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Put together two packages (12kg and 15kg) of trichos and kanna for some members some of whom where kind enough to trade with me. Still have enough of trichos for two more packages to give away to members. See photos of what was included. I just go and randomly pick out examples from my collection. I wrap each one carboard to reduce any damage from the spines. If I know the cultivar I label it for you. I get a box from Bunnings and as many as I can fit in the box and for about $50 postage will cover most people - if you live further from Vic, then postage will be more. Sharing the love.

Allylbenzene is correct, it's the crushed seed shell fragments that cause nausea, follow the instructions in my book in Chapter 5, illustrated with pictures...we are leaving behind the nausea causing seed fragments from the HBWR seeds at the bottom of the shot glass, these dust like fragments STICK to the bottom of the shot glass and get throw away, 100% eliminating nausea and any side effects, as the 1oz everclear (95% grain alcohol spirit) contain the active alkaloids which we pour off into the brownie dish and evaporate the everclear (or other high proof alcohol you want to use) leaving behind the pure LSA extract which we then scrape up with two razor blades, add this pure LSA extract to 2oz water, pour in your 3g of AOJIRU young barley grass powder from the individual nitrogen sealed packet (come 46 to a box) and stir for 10 minutes using a magnetic stirrer (cheap from amazon) and consume for a profound psychedelic experience even better than LSD imho, like a combination of ALD-52 (anxiety free version of LSD also discovered by Dr. Hoffman) and mescaline combined, my absolute favorite psychedelic. I promise you even with 40 seed extract converted to LSI + LSV (equivalent to 160ug LSD) there are ZERO side effects, no nausea, cramping or vasoconstriction at all, complete infinite euphoric psychedelic bliss for the entire night: 8 strong hours with 10 hour duration. I hear your concern flame_assay, you can do as Allylbenzene states above, or do what I did in the very beginning: -->I started out with just 5 seeds and noticed it felt about like 20ug LSD, then I went up to 25 seeds which felt like (25 x .04mg per seed) = 100ug LSD, then I moved up to 30 seeds which felt exactly like (30 x .04mg LSA per seed ) = 120ug LSD, then I moved up to 40 seeds (40 x .04mg LSA per seed) = 160ug LSD. This may help you to feel more comfortable, see here how Kash (very well respected, author of the LSA extract TEK) used up to 40 seeds: Kash said in the thread “Kash’s advanced LSA extraction” back in 2012: Kash's Advanced LSA Extraction - LSD, LSA, LSH - Welcome to the DMT-Nexus Kash is correct, in that if the LSA is not mixed with 3grams of the Aojiru 100% Japan domestic grown young barley grass powder, the experience is just like your typical LSA experience: uncomfortable and sedating with no visuals. LSI and LSV are stimulating and VERY POTENT psychedelics on the other hand. Don't use peppermint oil as it contains 100 times less isovaleraldehyde as barley, always use AOJIRU barley, it comes in 3grams nitrogen sealed packs. Just snip open the pack and pour it into your 2oz (60ml water) with the LSA extract, spin for 10 minutes, and consume. Keep in mind, we are extracting PURE LSA from the HBWR seeds, then converting it to LSI + LSV (main alkaloids) in record time in 3 super simple steps. There is ZERO or no side effects, as we are leaving the nausea causing seed pulp behind at the bottom of the shot glass, which gets thrown away. For decades, people have been consuming the whole seeds crushed, which is the wrong way, as the seed pulp is what is nauseating and has side effects galore, the pure LSA has none of this at all, just like Kash notes above. Start off with just 5 seeds if you want, just as I did....I was cautious just like you in the beginning. I have taken 40 seeds (equivalent to 160ug of LSD) x twice now, spaced 1 month apart, and she is my all time favorite psychedelic, that I will respect for the rest of my life: She is even better than LSD imho: No anxiety, hours and hours of closed eye colored visions just like LSD, extreme mescaline like euphoria all night, just as colorful and music enhancing as mescaline, tracers as powerful as lightning strikes, whereas LSD can have choppy visuals, the visuals are flowing with LSI, continuous diamond like shimmering of all visuals, LSI is the most bad ass psychedelic equal to mescaline and Ayahuasca that I've ever had the pleasure of trying, yes, she is that good, and she is super cheap to make, with no nastiness to the 2oz brew, down in 2 gulps. As there is zero or no anxiety with LSI + LSV, I plan on even taking her at 40 seed dose converted to LSI + LSV and walk down the street and trip all morning and early afternoon long at one of the world's largest waterparks, which we live down the street from. I know this will be absolutely incredible! As I used to take zero nausea bridgesii cactus tea at least 20 times at the waterpark. This LSI + LSV is just as incredible as mescaline, my other all time favorite psychedelic. From 2.1.2026: Read the last few sample pages from ebook to learn of the dozen bad ass psychedelic effects from LSI + LSV: Amazon.com --> Remember, even though LSI + LSV is stimulating just like LSD, it's way easier to fall asleep on than after LSD, I can take LSI + LSV 2oz brew at 3pm, and be able to fall asleep at midnight, whereas with LSD, I would still be up till 3 or 4am in the morning, a huge benefit to this very powerful no anxiety LSI + LSV Sacred ancient Elixir <-- Search amazon for "LSD", the book has been in the #1 spot for weeks now, with over 60 copies sold in 1 month, which is good as I will be able to make sizeable donations here to hip forums every 3 months to help support its operation. Don't forget my interview with Dr. Mckenna goes up in just a few days: Podcast McKenna Academy of Natural Philosophy | Archives perpetualdawn said: 1-s2.0-S2212429222000074-main-2.pdf 3.29MB 41 downloads Assessing the product quality and biological activities of barley Hordeum vulgare L grasses at different harvest times, 2022, see PAGE 5, ALDEHYDE TABLE: Isovaleraldehyde, Valeraldehyde & Crotonaldehyde levels eclipse the levels of the other 10 aldehydes in young barley, resulting in a triple action LSI, LSV and LSCr experience when simulating the Eleusis Kykeon. Aldehydes strongest at Z21 young growth stage: Propionaldehyde = 2.18 Isobutyraldehyde = 1.41 Butyraldehyde = 0.69 2-methylbutyraldehyde = 2.28 → Isovaleraldehyde or Butanal = 7.52 (converts LSA to LSI) Hexanal = 3.73 Trans-2-hexenal = 1.60 Trans-2,4-heptadienal = 1.17 Benzaldehyde = 1.12 2,6,6-trimethyl-1-cyclohexene-1-carboxaldehyde .3 → Valeraldehyde = 13.40 (converts LSA to LSV) → Crotonaldehyde or 2-Butenal = 7.63 (converts LSA to LSCr) 2-hexenal = 1.39 The levels of isovaleraldehyde in AOJIRU young barley grass powder is x100 (one hundred times) the levels found in peppermint, which is what we need (these super strong levels of these 3 aldehydes to form LSI + LSV + LSCr) for a profound triple psychedelic action when the 2oz Sacred Psychedelic Elixir is consumed. Last edited: Yesterday at 7:54 AM

Consider this a no-reserve auction. Whoever bids highest will receive this splendid Jourdaniana graft (on PC rootstock). All proceeds will be donated to offset the costs of Corroboree website/forum maintenance. Auction is open for bids until the end of next week (April 18). Please indicate below how much you're willing to pay for this fine specimen. * Flower is indicative only, from a comparable grafted specimen. Props to Trip for the mother of all scions!

$150 - For an absolutely awesome cause. It might go up depending on what i can scrounge up 😝 (hope that's OK if I double post..) absolute beauty

More's the reason to rehabilitate this humble forum. It'd be a shame to lose it.

It was pretty rad, well worth the trip, although I forgot my glasses so I had to squint. I didn’t take many photos

Hi all, The content of this post is going to be blaringly obvious to most people but I thought it was worth sharing my method of cloning B. caapi. I worry about my caapi for no particular reason so I take cuttings when I can. I had one not doing too good in early winter so I turned it into a number of cuttings. I took sections of 15 - 20cm, soaked the ends in Clonex (Hardwood 8g/L IBA) for approx. 5 mins and stuck them in a small plastic pot of moistened potting mix. I then put this pot into a round take away container and taped a ziplock bag around the whole thing to ensure humidity. I also had one cutting in a tube stock put hanging up in a ziplock bag. This worked great! The first thing I noticed was fungi growing from the tips of the cuttings but this quickly died out. As roots started to grow out of the pot and into the bottom container and leaves appeared I started to cut holes into the plastic bag to hardening them off. This was inside with no direct sun during a Sydney winter. Eventually I removed the bag all together and watered with a dilute seaweed fertiliser (OCP Eco-seaweed) to encourage root growth. Keeping the plants away from direct sun. After most of the plants had 2 sets of leaves I separated them into tube stock and they went outside! They looks great! Throughout the whole experiment I realised the best cuttings were the largest. Fastest to root and put out leaves etc Cheers all!! God bless rooting hormone

