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Lysergamides Rethinking the LSA aldehyde theory

SassysShrooms

Greenlighter
Joined
Oct 21, 2026
Messages
5
I’ve been a long-time believer and researcher of the classic LSA + aldehyde “adduct” theory. I want to say sorry in advance to Tregar if this alternative framing undercuts some of his work — I’ve always respected his research and the effort he’s put into the community.
Over the past 10 years I’ve done a lot of experiments with different aldehydes and aromatic compounds alongside LSA (morning glory / HBWR). Many of them produced noticeably different effects — sometimes it felt like a completely different drug than plain LSA.


I recently came across this Google patent from Goodcap Pharmaceuticals:


They researched combining 5-HT2A agonists (psilocybin, LSA / lysergic acid amide, lysergic acid α-hydroxyethylamide from morning glory and Hawaiian baby woodrose seeds, and others) with various TRP receptor agonists. The core idea is multimodal action at both 5-HT2A and TRP channels (TRPV1, TRPA1, TRPM8, TRPV3, etc.). This can allow lower doses of the 5-HT2A compound while changing the overall effect profile — more euphoria, altered duration, reduced anxiety or body load in some combinations, better anti-inflammatory effects, etc.
Interestingly, many of the classic “LSA adduct” herbs are listed in the patent as TRP agonists:

Peppermint (menthol → mainly TRPM8)
Cinnamon (cinnamaldehyde → strong TRPA1)
Clove (eugenol)
Cayenne (capsaicin → TRPV1)
Turmeric (curcumin)
Black pepper (piperine)
Nutmeg (myristicin — which they note can also have some 5-HT2A activity itself)
Plus oregano, thyme, ginger, garlic/onion (allicin), bergamot, cardamom, chocolate/cocoa, myrrh, frankincense, and others.

The patent’s strongest practical observations are mostly with psilocybin + the spice combination of cayenne + turmeric + clove + cinnamon + nutmeg (sometimes with chocolate or bergamot). They describe clear synergies: nutmeg increasing euphoria, turmeric prolonging effects and reducing anxiety, cayenne speeding onset and improving pain relief (while sometimes increasing anxiety), etc. Morning glory and HBWR seeds are explicitly listed as usable 5-HT2A sources in the same framework.

This made me rethink the old adduct idea. A lot of the same materials that people used for “aldehyde potentiation” are simply good TRP agonists. The change in effects may be coming from receptor-level interactions (5-HT2A + TRP) rather than a chemical adduct forming between LSA and the aldehyde.

That still left the question of wine, sherry, and other acetaldehyde-containing drinks, which many of us have noticed can also shift LSA in a similar stimulating/euphoric direction. Acetaldehyde itself is a documented TRPA1 agonist so it fits the same pattern without needing an adduct.

The notorious Isovaleraldehyde interacts with transient receptor potential (TRP) channels—primarily TRPA1 and TRPV1—acting as a chemical agonist that drives sensory irritancy, trigeminal pungency, and respiratory reflexes. reactive aldehydes like isovaleraldehyde typically interact with TRP channels via covalent protein modification

Other relevant points:

Garlic (allicin) has long been used for nausea with these seeds — it’s a TRP agonist.
Black pepper is a classic TRP agonist.
There’s an old report about mustard powder (allyl isothiocyanate is a strong TRPA1 agonist) producing more visual/LSD-like effects.
Cuminaldehyde (from cumin) is also a TRPA1 agonist.

I tested the idea with psilocybin: a packed 000 capsule of mushrooms (roughly 0.3–0.4 g) + 2 drops of peppermint oil. It produced the same kind of shift I used to get with LSA — noticeably more euphoric and stimulating, plus the candy-cane flavored burps.

I also suspect this framework explains a good chunk of the old “oilhuasca” / space-paste observations. Many of the classic space-paste ingredients (turmeric, black pepper, cinnamon, clove, cayenne, etc.) are exactly the TRP agonists the patent highlights. There are probably enzyme and absorption effects in the mix too, but the TRP angle seems like a big piece that was missing.

I did write this all myself but then used AI to touch it up. I am a drug using sasquatch, not an English professor.
 
We term that a 'genus patent application'.

