Curious concluding thought...
"Acetaldehyde is one of the most important sensory carbonyl compounds in wine and constitutes approximately 90% of the total aldehyde content in wine. Acetaldehyde can be formed by yeasts and acetic acid bacteria (AAB)."
1 shot of sherry wine which contains on avg 10mg of acetaldehyde is an important ingredient of the LSH saturating/stabilizing recipe given above, as is the fresh from foil packet Bigelow combination spearmint/peppermint "Mint Medley tea" and/or 5 peppermint extract drops mixed all together with the 500ml ph=4 DL tartaric acidified spring water.
Vin Mariani wine with coca leaf was drunk by the Pope and Thomas Edison & leagues of famous people back in the 1800's. It consisted of wine with at least an alcohol content of 15% and added coca leaf (coca leaf tea bags soaked in wine) which in vivo (in the liver) turned into coca-ethylene which was orally potent, the secret of it's strong activity was not even discovered until 1994.
Sometimes I wonder if an enzymatic reaction in the liver also has something to do with adducting acetaldehyde to ergine (LSA) to form LSH in-vivo in the liver (unlikely) and/or improving LSH stability in combination with ethanol & acetaldehyde, which is known to drive acetaldehyde adduct formation with tryptophans in a paper I read once still on-line "Tryptophan analogues form adducts by cooperative reaction with aldehydes and alcohols or with aldehydes alone" by J E Austin & H Fraenkel-Conrat (below). After-all we are only dealing with mg amounts.
But a more plausible explanation is that acetaldehyde is adducting on to the indole ring further below in it's structure, creating something more akin to what ald-52 looks like (see attached pic at bottom) according to the aldehydes adduct paper. How this plays out as far as effects-wise/stimulation/etc. in the human body is unknown.
https://www.ncbi.nlm.nih...v/pmc/articles/PMC49935/hxxps://www.ncbi.nlm.nih.gov/pmc/articles/PMC49935/
LSH is a labile adduct of ergine and acetaldehyde, which rearranges to LSA in neutral water, but we know from researchers that it is stable in acidic solutions.
The in-vivo liver adduction hypothesis of "adduction of acetaldehyde to LSA at the bottom of the indole ring" (like adducts paper saids can happen) to something more akin to looking like ALD-52 bottom indole wise ---> might likely help to explain why there is no sedation felt after solution is drunk, instead entire experience is energizing, as if only LSH effects are felt, along with the stimulating penniclavine, and whatever is created with the leftover LSA to something described above.
In The Hallucinogens by Hoffer and Osmond (1967), ALD-52 is listed as having a lower [approximately 1/5] intravenous toxicity (in rabbits), a lower [approximately 1/8] pyretogenic effect, an equal psychological effect in humans, and double the "antiserotonin" effect as compared with LSD.
So it appears that this "mystery compound" created by the adduction of acetaldehyde to LSA will be highly stimulating as we know that ALD-52 is double the anti-serotonin properties of LSD, and whenever a molecule is strongly anti-serotonin, it is also strongly stimulating.
Examples of strongly anti-serotonin (block serotonin) and thus highly stimulating molecules:
* LSD
* our mystery molecule made from adduction of acetaldehyde + LSA at the bottom of indole nitrogen in the liver according to J E Austin & H Fraenkel-Conrat's aldehyde adduction paper. Will look similar to what ALD-52 looks like at the bottom.
* cocaine
* orally active coca-ethylene (coca leaf + wine)
* ibogaine
* mescaline
* psilocybin
* 5-meo-dmt
* bufotenine
69ron earlier in this thread also backs up my claim that there are no LSA sedative effects left over or felt, only stimulating/energizing, euphoric and psychedelic qualities. He writes about this for 2 pages (quoted earlier in this thread) and rightly so, as it is a revelation the first time you experience it. I think the reason some of his conversions worked 100% and others failed completely was because: 1) he did not acidify his solution, and 2) he did not use high acetaldehyde containing wine, but rather mint tea only, and 3) at other times he used rum (not much acetaldehyde that I know of).