If anyone has input, feel free to comment. I was asked a question on what is the current view on differences between pachanoi vs bridgesii etc that impacts differing medicinal potency, if mescaline % is alone not always enough to deduce it. There's been a long-standing notion that there may be MAOI active phytochemicals that impact potency and this seems to be the current view in the literature? AI generated this viewpoint for me: Bridgesii: May contain higher levels of anhalonidine and hordenine, contributing to its sharper onset and intensity. Pachanoi: Often richer in simple phenolic PEAs, which may influence mood and cardiovascular response. On a more extensive level, some broader phytochemistry: Some alkaloids in Cactaceae: Particularly considering findings by Ogunbodede et. al. who hypothesised 'the cacti with the highest mescaline tissue concentrations would be more likely to be used in shamanic practice' but noted some analytical findings which dispute mesc. % as being the sole determinant of relative potency, such as a comparatively low level in TBM - E. lageniformis (monstrose) [0.48% of dry weight of cactus tissue], despite wide-spread consensus it's potently active, vs E. scopulicola [0.85% % of dry weight of cactus tissue], with some saying ones probably belonging into the range of the species Trichocereus scopulicola, like cordobensis, generally not even being worth exploration. I did some extra research and found a new book which explores this topic in some chapters and I found to be a very interesting read - Comprehensive Guide to Hallucinogenic Plants (2025) It took a long time to track down online but eventually found it - I won't upload pdf to forums but if you can't find it, message me and I'll send it through. Trichocereus/Echinopsis May contain things like mescaline, tyramine, 3-methoxytyramine, 3,4-dimethoxyphenylethylamine, 3,5-dimethoxy-4-hydroxy-phenylethylamine and anhalonidine etc. The book mentions: Pachanoid acid – enhances serotonin signaling Flavonoids – antioxidant and anti- inflammatory effects Kaempferol Quercetin Betalains (generally in coloured parts) – antioxidant nitrogenous pigments Sterols like ergosterol – antimicrobial effects Others: Triterpenes bridgesigenins A and B, along with aglycones The combination of alkaloids, lignans, and other compounds contributes to the psychotropic potency and medicinal properties. The phytochemistry varies between different samples and growth conditions (Moreno- Pedraza et al., 2019). Mescaline: The forgotten psychedelic Mescaline binds with a low μmolar affinity to the serotonin 5HT1A/2A/2B/2C, adrenergic, dopamine D1/2/3 and TAAR1 (trace amine-associated receptor 1 that regulates dopamine, noradrenaline, and serotonin neurotransmission) receptors. Mescaline also binds to the dopamine (DAT), norepinephrine (NET), and serotonin (SERT) transporters but with lower affinity At high doses, it potentially leads to an increase in the release and/or reuptake of serotonin (dos Santos et al., 2016; Freedman et al., 1970), although this is not proven. The nature of the psychoactive effects may be modulated by, among other things: Adrenergic α1A and α2A receptors may modulate the pharmacodynamics, together with broad serotonergic receptor activation. 5-HT2A vs 5-HT1A selectivity 5-HT2A vs 5-HT2C selectivity, etc 5-HT2A/2C interactions are not the only factors that influence potency in humans and pharmacokinetics may potentially have a significant impact on in vivo effects. Namely, interactions with other monoamine receptors, lipophilicity, receptor activation, functional selectivity, and metabolism via cytochrome P450 enzymes or amine oxidases could also play a role. The characteristic effects of mescaline in animal studies are not only mediated via serotonergic and noradrenergic receptors but also via dopamine receptors, as pre-treatment with low doses of either serotonin or dopamine antagonists almost completely blocked the effects of mescaline From the book earlier: In addition to mescaline, Trichocereus contains other phenethylamine and tetrahydroisoquinoline alkaloids such as tyramine, hordenine, 3-methoxytyramine, anhalamine, anhalinine, anhalonidine, and anhalidine (Ogunbodede et al., 2010). Some of these compounds act as MAO inhibitors and enhance or prolong the effects of mescaline (Kapadia & Fayez, 1970). Anhalonidine also shows activity at 5-HT2A receptors (Pardanani et al., 1977) [? is this correct]. More recently, it has been described as to act as a potent inverse agonist of the serotonin 5-HT7 receptor Small phenolic alkaloids may impact the resultant mood effects, or add peripheral side-effects: Tyramine was unable to cross the blood-brain barrier, resulting in only non-psychoactive peripheral sympathomimetic effects Hordenine has significant pharmacological activity and is used by some as a psychostimulant at low doses, including in the nootropic community. The sympathomimetic effect of hordenine is based on its structural similarity to various neurotransmitters (dopamine and adrenaline) and potentially has activity as a competitive MAOI substrate, more selective to MAO-B. It results in high blood pressure, and it also increases respiratory and cardiac functions (Frank et al. 1990). Inhibited noradrenaline uptake and stimulated noradrenaline release. Hordenine is a low-potency D2 dopamine receptor agonist and "might contribute to the mood elevating properties". Resembles both adrenaline and nicotine in activity 3-methoxytyramine is a neuromodulator that can exert physiological actions, partially via activating TAAR1. While likely rapidly degraded normally, concentrations increased notably by inhibiting MAO N-methylmescaline, although less potent than the parent alkaloid, may modulate the effect. 3,4-dimethoxyphenethylamine occurs naturally along with mescaline in various species of cacti. Said to potentially modulate the effect of other alkaloids. DMPEA has activity as a MAOI along with its naturally occurring N-methylated homologs see: https://doi.org/10.1002/jps.2600660741, it seems to produce no notable effects when tested even with very high doses, such as 1,000 mg orally Trichocereine (N,N-dimethylmescaline) in one study at 9 mg/kg orally (630 mg for a 70-kg person) was found to produce no notable mental disturbances in humans but others have noted potential psychoactivity eg @ 400 mg sublingually and reported that it produced moderate psychedelic effects with a one-hour onset (compared to two hours for mescaline) and a "proportionally shorter" duration and at doses of up to 800 mg (presumably orally), being less active than mescaline . In animals, produced marked excitation similar to that induced by amphetamine. [note: pharmacologically, for psychedelic activity: phenethylamines generally cannot tolerate even a single N-substitution, with the exception of derivatives like N-2-methoxybenzyl etc, which increases activity. Small groups such as N-methyl or ethyl abolish 5-HT2A activity.]. Trichocereine may have actions through monoamine transporters rather than receptors. Reported as the major component of the mescaline-containing cactus Trichocereus terscheckii The beta-hydroxylated macromerine, found in some cacti, is classified as psychoactive but not significantly MAOI inhibitory MMDPEA, with empathogenic-like action, is a minor alkaloid potentially found in cacti. It resulted in a peaceful elevation of mood, euphoria, enhancement of visual perception, and the generation of closed-eye mental imagery. At dosages above 300 mg, visual distortions that resemble those of standard doses of mescaline are said to begin to appear. Removal of the 5-methoxy group from mescaline caused about a 50% loss of previous activity, while demethylation of the 4- methoxy group resulted in a complete loss of all conventional activity. It is not clear how it's binding profile/pharmacological activity is altered by such A polar moiety such as a OH on the 4-position gives compounds with very low 5-HT2A affinity, probably in part through decreases in the overall hydrophobicity of the molecule, preventing it partitioning into the central nervous system The fairly potent MAO-A inhibitory action of carnegine suggests that this and similar alkaloids, if present in a cactus or one of its extracts, might potentiate the effects of mescaline. Candicine also penetrates a blood-brain barrier model and seems to have nicotine-like effects Coryneine stimulates acts like a weak D1 (or D1 + D5) dopamine receptor partial agonist but may not reach the CNS effectively THIQs - mildly psychoactive - calming /sedative Phenolic tetrahydroisoquinolines peyotline and anhalonidine were found to produce no sensory distortions, characteristic of the effects of mescaline, at doses of up to 250 mg. These compounds appear to induce a calming or sedative effect. Two methylenedioxy tetrahydroisoquinolines, lophophorine and anhalonine, were also found to lack any mescaline-like effects. Pellotine has sedative/hypnotic like effects. Trials note delayed onset (30–45 minutes post-administration) due to slow BBB penetration. Lophophora It can be concluded that the more than 60 alkaloids of Lophophora williamsii, in combination, exert the total psychopharmacological effect Peyote constituents: chemistry, biogenesis, and biological effects https://doi.org/10.1002/jps.2600591202 Things like L. diffusa contain higher amounts of tetrahydroisoquinolines like pellotine pellotine is the main abundant alkaloid (86.2%) in L. diffusa followed by anhalonidine (3.8%) and mescaline (1.2%) while contains zero to trace amounts of hordenine, anhalinine, and lophophine by using available limited literature studies. Pellotine is the inverse agonist for 5-HT7 receptor with an EC50 of 291 nM. Pellotine exhibits good affinity to 5-HT1DR and 5-HT6R with K of 117 nM and 170 nM. Pellotine reduces intracellular cAMP levels, thereby reducing neuronal excitability and neurotransmitter release.

The love of money is the root of all kinds of evil.

i think the problem is the same with most circles of people. When you're looking in from the outside the noisiest people are heard first. They're not always a good representative of the whole demographic; you might have to dig a little more to find the people that are genuine and humble

I'm not sure what circles you're mixing in there but this is absolutely the opposite of my experience. Try getting along to an APS event would be my best advice for a start. https://www.psychedelicsociety.org.au/ And "Drug Bros"? There are quite a few sisters about too, so again, maybe you've just been at the wrong events. EGA - another great org and more specifically plant orientated: https://www.entheogenesis.org/ I'm not saying the type of person you describe does not exist, but i'd say "very rarely" instead of "very often".

