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polytrip
#1 Posted : 7/4/2008 9:48:55 PM
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I've been hearing different stories about bufotenin. I thought that bufotenin is not the substance you would want to use because of toxic effects and that you would have to turn it into calcium-bufotenate. But now 69ron from this forum said that in fact bufotenin is OK and not toxic. I can easily get my hands on yopo but i heard you can get pretty sick so i'm wondering if anybody has any advise on yopo. do or don't?
 

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burnt
#2 Posted : 7/4/2008 10:21:41 PM

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yopo also contains DMT and 5-meo-dmt. Yopo itself it probably pretty safe to use its been used for hundreds of years as a snuff in the amazon. As far as taking pure bufotenin there is considerable controversy over whether it is or isn't a psychedelic in the literature. some people say it is some people say it isn't. SWIM never consumed it and has no plan too. however it seems according to some researchers like john ott that its psychoactive when vaporized and or snorted. early research into the substance involved injecting into schizophrenic patients which really didn't do much to answer whether or not it was psychoactive since they were injecting it into psychotics!
 
69ron
#3 Posted : 7/5/2008 7:15:50 PM

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Its very rare to find Yopo with enough DMT or 5-MeO-DMT to feel their effects. The effects are from bufotenine.

Bufotenine is definitely very hallucinogenic. The visual effects from it are stronger than any other hallucinogen. But it's hardly "psychedelic", in that there are next to no mental effects unless massive amounts are taken. It's quite unique in that way. It’s almost purely visual. It's effects are very unlike 5-MeO-DMT or DMT.

When you make Yopo you freebase bufotenine by adding lime and water. This makes it easier to absorb into the blood stream and into the brain. If its not in freebase form it takes too long to absorb through the nose and becomes a salt and most of it gets stuck in the body.

I don't know about this calcium bufotenate stuff I've read about, but freebase bufotenine is plenty hallucinogenic. Vaporizing 10 mg of it will produce tons of visuals; it's about equal to maybe 100 mg snorted.

The effects of Yopo are almost entirely from freebased bufotenine, but not completely. There are compounds other than DMT/5-MeO-DMT present that can be felt. It's almost impossible to feel the effects from the DMT/5-MeO-DMT present in most Yopo because it's usually so small. There's usually, but not always, far more bufotenine and bufotenine N-Oxide in Yopo than DMT and 5-MeO-DMT combined.

Bufotenine needs to be in freebase form when used, or it won't be very hallucinogenic. It's all about absorption. Water soluble drugs don't absorb into the brain as fast and will therefore have more effects on the body. Look at this quote

Quote:

The un-ionized form is usually lipid soluble (lipophilic) and diffuses readily across cell membranes. The ionized form has low lipid solubility (but high water solubility—ie, hydrophilic) and high electrical resistance and thus cannot penetrate cell membranes easily.


That quote is taken from http://www.merck.com/mmp.../sec20/ch303/ch303b.html

Here’s another page with similar info: http://www.4um.com/tutorial/science/pharmak.htm

Bufotenine must enter the body in un-ionized form to be an effective hallucinogen because it’s too water soluble in ionized form. The main problem is that bufotenine (5-HO-DMT) has a very high pKa of 9.67 (see http://lib.bioinfo.pl/pmid:6259355), which is higher than most other hallucinogens. Even its close cousin psilocin (4-HO-DMT) has a lower pKa of 8.47, and this is why it is a much stronger hallucinogen orally then bufotenine is. Bufotenine has a higher pKa than DMT as well. DMT has a pKa of 8.68 which is close to that of psilocin, and why, like psilocin it is effective orally (with MAOI) and by injection and bufotenine is not. It’s all about pKa. Your blood pH is about 7.4. The closer an alkaloid’s pKa is to your blood’s pKa the more effective it is at crossing the blood brain barrier because it is less ionized. Ionized alkaloids have a hard time entering the brain. Let me explain a little more and you’ll get what I’m talking about and understand why bufotenine must enter the body in freebase form while hallucinogens like psilocin and DMT with lower pKa’s don’t need to enter the body in freebase form.

