Ayahuasca healing: How easily are permanent changes aquired

[psyche]

For about a year SWIM has been steadily losing his personality and interest about everything. That has been accompanied and might even be caused by his impaired memory and concentration. Last sunday he finally made succesfull DMT trip with 10g mimosa and 5g syrian rue. It was wonderful, scary and lonely trip, which lasted a bit too long for SWIM. Next day and day after that he felt the most blissful afterglow: he felt like his memory would've been greatly improved and he was alive again and that he had forgot how great it was to be alive. After couple of days that faded away and now SWIM is thinking about trying that again, maybe two days in a row, for longer periods of time. Any healing experiences would be appreciated, especially info on what doses and for how long it took to get long-term benefits.

[CrookedEye]

SWIM has read studies of Shaman who used ayahuasca at least 2X a week, and after a few years had much higher serotonin levels than the normal population.. This resulted in a better sense of well being and better health.. SWIM thinks that it's mostly from the MAOI action, but the DMT sure probably makes it way fun..

[psyche]

You aren't talking about Grob's study of UDV members, who had significantly improved attention span and memory, right? It too found that long-term ayahuasca users had more serotonin receptors than the control group. I'd like to have some nearly first hand experiences.

[sunyata]

SWIM has also noticed this "afterglow", but he gets it from most tryptamines, like psilocybin, LSD, 5-meo-Dipt/Mipt.
I am not sure, but I am wondering if it might have something to with the tryptamines being broken down to plain tryptamine(or similar) and then being rebuilt into serotonin. Something like that.
For SWIM it has nothing to do with the psychedelic experience itself, since even un-psychedelic doses has this after-effect on him.
It makes SWIM think that 25-50mcg doses of LSD would be very a very good anti-depressants for some people. Though I suspect some people would just save their up their doses for the weekend.

With Ayahuasca I have the impression it is not a one-time-only kind of medicine, one needs to take it with a certain frequency, and one needs to actively direct the experience into those areas one wants to work on.
And there is also something about the medicine not being only in the ayahuasca, but in the application of it. That is, it is not enough to just drink the brew and lay back, you need to participate directly in the experience for the best results.
There are a lot of books on shamanism that will give you an idea on how to do this, Michael Harner has written a few. Or you might not read any books at all and just go on instinct if you please. The trick is to go from being someones patient to being you own doctor.

Anyway, 5g of peganum harmala is a bit on the heavy side and might account for your experience lasting long, the same happened to SWIM at that dose level.

[psyche]

SWIM will definately try next time about 3g of syrian rue. Also the trip was very uncomfortable all the time since SWIM didn't manage to puke anymore after an hour had passed and he had kept it in.

I am not sure, but I am wondering if it might have something to with the tryptamines being broken down to plain tryptamine(or similar) and then being rebuilt into serotonin. Something like that.

That's an interesting idea, but I think it isn't from serotonin (alone) based on SWIMs experience with 5-HTP. It was nothing like ayahuasca's afterglow, particularly it doesn't increases SWIM's mental abilities(or feel like they've increased) and doesn't make SWIM so profoundly happy. But ofcourse there's difference between tryptamine, l-troptophan and 5-HTP, tryptamine might have more complex effect on mood overall than the specific serotonine 'prodrug'.
SWIM should propably do some reading on shamanism, but he is a bit doubtful about it and feels like it's conflicting with his scientific worldview, it feels a bit dodgy on general.

[Nagognog2]

I've found the Shamanic view highly useful and complimentary to both understanding and employing psychology and science. So you might be surprised at what you find if you approach with your mind wide open.

[dreamatrix]

swim doesnt think you can take dmt or any ayahusca brew and not be permanently changed from the very first time,, the cosmic serpent takes you ,there is no choice ,surrender or you resist ,,

[Enfintity]

yes, the higher th dose of MAOI generally the longer the experience will last. 2 grams of harmala is enough to inhibit MAO
also, b. caapi is usually much preferred over harmala, definitely think about giving it a try. b. caapi IS ayahuasca.


