Nootropics as a tripblocker

[lunac]

Hi,

It is known that certain nootropics may block a k-hole for ketamine but I have found out that certain nootropics may (at least for me) block a breakthrough with DMT. These effects that come with the blocks seem similar.
I have consumed the following nootropics-stack during the day before my attempted breakthrough and k-hole:
200 mg Cafeïne Anhydrous
400 mg L-Theanine
400 mg Sulbutiamine
350 mg NALT (N-Acetyl L-Tyrosine)
1500 mg Choline Bitartrate
1000 mg Aniracetam
30 mg Noopept
The DMT was smoked after 25mgs of 2c-b and the ketamine was snorted followed by a balloon with NOS.
Where a DMT-breakthrough or K-Hole usually launches me into another realm when I close my eyes, the nootropics-stack seemed to put up a white solid wall in front of me with a few coloured lines or shapes. I kept hearing music but that was it. It also "felt" very empty (and very scary the first time this happened)
I have smoked DMT before while on aniracetam only, this had no effects on the trip so I am inclined to say one or a combination of the other substances act as a "tripblocker".
I have searched google and the nexus for known interactions but all I can find is that nootropics may act as an enhancer on triptamines.

I wanted to share this experience and I am wondering if you guys are familiar with any combinations of DMT with above substances.

 

[entheogenic-gnosis]

To "block" a trip you would probably need a 5HT2a/c antagonist, while nothing you listed strikes me as being able to serve this purpose...

I think it's more likely that the phenethylamine (2C-B) you consumed, which is also a 5HT2a/c agonist, had some type of cross tolerance with the DMT...

...or sometimes DMT will simply refuse to let you in...

Was there nicotinic acid (Niacin) in this "nootropic stack"?

It's been claimed that Niacin can reverse an LSD experience:

Niacin (NADH-dependent enzyme) "One of the metabolites of LSD in the human body is 2-oxy-lsd. It is formed by liver microsomes by an NADH-dependent enzyme," Nicholas J. Giarman (1967). ref. (Axelrod 1957; Hoffer 1955) Use of nicotinic acid (niacin, B3) to abort psychosis - "We have given the subject 100 ug. of LSD; at the height of the experience we injected intravenously 200 mg. of nicotinic acid. Our experience has been that, within a matter of two to five minutes, almost all of the LSD phenomena disappeared, and the subject claimed that he was entirely normal," Abraham Hoffer (1956)

-Otto snow ; LSD

HOFFER A
Studies with niacin and LSD.
Lysergic Acid Diethylamide and Mescaline in Experimental Psychiatry, Grune & Stratton Inc. 1956, p 44
200 mg nicotinic acid given i.v. at the height of the effects of LSD (100 mcg) caused almost all the LSD phenomena to disappear with 2-5 minutes. 3 Gm. nicotinic acid given daily for 3 days prior to 100 mcg LSD caused the LSD phenomena to appear after about 1 hour instead of after 15-30 minutes and seemed to prevent most of the perceptual phenomena, the main changes noted being feelings of unreality and depersonalization

https://www.anoniem.org/?http://www.lycaeum.org/mv/mu/LSD_niacin.html

AGNEW N, HOFFER A
Nicotinic acid modified lysergic acid diethylamide psychosis.
J.Ment.Sc. London 101:12 (1955)
200 mg nicotinic acid given i.v. to 5 normal subjects at the height of the LSD experience (100 mg orally) strikingly reduced the LSD-induced disturbances in all subjects except one. 3 Gm. nicotinic acid given by mouth daily for 3 days prior to 100 mcg. LSD orally in 5 normal cases reduced the LSD-induced disturbances in concentration and vision, but in some instances produced a psychosis more closely resembling schizophrenia than that observed after LSD alone

MILLER A I,WILLIAMS H L, MURPHREE H B
Niacin, niacinamide, or atropine versus LSD-25 model psychoses in human volunteers.
J.Pharmacol.& Exper.Therap., 119:169 (1957)
Studies in 16 volunteers using the double blind method showed that atropine (1 mg orally), niacin (up to 600 mg orally), and niacinamide (up to 600 mg orally) did not alter the pattern of response to LSD when they were given in combination with LSD (75 mcg orally). Niacin seemed to produce a release from the anxiety associated with the LSD-induced illusions without lessening or eliminating the illusions.

-eg

 

[entheogenic-gnosis]

A ha!

After a confirmed test of the anxiolytic efficacy in a mouse model, haloperidol, mecamylamine, and ketanserin were applied to determine the pathways aniracetam depends on to exert its anti-anxiety effects. Haloperidol completely reversed the anxiolytic effects, and mecamylamine and ketanserin nearly completely reversed the effects. These respectively suggest that aniracetam's anxiolytic mechanism may be mediated through D2, nAChR, and/or 5-HT2A receptor activity. -Wikipedia

Aniracetam interacts with the 5HT2c receptor!

You may be on to something with the Aniracetam, I have to do some research...