At pH 7.4 about 90% of DMT gets ionized, so that 10% can easily cross the blood brain barrier to produce hallucinogenic effects. This is why DMT is still very effective even when injected as a salt, because once in the blood about 10% becomes freebase and enters the brain. After that 10% enters the brain, 10% more becomes freebased. That continues until all of the DMT enters the brain. This is why injected DMT takes longer to hit and lasts longer than vaporized freebase DMT. It enters the blood stream in pre-ionized solution where only 10% enter the brain at a time. When vaporized as freebase nearly 100% enters the brain at once because its not ionized.

At pH 7.4 over 99% of bufotenine gets ionized, so as soon as it enters the blood stream it starts to rapidly ionize to maintain over 99% in ionized form, so it needs to be absorbed into the brain in freebase form really fast before it gets ionized by the blood. If taken orally, it is 100% ionized in the digestive system before entering the blood stream. When injecting it, a 99% or greater ionized form is always used. Ionized bufotenine can’t enter the brain. Only freebase bufotenine can enter the brain. When in the blood, at pH 7.4, whether it enters as freebase form (0% ionized) or salt form (100% ionized), given enough time, over 99% becomes ionized. This means less that 1% can enter the brain at a time. After that less than 1% enters the brain, less then 1% becomes freebased again. But this happens too slowly, so that hallucinogenic effects are extremely weak. If the bufotenine enters the blood in freebase form (by vaporizing it or snorting it in freebase form) quite a lot freely enters the brain before it gets ionized by the blood. Ionization is not instant, it takes time, and fortunately it’s not fast enough to prevent the freebase bufotenine from entering the brain if it enters the blood stream in un-ionized freebase form.

Freebase bufotenine is quite water soluble and has a hard time entering the brain as is, if made into a more water soluble salt, it’s extremely difficult for it to enter the brain fast enough to have much hallucinogenic effects. This is one reason why injecting it in salt form produces mostly bodily effects. Also, bufotenine easily oxidizes into bufotenine N-Oxide which pretty much only produces bodily effects and next to no visual effects even at very high doses. It’s also very likely that the tests performed by injection on those schizophrenic patients was done using old bufotenine that oxidized into bufotenine N-Oxide, accounting for the almost total lack of visual effects. SWIM has tried bufotenine N-Oxide and it’s effects are the same as those reported by those schizophrenic patients. Bufotenine N-Oxide falsely gets identified as being bufotenine by most chemical analysis procedures. So even if the scientists performing those tests checked the purity of their “bufotenine” and if it was all oxidized into bufotenine N-Oxide at the time, it’s very likely that their tests showed a positive for bufotenine, even though it could have all been bufotenine N-Oxide.

We know for sure that bufotenine is hallucinogenic because some fresh snuff samples that were very effective hallucinogens were analyzed and found to only contain bufotenine. If it was not hallucinogenic, that could not be possible. Also SWIM has taken DMT and 5-MeO-DMT many times and knows their effects very well, and the effects of Yopo are very different from either of those. It's more visual than DMT, not as mental as DMT or 5-MeO-DMT, and it's effects last 2-4 times longer. SWIM has tried freebase bufotenine many times and knows for sure that this is the main active principle in Yopo because the effects are almost identical.

Remember that the key to getting bufotenine into the brain is to have it enter the blood un-ionized. So that means it must be smoked in freebase form, snorted in freebase form, taken sublingually in freebase form, or taken rectally in freebase form. Any other method requires that it be ionized before entering the blood stream, so it cannot be injected in pH 7.4 solution, taken orally, etc., or it won’t enter the brain fast enough to be an effective hallucinogen. It’s all about pKa. With the high pKa of bufotenine being 9.67, at blood pH of 7.4, over 99% of the bufotenine cannot enter the brain. So it must enter the blood as freebase and enter the brain before the blood ionizes it. The longer it sits in the blood the more it gets ionized. If in the blood long enough over 99% becomes ionized and cannot enter the brain.

