipe that I was given by a very, very conservative fellow-club member, one evening, after rehearsal. He told me of a formula that had provided him with the most complete relief from arthritic pain he had ever known. It was a native decoction he had learned of many years eariler, when he was traveling in Mexico. One took equal quantities of three plants, Ruta graveolens (or our common rue), Rosmarinus officinalis (better known as rosemary), and Cannabis sativa (which is recognized in many households simply as marijuana). Three plants all known in folklore, rue as a symbol for repentance, rosemary as a symbol of remembrance, and pot, well, I guess it is a symbol of a lot of things to a lot of people. Anyway, equal quantities of these three plants are allowed to soak in a large quantity of rubbing alcohol for a few weeks. Then the alcoholic extracts are clarified, and allowed to evaporate in the open air to a thick sludge. This then was rubbed on the skin, where the arthritis was troublesome, and always rubbed in the direction of the extremity. It was not into, but onto the body that it was applied. All this from a very conservative Republican friend!

The methoxy-methylenedioxy pattern is also found in nature with the 2,4,5-orientation pattern. The allyl-2,4,5-isomer is called asaricin. It, and its propenyl-isomer, carpacin, are from the Carpano tree which grows in the Solomon Islands. All these plants are used in folk medicine. These two systems, the 2,3,4- and the 2,4,5-orientations, potentially give rise, with ammonia, to MMDA-3a and MMDA-2.

(6) The 3,4,5-trimethoxy pattern. Elemicin is the well studied essential oil, 5-allyl-1,2,3-trimethoxybenzene, primarily from the oil of elemi. It is, like myristicin, a component of the Oil of Nutmeg, but it is also found in several of the Oils of Camphor, and in the resin of the Pili in the Philippines. This tree is the source of the Oil of Elemi. I had found a trace component in nutmeg many years ago that proved to be 5-methoxyeugenol, or elemicin without the 4-methyl group; it is also present in the magnolia plant. The aldehyde that corresponds to this is syringaldehyde, and its prefix has been spun into many natural products. Any natural product with a syring somewhere in it has a hydroxy between two methoxys. The amphetamine base from elemicin or isoelemicin would be TMA, the topic of this very recipe.

(7) The 2,4,5-trimethoxy pattern. There is an essential oil called asarone that is 2,4,5-trimethoxy-1-propenylbenzene. It is the trans- or alpha-isomer, and the cis-isomer is known as beta-asarone. It is the isomerization analogue of the much more rare 1-allyl-2,4,5-trimethoxybenzene, gamma-asarone, or euasarone, or sekishone. Asarone is the major component of Oil of Calamus obtained from the rhizomes of Acorus calamus, the common Sweet Flag that grows wild on the edges of swamps throughout North America, Europe, and Asia. It has been used as a flavoring of liqueurs and, as almost every other plant known to man, has been used as a medicine. In fact, in Manitoba this plant was called Rat-root by the Cree Indians in the Lake Winnipeg area known as New Iceland, and Indian-root by the Icelandic pioneers. It was used externally for the treatment of wounds, and internally for most illnesses. There apparently is no report of central effects. The corresponding propanone, acoramone (or 2,4,5-trimethoxyphenylacetone), is also present in Oil of Calamus. The styrene that corresponds to asarone is found in a number of plants, and is surprisingly toxic to brine shrimp. The older literature describes an allyl-trimethoxy benzene called calamol, but it has never been pinned down as to structure. The isolation of gamma-asarone or euasarone from Oil of Xixin (from wild ginger) has given rise to a potential problem of nomenclature. One of the Genus names associated with wild ginger is Asiasarum which looks very much like the name asarone, which comes from the Genus Acorus. And a second Genus of medical plants also called wild ginger is simply called Asarum. There is an Asarum forbesi from central China, and it is known to give a pleasant smell to the body. And there is Asarum seiboldi which is largely from Korea and Manchuria. It has many medical uses, including the treatment of deafness, epilepsy, and rheumatism. The amphetamine that would arise from this natural treasure chest is TMA-2.