DO NOT POST LINKS TO OTHER FORUMS. READ THE RULES.

[Orchid_Suspiria]

SWIM has discovered it takes more than a substance to make a change.Sure substances can be teachers and helpers but one has to want that change enough.

[psyche]

Last time I met SWIM he mentioned to me that he has begun to question whether the aferglow (and all healing power) from ayahuasca is only form peganum harmala. After all there are products like moclobemide for depression. Has any of your friends treated depression with peganum? SWIM should test peganum alone to see if it clears his head as ayahuasca.

The 'healing' or whatever is going on with ayahuasca helps with SWIM's short-term memory, concentration and imagination remarkably. SWIM has lived not-so-vivid life of his for about half a year: nothing interests, everything is flat and lacks details, everything is stressing and needs alot of effort. He has been pondering on what is going on, but the most likely explanation would be that he is just becoming exactly like he's father is. Genes. He has in doubt if it could be the cannabis that is doing this to him, if he's prone for this kind of nasty side-effect of weed. He's been thinking to see a psych for some time but never got around doing it...

Enfintity why should I tell SWIM to try caapi? Why is it preferred?

[Enfintity]

i just suggest it because b caapi is ayahuasca, even without anything else added, while harmala is what is referred to as an ayahuasca analogue.
they have their own personality and ways of 'teaching'. and most report that caapi feels as though it has a longer history working with humans, and that it feels more 'friendly' and 'teacherly'(new word) than harmala.


here is some interesting info:
taken from the nook and ayahuasca forums:

posted by Archaea:
"I found this interesting bit of info/knowledge on another forum from Archaea (May 25 2006) and I hope it clears up some misunderstandings about food interactions with betacarbolines and the role that THH plays in the brew in potentiating the dmt effects from psychotria and other dmt containing plants admixture to the brew:

"With caapi you really don't have to worry about foods so much as medications, caapi is not much of an MAOI compared to its other effects.

This will be explained below.

Harmine & Harmaline are betacarbolines, but in caapi THH (tetrahydroharmine) is also present, a betacarboline that is an SSRI and has a lot to do with the activity of caapi on its own. Caapi is used by itself and that is called ayahuasca, any ayahuasca brew containing DMT is an ayahuasca admixture.

MAOI is an effect, not a chemical class. Many different alkaloids can have MAOI effects, MDA and mescaline for example, have some MAOI properties.

Also harmine and THH, the major constituents of most caapi, are only selective MAOI type A short term reversible inhibitors, they are nothing like long term type B ireversible inhibitors that all those medical precautions are about. Mescaline is more likely to cause a hypertensive reaction with tyramine for example, than caapi or rue would, because the MAO enzyme has a higher affinity for tyramine that it does for the betacarbolines. In other words you can violate the MAOI diet with caapi and rue without signifigant risk, the single expection to this is medications that are SSRI or MAOI themselves but those can cause things like seizures when taken with LSD and mushrooms and it is just unwise for someone on prescription meds to take a psychoactive.

Harmaline BTW is the major alkaloid in rue and can be very unpleasant to take, Shulgins tests with it are a good example, but he never did explore the betacarbolines much.
Betacarbolines have complex action, they are not just MAOI type a reversible selective inhibitors, they have a pronounced sedative action and their own psychoactive potential, some as I mentioned are SSRI's that may not be active themselves without taking an MAOI with them.

As for mushrooms you can potentiate the experience of mushrooms without an MAOI inhibitory dose. The betacarboline potentiation of tryptamines is due to their SSRI properties. MAOI's attenuate the effects of tryptamines while SSRI's potentiate them. Because the betacarbolines have both MAOI and SSRI actions, among others, they can allow oral activation of DMT and potentiate it.

Rue contains other alkaloids that caapi doesn't and a doctor who has testified to the supreme court over the saftey of caapi once told me I should avoid playing with rue (and other non-traditional MAOIs) and that it was not tried and true like caapi. There are other MAO-Inhibition causing alkaloids in rue that can promote hypertensive crisis with massive doses.