Adding lime to bufotenine when snorting it, helps prevent it from getting ionized in the nose. This way it can enter the blood in freebase form. This is why the natives add lime and don't use it without lime.
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polytrip
#4 Posted : 7/5/2008 9:11:48 PM
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This makes sense. It would explain why people who smoked bufotenine are most of the time more positive about it then those who snorted it. Would it be wise to add a little more lime then the official recipe's require, just to make sure ALL the bufotenin is free-based? I've heard of people getting sick when using yopo, so they must have done something wrong in preparing the snuff. Maybe they didn't mix it well enough or they gave it too little time to turn into free-base. I don't want to make those type of mistakes. I definately like to try this it.
 
Entropymancer
#5 Posted : 7/5/2008 10:12:33 PM

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People get sick with yopo. This seems to occur regardless of the method of administration. It may be a result of a non-bufotenine chemical in the seeds, or it could just be a side-effect of the serum concentration of bufotenine changing so rapidly as the drug gets taken up. SWIM didn't vomit when he snuffed the seeds, but there was substantial nausea on the come-up.

I'm not sure what your recipe is, but 1:4 lime to yopo seems like the most you could possibly need. Lime is pretty alkaline material.

Also, just to be clear, not everyone enjoys bufotenine. It's definitely not going to catch on as a recreational drug. That said, SWIM found it a worthwhile experience. Once, after taking the snuff by itself to become acquainted, he took the snuff on the plateau of a mushroom trip, and found the two to complement wonderfully... there's also something a little poetic about pairing 4- and 5- hydroxy-DMT on a visionary jounrney.
 
LemonScented
#6 Posted : 7/6/2008 4:33:34 AM
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polytrip wrote:
This makes sense. It would explain why people who smoked bufotenine are most of the time more positive about it then those who snorted it. Would it be wise to add a little more lime then the official recipe's require, just to make sure ALL the bufotenin is free-based? I've heard of people getting sick when using yopo, so they must have done something wrong in preparing the snuff. Maybe they didn't mix it well enough or they gave it too little time to turn into free-base. I don't want to make those type of mistakes. I definately like to try this it.



true. it has to do with how well the yopo snuff is prepared, but beyond that the shit is extremely painful to snort. you become horribly congested instantly and can't help but gag. next thing you know your vomiting and blowing your nose, at the same time. SWIM was clogged up for the rest of the week! it worked very well but it was a hard experience. overall, it's just part of the ritual.
 
69ron
#7 Posted : 7/6/2008 6:42:43 AM

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Entropymancer wrote:
People get sick with yopo. This seems to occur regardless of the method of administration. It may be a result of a non-bufotenine chemical in the seeds, or it could just be a side-effect of the serum concentration of bufotenine changing so rapidly as the drug gets taken up. SWIM didn't vomit when he snuffed the seeds, but there was substantial nausea on the come-up.

I'm not sure what your recipe is, but 1:4 lime to yopo seems like the most you could possibly need. Lime is pretty alkaline material.

Also, just to be clear, not everyone enjoys bufotenine. It's definitely not going to catch on as a recreational drug. That said, SWIM found it a worthwhile experience. Once, after taking the snuff by itself to become acquainted, he took the snuff on the plateau of a mushroom trip, and found the two to complement wonderfully... there's also something a little poetic about pairing 4- and 5- hydroxy-DMT on a visionary jounrney.


Combining psilocin with bufotenine? Now there’s an interesting idea. SWIM will try that next time he has a batch of fresh shrooms Smile

Bufotenine, even pure, has a body load that some people really don’t like. It’s not as bad as the snuff though. It’s not painful to snort freebase bufotenine. SWIM tried freebase bufotenine by every method imaginable except by injection. Snorting freebase bufotenine works very well, there’s no pain, but it gives SWIM a headache and nausea at 75 mg and up. He really doesn’t like it that way. Maybe he’ll try freebase bufotenine with lime or baking soda next time to see if that helps stop the side effects by keeping the nasal pH high.

When the natives make snuff the pH is normally adjusted to about 9.2-9.4. This is very close to the pKa of bufotenine.