Congratulations and thanks to misteek, thanks also to Starward and Trip and everyone else who supported this.

Saguaro said: Yes! Micromegas said: Thanks for the kind words Micromegas. I would love to contribute to this valuable site to keep her running forever, which I plan to do once every 3 months. Search my user name to see that I contributed many years ago on subject Myristicin. Alchemica said: Nice research there Alchemica, yes I wrote the paper at reddit you dug up there ages ago with the pics of LSA and LSH. I write about my earlier discovery of LSH in the book, however LSI is WAY, WAY, WAY beyond LSH. LSI is like a combination of ALD-52 (anxiety free version of LSD also discovered by Dr. Hoffman) combined with mescaline, just as powerful as LSD but no anxiety! I love, love, love her! I can feel this extra carbon donated from isovaleraldehyde and valeraldehyde are hitting all the extra adrenal receptors (A2A, A2B, A2C) and beyond that mescaline and DMT both hit with great strength, while LSD only hits one adrenal receptor (A2A). No other herb on the planet has this magnificent very high levels of all 3 aldehydes forming LSI, LSV, and LSCr for a triple psychedelic combo that feels exactly like a combo of ALD-52 and mescaline at the same time to me. LSI is forming from LSA + isovaleraldehyde with stirring at ph=4, but is also forming in the liver via an in-vivo condensation reaction, isovaleraldehyde is an aldehyde, these aldehydes are attracted to the "NH" amide of LSA like a magnet, and condense onto LSA forming LSI or Lysergic Acid Isovaleraldamide, where it reaches the brain from the liver. Under specific acidic conditions involving catalysts to speed up the reaction, chemists can force amides and aldehydes to form new condensation products. Aldehydes and the N-H group of amides such as our LSA are attracted to each other primarily through hydrogen bonding and dipole-dipole interactions. These intermolecular forces influence the physical properties and potential chemical reactions between the two types of molecules. In the 1992 paper titled "Tryptophan analogues form adducts by cooperative reaction with aldehydes and alcohols or with aldehydes alone: Possible role in ethanol toxicity," researchers James E. Austin and Heinz Fraenkel-Conrat demonstrated that while some tryptophan analogues require both an aldehyde and an alcohol to form stable adducts, others—specifically unsubstituted indole (our LSA)—can form adducts with aldehydes alone in vivo (in the liver) or with stirring in acidified water to form LSI, LSV and LSCr. pnas01092-0040.pdf Yes, since LSA from the HBWR seeds (makes up 83% of the seed alkaloids) is an indole ergoline, it easily forms adducts WITHOUT THE USE OF ALCOHOL with isovaleraldehyde, valeraldehyde, and crotonaldehyde to form LSI + LSV + LSCr. No alcohol is required when forming adducts with indole, just incubation or stirring in acidified water for 10 minutes (hence the use of the cheap magnetic stirrer from amazon). My brew is 60ml (2oz) and is non-alcoholic, no nastiness to the brew, just a slight herbal taste from the 3grams of Aojiru young barley grass powder (available worldwide from amazon or auction or stores) which supplies the 3 aldehydes in sky high amounts, which is what we need to form LSI + LSV + LSCr, for a triple psychedelic action when the Sacred Elixir is consumed. My discovery (isovaleraldehyde) and Dr. Nichol's discovery (3-aminopentane) are both extremely similar, see how Dr. Nichol's has a paper on line about his discovery called "LSD and it's Lysergamide Cousins" from the Heffter institute, link below. My discovery of isovaleraldehyde relates directly to Dr. Nichols discovery: 1) This aldehyde: isovaleraldehyde discovery that works has 5 carbon groups and 11 hydrogens just like 3-aminopentane which was found by Dr. Nichols to have activity very similar to LSD in the rat assays, as the rats reacted to it as if they had been given LSD. Anything beyond this, like cinnamaldehyde with a very high molecular weight has way too many carbons and hydrogens (almost double) and will result in weak effects, as it does not fit into the receptor. 2) The important thing to note from the Dr. Nichol's table, in the far right column, is the fact that LSD has a potency in rats in the drug discrimination behavioral assay of 48 nanomoles per kilogram of rat body weight. Only two other compounds have comparable activity: entries 6 and 16. Entry 16 is 3-aminopentane, and has a potency in rats in the drug discrimination behavioral assay of 52 nanomoles per kilogram of rat body weight. 3) Isovaleraldehyde looks identical to the tail end of DMT and psilocin once it condenses onto the amide (NH) of LSA with the exact same number of carbons and hydrogens with the same chemical formula of CHO CH2 CH2 2(CH3). 4) BOTH have exact same molecular weights of 87 similar to diethylamine molecular weight of LSD at 73g/mol. See table 3, entry 16 for 3-aminopentane which is extremely similar to my discovery of the aldehyde: isovaleraldehyde and valeraldehyde in young barley grass: chap6.pdf I promise everyone, this LSI + LSV + LSCr is the most incredible psychedelic that I plan to respect once a month for the rest of my life, she is absolutely incredible: I have taken 40 seeds (equivalent to 160ug of LSD) x twice now, spaced 1 month apart, and she is my all time favorite psychedelic, that I will respect for the rest of my life: She is even better than LSD imho: No anxiety, hours and hours of closed eye colored visions just like LSD, extreme mescaline like euphoria all night, just as colorful and music enhancing as mescaline, tracers as powerful as lightning strikes, whereas LSD can have choppy visuals, the visuals are flowing with LSI, continuous diamond like shimmering of all visuals, LSI is the most bad ass psychedelic equal to mescaline and Ayahuasca that I've ever had the pleasure of trying, yes, she is that good, and she is super cheap to make, with no nastiness to the 2oz brew, down in 2 gulps. As there is zero or no anxiety with LSI + LSV, I plan on even taking her at 40 seed dose converted to LSI + LSV and walk down the street and trip all morning and early afternoon long at one of the world's largest waterparks, which we live down the street from. I know this will be absolutely incredible! As I used to take zero nausea bridgesii cactus tea at least 20 times at the waterpark. This LSI + LSV is just as incredible as mescaline, my other all time favorite psychedelic. -->I started out with just 5 seeds converted to LSI + LSV + LSCr and noticed it felt about like 20ug LSD, then I went up to 25 seeds which felt like (25 x .04mg per seed) = 100ug LSD, then I moved up to 30 seeds which felt exactly like (30 x .04mg LSA per seed ) = 120ug LSD, then I moved up to 40 seeds (40 x .04mg LSA per seed) = 160ug LSD. Wachumacallit said: The authentic argyreia nervosa seeds can be smaller like the ones I use from Hawaii (a mix of black and brown color) or bigger and rounder and tan in color like the ones from India where they originate. I have tried both of them, and they both work exact same in the recipe. If using the bigger India round seeds, just count them out similar to the way I count them out in Chapter 5 of the book, with illustrated pictures. My publisher is Sacred Forest Botanicals, see their trademark copyright logo on 1st page of book when viewing sample of book on-line. Starward said: Thanks Starward for kind words. Search the USA Amazon for "LSD", the paperback and very inexpensive kindle (opens on a phone or pc with the free kindle app) are consistently in the #1 or #2 best selling book under "LSD" search. I highly recommend getting the kindle or paperback before it could possibly one day get banned in Australia like Starward mentioned. Au herbalistics has 5g (50 seed) and 10g (100 seed) for growing purposes, I have searched and located a few botanicals in Australia that offer the seeds for growing. All of the psychedelic discoveries in the book (5 of them) were given to me by an ancient dead Aztec Shaman who visited me for 20 minutes during a profound very high dose LSD trip around 20 years ago. I take no credit for these discoveries, as they all originated from the Shaman in the Spirit world, this is all recounted in Chapter 1 of the book "Shaman on the Wall". I have had 5 near death experiences in my life, and after each one of these profound very close encounters with death, a discovery he gave to me would rise to the front of my consciousness in detail in the form of a vision, all recounted in Chapter 1. The Shaman uses my chemical background to "expose" these discoveries to the rest of the world. We may only have 50 years left on this planet before earth's population takes a serious nosedive due to extreme climate disasters and events, there is way too much carbon in the atmosphere, and no way to remove it. My Interview with Dr. Mckenna (Terrence Mckenna's older brother) goes up around Valentines day Feb 14: Podcast McKenna Academy of Natural Philosophy | Archives New paper on LSI goes up at Graham Hancock's site in month: The Official Graham Hancock Website - Graham Hancock Official Website Attached scientific papers backing up my discovery of LSI, LSV and LSCr, several more papers backing up discovery in the book. Notice last paper from School of Health Sciences, University of South Australia. Just remember that cinnamaldehyde from the paper has too many carbons and hydrogens for it to work: 1) This aldehyde: isovaleraldehyde discovery that works has 5 carbon groups and 11 hydrogens just like 3-aminopentane which was found by Dr. Nichols to have activity very similar to LSD in the rat assays, as the rats reacted to it as if they had been given LSD. Anything beyond this, like cinnamaldehyde with a very high molecular weight has way too many carbons and hydrogens (almost double) and will result in weak effects, as it does not fit into the receptor. But pay close attention to reference 6: [6] Mehra, R. K., & Pandya, K. C. (1938). The condensation of aldehydes with amides - Part II. The condensation of cinnamaldehyde. Proc Natl Acad Sci India - Phys Sci, 7(6), 376-380. The 3 super simple steps from HBWR seeds to LSI + LSV + LSCr are illustrated with pictures and full trip reports in Chapter 5 of my book: LSI, Ancient LSD, Secret of the Eleusis Kykeon and Vedic SOMA eBook : Stahl, Matthew : Amazon.com.au: Kindle Store In the USA, we are able to purchase 400 seeds very cheap (around the price of a few movie tickets) from various botanicals for growing. As mentioned in post #4, we absolutely love Australia and the people, the friendliest and most gorgeous people, beaches & nature in the world. My beautiful wife and I constantly watch Australian TV and movies on Netflix and 4k walking of Australia on you tube. I am a former beach and deep water waterpark lifeguard, so you know I love your beaches. pnas01092-0040.pdf 1-s2.0-S2212429222000074-main-2 (34).pdf chap6.pdf Paper+1+(2022.1.1)+The+Theoretical+Synthesis+and+in+silico+Modelling+of+Lysergic+Acid+Biscinnamylidene+Amide+from+the+Adduct+Formation+of+d-Lysergic (1).pdf