-eg

 

[lunac]

I have multiple experiences with the 2c-b DMT combo (without nootropics), this has worked fine to say the least
Maybe "block" is not the right word in the sense that receptors were blocked, because something does happen. It is more that something else put up this "wall". I have had experiences where DMT didn't let me in, those were very different.
I realise DMT has almost unlimited possibilities but the similarity with the K-Hole "block" is what got me thinking about this.

 

[lunac]

A ha!

After a confirmed test of the anxiolytic efficacy in a mouse model, haloperidol, mecamylamine, and ketanserin were applied to determine the pathways aniracetam depends on to exert its anti-anxiety effects. Haloperidol completely reversed the anxiolytic effects, and mecamylamine and ketanserin nearly completely reversed the effects. These respectively suggest that aniracetam's anxiolytic mechanism may be mediated through D2, nAChR, and/or 5-HT2A receptor activity. -Wikipedia

Aniracetam interacts with the 5HT2c receptor!

You may be on to something with the Aniracetam, I have to do some research...

-eg

Thnx
I am wondering how noopept fits in, seeing how much more powerful it is claimed to be

 

[entheogenic-gnosis]

I'm also looking into the function of metabolites of aniracetam

When ingested orally aniracetam is quickly broken down via first pass hepatic metabolism. The primary metabolites of aniracetam are N-anisoyl-GABA, 2-pyrrolidone, and anisic acid.[10] Plasma concentrations are generally in the 5–15 μg/L range for aniracetam and 5–15 mg/L range for N-anisoyl-GABA, a pharmacologically-active metabolite, during the first few hours after oral administration of the drug. These two plasma species may be measured by liquid chromatography-mass spectrometry -Wikipedia

I'm running out the door, so I'll have to return to this topic, but I think there might be something interesting going on here, so I am going to do further research.

--------

Misc. Research

Aniracetam enhances cortical dopamine and serotonin release via cholinergic and glutamatergic mechanisms in SHRSP
Abstract
Aniracetam, a cognition enhancer, has been recently found to preferentially increase extracellular levels of dopamine (DA) and serotonin (5-HT) in the prefrontal cortex (PFC), basolateral amygdala and dorsal hippocampus of the mesocorticolimbic system in stroke-prone spontaneously hypertensive rats. In the present study, we aimed to identify actually active substances among aniracetam and its major metabolites and to clarify the mode of action in DA and 5-HT release in the PFC. Local perfusion of mecamylamine, a nicotinic acetylcholine (nACh) and N-methyl-D-aspartate (NMDA) receptor antagonist, into the ventral tegmental area (VTA) and dorsal raphe nucleus (DRN) completely blocked DA and 5-HT release, respectively, in the PFC elicited by orally administered aniracetam. The effects of aniracetam were mimicked by local perfusion of N-anisoyl-gamma-aminobutyric acid [corrected] (N-anisoyl-GABA), one of the major metabolites of aniracetam, into the VTA and DRN. The cortical DA release induced by N-anisoyl-GABA applied to the VTA was also completely abolished by co-perfusion of mecamylamine. Additionally, when p-anisic acid, another metabolite of aniracetam, and N-anisoyl-GABA were locally perfused into the PFC, they induced DA and 5-HT release in the same region, respectively. These results indicate that aniracetam enhances DA and 5-HT release by mainly mediating the action of N-anisoyl-GABA that targets not only somatodendritic nACh and NMDA receptors but also presynaptic nACh receptors.

-eg

 

[○]

No science from my end. Purely anecdotal

I used to take 30mg noopept/2g aniracetam daily. I did this for close to 4 months or so.

I had smoked some old enhanced leaf I had laying around at the time. If anything, those two nootropics made me moar susceptible to the experience, moar sensitive. I was obliterated without question.

 

[Shrugs]

No science from my end. Purely anecdotal

I used to take 30mg noopept/2g aniracetam daily. I did this for close to 4 months or so.

I had smoked some old enhanced leaf I had laying around at the time. If anything, those two nootropics made me moar susceptible to the experience, moar sensitive. I was obliterated without question.

^ Same here.
using a little noopept during the week made the visuals massively more defined, vibrant.

 

[Infectedlsd]

I think from a biological standpoint. The NOS you smoked in combination with Ketamine might be the culprit for using up the "light" in ur brain. Namely it's reaction with N2. This sounds like a powerful combination that culminates and uses up all the N2 in ur body. I personally suspect this one chemical is responsible for most visuals.

If this is so, someone else who is more experienced with using NOS might be able to confirm my feelings surrounding this subject

 

[lunac]

I think from a biological standpoint. The NOS you smoked in combination with Ketamine might be the culprit for using up the "light" in ur brain. Namely it's reaction with N2. This sounds like a powerful combination that culminates and uses up all the N2 in ur body. I personally suspect this one chemical is responsible for most visuals.

If this is so, someone else who is more experienced with using NOS might be able to confirm my feelings surrounding this subject

I also have a lot of experience combining ketamine with NOS (inhaling, it smoking!) It's a great way to induce a very profound "godlike" K-Hole. For me at least. This always works resulting in similar trips, except for this last time where I had nootropics in my system.