SWIM likes freebase bufotenine vaporized most of all and can take up to 30 mg that way for a real intense trip (there’s a little nausea on the come up though, but only for about 1-2 minutes). SWIM usually uses 10 mg at night and lays in bed to watch the very intense eyes closed visions. At that dose it’s extremely visual but not at all intense. The visual effects are phenomenal! By vaporizing it you avoid most of the side effects because it gets rocket launched right into the brain as freebase via the lungs and has little time to ionize in the blood. A small amount vaporized, about 5 mg, will greatly intensify the visuals of most other hallucinogens without causing side effects. At 10 mg and up, nausea starts to creep in for SWIM, but its light nausea and only lasts 1-2 minutes. SWIM never vomited from it. The nausea is from the peripheral vasodilation effects it has on the body. It’s the same type of nausea one gets from taking too much vitamin B3.

500-1000 mg of ginger root taken 30 minutes before hand is very effective at relieving the nausea even from snuff. It works for SWIM.
You may remember me as 69Ron. I was suspended years ago for selling bunk products under false pretenses. I try to sneak back from time to time under different names, but unfortunately, the moderators of the DMT-Nexus are infinitely smarter than I am.

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LemonScented
#8 Posted : 7/6/2008 7:07:45 AM
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swim once smoked calcium bufotenate and he experienced this temporary nausea. if he recalls it was pretty manageable. the nausea associated with the snuff on the other hand, feels more like a gag reflex than being chemically induced. sounds like it could be the other way around tho. in which case ginger is definately a good idea.
 
burnt
#9 Posted : 7/6/2008 10:08:18 AM

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interesting. yea i get the solubility and distribution stuff. so it seems that bufotine needs to be in freebase form. could this explain the strange results from early researchers who were probably injecting it as a salt?
 
polytrip
#10 Posted : 7/6/2008 5:40:10 PM
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If bufotenin is so water solluble, could i just extract it with water then, and mix the yopo-tea with lime, let it dry and then vaporise it?
This seems pretty easy to me. I'm not fond of the smell of naphta and the naphta that's widely available contains some toxic chemicals as well, of wich i don't even like to take the slightest risk of inhaling them, so if a simple water extraction would do.......
 
Entropymancer
#11 Posted : 7/6/2008 6:04:05 PM

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The problem there is all of the plant fats that would also extract into the water. Rather than snorting/smoking seed powder, you'd be attempting to snort/smoke fatty plant goo + bufotenine. I guess that would probably work with vaporizing, though it would probably be about the same as smoking the raw seeds; the thing that makes the smoke unpleasant is all the plant fats, some of which form an irritant chemical called acreolin on combustion. I'm not sure whether you could get the material into a snortable consistency if you're interested in the intranasal route.

But the good news is, bufotenin extraction doesn't require naphtha. There's an extraction tek on drug-forums posted by 69Ron (it may be on this forum too, I didn't check) using acetone, citric acid, and pickling lime. So it looks easy enough to get clean bufotenin of a fairly high purity. (SWIM can't yet confirm, but says he has some seeds on the way to his boathouse in international waters).

I have to admit though, its water solubility makes me intrigued by the idea of harmala/yopo espresso Very happy
 
polytrip
#12 Posted : 7/6/2008 6:18:40 PM
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with drinking it, i think you would have a problem, with it turning into a salt even before it enters the bloodstream. But i think and also hope that yopo-tea/espresso would vaporise well, when mixed with lime and then dried. The mixing with lime would at least go better than with yopo powder.
 
Entropymancer
#13 Posted : 7/6/2008 6:48:51 PM

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No, as far as I know there's no indication that injesting a bufotenin salt orally causes any problems. We only have any indication that the salts are unpleasant intravenously and intramuscularly. Intranasally they appeared to cause no ill effects (no psychoptic effects either though).

Yopo seeds have been reported as being used orally by indigenous peoples. It's possible this was a misunderstanding on the part of the ethnographer, and the ingestion was really buccal (holding the seeds in the mouth). But regardless, Ott has shown pure bufotenin provides psychoptics effects without substantial nausea when taken orally, and by this route is drastically potentiated by the use of an MAOI.