A psychiatrist asked me about this very concept after it was mentioned to him and below was my reply. We're on the same page for the gist of it @tregar ? "Yeah the concept of adding aldehydes to enhance the potency of LSAs has been a fringe thing for a long time. Even things as wild add peppermint to condense with the LSAs before consuming etc etc. It's not all totally without some slight merit It's been proposed that the LSH and LSA (LSA is actually a decomposition product of LSH in the seeds) is converting to the 1-aldehyde condensation products (with the bottom of the NH group on the indole), see my sketch. "For 2 decades people have been thinking that LSA is turning into LSH, but no such thing can happen without a catalysts and long chemical procedure." I'd agree that in my mind, it's probably not likely the -CONHR amide at the top of the LSA molecule is being modified to give new amides that are more active, rather something simpler? The amides that are already formed in the seeds are unlikely to undergo chemical reactions at that -CON- region simply by adding an aldehyde The formation of condensation products (such as the aldimine) at the 1-indolic N position seems to occur on structurally related molecules and one could speculate that these substitutions could impact potency, compare to ALD-52/1P-LSD etc if they are stable. It's been studied on simple tryptophan derivatives like indole-3-acetic acid, IAA in: "Tryptophan analogues form adducts by cooperative reaction with aldehydes and alcohols or with aldehydes alone: Possible role in ethanol toxicity" https://www.pnas.org/doi/epdf/10.1073/pnas.89.18.8439 "...condensation with the primary aldehyde took place, followed by that with the alcohol to produce stable derivatives" IAA + CH3CHO (acetaldehyde) --> IAA>N-CH(CH3)-OH (indole N- 1-substituted aldimine) Thing is, these compounds are quite unstable and hydrolyse easily and would probably rapidly be destroyed in vivo but the N-acyl hemiaminal in combination with an alcohol might be more stable. On adding ethanol, a stable derivative could be formed: IAA>N-CH(CH3)-O-C2H5 Tryptophan analogues require both an aldehyde and an alcohol to form stable adducts. LSA is an ergoline alkaloid with an indole structure as its core, and aldehydes (such as isovaleraldehyde, valeraldehyde, and crotonaldehyde) could possibly form a stable adduct with LSA in vivo via a simple condensation reaction forming LSI, LSV, and LSCRr etc See more: https://www.reddit.com/r/LSD/comments/hkieqc/alchemy_conversion_of_lsh_lsa_in_morning_glory_to/ https://www.bluelight.org/community/threads/lsi-ancient-lsd-secret-of-the-eleusis-kykeon-and-vedic-soma.950819/

I have a theory around psychedelics and tinnitus. Interesting I quick search turned up a few planned or theoretical research on possible benefits of psychedelics and tinnitus. I have tinnitus, which for those who do not know is a clicking, ringing or zapping sound. You might develop tinnitus symptoms from being exposed to loud noise or medication. The basic explanation for tinnitus is hearing loss. The fine hair in the cochlear are damaged and no longer convert vibration from sound into neural signal. In a response to this drop in input coming into the brain, some brains respond by produce these phantom tinnitus sounds. The issue is that tinnitus can become debilitating, destroying sleep and it is linked to cognitive decline, and dementia. In essence tinnitus is a problem not with the hearing per say but with the brain, mall-adaptive response, that some people with hearing loss experience but not all. Therefor treatment should focus on the brain rather the ear, which is where most tinnitus treatments focus their efforts. Knowing this it made me notice that during a psychedelic experience, that my tinnitus, faded in intensity, also the perception of the sound within my brain seems to change location. Also post dosing there has been a significant improvement in my tinnitus symptoms. I would like to propose a spit balling theory, that the increase in neural connections between different regions of the brain during psychedelics, compensates for the lack of signal from the cochlear thereby reducing the perception of tinnitus. Thoughts opinions? Has anyone else noticed improvements in their tinnitus due to psychedelics?

Very Interesting, I cannot wait for other to replicated your method. If it turns out to be verified by others, @tregar would have contributed significantly to resolving two great mysteries in psychedelic history. And shortly afterwards to having your book banned by the government, under new emergency legislation.

FREE Cuttings - Downsizing Tricho Cactus Cultivars Available For Free or Trade. With over 200 cacti from seedlings to full grown samples. I am certain to have something of interest the connoisseur or those just starting out. A small sample of my collection includes: Eileen, J30 OP, NZ Timewarp OP, Psycho0, Yowie, Sir Jean, Rosei 2, Hoffs 3", Jada, Shark XXXX, Foolsbreath, Ogen, Monstrose, Crested, Super Pedro, Dr Funkenstein, Matucana and many more interesting cultivar crosses as well as no-label Pachanoi, Bridgesii and Peruvianus. Message me for further details. Just pay postage, and they are yours.

https://ebay.us/m/wnDZMq

Thought I's share this trip report as it's science-y without as much of the over-complication that often comes with the published literature Longevity expert, Bryan Johnson released the full date of his mushroom trip and the effects of psilocybin on his brain: "First mushroom trip data is out: my brain activity. Dose: 5 g dried Psilocybe cubensis (B+ strain) Containing 24.9 mg psilocybin Psilocybin longevity experiment. What we see in the brain: + brain activity data mirror my subjective experience + strong decrease in my brain’s control center (prefrontal + premotor cortex) + strong increase in sensory, auditory and speech integration + higher entropic brain patterns: open, flexible, less predictable, exploratory + brain network patterns resembling a youthful state vs aged and rigid Matching what I reported experiencing: + “felt like my consciousness was dialed up to 10/10.” + “I felt hyper aware and hyper alive.” + “I experienced sense of touch with awe.” + “my mind was insatiably curious and wanted to deploy its sensors into the world and discover all things.” + “My brain wanted to stare, study and marvel.” + “The flavor exploded in my mouth.” + “...restored my perception to youthful levels, returning them to factory settings and dissolving my aged numbness.” Why this could matter for longevity: + In people aged 65-85, higher happiness was linked to a 22% reduced risk of all-cause mortality over 15 years. + A meta-analysis showed that optimism correlated with a 35% decrease in heart attacks and a 16% decrease in all-cause mortality. + Having a strong purpose in life is associated with a 17% reduction in both heart attacks and all-cause mortality. + In psychedelic medicine, treating depression with ketamine has been shown to reverse biological age by up to 3 years. Together, these findings suggest a plausible mechanism by which psychedelics, including psilocybin, can prolong both health and lifespan by improving mental well-being and rewiring the brain to a more positive, creative, and curious state. My team and I hypothesized that neuroplasticity, the loosening of rigid inhibitory patterns that makes the brain more flexible, creative, and relaxed, and even the subjective psychedelic state itself may be as meaningful for longevity as methylation shifts, senescence reversal, or telomere biology. What’s happening mechanistically Earlier work shows that psilocin (the active metabolite of psilocybin) acts primarily as an agonist at 5-HT₂A serotonin receptors in the cortex. These receptors are especially dense in high-level association and sensory regions, as mapped in a high-resolution PET/MRI atlas of the human serotonin system. When these receptors are activated, brain imaging studies show an induced state of desynchronization, entropy, and neuroplasticity. This process erodes the rigid brain hierarchy and default mode networks in favor of a brain-wide spontaneous, creative, curious, and child-like state. Kernel Flow data shows the same pattern: The recorded timepoints included: + baseline: directly before session start (not shown) + timepoint 1: 4 hrs after dose (acute phase effects). + timepoint 2: end of the day, before bedtime. + timepoint 3: the following morning. I continue to measure my brain daily. Image notes + The three maps show changes vs. baseline (not absolute activity) + Red = increased connectivity, blue = decreased connectivity vs. my baseline. + The left reference map shows the 5-HT₂A receptor distribution from PET, the main psilocybin target. Time Point 1 - 3 hrs post dose + Reduced connectivity in the prefrontal and premotor cortex, correlating with acute brain desynchronization. + Increased connectivity and hyperintegration between the primary motor and sensory cortex regions. + Enhanced connectivity in the auditory and speech areas of the cortex. + Inhibited connectivity in the medial prefrontal and posterior zones, areas associated with the Default Mode Network (DMN). Subjective experience: + Enhanced sensory vividness and bodily presence: The brain's top-down hierarchy, originating in the pre-frontal cortex, was attenuated. This reduced predictive filtering, leading to a flood of bottom-up sensory information and heightened bodily perception (e.g., a fascination with water and light dynamics in a jar, a restored, primal joy of touch and sensation). + Peak neuroplasticity and cortical entropy: A peak in cortical entropy and neuroplasticity contributed to a feeling of hyperawareness (e.g., heightened sensory perception, feeling "at one with existence," hyper-aware and hyper-alive). + Deeper appreciation of music and uninhibited movement and expression: Sharpened auditory senses and reduced top-down inhibition allowed music to be enjoyed on a profound level. Concomitant functional connectivity in speech-motor and auditory-motor integration areas facilitated uninhibited expression through both speech and movement (a restored, uninhibited, child-like joy of music). + Note: Full ego dissolution was not experienced, which may necessitate a higher dose to achieve more advanced desynchronization of the prefrontal and parietal cortices. Time point 2 - 5 hrs post dose, end of trip + Intensified sensory and motor hyperconnectivity. + Continued increased connectivity in auditory and speech centers, with a relative restoration of connectivity to the speech understanding area. + Partial re-emergence of the prefrontal parietal coupling, while prefrontal context remains partially inhibited. + Partial re-emergence of connectivity in areas related to the default mode network. Subjective Experience + High-order brain networks begin to restabilize, alongside persisting sensory, motor, auditory, and speech hyperconnectivity, suggesting neuroplasticity in action. + The narrative shifts from pure sensation and experience to meaning generation, accompanied by deep philosophical reflection (e.g., reconsidering the meaning of life and one's relationship with mortality in the time of AI, and pondering the future of human evolution). Time point 3 - next morning (afterglow) + Persistence: Patterns from the acute phase continue, including general prefrontal cortex inhibition, ongoing neuronal plasticity, and heightened senses. + Intensified connectivity: Increased connectivity is noted in the speech generation area and the somatic sensory association area. + DMN inhibition: The default mode network remains inhibited. Subjective Experience: + "Afterglow" effect: Characterized by continued sharpened senses, calm clarity, emotional openness, and low inhibitions. For instance, I felt more comfortable expressing uninhibited, self-deprecating humor (i.e. my post making fun of myself about the insane lengths I go for my Don’t Die experiment) + Integration of experience learnings: The heightened activity in the somatic sensory association area aligns with the process of integrating and "making sense" of the raw sensory experience of both the self and the external world. + Enhanced creativity: The intensified connectivity in the speech generation area contributed to the uninhibited bout of creative writing I undertook to report my experience."