I find the the betacarbolines (such as found in caapi) are, in my opinion, the most misunderstood alkaloids out there, with a plethora of flawed information on them still being perpetuated in entheogenic circles and I have posted a bit about that opinion before:



Betacarbolines: Fact, Fiction and Mystery.

[B]Beta-carbolines are often considered in counterculture literature and forums, to be monoamine oxidase inhibitors used for the oral activation and the potentiation of psychoactive tryptamines including DMT, NMT and others. It is true that betacarbolines, a rather large group of molecules, is known to have MAOI effects, however the action of beta-carbolines, even those used for the purpose of potentiation or activation, is complex and the resulting effects cannot be attributed to MAOI properties alone. Moreover the effects of potentiation do not seem due to the MAOI properties.


QUOTE
beta-Carbolines regulate acetylcholine secretion through the benzodiazepine-GABA complex and through the secretion of GABA (a neurotransmitter). Acetylcholine is a primal neurotransmitter, involved in our behavior, cognitive functions and muscle contractions. Acetylcholine is made of choline, and the transportation of choline is also regulated by beta-carbolines. (4) beta-Carbolines also influence secretion and decomposition of other neurotransmitters, like serotonine, dopamine and norepinephrine.



QUOTE
Tomas Herraiz, a Spanish chemist, has isolated one more chemical from chocolate. Dr. Herraiz has found alkaloids called tetrahydro-beta-carbolines in chocolate and cocoa. The newly discovered compound, tetrahydro-beta-carboline, and the family of chemicals it belongs to, beta-carboline alkaloids, affect the central nervous system in several ways:

* They are mild inhibitors of an enzyme called monoamine oxidase (MAO). MAO is an enzyme that destroys monoamine neurotransmitters (norepinephrine, dopamine, serotonin).

* They work by inhibiting the reuptake of the serotonin. The net result is an increase in the amount of serotonin within the synapse.

* They inhibit the binding of benzodiazepines on their receptors. This results in a decrease in the level of the neurotransmitter GABA.



b-Carbolines antagonize the anxiolytic, anticonvulsant and sedative effects of the benzodiazepines. These compounds also can differentiate between the anticonvulsant and anxiolytic actions of the benzodiazepines. Early studies suggested that the b-carbolines may be produced endogenously to modulate GABA receptors in vivo although a physiolgical role of the b-carbolines has been refuted.

Within the class of b-carbolines, molecules with varying potency and efficacy have been developed for benzodiazepine binding sites. Both methyl- and ethyl-b-carboline-3-carboxylate are proconvulsant. They block the binding of benzodiazepines and act as inverse agonists since they produce the opposite effect of diazepam.


One common mistake often encountered in subversive literature is that betacarbolines are regarded as MAOI, they should be though of as Beta-carbolines and as having some MAOI effects, however they are selective reversible short-term inhibitors of MAOI-A and as such should not be classed along with MAOI in general. One common tidbit of misinformation that keeps being recycled is that the dietary precautions for MAOI's in general apply to Beta-carbolines that are used in Ayahuasca, this simply isn't substantiated or even indicated. On the contrary at dosages normally used for Ayahuasca, breaking dietary precautions for prescription MAOI's will cause no ill effects. A much greater risk comes from combining betacarbolines with prescriptions drugs such as anti-depressants, than from eating tyramine rich foods while under the influence of betacarbolines.