The only warnings about injesting bufotenin salt (other than by IV and IM) come from the charlatan Adam Smyth / Anadenathera, who doesn't appear to have actually tried injesting the salts himself, so the source of his info is unclear and likely fictional.
 
Entropymancer
#14 Posted : 7/7/2008 6:00:18 AM

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Also of interest to the original post is a summary of the published scientific literature on bufotenin's activity in man:



(As has been mentioned, the frequent use of bufotenin salts limits the applicability of some of these findings to the actual use of the drug by typical routes (intranasal, vaporized, etc. administration of the free-base).




Fabing & Hawkins (1955)

These two have the dubious honor of having been the first to explore bufotenine's activity. They injected it intravenously into four inmates at the Ohio State Penitentiary, in doses ranging up to 16 mg of bufotenine creatinine sulfate. The higher doses in this study caused the subjects faces to turn "the color of an egglant." These subjects apparently also experienced minor short-duration visual phenomena, leading Fabing & Hawkins to classify the drug as "hallucinogenic". (Fabing & Hawkins 1956, Ott 1996)


Isbell (1955)

Working under the auspices of the CIA's infamous project MKULTRA, Isbell administered both bufotenin and cohoba snuff to inmates at the Lexington, Kentucky Federal Narcotics Farm (at this facility, nominally a drug rehab center, incarcerated addicts were offered heroin in exchange for cooperation in the experiments). The snuff was found to be inactive at doses up to a gram (the quality of the snuff is unknown, as this report comes secondhand through Turner and Merliss). Doses of up to 40 mg of bufotenine creatine sulfate were found to be inactive when administered intranasally. With 10-12.5 mg of the same salt administered intramuscularly, subjects experienced "visual hallucinations... a play of colors, lights, and patterns." (Turner & Merliss 1959, Ott 1996).


Turner & Merliss (1959)

Having the leisure of captive subjects in a New York mental institution, Turner and Merliss investigated the effects of both bufotenin and DMT in 14 schizophrenics (their trials with the latter drug will be relevant to the discussion of bufotenin's reported toxicity). They reported dramatic physical symptoms following the intravenous administration of 10 mg bufotenin.

It must be recalled that the subjects in these trials were almost certainly on other medications which could have played a role. In some of the cases, bufotenin injections were administered as "[the 'patients'] were coming out of insulin coma or following EST" (electroshock therapy). In their own words, "each of these injections almost proved fatal in small amounts (between 2.5 and 5.0 mg)," with cessation of breathing and the developement of a "plum-colored" face. They note that "the patients become frightened to an extreme degree," which prompts Ott to wonders "whether this 'paranoia' may have conttributed to their continued incarceration and 'treatment' for 'schizophrenia'."

After finsihing their work with bufotenin, Turner and Merliss concluded that bufotenine was not capable of producing the snuff intoxication.

Next, dynamic duo went on to experiment with the human effects of DMT, finding it quite active when 25 mg or more was administered intravenously. In one case, a female patient suffered cardiac arrest and nearly died after the intravenous administration of 40 mg DMT (not bufotenin, which only caused respiratory arrest). This has been reported mistakenly in the literature as a case of "bufotenine toxicity". Based on the work of Dr. Rick Strassman, it would appear that interactions with other medications must have played a role in this instance. (Turner & Merliss 1959, Ott 1996).


Bonhour et al (1967)

Intravenous injection of 12-16 mg bufotenin (again as a water-soluble salt) essentially confirmed the fidings of Fabing & Hawkins. (Bonhour et al 1967, Ott 1996).




In the bufotenin entry of TiHKAL, Dr. Shulgin presents a couple of quotes from patients exemplifying the somatic and visual effects typically encountered with lower-dose IV administration. At higher doses, the unpleasant somatic effects from intravenous administration appear to largely drown out the psychoactive effects.