It wouldn't matter which path performed best in clinical trials. The profitable, proprietary option wins out -- no contest. It's potentially risky though, since everyone knows that isolating, concentrating, and commodifying plant alkaloids typically ends in social disaster. I'm not saying the novel drug is anything like crack cocaine (versus coca leaf). But it might prove just as harmful as, say, Prozac. Most westerners -- health bureaucrats, prescribing doctors, as well as consumers themselves -- prefer the (illusory) "magic bullet." Personalised plant therapeutics sounds like a time-consuming affair. At least in cultures with no established history of traditional use. But isn't that a basic principle of shamanic healing? I can see the market opening up to accommodate both pathways. Big wins for Big Pharma (via the government-subsidised masses) and bespoke plant remedies (for economic and cultural elites). What I don't see, necessarily, is just compensation being paid to the custodians of traditional plant knowledge. Colonialism in Africa, under the aegis of western biomedicine, is abysmal. It's essentially organised biopiracy, sanctified in the name of global health. And wouldn't it be a prudent strategy to ameliorate (if not remedy) the causes of social anxiety in the first place? LOL, bitterly. Such questions only should play a more prominent role in determining how we should proceed.

Packed another box - I think that I only have enough left for maybe 1.5 boxes worth of cactus. Almost all gone. \

@Wood Chuck box has been packed - Fitted most of what I had planed to include, minus one, ran out of space. Threw in some kanna in a zip lock bag hopefully it makes it before rotting. Will be in the post today. Have to fill another order by this week. Best to post on Mondays. Still have enough for 4 plus boxes worth, or if you come for a visit you can have a large ute load. Appreciate those who are willing to swap for ANYTHING interesting. Would love to find Khat, Neem, Mexian Dream Herb, and Vilca/Yope.

I've been doing some research for a previously active member who is now blind, if you have input that would be great. He believes Heimia is a potent medicinal plant and can sometimes have an effect where it causes a 'detached life-review' where one can allow processing of negative life experiences and memories in a more compassionate, less self-critical and non-judgmental way and thus, has potential for PTSD etc. I'm yet to encounter such effects but would be interested in hearing if anyone has had that sort of effect, or otherwise therapeutic experience with it? He also states significant potentiation of more classical serotonergics. I'm trying to get him to do a recorded talk or something at a later stage but curious on other's experiences with it so I can give him feedback. Compared to other entheogenic plants, H. salicifolia has been said to have softer, less potent effects [1]. Though H. salicifolia has a long history of traditional use, little is properly known about its possible therapeutic effects, particularly psychopharmacologically. While some people seem to hold Heimia in high regard, it seems to sometimes gain a reputation of being "not worth it" due to unpleasant experiences, including muscle aches, fatigue etc There are 24 known alkaloids from the plant, the three most abundant (in order) being cryogenine/vertine, lyfoline, and lythrine (Rother, 1990) with others including nesodine, heimidine, sinicuichine, dehydrodecodine, lythridine (Kitajima et al., 2018; Kitajima et al., 2019). They all belong to a class of alkaloids known as biphenyl quinolizidine lactones, which are the primary biologically active compounds. Within the genus, there are marked differences in the concentration of the individual alkaloids (Rother, 1990). Heimia alkaloids The Lythraceae alkaloids have four centers of chirality-three chiral carbon atoms at the quinolizidine ring C-1, C-3, and C-5, and the biphenyl or biphenyl ether link. The quinolizidine ring of Lythraceae alkaloids can exist in both trans and cis configurations. Structurally, vertine has a cis-fused quinolizidine ring while lythrine, lyfoline and nesodine possess trans-fused quinolizidine rings. The nitrogen lone pair in those alkaloids with a cis ring juncture is less hindered, as below: Cryogenine/vertine Lythrine Various alkaloids present and their configuration Rother in 1994 reported absence of any 'psychodysleptic' effects in a “double blind” screening of both vertine and lythrine. Cryogenine/vertine: - cholinergic affinity/mAChR/anti-cholinergic? - anti-inflammatory/ prostaglandin synthetase inhibitor - induces sedation/tranquilising - spasmolytic activities - decreases spontaneous motor activity - dose-related hypothermia - skeletal and passivity without muscle involvement - hyperglycemic - hypotensive - vasodilator Cryogenine/vertine has been reported to have tranquilising properties - the central nervous system depression caused by it is selective in nature and pharmacologically distinct from that caused by conventional major tranquilisers. Lythrine may have psychological benefits, particularly in terms of reducing anxiety, in addition to its diuretic, anti-inflammatory, sedative, anti-hypertensive, and vasorelaxant properties. Given lythrine’s vasodilation and resulting blood pressure and heart rate reduction, it was reasonable to assume that it may have anxiolytic effects similar to clonidine. So far, previous research noted, at the doses tested, lythrine did not produce significant anxiolytic effects. Lythrine is the most effective vasorelaxant alkaloid in the plant and potentially has an effect mediated in part, by muscarinic receptors Four major alkaloids were isolated with their abundance varying considerably: cryogenine/vertine (2.0-8.6 mg/g of dry-weight aerial parts), lyfoline (1.8-6.6 mg/g), lythrine (0.55-0.66 mg/g) and nesodine (0.09-0.55 mg/g) (Blomster et al., 1964; Appel et al., 1965; Dobberstein et al., 1975; Rother, 1989). Sinicuichine and lyfoline were shown to undergo catabolism, while cryogenine was degraded very slowly, if at all. Evidence is presented for the conversion of lyfoline to lythrine The sequential appearance and metabolism of alkaloids in Heimia salicifolia Whereas vertine and lyfoline are the major compounds, the biphenyl quinolizidines sinicuichine, heimidine, lythrine, nesodine, dehydrodecodine and lythridine accumulate in the field-grown plants, and in much larger amounts than the biogenetically simpler phenylquinolizidinyl esters abresoline, demethoxyabresoline and its H-l0 epimer. The phenylquinolizidinols demethyllasubine-I and -II are only metabolites of young (5- to 10-day-old) plantlets. - roots and seeds have been shown to be alkaloid-free In explaining it's diverse herbal action and multitude of potential applications, such treating inflammation, fever, bladder control, constipation, and syphilis, some phytotherapists suggest it may be important to consider how it acts synergistically with other plants/phytoconstituents: It "may contain a variety of active constituents, which must be selected either through the process of preparation, or by the addition of other plant extracts which "turn on" or "turn off' particular chemical compounds. " None of the reported psychoactive effects brought on by the consumption of the entire plant have yet been matched by any of the single alkaloids discovered so far, but serotonin and dopamine systems in the brain have been hypothesised [1] to potentially interact with Heimia alkaloids, which may help explain the plant's mental effects. Effects normally reported: • Pleasant drowsiness • Relaxation of skeletal muscle • Slowing of the heartbeat • Dilation of coronary vessels • Inhibition of acetylcholine • Enhancement of epinephrine • Mild reduction in blood pressure • Cooling of the body • Mild intoxication and lightheadedness • Blurred vision • Auditory changes (sounds seem distant); and • Altered memory function. Some have mentioned that it may be important to study the correctly prepared material, which may have novel constituents; "It is necessary to study both the fermented product and the dry leaf infusion in order to isolate the compound responsible for the reported mental effects" What is the (sun) fermentation doing to potentially change Heimia's chemistry and psychoactivity? It has long been believed that fermenting tea before drinking it lessens associated negative effects Is such a process accomplishing: enzymatic bioconversions in plant material post-harvest? chemical oxidation reactions or degradations, similar to tea fermentation? something like a a light/UV mediated photoisomerisation/conversion of alkaloids? Light-induced (can also be enzyme-catalyzed) cis-trans (geometric) isomerisations (photoisomerisations) of double bonds can impact the biological activity eg The pungent amides in black pepper undergo light-induced photoisomerisations to differing compounds with altered levels of biological pungency a bioconversion of alkaloids by yeasts/lactic acid bacteria? [seems unlikely with short duration fermentation normally mentioned] Fermentation can substantially alter the secondary metabolite composition of plant-based products due to a series of microbial actions such as hydrolysis, methylation, and carboxylation etc. Microbial fermentation is considered to provide a multi-enzyme complex consisting of esterases, dihydrogenases, decarboxylases, and de-aminating and CC-cleaving enzymes etc Something else? In a case-study, analysis has been undertaken of a sample from a person who created a brew of Heimia fermented over 24 h by adding yeast and sugar. No mention of light exposure during fermentation was made. Undesirable effects were noted, it resulted in muscle pain of the extremities and the tongue as well as slightly raised temperature, night nausea, headache This (yeast-enhanced) fermentation created an alkaloid profile of demethyllasubine I, demethyllasubine II, heimidine, lythridine, abresoline, 10-epi-desmethoxyabresoline, desmethoxyabresoline, lyfoline, anelisine, dehydrocodine, vertine, nesodine, sinicuichine and lythrine Other constituents: Presence of chlorophyll, mucilage, fatty oils, tannins, quinones, polyphenols, pigments, gum, glucose, starch, and alkaloids within the members of the family. Flavonoids like quercetin and kaempferol have been detected, ellagic acid, a sterol known as stigmasterol, as well as triterpenes like ursolic acid It is a good source of phenolic compounds: Apigenin-7-O-rutinoside, protocatechuic acid; vanillic acid; apigenin-4'-O-methyl ether 7-O-glucoside (acacetin-7-O-β-glucoside); methyl gallate; gallic acid; apigenin-7-O-β-D-4C1-glucoside; 5,7,4'-trihydroxy-3-methoxyflavanone (dihydrokaempferol-3-O-methyl ether); dehydrotrigallic acid; 3,4,3'-trimethoxyellagic acid; 3,3'-dimethoxyellagic acid; 3-methoxyellagic acid; ellagic acid; apigenin; and kaempferol. 1,6-di-O-dehydrotrigalloyl-β-D-4C1-glucopyranose, 5,7,4'-trihydroxy-3-methoxyflavanone (dihydrokaempferol-3-O-methyl ether) Properties of the individual alkaloids including colour, crystal morphology and mp etc can be found here [1] Chapter 30 Sinicuichi (Heimia salicifolia (Kunth) Link Lythraceae) Rahmatullah Qureshi, Bushra Jabeen, and Noureddine Chaachouay The effect of light on the production of Heimia alkaloids Heimia salicifolia: A phytochemical and phytopharmacologic review Biosynthesis of Lythraceae Alkaloids