( 8 ) The 2,5-dimethoxy-3,4-methylenedioxy pattern. The parent allyl benzene is apiole (with a final "e") or parsley camphor, and it is the major component of parsley seed oil. Its conjugated isomer is called isoapiole, and they are valuable as the chemical precurors to the amination product, DMMDA. Whereas both of these essential oils are white solids, there is a green oily liquid that had been broadly used years ago in medicine, called green, or liquid apiol (without the final "e"). It comes from the seeds of parsley by ether extraction, and when the chlorophyll has been removed, it is known as yellow apiol. With the fats removed by saponification and distillation, the old term for the medicine was apiolin. I would assume that any of these would give rise to white, crystalline apiole on careful distillation, but I have never tried to do it. The commercial Oil of Parsley is so readily available.

(9) The 2,3-dimethoxy-4,5-methylenedioxy pattern. The second of the three tetraoxygenated essential oils is 1-allyl-2,3-dimethoxy-4,5-methylenedioxybenzene, commonly called dillapiole and it comes, not surprisingly, from the oils of any of the several dill plants around the world. It is a thick, almost colorless liquid, but its isomerization product, isodillapiole, is a white crystalline product which melts sharply. This, by the theoretical addition of ammonia, gives DMMDA-2.

(10) The tetramethoxy pattern. The third and last of the tetra-oxygenated essential oils, is 1-allyl-2,3,4,5-tetramethoxybenzene. This is present as a minor component in the oil of parsley, but it is much more easily obtained by synthesis. It, and its iso-compound, and the amination product, are discussed under the last of theTen Essential Amphetamines, TA.

One must remember that the term "essential" has nothing to do with the meaning of needed, or required. The word's origin is essence, something with an odor or smell. Thus, the essential oils are those oils that have a fragrance, and the Essential Amphetamines are those compounds that can, in principle, be made from them by the addition of ammonia in the body.

There were a few interesting experimental trials that were based on these natural oils. Methoxyeugenol was assayed up to a 10 milligram level, and asarone at up to a 70 milligram level, and neither had any effects at all. And, in an attempt to challenge the "oil-to-amphetamine" concept, I made up a mixture of 1 part MDA, 2 parts TMA and 5 parts MMDA. A total of 100 milligrams of this combination (which I had named the "Pseunut Cocktail" for pseudo-nutmeg) should be equivalent to the safrole, elemicin and myristicin that would be in 5 grams of nutmeg. And 100 milligrams indeed produced quite a sparkle and considerable eye-dilation. But then, I have never taken 5 grams of nutmeg, so I cannot make any comparisons.
 
When people say X Country is committing Human Rights Violations, this is where that comes from.

UN Universal Declaration of Human Rights
http://www.un.org/en/universal-declaration-human-rights/

Article 18
Everyone has the right to freedom of thought, conscience and religion; this right includes freedom to change his religion or belief, and freedom, either alone or in community with others and in public or private, to manifest his religion or belief in teaching, practice, worship and observance.

Article 27
(1) Everyone has the right freely to participate in the cultural life of the community, to enjoy the arts and to share in scientific advancement and its benefits.
(2) Everyone has the right to the protection of the moral and material interests resulting from any scientific, literary or artistic production of which he is the author.
 
Sasha's Words on Syllogisms

What is the train of thought that leads from the structure of a known compound (which is active) to the structure of an unknown one (which may or may not be active)? Certainly the extrapolations involve many what-if's and maybe's. The path can be humorous, it certainly can be tortuous, and it often calls for special things such as faith, insight, and intuition. But can one say that it is logical?

Logic is a tricky thing to evaluate. One of the earliest approaches was laid down by Aristotle, in the form of the syllogism. In it there are three lines consisting of two premises and a conclusion, a form that is called a "mood." All are statements of relationships and, if the premises are true, there are only certain conclusions that may logically follow. For example:

Every man is a lover.
Every chemist is a man.
Therefore, every chemist is a lover.



