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/...rg/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.

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

A ha!



Aniracetam interacts with the 5HT2c receptor!

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

-eg

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

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.

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.

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