I can't talk much on drinking or preparation but nothing will stop this plant growing (maybe frost). These things really take off and readily set seed. There is a nice H. salicifolia hedge in the Sydney botanic gardens if anyone is interested. I can't really describe the location but I believe its behind a bench near one of the ponds near the cafe.

You trying to see if these guys are millionaires now? In all likelihood they sent it all to the silkroad haha

I have so many good memories from 15+ years ago, I had been to my 2nd EGA conference and had a wonderful time and met so many sound folks. I think the problems are often associated with those who are trying to monetise the hobby in some way. When $$ are involved the unsavoury do seem to follow. Outside of people who are trying to make a dollar, I reckon a vast majority of plant heads I have met are great people. Facebook has diminished the forum for sure.

What could he be basing this on? As far as I'm aware there's been no public proposal to amend laws to criminalise growing certain cacti, and I doubt this grower has an insider in Parliament. People have been discussing whether peyote/trichos will be made illegal on this forum and elsewhere for decades now. The recent media is probably the most mainstream exposure these cacti have ever received. That is the only thing I can think of that would prompt pearl-clutchers to write to their MP about the cactus scourge destroying our youth. Even still, I doubt it would earn enough political brownie points to prioritise it as an issue. The TGA angle is possible, but I also agree the therapeutic uses in a mainstream context of mescaline are limited for a few reasons compared to something like psilocybin. The cost of a 12 hour session + burnout of practitioners etc.

Yeah this forum is super slow compared to 15 or so years ago. I keep coming back because of how awesome and inspiring it was when I was younger.

It is well established that psychedelic substances do occasion mystical experiences, and they continue to be used for religious and spiritual reasons. Despite the link between psychedelics and spirituality, there seems to be little follow-up in regard to the long-term changes in regards to specific religious and spiritual practices that psychedelic mystical experiences instigate and maintain. My questions to you are: How have psychedelics altered your religious and/or spiritual practice, and if so, where has it led you? Did psychedelics reinforce your existing believes or did psychedelics cause a major redirection in your religious and/or spiritual practice? My journey started by being raised in the Seventh Day Adventist Church, an experience completely devoid of any notion of a direct ecstatic experience of the divine. Interestingly enough, my first true transformative experience was through participation in a Voodoo ritual complete with animal sacrifice and fire worship, where for the first time I experienced a trance-like state akin to spirit possession. The next was a physical ordeal as part of martial arts practice tied to Shinto and Buddhist practices; over a period of several hours of rhythmic group vocalization under physical stress, I transcended my body, becoming an energetic wave. However, the mainstay of my everyday personal religious life was Soto Zen Buddhism; however, this was a more gradual transformative practice. It was only when I sought out psychedelics to address questions that had remained unanswered that I came to realize that I have always sought those experiences hinted at but that institutionalized religion could never provide: a direct becoming of existence, a non-dualism of Being. My exposure to psychedelics, admittedly later in life, has radically fractured and transformed the quality of my religious feeling and sentiment; it could not have been more distinct. It has transformed my own understanding of what it means to live and instigated within me a deep appreciation for the profundity contained within millennia of classical religious wisdom and practice. Through a process of serendipity and synchronicity, I am now able to draw upon a classical lineage of teachers that ensures me with "corrective thought" while providing me a scaffolding for a sustaining a burgeoning spirituality sustained beyond the transient well spring of psychedelics.

A heavily biomedical psychopharmacologist was once asked what would he say the best antidepressant was and it was "to go out and find someone to help". I'd agree that the multifaceted behavioural activation towards something valued and greater than one's self is a vital ingredient to escape the woe. Doesn't have to be changing the world but just something small and simple that induces the sense that "it was a good day that mattered" is a nice start. I could list ad infinitum potential antidepressants, which you could try and see if they work but in reality that's where I'd start. I find novelty is an important dopamine effluxer so find novel things to do. Exercise, diet as mainstays. Here's a list of potential nutritional etc options https://1drv.ms/x/c/a157359194a53c21/ESE8pZSRNVcggKF-CgAAAAABlsQ51KStyjW4ly8V9_-FlQ?e=IIMmSg&nav=MTVfezAwMDAwMDAwLTAwMDEtMDAwMC0wMDAwLTAwMDAwMDAwMDAwMH0 that could be coupled with such.

$50 - In the spirit of getting the ball rolling.

Hi, I am downsizing my collection of 300 plus Trichocereus mostly Bridgesii, some Pachanoi, as I have way too many to effectively care for and I am running out of space. My aim is to downsize and to re-home 100's of plants; therefore, I am GIVING THESE AWAY just as long as you cover postage cost OR pick up by arrangements in Gippsland, Victoria I will start posting photos of lots of cacti that would be of interest to people. So follow along and message now.

Alchemia is smart. Listen to Alchemia. But in addition, the lock and key analogy is also works in the sense that a lock must be opened by a key. After this, you need to stretch the analogy somewhat. So if these molecules are the keys, consider that some of these molecules are large keyrings with multiple keys on them. They can unlock several locks. But because I like straining analogies beyond their useful limit, imagine that the keys have another property; variance. Some keys don't work very well. Perhaps they were poorly made and only fit some of the locks of a certain type rather than all of the ones of that type. Now, imagine that these locks can only be opened whilst the key is in them and they automatically lock when the key is removed. But some of the keys are "stickier" than others and are harder to remove from locks. Now you've got molecules that can release many different neurotransmitters in different quantities for varying periods of time. Each of these neurotransmitters has a different effect depending on amount released, duration and how they are combined with other neurotransmitters. They all cause a cascade of release of other neurotransmitters and enzymes too. This results in significant variation in experience between molecules and even when taking the same substance.