Quote:
(with 4 mg, intravenously, over a 3 minute period) "During the injection, I first felt a burning sensation in my face, then a load pressing down from above, and then a numbness of the entire body. I saw red and black spots -- a vivid orange-red -- moving around. Apparently my purplish face color lasted some 15 minutes, well after my visual things had disappeared."


Quote:
(with 8 mg, intravenously, over a 3 minute period) "I became lightheaded as soon as the injection started, and then my face turned purple and I became nauseated and I felt I couldn't breathe. I see white, straight lines with a black background. I can't trace a pattern. Now there are red, green and yellow dots, very bright like they were made out of fluorescent cloth, moving like blood cells through capillaries, weaving in and out of the white lines. I another two minutes, everything was pretty much gone."











This was essentially the state of the inquiry into bufotenin's activity prior to the pbulication of Jonathan Ott's landmark Pharmanopo Psychonautics. Shulgin summed up the state of the literature with respect to the activity in bufotenin in the late 1990s:

Quote:
Some clinicians demand that the compound is unquestionably a psychotomimetic and it must be catalogued right up there along with LSD and psilocybin. Others, equally sincere, present human trials that suggest only peripheral toxicity and conclude that there is no central action to be seen. And there are many who state that there are no effects for it at all, either inside or outside the CNS. The psychopharmacological status of bufotenine... may be essentially unanswerable... At the bottom line, I do not really know if bufotenine is a psychedelic drug. Maybe yes and maybe no.


However, he also notes a very compelling bit of evidence for bufotenin's role in the psychoactivity of Anadenanthera snuffs:

Quote:
A study of the use of the seeds of a South American legume, Anadenanthera colubrina var. Cebil by the Argentine Shamans in Chaco Central, shows then to be dramatically psychedelic. And yet, extremely sophisticated spectroscopic analysis has shown them to contain bufotenine and only bufotenine as their alkaloid component.


Referencing this fact (and the bulk of older literature which confirms bufotenin to be the primary alkaloid in the seeds), Ott points to psychonautic bioassays by himself, CM Torres, Christian Raetsch, Pages Laraya, and Castillo, which clearly indicate the seeds to be a psychoptic (psychoactive visonary) agent. He then details his experiences with a range of doses by various routes of administration, both in the presence and absence of an MAOI (read the article if you haven't). This work seems to definitively establish that the concerning somatic effects of IV bufotenin salts don't appear to be so much of an issue when administering the free-base orally, buccally, parenterally as vapor, or intrarectally.

Ott's bioassays would firmly establish bufotenine as the chemical reponsible for the psychoptic effects of Anadenanthera snuffs, were it not for the tremendous disparity between the timeline of his intranasal bufotenin freebase experiences (peaking around 35 minutes in), compared to SWIM and many others' experiences with Anadenanthera snuffs (peaking 3 to 5 minutes in).

And so that's how it stands today: Anadenanthera seeds are without a doubt a psychoptic agent. Bufotenin is without a doubt a psychoptic agent. All the literature suggest bufotenin is the only alkaloid present in the seeds at a high enough concentration to account for psychoactive effects. And yet, the fundamental question, whether bufotenin is solely responsible for the psychoptic effects of the seed snuff, has still not been answered to a satisfactory extent.

Kind of ironic, when we consider the words of Safford, in his 1916 article providing a definitive botanical identification of the source of the snuff:

Quote:
The most remarkable fact associated with this narcotic [sic] is that... the source of its intoxicating properties still remains unknown.
 
69ron
#15 Posted : 7/7/2008 8:52:36 AM

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Entropymancer wrote:

Fabing & Hawkins (1955)

These two have the dubious honor of having been the first to explore bufotenine's activity. They injected it intravenously into four inmates at the Ohio State Penitentiary, in doses ranging up to 16 mg of bufotenine creatinine sulfate. The higher doses in this study caused the subjects faces to turn "the color of an egglant." These subjects apparently also experienced minor short-duration visual phenomena, leading Fabing & Hawkins to classify the drug as "hallucinogenic". (Fabing & Hawkins 1956, Ott 1996)


It’s SWIM’s belief that many of these types of tests were invalid because they actually unintentionally tested bufotenine N-Oxide. The effects that most of their test subjects reported sound to SWIM to be identical to the effects of bufotenine N-Oxide and not bufotenine. Bufotenine can rapidly oxidize into bufotenine N-Oxide in some cases in as little as a few minutes if the environment is right.