Letting lover be the major term "a" and letting chemist be the minor term "b" and letting man be the middle term "m", this reduces to:

Every m is a,
Every b is m.
Therefore, every b is a



and it is a valid mood called Barbara.

Of the 256 possible combinations of all's and some's and none's and are's and are-not's, only 24 moods are valid. The reasoning here with MDPH goes:

Some stimulants when given a methylenedioxy ring are MDMA-like.
Some ring-unsubstituted 1,1-dimethylphenylethylamines are stimulants.
Therefore, some ring-unsubstituted 1,1-dimethylphenylethyl
amines when given a methylenedioxy ring are MDMA-like.



In symbolic form this is:

Some m is a, and
Some b is m, then
Some b is a



and this is not one of the 24 valid moods. Given the first premise as some m is a, there is only one valid syllogism form that can follow, and this is known as Disamis, or:

Some m is a, and
Every m is b, then
Some b is a



which translates as:

Some stimulants when given a methylenedioxy group are MDMA-like.
Every stimulant is a ring-unsubstituted 1,1-dimethylphenyl ethylamine.
Therefore, some ring-unsubstituted 1,1-dimethylphenylethyl
amines when given a methylenedioxy group are MDMA-like.



The conclusion is the same. But the second premise is false so the entire reasoning is illogical. What is the false second premise? It is not a fact that every stimulant is a phentermine. There are lots of stimulants that are not phentermines.

So much for applying syllogistics to pharmacology.
 
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Sasha's Words on Structure Activity Relationship and the Failures of the Modern Medical World

There was absolutely no reason to suspect that the simple rearrangement of the methoxy groups of TMA from the classic 3,4,5-positions to this new, 2,4,5-orientation, would dramatically increase potency like this. Mescaline, 3,4,5-trimethoxyphenethylamine, is an extraordinary compound, but it is not particularly potent, requiring hundreds of milligrams for a trip. And going from its 3,4,5-pattern to the 2,4,5-pattern of TMPEA makes the compound even less potent. There was essentially nothing reported in the scientific literature about central activity of 2,4,5-substituted stuff, so there could not have been any logical preparation for the activity of TMA-2. My very first trials were with a rather liberal 400 micrograms, and the levels being explored leaped up in fairly large steps, mostly on separate days. On November 26, 1962, at 6:00 AM, when 12 milligrams proved to be inactive, another 12 milligrams went in and down an hour later. This was the 24 milligram discovery experiment, a fragment of which is given above. The anxiety of being thrust into the unknown certainly played a role in what can now be seen as obvious psychosomatic difficulties.

The unexpected ten-fold increase of effectiveness uncovered by the simple relocation of a single methoxy group of TMA gave the further juggling of methoxy groups a very high priority. There are a total of six arrangements possible for the three groups, namely, 3,4,5- (the original TMA), 2,4,5- (the present TMA-2), and then and in systematic sequence, 2,3,4-, 2,3,5-, 2,3,6-, and 2,4,6. These compounds were totally unknown at that time, and they could and would be assigned the sequential names TMA-3, TMA-4, TMA-5 and TMA-6, respectively. I made them all, and they are all included in this book.

Having found the treasure of 2,4,5-ness, it is instructive to look back at nature, to see what its plant equivalents might be. There are indeed a few essential oils that have their methoxy groups in this arrangement. TMA-2 is thus one of the Essential Amphetamines, and most of the botanical connections are discussed under TMA. The natural skeleton is found in asarone, with alpha-asarone being trans-propenyl, beta-asarone the cis-propenyl and gamma-asarone (also called euasarone) being the allyl-isomer. I had mentioned, in the spice cabinet discussion under TMA, the tasting of asarone at up to 70 milligrams without any effects.

A couple of additional experiments involving TMA-2 had been set up and started, but somehow never had enough fire to get completed. Studies on the optical isomers had gotten up to assays of 6 milligrams on each of the separate isomers, but had never been taken higher. The "R" isomer is much the more potent in rabbit assays, but the human comparisons remain unknown at present. Also, a study of the 14C labeled racemate (5 microcuries in 40 milligrams) was conducted with a view to metabolite analysis, but again, the project was abandoned before any results were obtained. In the rat, the 4-methoxyl carbon appeared as expired carbon dioxide to the extent of about 20%. And this is some four times the amount seen from either of the other two methoxyl carbon atoms.