So in the spirit of sharing the love the next person who wants an assorted cactii parcel from starward let us both know and i'll give him/her/they the $50

A readily available, plant-derived MAO-B inhibitor with neuroprotective properties Inside the brain, MAOs are present in two isoforms: MAO-A and MAO-B which differ in preferred substrates and regional location. MAO-A preferentially deaminates 5-HT and NE and MAO-B, small amines like benzylamine and phenethylamine. DA and p-tyramine are common substrates of both isoforms. MAO-A is often the target of antidepressant therapies. The activity of MAO-B is generally higher in patients affected by neurodegenerative diseases like Alzheimer's and Parkinson's, as such being used therapeutically, particularly in PD. Renewed interest in the field has come also from the recent findings that MAO-B inhibitors have neuroprotective and antioxidant effects and play a role in delaying apoptotic neuronal death and in protecting crucial mitochondrial functions. Figure 1. Structures of some synthetic MAO-B inhibitors Kava pyrones can inhibit MAO-B reversibly: The order of potency was desmethoxyyangonin > (±)-methysticin > yangonin > (±)-dihydromethysticin > (+)- dihydrokavain > (±)-kavain. A long time ago, I was interested in simple molecules that could effectively and selectively inhibit MAO-B. About the simplest one I could find was Ro 16 6491, a metabolite of moclobemide. Some of the pharmaceutical options such as selegiline have additional non-MAOI benefits such as acting as catecholamine activity enhancers, or for safinamide, inhibition of glutamate release, SERT and DAT, affinity to sigma receptors and blockade of calcium and sodium channels An endogenous MAO-B inhibitor is isatin: Isatin (indole-2,3-dione) is an endogenous indole found in the mammalian brain, peripheral tissues and body fluids. It is proposed isatin can be formed from indole in the body, typically produced by tryptophan catabolism in the gut. It accumulates in the brain, modulating brain function and produces multiple CNS effects, which include changes in gene expression. It exerts neuroprotective effects. can be present in humans in the <0.1 to > 10 µM range and levels increase in response to stress able to cross the blood-brain barrier endogenous inhibitor of monoamine oxidase (MAO), more selective for MAO-B than for MAO-A (Ki for MAO-A = 60-70 μM; Ki for MAO-B = 3 μM). Physiological concentrations of isatin in vitro inhibit monoamine oxidase B but administered at high doses, it can act on both MAO isoforms Induces dopamine release - intrastriatal administration of 1, 5 or 10 μM isatin, for 1 h, significantly increased dopamine levels to 355 ± 104%, 700 ± 72%, and 1241 ± 146%, when compared with basal values, respectively. These dopamine enhancements were synergistically enhanced by co-administration of L-dopa, caffeine etc anxiogenic/proconvulsant effect with lower dose-levels (around 20 mg/kg in animal models), an effect lost at higher doses (above 50 mg/kg) instead becoming sedative, potentially though inhibitory effect on central atrial natriuretic peptide receptors and stimulation of 5-HT3 increases glutamate levels, possibly activates NMDA receptors and nitric oxide production, which can promote a further increase in the dopamine release. significantly increased 5-HT concentrations in the hypothalamus and cortex weak inhibition of D-amino acid oxidase (DAAO) by isatin (about 20% at 20 μM), leading to modulation of NMDAR regulation of the brain levels of ACh There has been extensive research around natural products which can inhibit MAO-B but ones that are sufficiently potent, selective and available in pure form for convenient dosing are more limited. Unfortunately, most natural products are generally comparatively poor MAO-B inhibitors relative to synthetic options, in the micromolar-millimolar affinity range. Some classes of natural MAO-B inhibitors include β-carbolines, flavonoids, xanthines, xanthones, and alkaloids, a review can be found in [1]. Natural • Geiparvarin • Desmethoxyyangonin, a constituent of kava extract; modest affinity • Catechin and epicatechin, poor affinity • Garlic • Rosiridin Figure 2. Some natural MAO-B inhibitors from [1] An Australian plant, Geijera parviflora, contains geiparvarin, a coumarin derivative in the leaves which inhibits MAO-B Some simple small molecule MAO-B inhibitors include methyl piperate, a derivative of piperine from black pepper. Whilst there is some dispute on the MAO-A/B selectivity, one source claims it is more selective for, and relatively potent towards MAO-B [2]. Figure 3. Structure of methyl piperate Recent research [3] identified ethyl ferulate as a novel neuroprotective MAO-B inhibitor, displaying greater affinity than rasagiline Figure 4. Structure of ethyl ferulate Ferulic acid is conveniently available pure in small and bulk quantities fairly cheaply and serves as a convenient material for the simple synthesis of ethyl ferulate via a Fisher esterification with ethanol [4]. Figure 5. Binding of ethyl ferulate to hMAO-B from [3] “Ethyl ferulate could bind to the active site (substrate-binding site) of human MAO-B (hMAO-B) by hydrogen bound in a relative low binding energy (Binding energy = -6.47 kcal/mol …analysis showed that ethyl ferulate exhibited a higher affinity with hMAO-B than rasagiline mesylate, suggesting hMAO-B was a molecular target of ethyl ferulate.” One benefit to ethyl ferulate is it is a lipophilic ester derivative of a well-studied molecule, also with it’s own beneficial properties. That said, being an ester, it is likely subject to extensive hydrolysis in the GI tract and on first pass metabolism, which could hinder it's use. Ferulic acid is a phenolic compound that exhibits neuroprotective effects in the central nervous system [5, 6]. It has antidepressant properties by increasing the 5‐HT, NE, and DA levels in the synaptic cleft of frontal cortex and hippocampus via regulating the monoamine system. It also has antioxidant, anti-inflammatory and neurotrophic effects. Ethyl ferulate -novel natural compound that could be used for therapeutic purposes as a potent inducer of HO-1 for the protection of brain cells against oxidative and neurodegenerative conditions. - Potently suppress microglia-mediated neuroinflammation by binding to MAO-B Improving the properties of ferulates Both the phenethyl ester and phenethylamide [7,8] of ferulic acid seem to have potent MAO-B inhibitory properties, the amide having the properties of resistance to hydrolysis in vivo by esterases Figure 6. Ferulamides [1] Carradori, S., D’Ascenzio, M., Chimenti, P., Secci, D., & Bolasco, A. Selective MAO-B inhibitors: a lesson from natural products. Molecular Diversity, 18(1), 219–243. (2013) doi:10.1007/s11030-013-9490-6 [2] Lee SA, Hwang JS, Han XH, Lee C, Lee MH, Choe SG, Hong SS, Lee D, Lee MK, Hwang BY. Methylpiperate derivatives from Piper longum and their inhibition of monoamine oxidase. Arch Pharm Res. (2008) Jun;31(6):679-83. doi: 10.1007/s12272-001-1212-7. [3] Zou X, Gao S, Li J, Li C, Wu C, Cao X, Xia S, Shao P, Bao X, Yang H, Liu P, Xu Y. A monoamine oxidase B inhibitor ethyl ferulate suppresses microglia-mediated neuroinflammation and alleviates ischemic brain injury. Front Pharmacol. (2022) Oct 13;13:1004215. doi: 10.3389/fphar.2022.1004215. [4] Esterification, Purification and Identification of Cinnamic Acid Esters [5] Dong X, Zhao D. Ferulic acid as a therapeutic agent in depression: Evidence from preclinical studies. CNS Neurosci Ther. (2023) Sep;29(9):2397-2412. doi: 10.1111/cns.14265. [6] Sgarbossa A, Giacomazza D, di Carlo M. Ferulic Acid: A Hope for Alzheimer's Disease Therapy from Plants. Nutrients. (2015) Jul 15;7(7):5764-82. doi: 10.3390/nu7075246. [7] Badavath, V. N., Baysal, İ., Uçar, G., Mondal, S. K., Sinha, B. N., & Jayaprakash, V. (2015). Monoamine Oxidase Inhibitory Activity of Ferulic Acid Amides: Curcumin-Based Design and Synthesis. Archiv Der Pharmazie, 349(1), 9–19. doi:10.1002/ardp.201500317 [8] Koichi Takao, Kazuhiro Toda, Takayuki Saito, Yoshiaki Sugita, Synthesis of Amide and Ester Derivatives of Cinnamic Acid and Its Analogs: Evaluation of Their Free Radical Scavenging and Monoamine Oxidase and Cholinesterase Inhibitory Activities, Chemical and Pharmaceutical Bulletin, 2017, Volume 65, Issue 11, Pages 1020-1027, Released on J-STAGE November 01, 2017, Online ISSN 1347-5223, Print ISSN 0009-2363, https://doi.org/10.1248/cpb.c17-00416