Bufotenine is not a commonly sold drug. Many companies have bufotenine sitting on the shelf for years before it’s actually sold. If one purchases bufotenine for testing purposes and it is old and wasn’t kept properly, it will have all oxidized to bufotenine N-Oxide.

Entropymancer wrote:

However, he also notes a very compelling bit of evidence for bufotenin's role in the psychoactivity of Anadenanthera snuffs:

Quote:
A study of the use of the seeds of a South American legume, Anadenanthera colubrina var. Cebil by the Argentine Shamans in Chaco Central, shows then to be dramatically psychedelic. And yet, extremely sophisticated spectroscopic analysis has shown them to contain bufotenine and only bufotenine as their alkaloid component.



SWIM has found in his seeds that nearly all of them contain lots of bufotenine AND nearly equal amounts of bufotenine N-Oxide. Why is no one talking about bufotenine N-Oxide? This is a major alkaloid in the seeds and its effects are quite different from bufotenine. Please correct me if I’m wrong but I believe that spectroscopic analysis falsely identifies bufotenine N-Oxide as bufotenine because it cannot distinguish one from the other.

Entropymancer wrote:

Referencing this fact (and the bulk of older literature which confirms bufotenin to be the primary alkaloid in the seeds), Ott points to psychonautic bioassays by himself, CM Torres, Christian Raetsch, Pages Laraya, and Castillo, which clearly indicate the seeds to be a psychoptic (psychoactive visonary) agent. He then details his experiences with a range of doses by various routes of administration, both in the presence and absence of an MAOI (read the article if you haven't). This work seems to definitively establish that the concerning somatic effects of IV bufotenin salts don't appear to be so much of an issue when administering the free-base orally, buccally, parenterally as vapor, or intrarectally.


It must be kept in mind that different salt forms of drugs have different toxicity profiles and different potencies, and sometimes the differences are huge. This is why, in the US, only certain salt forms of some drugs are approved while others are banned because they are too toxic. If you are interested there is an entire book on this subject called “Handbook of pharmaceutical salts: Properties, Selection, and Use” which talks about how the effects of drugs can dramatically change by simply changing the salt form of it from one to another.

One thing that could have contributed to the toxicity of some of the earlier bufotenine injection tests was that a salt form that is specifically toxic may have been used. No one tested all the salt forms of bufotenine to find the least toxic form.

It’s known by many SWIMs that DMT phosphate is best form of DMT for making ayahuasca. It seems to produce the least toxic side effects with other forms producing much more nausea. I’m sure there is a best salt form for bufotenine as well, but it’s currently unknown.

Entropymancer wrote:

Ott's bioassays would firmly establish bufotenine as the chemical reponsible for the psychoptic effects of Anadenanthera snuffs, were it not for the tremendous disparity between the timeline of his intranasal bufotenin freebase experiences (peaking around 35 minutes in), compared to SWIM and many others' experiences with Anadenanthera snuffs (peaking 3 to 5 minutes in).


In all SWIM’s experience the snuff, like pure bufotenine, always takes about 2-5 minutes to start and 30-45 minutes to peak. SWIM doesn’t know why there’s such a difference in some reports, but there is. SWIM knows some people personally who say the snuff peaks after 10 minutes for them. SWIM is baffled by this info. What could cause such a huge differences in onset and peak time?
You may remember me as 69Ron. I was suspended years ago for selling bunk products under false pretenses. I try to sneak back from time to time under different names, but unfortunately, the moderators of the DMT-Nexus are infinitely smarter than I am.

If you see me at the waterpark, please say hello. I'll be the delusional 50 something in the American flag Speedo, oiling up his monster guns while responding to imaginary requests for selfies from invisible teenage girls.
 
 
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