The original recipe I used over 20 years ago calls for 500ml of DL tartaric acidified to ph=4 chilled spring water + 1 shot of cold sherry + chilled fresh spearmint/peppermint tea from sealed foiled packet and/or 5 peppermint extract drops added.
Also don't forget Krystle Cole's "ergot wine" experience (several pages long) in this thread.
Penniclavine (found in high amounts in the seeds, found to be CNS stimulating, Yui & Takeo) is a metabolite of agroclavine, and is active at the following brain receptor sites: Dopamine D1A, Dopamine D1B, 5-ht2a, Adrenal A2A, Adrenal A2B & Adrenal A2D, in comparison LSD (as far as adrenal sites are concerned) only has activity at A2A, but zero activity at A2B, A2C, and A2D.
The teamwork between LSH and Penniclavine in the seeds is what imho results in the potent & very euphoric experience. Learned the value of teamwork when I trained & worked as a deep water lifeguard for many years...believe I'm a water spirit...the importance of the team working together at all times can mean the difference between saving a life or not. More examples of "entheogenic teamwork between molecules" below:
Thomas S. Ray, Psychedelics and the Human Receptorome (2010):
https://journals.plos.or...371/journal.pone.0009019hxxp://journals.plos.org/plosone/article?id=10.1371/journal.pone.0009019
Breadth of Receptor Binding, 4.00=max, 0.00=min
Quote:LSD: 5ht1a = 3.73, DMT: = 0.00, psilocin = 2.88, mescaline = 3.61, 5-meo-DMT: = 4.00 (make up >80% of brain 5-ht)
LSD: 5ht1b = 4.00, DMT: = 0.00, psilocin = 2.19, mescaline = 0.00, 5-meo-DMT: = 2.41
LSD: 5ht1d = 3.70, DMT: = 3.91, psilocin = 3.40, mescaline = 0.00, 5-meo-DMT: = 3.48
LSD: 5ht1e = 2.62, DMT: = 3.28, psilocin = 3.03, mescaline = 3.16, 5-meo-DMT: = 1.72
LSD: 5ht2a = 3.54, DMT: = 2.58, psilocin = 2.14, mescaline = 0.00, 5-meo-DMT: = 0.98
LSD: 5ht2b = 3.11, DMT: = 3.91, psilocin = 4.00, mescaline = 3.97, 5-meo-DMT: = 0.69
LSD: 5ht2c = 3.11, DMT: = 3.42, psilocin = 2.52, mescaline = 0.00, 5-meo-DMT: = 1.55
LSD: 5ht5a = 3.64, DMT: = 3.16, psilocin = 2.83, mescaline = 0.00, 5-meo-DMT: = 1.84
LSD: -5ht6 = 3.75, DMT: = 3.35, psilocin = 2.82, mescaline = 0.00, 5-meo-DMT: = 2.73
LSD: -5ht7 = 3.77, DMT: = 4.00, psilocin = 2.82, mescaline = 0.00, 5-meo-DMT: = 3.69
LSD: ---D1 = 2.34, DMT: = 3.51, psilocin = 3.37, mescaline = 0.00, 5-meo-DMT: = 2.38
LSD: -A-2A = 2.93, DMT: = 2.75, psilocin = 1.36, mescaline = 2.92, 5-meo-DMT: = 0.00 (aesthetic/beauty adrenal a2a)
LSD: -A-2B = 0.00, DMT: = 3.53, psilocin = 1.57, mescaline = 0.00, 5-meo-DMT: = 0.86 (aesthetic/beauty adrenal a2b)
LSD: -A-2C = 0.00, DMT: = 3.53, psilocin = 1.03, mescaline = 4.00, 5-meo-DMT: = 1.57 (aesthetic/beauty adrenal a2c)
Ibogaine binds directly to the serotonin transporter (SERT), so it does not have to target the 5-ht1a substrate pathway. This could be likely what happens with tetrahydroharmine, as THH in caapi (2nd highest ingredient in caapi after harmine) and ibogaine have similar basic beta-carboline structures.
Thomas S. Ray's study shows a value of 3.57 at SERT for Ibogaine (4.00 is max). Ibogaine has been shown to inhibit serotonin transporter (SERT) noncompetitively, in contrast to all other known inhibitors, which are competitive with substrate.