Prolonged adverse effects from repeated psilocybin use in an underground psychedelic therapy training program: a case report I thought this article was interesting, in having to consider at what point does one's mindset switch from psychedelically-minded, allowing a natural unfolding process of self-healing, to wait a minute, something is really wrong here, they need professional medical help kind of thing happen? Are facilitators open to, and knowing of when, a change of approach, ie professional help is needed? It presents a case of a (Dr) clinical psychologist undergoing 'training', who had prior experience with psychedelics, and no history of mental illness undergoing a long-term psychedelic adverse experience after multiple psilocybin doses. It illustrates: - adverse experiences may need not result from an underlying psychiatric vulnerability exposed by psychedelics, and can occur in those with multiple psychological, social, and environmental protective factors -factors of the broader set and setting that contributed to this use pattern and perpetuated it by denying, obscuring, or reframing harms, despite the patient having recurrent and escalating distress

I have been growing Ashwagandha over spring and summer and have started to harvest seeds. With winter coming up I am hoping to harvest the leaves when I trim the plant back. I plan to let it grow for another year to get more sizable roots before harvesting next year. Has anyone any experience with using Ashwagandha Leaf and Fruit? The basic idea is that only the roots are safe, with differing ideas around the fruit and leaves; however, I have been able to dig up academic papers in which they have used the leaves and the fruit. However, there is no information on how they were used/extracted and at what dose. I assume that a simple water extraction would suffice. Any insights would be appreciated. https://ayush.gov.in/images/domains/quality_standards/safetyReportAshwagandha.pdf https://www.longecity.org/forum/topic/34419-ashwagandha-is-toxic/ This post is interesting by coin who makes an interesting point about the pitta and "if you lean toward these tendencies you need to combine with other herbs"

I have two new channels for my rap music if anyone would like to listen. I'm improving! http://www.youtube.com/@longjetty http://www.youtube.com/@ForSmith-o2t

Harmine is a high potency reversible inhibitor of MAO-A with specificity for the MAO-A isoform and does not, at most relevant doses, inhibit MAO-B. In general, both harmine and harmaline are considered reversible MAO-A inhibitors. Norharman is more selective for MAO-B Samoylenko et al., 2010 and Wang et al., 2010 reported the inhibition of MAO-A and MAO-B by harmine, harmaline, and tetrahydroharmine. In that case, the selectivity for MAO-A for both alkaloids was much greater for MAO-A than the -B isoform, IC50 2.5 and 2.0 nM for MAO-A, and 25 and 20 μM for MAO-B, respectively. However, Wang et al., 2010 did not find any MAO-B inhibitory activity by the aforesaid alkaloids

I have heard that it does grow from cuttings. Honestly the seeds grows like a weed. I grew it a grow tent with high humidity. @fyzygy Happy to send you fresh seeds. Message me.

@rottenjonny A very generous offer. Maybe I have something I can give you as well.

Think of it as even though both bind to the 5-HT2A receptor, there's a variety of things that different molecules can make the receptor to do after activation. Serotonin is the wise old soul that tells the receptor to signal one way that isn't too funky but if you add a hallucinogenic agonist, the party animal system gets activated and all systems go turbo That's over-simplistic, as the substances aren't normally purely active at the 5-HT2A receptor but still. You get the initial binding of substance to the receptor but then there is a cascade of signaling that follows, the secondary messengers. - The distinct signaling signatures evoked by hallucinogenic versus non-hallucinogenic 5-HT2A receptor agonists as seen by differences in the magnitude of production of the secondary messengers - hallucinogenic agonists show differential desensitisation as well as signaling responses as seen by the higher production of inositol phosphates and pERK levels as compared to non-hallucinogenic agonists - fingerprints have been mapped that distinguish the hallucinogenic and non-hallucinogenic 5-HT2A receptor agonists eg upregulation of levels of c-fos and egr-1 mRNA There's also complexes that form between the 5-HT2A receptor and another type of receptor: -5-HT2AR-mGluR2 complex is necessary for the neuropsychological responses induced by hallucinogens. Banerjee AA, Vaidya VA. Differential signaling signatures evoked by DOI versus lisuride stimulation of the 5-HT2A receptor. Biochem Biophys Res Commun. 2020 Oct 22;531(4):609-614. doi: 10.1016/j.bbrc.2020.08.022. Moreno JL, Holloway T, Albizu L, Sealfon SC, González-Maeso J. Metabotropic glutamate mGlu2 receptor is necessary for the pharmacological and behavioral effects induced by hallucinogenic 5-HT2A receptor agonists. Neurosci Lett. 2011 Apr 15;493(3):76-9. doi: 10.1016/j.neulet.2011.01.046.

Hi Starward I wouldn't mind getting a Pachanoi How much for postage to Sydney. Thanks Luke

I picked 9 large leaves and washed them, then added them to a pot containing 1.5 cups of cold tap water. I brought the water to a boil, and then reduced it to a simmer and reduced it to 1 cup of water. The end product looks like oolong tea, has a slightly green grass smell, the taste is not bad, the taste starts like tasting like nothing much but fades to a solid bitter. It leaves the mouth feeling parched almost like the feeling you get from tannins. I will start with one glass a day and see what effect it has on my blood sugar and weight over a month. I am also due for a blood test and will get results for my liver function to see if there are any downsides. PS. my interest in the leaves is my frugality, if I can avoid digging up a plant by harvesting leaves then all the better. The leaves seem to be a more sustainable resource management option.

I've used the leaf, it seems personally friendly enough but caution is still advised. Perhaps the most off-putting bit of the leaf is it's weird flavour, I used to make a glycerite to cover it a bit Some mention of the leaves being used by Indians has been made, in tea "When brewed as a tea, the leaves may help to regulate blood glucose (blood sugar) in the body, increase energy and support mental clarity and attention." It seems to require more cautious dosing, the leaf due to the high levels of withaferin A, one withanolide which is cytotoxic, needs some caution. The leaves possess higher content of active withanolides, withaferin-A and withanone, as compared to the roots [1]. Nootropic and CNS therapeutic properties of the leaf have been claimed [2]. Withaferin-A is a potent leptin sensitiser with additional antidiabetic actions and resulted in a 20-25% reduction of body weight in overweight mice [3]. It improves insulin sensitivity [4]. Anti-neuroinflammatory properties have been ascribed to the leaf [5] along with neuroprotective properties [6] Withaferin-A shows anti-neuroinflammatory [7] anti-Aβ properties [8] and dopamine-restoring [9] properties. Improvement of cognitive dysfunction has been ascribed to Withanone [10] including inhibition of AChE, anti-Aβ, protection against oxidative stress and anti-inflammatory effects. Many toxicological studies have demonstrated that Ashwagandha, in its reasonable dose, is a non-toxic, safe and edible herb - despite that, there is sometimes movement away from the cytotoxic constituents towards root extracts which may be less effective Fruits of Withania are reported to possess several bioactive compounds as curative agents for various clinical conditions. 82 chemically diverse metabolites consisting of organic acids, fatty acids, aliphatic and aromatic amino acids, polyols, sugars, sterols, tocopherols, phenolic acids and withanamides were found in the fruits of W. somnifera. Withanamides, the primary active constituents in W. somnifera fruit extract exhibited neuroprotective effects. The fruits have relatively strong antiproliferative activity. They may improve antioxidant status and reduce proinflammatory markers. [1] https://www.ncbi.nlm.nih.gov/pubmed/27936030 [2] https://www.ncbi.nlm.nih.gov/pubmed/26361721 [3] https://www.ncbi.nlm.nih.gov/pubmed/27479085 [4] https://www.ncbi.nlm.nih.gov/pubmed/30417321 [5] https://www.ncbi.nlm.nih.gov/pubmed/27550017 [6] https://www.ncbi.nlm.nih.gov/pubmed/25789768 [7] https://www.ncbi.nlm.nih.gov/pubmed/26266054 [8] https://www.ncbi.nlm.nih.gov/pubmed/30356847 [9] https://www.ncbi.nlm.nih.gov/pubmed/30544122 [10] https://www.ncbi.nlm.nih.gov/pubmed/29108796

Early visualisation of mesembrine-type alkaloids via TLC was plagued by the use of crude iodine vapor visualisation which was non-specific, making accurate detection of alkaloids problematic. As noted previously, there are several distinct Sceletium chemotypes which makes having a specific reference material a challenge, coupled with extremely variable alkaloid levels in the raw plant material. To improve the visualisation technique, Dragendorff's reagent was selected as an alkaloid-selective method. This uses a potassium bismuth iodide complex which forms with (mainly tertiary nitrogenous) alkaloids to form a yellow-red-orange-brown colouration revisited tlc | PDF Host

Hey all, it's been a long time. Slowly trying to build up a collection after a long time without... Anyone have a cutting of TPM x Sharxx Blue for sale? Other blue crests or monstrose clones would be cool too, as would classics like Psycho0 or Sharxx Blue itself. Still chasing that clone that someone named after me too - Tripsis. It was an amazing blue peruvianus.

I've done this many times. It does absolutely work to convert all the ibotanic acid into Muscimol. I'll post a link of how it's done. It's a form of kombucha called "Ginger bug soda" only that you add the Amanita into the ferment and just a little tip. Once you have your finished product you can add extracts , tinctures or boiled down teas from other plants and herbs to the mix. It's also very tasty on it's on, not a hint of Amanita taste. Link to come.