Goodcap Pharmaceuticals Ltd is a 2019 startup and being able to claim 'patent pending' makes ignorant investors believe they will get the patent; which they won't.

You really do need to be deeply cynical when the goal isn't and never was to reduce human suffering but to take as much money from investors as possible.

I tell the story of Nutt offering us cash or shares (in Alcorelle) and without drawing breathe was said 'cash'. That was a decade ago, Alcorelle became GABA Laboratories BUT Alcorelle shares were diluted.

So we made the correct choice because now we know even as the offer was made, the goal was in essence to give us nothing.

If someone ever offers 'cash or shares' - take the cash. You can buy shares with cash BUT not the other way around.
 
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Not saying this is the magic bullet proven research... Just showing it as a promising alternative theory to the lsa adduct theory 😊 food for thought.

And I understand that must be a joke about me being tregar? Why would I post a bunch of research completely debunking the years of research and a whole book he has written 😆
 
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I think tregar is a touchy subject for some here, but it may cloud judgement at times given the strong emotional response :p

One suggestion is to repeat your experiment. I think if there is something to that adduct theory* -- and there may very well be something, considering multiple reports which are not all attributable to tregar -- it would be worthwhile to rule out placebo as an influence. Three experiences at the same dose, each with and without peppermint oil, self-blinded, could do the trick. Only unblind yourself after all 6 experiences have been made. I'm curious about replicating the findings after doing some more research about your hypothesis. 2C-D could be a nice basis for me. It is usually rather neutral, so if there is significantly more euphoria it could be a relevant finding. I'll just need to see how I go about the blinding. I am worried I may smell the peppermint through a gel cap and it may need to be absorbed on some inert carrier. I proposed this sort of experiment to tregar but it was only met with endless walls of text, oh, and have you already bought his book on how you can alter the experience to be like MESCALINE and LSD at the same time (the same he said about complexed NBOx, sketchy bufotenine extracts and what-not)??

* in terms of ketones/aldehydes/menthol etc altering the experience, which is not unthinkable, unlike the adducts for which there is, at least in my opinion, not a lot of basis

Edit: Just ate a cap of 70 mg menthol to see if unblinding would be an issue, no psychedelic. Feeling more comfortable somehow.
 
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The fact that acetaldehyde is a TRPA1 agonist is the piece that ties it all together. You don't need an adduct to explain wine or sherry changing the experience; the acetaldehyde is just hitting the same receptors as the spices. It's a much simpler explanation that fits the data better than the old chemical theory.
 
Hi, I just want to share my two cents as I didn't have a lot of knowledge about the science behind it.

I eat a lot of peppers and like to grow them so if I can say I'm experienced with the effect of capsaicin and there is an euphoria induced by it.

I never tried it with any psychedelic yet, but I will try it in my future experience as I have a lot of peppers from the season 😁

Not related but I remember eating high quality chocolate and feeling a surge of euphoria and my partner too, with a low dosage of 1cP-LSD (75ug)
 
Edit: Just ate a cap of 70 mg menthol to see if unblinding would be an issue, no psychedelic. Feeling more comfortable somehow.

Potentially it's a GABAA PAM:
Menthol acts via TRPM8 and TRPA1 channels and as a positive allosteric modulator of recombinant GABAA receptors.
...
These results suggest that menthol positively modulates both synaptic and extrasynaptic populations of GABAA receptors in native PAG neurons.
10.1111/bph.12602

BDNF/TrkB:
Antidepressant-like effects of L-menthol mediated by alleviating neuroinflammation and upregulating the BDNF/TrkB signaling pathway in subchronically lipopolysaccharide-exposed mice
10.1016/j.brainres.2023.148472

Potential influence on DA:
These observations indicated that after subcutaneous administration, l-menthol enhances dopamine-mediated neurotransmission, and activates neuronal activity in the dorsal striatum, thereby promoting motor activity in mice.
10.1371/journal.pone.0260713

Possible mGluR involvement:
Recent reports have recapitulated the requirement of central group II/III metabotropic glutamate receptors (mGluR) with endogenous κ-opioid signaling pathways for menthol analgesia.
10.3389/fnmol.2022.1006908
 
...some materials that people used for “aldehyde potentiation” are simply good TRP agonists.