One final memory in the TMA-2 area. About twenty years ago I co-authored a rather thorough review article in the British journal Nature, that described the structure-activity relationships between the simpler one-ringed psychotomimetics. It also quietly served as a vehicle for mentioning a number of newly-discovered compounds and their human activities. But as a magnificent attestment to youth and brashness, we proposed a complex compound that embraced each and every clue and hint that might tie it to the neurological process. This hybrid monster was 2,beta-dihydroxy-4,5-dimethoxyphenethylamine. It had everything. The 6-hydroxydopamine hydroxy group and the rest of the dopamine molecule intact as represented by the two methoxyl groups. And the beta-hydroxy group gave it the final "norepinephrine" touch. And, with due modesty, we proposed that it might be "an endogenous psychotogen." Why not "the endogenous psychotogen?" And then, to compound the picture, what should arrive in the mail a month or two later, and from a most respected scientist, but a sample of just this stuff, synthesized for our investigations. I must have bought a little of my own promotion, as I noted that even after my first four graded dosages with the compound, I was still only up to a 250 microgram dose. And then, as the sample became increasingly brown and was clearly decomposing, the project was finally abandoned.

A sad note on how things have changed since that time. I recently queried the editors of Nature, about their thoughts concerning a twenty year retrospective of this area, written by the three authors of the original review. We had each followed quite divergent paths, but each of us was still keenly the researcher. It would have been a marvelous paper to put together, and it would have delighted the reading audience of Nature, had it been the audience of twenty years ago. But not today. The journal is now dedicated to neutron stars and x-ray sources. The respected old English journal of interdisciplinary interests is not the grand and curious lady she used to be. The Editor's reply was polite, but negative. "Such an article would be unsuitable for publication in Nature at present," they said. And, I am sad to say, they're right.

And I am afraid that the American counterpart journal, Science, has suffered a similar deterioration. It, too, has abandoned multidisciplinary interest, but in a different direction. They are now dedicated to chromosomes, and nucleotide identification, and are totally captivated by the attention paid to, and the apparent importance of, the human genome project. There is where you automatically go to publish, now, if you have unraveled some DNA sequence from the Latvian cockroach.
 
Sasha Explains Structure Activity Relationship

There is a sadness felt with most of the published efforts to form sweeping correlations between the structure of a molecule and its biological activity. This relationship is called a SAR, or a Structure Activity Relationship, and there are journals that are dedicated to just this form of analysis.

One needs a large collection of compounds of known structure, and all of them must be of known pharmacological activity. And one needs a computer of some sort. One considers all aspects of the structure such as bond energies, electronic charge densities, molecular lengths, widths and thicknesses, degrees of freedom or of constraint, anything that can be calculated or measured. Then one assigns an independent variable coefficient to everything, constructs some additive equation where these coefficients equal something else, and then compares that something else to the biological activity. Push the "go" button on the computer, and let everything be varied clear across the map, until the calculated solution of the equation makes the best match with the value of pharmacological activity. Then one has a SAR with a statistical measure of goodness of fit, and it then can be used to predict the activity of new structures, which are yet untried, pharmacologically.

And there is the essence of why this entire process is ineffective. Prediction is the heart of this procedure, and prediction is never brought to bear. Let us take a new structure that is not in the original collection of structures, and let us make a prediction as to its, let us say, psychedelic potency. But no one ever tries it out for any of a number of reasons. Maybe the new compound is never synthesized. Or maybe it is synthesized, but never evaluated pharmacologically. The synthesist does not care, or is uninterested, or is restrained by the legal complications that might ensue. Or he does explore it, but chooses not to publish. Almost never is a prediction tested. What is more likely to happen, is that a new input of biological activity and structure variation is uncovered (for which there is no published prediction) and this data is tossed into the mill, and a new set of "more valid" coefficients is calculated, and the SAR becomes touted as a more accurate predictor. But, always remember, that without prediction and challenge, there is no inventive value from the SAR game. It simply organizes what is known, but creates nothing new.

