Why is B. Caapi active by itself? - Euphoric, awareness expanding sensations

[Seeking_Similarity]

Hello folks. A few weeks ago I brewed some B. Caapi into a tea for my ingestion as a MAOI primarily so that I could have a longer vaped DMT trip. I didn't think I would feel the effects too much, but that was definitely very active. Without taking too much, I felt a sense of euphoria, awareness expansion... similar to what I experienced at the beginning of my Ayahuasca trip.

What causes B. Caapi to be active like this? I imagine it does have some amount of DMT, although not much. As far as I know, it can't be the MAOIs present in it like THH, Harmine and Harmaline as they produce no real noticeable effects other than nausea (again, as far as I know)

What other alkaloids are present in B. Caapi? And why can it be vision inducing by itself without the Chacruna leaves?

 

[Prima Materia]

The harmala alkakoids present in caapi are responsible for the effects you are describing.
I am sure there are other compounds in there that contribute to the effect but are not as important as the harmala alkaloids. One can experience visions and visuals under the influence of these alkaloids. And the same alkaloids are responsible for the MAO inhibition as well. The exception is THH though, which supposedly acts as a SRI (serotonin reuptake inhibitor).

 

[Jees]

Hi S_S, Triglav is right.

caapi only seems to be the base definition of ayahuasca, go reckon it works on itself.
The other plants are admixtures, and as I've read somewhere the term Chacruna should be the Quechua word for 'admixture', sort of.
According to ayahuasca.com:

Ayahuasca derives from the Quechua aya-spirit/dead, waska-vine/rope.

In this definition only the vine is to be recognized.
Later on, the word ayahuasca became the 'container' word for the base (the vine) plus all the different admixtures possible, and eventually also the word for brews that even did not even contain the vine anymore like rue+mimosa etc..
But ideally we would make the differences and reserve 'ayahuasca' for caapi containing brews.

In short, you've rediscovered the most original form of ayahuasca :thumb_up:

 

[Seeking_Similarity]

The harmala alkakoids present in caapi are responsible for the effects you are describing.
I am sure here are other compounds in there that contribute to the effect but are not as important as the harmala alkaloids. One can experience visions and visuals under the influence of these alkaloids. And the same alkaloids are responsible for the MAO inhibition as well. The exception is THH though, which supposedly acts as a SRI (serotonin reuptake inhibitor).

That's fascinating by itself... If I had pure Harmine and Harmaline (pure extraction) and took them, I would feel the same effects I did when I drank the tea then?

As you said, there could be other alkaloids present in the vine. Would really appreciate it if there was a list of all compounds that act as a psychoactive component in it. I'm sure there should be some NMT, DMT or other stuff in there.

 

[der-seemann]

AFAIK the main active molecules are harmine and harmaline, both acting as MAO-inhibitors and THH, acting NOT as MAOI but as SSRI. The effect of the THH probably gets enhanced significantly by the MAOIs.

So taking only harmine and harmaline will be quite different as it lacks the SSRI-effect of the THH.

All the other alkaloids (sorry, German names: Harmol, Harmalol, Harmin-N-oxid, Harminamid, Harminsäure, Harminsäuremethylester, Harmalinsäure, 6-Methoxytryptamin, Banistenosid A, Banistenosid B, Acetylnorharmin, Ketotetrahydronorharmin, Tetrahydronorharmin, Shihunin and Dihydroshihunin) will contribute to the Caapi experience as well.

 

[endlessness]

Harmalas have been thought to merely orally activate DMT through their MAOI properties. Nevertheless, both traditional ethnobotanical use as well as modern pharmacological data (and bioassays too) show there is much more going on with harmalas than merely activating DMT.

It is likely that initially, historically, ayahuasca started as a caapi-only preparation. There is ethnological evidence showing caapi-only use in some tribes (I can try and dig some sources later if someone is interested). Seems some of these people consider the vine to be incredibly powerful and spiritual on its own.

When looking at modern pharmacological studies, we can see, apart from the MAOI properties, harmalas act on a host of receptors which may explain those effects, including GABA, opioid, and others (Moloudizargari et al 2013)

From a personal perspective, I have taken caapi-only brews several times and they definitely have psychoactive effect on their own. Sometimes I describe the effects as dreamy, inducing an altered headspace, feeling in a bubble of sorts, in higher doses there are visual effects but they aren't geometrical like tryptamines, more like, a potentiated imagination where realistic scenes can be seen. Plus feeling dizzy, being sensitive to stimulus, specially light, and seeing tracers too. It's been a while, but that's kinda how I remember it.