Cuminaldehyde, anisaldehyde and citral also have TRP activity. Citral appears to have psychoactivity via other mechanisms (potentially serotonergic/cannabinoid) which could influence results.

Recently, it has been reported that anisaldehyde, tiglic aldehyde, and cuminaldehyde activate TRPA1.
10.2220/biomedres.46.51

Citral has been shown to act as a partial TRPV1, TRPV2, TRPV3, TRPM8, and TRPA1 channel agonist, and prolonged inhibition of TRPV1, TRPV2, TRPV3 and TRPM8 following their activation is considered an important pharmacological effect of this monoterpene
10.17179/excli2022-5042

Early paper mentioning citral:5-HT2A link (recent papers allude no 5-HT2A involvement):
Citral exerts antinociceptive effects in both eutrophic and obese mice, with enhanced efficacy in obese mice. Its action is mediated, at least in part, by CB2 receptor modulation
10.1016/j.ejphar.2026.178894

Citral-induced analgesia is associated with increased spinal serotonin, reduced spinal nociceptive signaling, and reduced systemic oxidative stress in arthritis
...
We assessed the levels of serotonin...and the profiles of expression of the glycogen synthase kinase-3β (GSK3β), which is a 5-HT-regulated intracellular protein...

Oral administration of citral reversed mechanical allodynia, increased endogenous spinal 5-HT levels, reduced spinal SAPK/JNK phosphorylation, and reduced plasma SOD levels.
10.1016/j.jep.2019.112486
 
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Why would I post a bunch of research completely debunking the years of research and a whole book he has written
Ima think... what a tregar would do... They're kind of hard to predict sometimes but the threads usually go like this.


1) Create a brand new schill account with zero comments on any other post
2) write anything about LSI and isoveraldehyde to get people's attention and stimulate conversation. Say things like "notorious isovaleraldehyde" to try and preestablish credibility even when the word "isovaleraldehyde" has probably never been mentioned in a single thread that does not have posts by tregar/allylbenzene/quantamide/or some suspiciouly new user that has only posted in that specific thread or other threads related to LSI.
3) have alterego allylbenzene swoop in to talk flawed SAR theories, TRP activity, procholinergic drugs and ADL and inhibitors or other gibberish or pseudoscience that has no basis in reality.
4) post giant walls of text when anyone disagrees or makes a valid point that contradicts the pseudoscience or direct reports personal experiences refuting the original post.


so far 3/4

It's a good thing allylbenzene has me blocked and can't see the comments I write. I doubt he'd appreciate that fact that I almost bought Tregars book off of amazon. I was going to have it delivered to some city's municipal dump knowing that Tregar/Matthew Stahl would personally see the address it's to be delivered to and that way I could also avoid the personal responsiblity of taking the book out of my mail box and walking over to and throwing it in the trash where it belongs. Better to just skip the middle part of the process. But then I decided I really didn't want fo financially support such a manipulative liar.
 
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Am I reading the same patent? 'Compositions for reducing inflammation to improve or maintain mental or physical health'?

Because it's only novel aspect is adding a psychedelic to a range of herbal medicines.

You would need to locate, read and understand supporting academic papers since patents be default provide the absolute minimum amount of detail.

I would wager £1 the REAL goal is the hope that a patent zombie will buy it up cheap and as you know, patent zombies just use legal process to halt the commercialization of someone else's work not because they think they are in the right, not even because they think they can win - but because tying a novel medication up in legal process for years just means it's cheaper for the true patent-holder to pay off said patent zombie.

Awful, isn't it?

But as I said, one has to view any and every patent with deep suspicion as we have now reached the point where those whose goal really IS to improve the lives of others is a tiny minority.
 
ddddigital said:
have alterego allylbenzene swoop in to talk flawed SAR theories, TRP activity, procholinergic drugs and ADL and inhibitors or other gibberish or pseudoscience that has no basis in reality

Your flawed theory was worth this comment, but at least get the enzymes right unless your goal was gibberish (which I'll let you get back to).