This is a role that I would have loved to see a,N,O-TMS play. At the time of its first synthesis its biological activity was, by definition, completely unknown. Let's cast its shadow up against the structures that were known, and with known activity. What would you predict? The most logical archetype to use as a starting point is the primary amine homologue, a,O-DMS. This is an extremely potent, quite long-lived tryptamine that still ranks up there as the most potent, or nearly so, of all the simple substituted tryptamines. It is orally active. It lasts for many hours. It is completely wild as to visual distortions and illusions. It consistently leads to dramatic, perhaps frightening, but certainly memorable dreams. Three or four milligrams are unmistakably adequate. I would have loved to have had an SAR jock predict what changes would come from the simple addition of an N-methyl group. No one out there predicted this for me, and I have now completely abandoned the art of prediction, at least via the SAR technique. My motto is, make 'em, and taste 'em.

To base structures that are stimulants (amphetamine, for example) an added N-methyl group enhances potency and richness. With MDA, for example, one gets MDMA, not more potent, but of an entirely different form of psychological magic. However, with all the other explored primary amine phenethylamine psychedelics, the potency and the quality of action are effectively lost. With tryptamines, however, the N-methyl groups appear to be needed for full, robust activity. Here, the loss of an N-methyl group might well detract from full potency, and the final unmethylated product (DMT becoming simply tryptamine) will be relatively weak and uninteresting. If a,N,O-TMS had been active at one milligram, then the MDMA explanation is obviously correct. If a,N,O-TMS had been active only at a meager level of twenty milligrams, then the DMT explanation would appear to be correct. It is much less active. It is not spectacular. All you SAR scientists, take this new data, toss it into the maws of computer calculation, and come out with better coefficients.

With this, now, as a challenge, predict for me the potency of a,N,N,O-tetramethylserotonin. Here is a compound that has not been yet synthesized, but which carries the second N-methyl group (yet closer to DMT at the nitrogen atom and probably more potent) and yet a structural kiss of death (as to potency) in the MDA/MDMA world. Will it be up? Will it be down? I am afraid that the "make 'em and taste 'em" procedure is the only one that I can trust.

Good luck
 
Sasha's Words on Psychedelics and Biology

In 1956, Humphry Osmond suggested, at a New York Academy of Science meeting that it might be less pejorative to soften the prefix that was used to relate to the mind from psychoto- or psycho-(used in medical diagnoses that are largely negative) to a misspelled but softer alternative, psyche- (which had not yet been tarred by the image of medical pathology). His suggestion was "psychedelic," it was aped in many trials with such creations as "psychephoric" (mind-moving), "psychehormic" (mind-rousing), "psycheplastic" (mind-molding), "psychezymic" (mind-fermenting), "psycherhexic" (mind-bursting-forth) and "psychelytic" (mind-releasing). But, psychedelic (mind-manifesting) has weathered all storms, and is now a fixed component of our vocabulary. There are several recent contributions for possible class names for some of these compounds, such as entheogen (God-created-within), entactogen (touching-within) or empathogen (the discovery of empathy), are creations that try to address the integrity and warmth that can be part of the psychedelic experience. Each uses the suffix, "-gen," that suggests genesis, or creation. Each has its use, and each has its limitations. One must remember that none of these terms describe what occurs within an experience. Their value is limited to the search for a label for the drugs that allow these experiences to happen.

Back to the metabolism discussion. And to the search for the actual drug, the magic bullet, that actually precipitated a model schizophrenic state. If one were to find it, one could look skillfully for the counterpart in the human animal, the one that simply appeared on the scene from some mismanaged metabolic process, and thus could be blamed for mental illness. It had been observed that the longer the chains on the N,N-disubstituted tryptamine, the less the potency. And the longer the chains, the less of the drug was excreted as the 6-hydroxyl metabolite. This focused attention on the hydroxy metabolites of the two simplest and most potent of the dialkyltryptamines, DMT and DET.