Its all good to experiment and see what works for each person. I do think there is value to caapi-only but eventually I've always preferred taking it with tryptamines too.. Nevertheless, when brewing a new batch of aya, I always preferred brewing first a caapi-only brew to find the potency, taking it in gradually increasing doses until I found the exact dosage needed to get that slight dizzyness, headspace and light-sensitivity, but not so much that it becomes overwhelming. When I found that dosage, then in another session I will take that same dose but with added DMT. Taking caapi orally and vapping DMT on top as OP is doing can also be nice...

 

[doubledog]

Could it be that the effect of harmalas is also due to effects of endogenous monoamines, which becomes more active when MAO are inhibited?

 

[Prima Materia]

Could it be that the effect of harmalas is also due to effects of endogenous monoamines, which becomes more active when MAO are inhibited?

You certainly have a point.

quoted from wikipedia --- serach: trace amine

Trace amines are an endogenous group of trace amine-associated receptor 1 (TAAR1) agonists[1] – and hence, monoaminergic neuromodulators[2][3][4] – that are structurally and metabolically related to classical monoamine neurotransmitters.[5] Compared to the classical monoamines, they are present in trace concentrations.[5] They are distributed heterogeneously throughout the mammalian brain and peripheral nervous tissues and exhibit high rates of metabolism.[5][6] Although they can be synthesized within parent monoamine neurotransmitter systems,[7] there is evidence that suggests that some of them may comprise their own independent neurotransmitter systems.[2]

The human trace amines include:

quoted from wikipedia:

Phenethylamines (related to catecholamines):
Phenethylamine[5][6][15] (PEA)
N-Methylphenethylamine[4][5][15] (endogenous amphetamine isomer)
Phenylethanolamine[16][15]
m-Tyramine[5][15]
p-Tyramine[5][15]
3-Methoxytyramine[4][15]
N-Methyltyramine[4][5][15]
m-Octopamine[5][15]
p-Octopamine[5][15]
Synephrine[4][15]
Thyronamine compounds:
3-Iodothyronamine[6][15]
Tryptamine[4][6][15]

Also there are TAAR (trace amine associated receptor) receptors in the human brain. The wikipedia yields interesting information about that as well.

quoted from wikipedia: search - trace amine-associated receptor

Trace amine-associated receptors (TAARs), sometimes referred to as trace amine receptors (TAs or TARs), are a class of G protein-coupled receptors that were discovered in 2001.[1][2] TAAR1, the first of six functional human TAARs, has gained considerable interest in academic and proprietary pharmaceutical research due to its role as the endogenous receptor for the trace amines phenylethylamine, tyramine, and tryptamine – metabolic derivatives of the amino acids phenylalanine, tyrosine and tryptophan, respectively – ephedrine, as well as the synthetic psychostimulants, amphetamine, methamphetamine and methylenedioxymethamphetamine (MDMA, ecstasy).[3][4][5][6][7][8] In 2004, it was shown that mammalian TAAR1 is also a receptor for thyronamines, decarboxylated and deiodinated relatives of thyroid hormones.[5] TAAR2–TAAR9 function as olfactory receptors for volatile amine odorants in vertebrates.[9]

 

[jamie]

The structure of harmine and harmaline share a lot in common with ibogaine and iboga alkaloids. The effects of these harmaloids are in my experiences also most similar to the effects of Iboga. This is commonly reported.

Mystery solved...not entirely, but I am surprised more people have not started utilizing high dose harmalas because they are invaluable tools.

 

[downwardsfromzero]

All the other alkaloids (sorry, German names: Harmol, Harmalol, Harmin-N-oxid, Harminamid, Harminsäure, Harminsäuremethylester, Harmalinsäure, 6-Methoxytryptamin, Banistenosid A, Banistenosid B, Acetylnorharmin, Ketotetrahydronorharmin, Tetrahydronorharmin, Shihunin and Dihydroshihunin) will contribute to the Caapi experience as well.

Most of these can be translated to English by sticking an 'e' on the end (and they're not of the special grammatical class 'proper nouns' so they start with a lower case letter, unlike German nouns):
harmine-n-oxide, harminic acid amide, harminic acid, harminic acid methyl ester, harmalinic acid, 6-methoxytryptamine, banistenoside A, banistenoside B, acetylnorharmine, ketotetrahydronorharmine, tetrahydronorharmine, shihunine and dihydroshihunine.

Harmol and harmalol translate identically, capital letters notwithstanding.