- ADH (oxidises alcohols)
- ALDH (oxidises aldehydes)

Interestingly, menthol has ALDH inhibitory activity:
Menthol or menthone, or both, like progesterone, have been shown to have the following biological activities: (i) an inhibitory action on liver and kidney aldehyde dehydrogenase activity

doi: 10.1126/science.132.3421.225

Kash from dmt-nexus always recommended combining LSA with peppermint & lemon juice (lemon is another ALDH inhibitor, ref). Intriguingly the ancient Greek Kykeon recipe includes Pennyroyal which contains 4+ ALDH inhibitors (eg pulegone: ref).

...the entire plant contains a variety of compounds including Pulegone, Isomenthone, Carvone, Menthofuran, Menthol, 1,8-Cineole, Piperitone, Piperitenone, Neomenthol, -humulene, and 3-octanol. Eriocitrin, Hesperidin, Narirutin, Luteolin, Isorhoifolin, Galic acid, Rosmarinic acid, Quercetin...

doi: 10.2174/1871530323666230914103731

Aside: info on the enzymes that produce acetaldehyde from ethanol consumption (CYP2E1 & catalase):
Within the cerebellum, ethanol (EtOH) is primarily metabolized through enzymatic pathways, with approximately 60% metabolized by catalase and 20% by CYP2E1. However, these proportions are not universal and may vary by species, ethanol concentration, and exposure paradigm. . This metabolic pattern differs from hepatic ethanol metabolism, where alcohol dehydrogenase (ADH) is the predominant first-step enzyme that oxidizes ethanol to acetaldehyde, followed by ALDH2-mediated conversion of acetaldehyde to acetate.

doi: 10.3390/ijms27156825
 
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unless your goal was gibberish.
GB2 receptor affinity xbox aldehyde dehygrogenase fumarate mescaline potentiates florida AND texas inhibitors!

It's like old times when I used to make a comment and get a reply from allylbenzene within minutes. I wonder if we'll get to see classic tregar altering prior comments or direct messages or his "wife's" little angry faces?
 
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Hmm. So far we only have 3 greenlighters commenting :( Tregar must have been preparing. But at least we had warning he was back from the social thread.

Apologies. It was worthwhile replying before setting him to 'ignore'. The beef is off the proverbial table.


Here (Paris) the flowers are still going. I see the occasional sage plant but there's a park not too far away with wild lavender growing. Unlike in summer when you used to hear them all the time, the green parrots have moved somewhere else (there's a bunch of these parrots that live in and around Paris, since several years apparently).
 
Well by all mean, provide hyperlinks to the supporting academic papers. Do you mean theory or in fact hypothesis, because a theory does at least have a weight of evidence and after a decade of research one tends to assume someone might provide something a little more well... vaguely related, if you see what I mean.

We tend to apply Hitchen's Razor.

You provide them and they WILL be read top-to-tail, not just the 'results' section as methodology matters.
 
Yes I have posted this because I think tregars "adduct theory" is wrong.

I believe these herbs are making a massive change to effects. But it don't think it's actually a chemical reaction with the adduct and amide causing it.

Also I wrote the "notorious isoveraldehyde" as a bit of a piss take.....
So.. are you saying that Tregar is completely full of shit? Because I don't see anything in your actual post that suggests that.
 
Everything is a drug if you look hard enough. I think you should look up the affinities for porridge, potatoes and beef.
"Yeah bob from Goodcap pharmaceuticals told me in a personal communication that beef is a very strong allosteric modulating mGluR7 triple inverse agonist but only when you complex it with paprika derived RAMEB cyclodextrin to form an adduct neutral zwitterion with potates while injecting anti malarial porridge to inhibit MAO-D inhibitors and mason jar oxidase.

It's obvious because of negative Ki values and it's distinct structural overlap from 5-Fluorotryptophan and 1-oxopork-elemicin. Dr. Miri Halperin from mindmed agrees with me.


Sources:
https://patents.google.com/patent/US7022007B2/en"

If it didn't feel like 6-chloro-2-bromo-TMA it's probably because you sourced low quality Tonkotsu Ramen. You can find quality here at this site that I have no financial links to:
https://www.tregar.com/orig.html"

I'm Allylbenzene/Tregar for halloween this year.
 
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