6-HO-DET has been observed to be a minor human metabolite of DET, with the excretion of about 20% of the administered dose as the glucoronide conjugate. In a study with normal and schizophrenic patients, a positive correlation was observed between the amount of 6-HO-DET excreted and the intensity of the experience. Also, there was a suggestion that the schizophrenics produced greater amounts of this metabolite. This led to a hypothesis that perhaps it was an active factor in the generation of the intoxicated state. In principle, as with bufotenine, that bare, exposed polar hydroxyl group should make its entry to the brain quite difficult. But, on the other hand, if it were generated there from DET after it had gotten into the brain, entry would not be a concern and the lipophilic barrier could serve to make its exit difficult. Then, if it were an effective compound, it might well be a long acting one. There is an early report of the self-administration intramuscularly, within a single subject, of 10 milligrams 6-HO-DET with the description of what appeared to be DET-like effects from about the second to fourth hour. Although this report suggested that it was several times more potent than DET, it has never been replicated and it does not jibe too well with the 6-HO-DMT report below.

As a challenge to the hypothesis that hydroxylation at the 6-position of the N,N-dialkyltryptamines might play some role in the expression of the activity, this position was metabolically blocked by the insertion of a fluorine atom there, giving 6-F-DET. This compound, with DET as the control, was studied in some twelve hospitalized alcoholics at doses of about 60, 80 and 100 milligrams intramuscularly. It "does produce autonomic effects, pupillary changes, blood pressure changes; but it does not produce the drifting away into a dream world and other phenomena characteristic for the hallucinogenic activity." The experimenters considered its possible experimental role as an "active placebo" but nothing more was done with it.

6-HO-DMT is a minor metabolite of DMT in man, and it was studied for the same reasons. Could this compound play a role in explaining the activity of the parent dialkylamine? It was explored in a series of subjects who had responded spectacularly to DMT. The five volunteers in this study were former opium addicts who were serving sentences for violation of United States narcotics laws. They were administered 6-HO-DMT at either 0.75 mg/Kg (one subject) or 1.0 mg/Kg (four subjects) and reported no differences from the inactive placebo control. The objective measures (blood pressure, respiration and heart rate, pupillary dilation) confirmed this absence of activity at this level. The active control drug was DMT itself, and it showed the expected responses in all regards.

I have always been quite skeptical, and just a little embarrassed, that so many of these early studies used hospitalized patients, schizophrenics, alcoholics, and prisoners as subjects. These latter experiments were carried out at the Lexington, Kentucky Public Health Service Hospital. This has been for years a major site for human research in the area of addictive or psychotropic drugs. But it cannot be forgotten that it was first, and foremost, a prison and the people there were prisoners. A complete objectivity of reporting, from a person who is in custody and who might wish to please his jailers, is unlikely. The whole scene started shortly after the Harrison Narcotics Act passed back near the time of World War I. The medical profession held that narcotics addiction was a medical problem, and the legal authorities held that it was a legal problem. In other words, was a heroin user sick, or was he a criminal? The law enforcement viewpoint prevailed, the physicians who objected went to jail, and the addicts went to what were called "narcotics farms." They were indeed prisons, but the name carried the suggestion of rehabilitation. And it was at the last of these, at Lexington, that this hydroxylated DMT study was done.

The results were negative, to the disappointment of the researchers. It is pretty generally accepted that 6-HO-DMT is inactive. I am not too surprised. There are so few things with open and exposed hydroxyl groups that succeed in making it through the lipid barriers to the brain.
 
There is another mixture that is as simple as the Coffee, Almond, Cinnamon, Vanilla and Nutmeg.

Someone reported having eaten some Nutmeg, but not enough to cause effects. Then took some Calamus Root Extract, but not enough to cause effects. Then smoked some Parsley seed and Dill seed, and reported noticeable Psychedelic effects.
 
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