Thomas S. Ray Receptorome study, 4.00=max, 0.00=min.
Quote:Ibogaine: 4.00 Sigma2, 3.57 SERT, 3.02 DAT, 3.01 NMDA, 2.88 KOR, 2.67 MOR, 2.55 Sigma1, 2.22 M3, 2.16 5ht2a, 1.96 M1, 1.72 M2, 1.47 D3;
0.00: DOR, 5ht1b, 5ht1d, 5ht1a, H1, 5ht2c, D2, D1, Beta1; ND: Alpha2C, D5, D4, Alpha2B, Imidazoline1, NET, Alpha2A, 5ht5a, 5ht6, 5ht7, Alpha1B, 5ht1e, 5ht2b, M4, M5, Alpha1A, H2, CB2, CB1, Ca+Channel, Beta2
Ibogaine (inhibits both serotonin and dopamine reuptake transporters, it is an SDRI or serotonin & dopamine reuptake inhibitor). Tetrahydroharmine (serotonin reuptake inhibitor, it is an SRI found in caapi.)
Additional 1988 study which backs up the 2011 Thomas S. Ray receptorome study:
Pharmacology of 5-hydroxytryptamine-1A receptors which inhibit cAMP production in hippocampal and cortical neurons in primary culture.
https://www.ncbi.nlm.nih.gov/pubmed/2828913 Quote:5-HT1A agonist: All the tryptamine derivatives substituted in position 5 of the indol were potent agonists [5-HT, 5-CT, 5-MeO-N,N-DMT, 5-methoxytryptamine, and bufotenine (5-ho-DMT), whereas tryptamine, N-methyltryptamine (NMT), and N,N-dimethyltryptamine (DMT) were very poor agonists.
As we go thru day to day life, the brain serotonin filters (or gates) are in place so that we will not be overwhelmed by the perception of the way things would appear to an un-filtered mind, or "Mind at Large" as Aldous Huxley describes it in "Doors of Perception" as "infinite or eternal". He also referred to the visions as coming from "the other world" in his book "Moksha". I prefer to think of it in similar terms as well "the spirit world" or "the other world".
5-ht1a inhibition (in green above) theoretically causes this filter system to be lifted, and the infinite mind to manifest in combination with oral dmt from traditional psychotria for example.
Dr. Nichols:
Quote:LSD has very strong potency in blocking the action of serotonin. LSD is strongly "anti-serotonin". The morpholide lysergamide cousin had only about 1/10th the potency in blocking serotonin. Of the 5 diferent dialkylamides we studied LSD was the most potent and specific serotonin antagonist. 5-ht1a makes up >80% of brain 5-ht receptors.
An example of the importance of adding the serotonin reuptake inhibition properties of 5-meo-dmt for example to dmt (which totally lacks 5-ht1 reuptake properites on it's own) is described in combination experiments in James Oroc's book "Tryptamine Palace". This is the same way the snuff's are used in the amazon, as they naturally combine dmt with additives which cause the reuptake of 5-ht like bufotenin for example (giving effects which last 3 hours)...or as Ayahuasca is used traditionally in the Amazon, teamwork combining caapi with admixture. This way, the dmt in admixture leaf psychotria targets the other 20% of brain receptors very heavily (see dmt receptorome in chart above), while caapi being an SRI inhibits the other 80% of brain 5-ht at 5-ht1a (inhibiting the brain filters normally used day to day in survival mode) just like the other oral entheogens above like LSD, mescaline, ibogaine, shrooms, 5-meo-dmt, bufotenine in snuffs.
tregar attached the following image(s):
pic20.JPG
(14kb) downloaded 146 time(s).You may remember me as 69Ron. I was suspended years ago for selling bunk products under false pretenses. I try to sneak back from time to time under different names, but unfortunately, the moderators of the DMT-Nexus are infinitely smarter than I am.
If you see me at the waterpark, please say hello. I'll be the delusional 50 something in the American flag Speedo, oiling up his monster guns while responding to imaginary requests for selfies from invisible teenage girls.