http://www.erowid.org/chemicals/ayahuasca/..._journal3.shtml
QUOTE


] The primary action of ß-carbolines in the ayahuasca beverage is their inhibition of peripheral MAO, which protects the DMT in the brew from peripheral degradation and thus renders it orally active. There is some evidence, however, that tetrahydroharmine (THH), the second most abundant ß-carboline in the beverage, acts as a weak 5-HT uptake inhibitor and MAOI. Thus, THH may prolong the half-life of DMT by blocking its intraneuronal uptake, and hence, its inactivation by MAO, localized in mitochondria within the neuron. On the other hand, THH may block serotonin uptake into the neuron, resulting in higher levels of 5HT in the synaptic cleft; this 5-HT, in turn, may attenuate the subjective effects of orally ingested DMT by competing with it at post-synaptic receptor sites (Callaway, et al., 1997). It is worthy of note that ß-carbolines are highly selective inhibitors of MAO-A, the form of the enzyme for which serotonin, and presumably other tryptamines, including DMT, are the preferred substrates (Yasuhara, et al., 1972; Yasuhara, 1974). This selectivity of ß-carbolines for MAO-A over MAO-B, combined with their relatively low affinity for liver MAO compared to brain MAO, may explain why reports of hypertensive crises following the ingestion of ayahuasca have not been documented. On the other hand, Suzuki, et al., (1981) has reported that DMT is primarily oxidized by MAO-B; it is possible, therefore, that high concentrations of ß-carbolines, partially inhibit MAO-B as well as MAO-A; but the greater affinity of tyramine for MAO-B enables it to compete for binding to the enzyme and displace any residual ß-carbolines. This mechanism would explain the lack of any reports of peripheral autonomic stimulation associated with the ingestion of ayahuasca in combination with foods containing tyramine (Callaway, et al., 1997)…

ß-carbolines exert a variety of neurophysiological and biological effects (McKenna and Towers, 1984). ß-carboline derivatives are selective, reversible, competitive inhibitors of MAO-A (Buckholtz and Boggan, 1976, 1977). Other neurophysiological actions of ß-carbolines include competitive inhibition of the uptake of 5-HT, dopamine, epinephrine, and norepinephrine into synaptosomes (Buckholtz and Boggan, 1976; P·hkla, et al., 1997), inhibition of Na+ dependent membrane ATPases (Canessa, et al. 1973), interference with biosynthesis of biogenic amines (Ho, 1977), and vasopressin-like effects on sodium and water transport in isolated toad skin (de Sousa and Gross, 1978). ß-carboline-3-carboxylate and various esterified derivatives have been implicated as possible endogenous ligands for benzodiazepine receptors (Lippke et al. 1983). ß-carboline ligands of these receptors can induce epileptiform seizures in rats and in chickens homozygous for the epileptic gene (Morin, 1984; Johnson, et al. 1984); this proconvulsant action can be blocked by other receptor ligands, including diazepam and ß-carboline-carboxylate propyl ester (Morin, 1984; Johnson, et al. 1984).





I know of one study that found the effects of DMT were attenuated IE cancelled by MAOI inhibition and potentiated by SSRI, it should be noted that taking an SSRI with a MAOI can be deadly in terms of prescription medicine, however some beta-carbolines clearly have both MAOI and SSRI function and have no detrimental symptoms or side effects that have been observed. Particularly interesting is the clandestine work that has been done on potentiation.

We had developed this technique for smoking the passion flower to potentiate Psilocybian mushrooms (see below) and wished to have the data from this set of experiments be comparable…

In each case we smoked the extract until we had reached subjectively the same high…

The high is not particularly psychedelic or hallucinogenic. One feels calm. This calming effect is particularly noted by an observer as a significant change in facial expression and tone of voice. The limbs become heavy and lethargic and visibly tremble. Hypersalivation occurs, particularly at the back of the mouth, making for a particularly smooth smoke. A slight irritation of urethra and anus is sometimes noted. At higher dosages, dizziness and nausea sets in with very little increase in the high. Closed eye imagery is at best hypnagogic. That is to say, faint, moving outlines can be discerned with closed eyes. If one has a particularly vivid imagination, ghostly outlines of figures can be discerned. The more literal minded just see dim shifting blobs of light and dark. No one who has experienced DMT or high dose mushrooms would ever call them visions.

The high comes on and stabilizes after about 5 to 10 minutes or smoking. As mentioned before, it is very difficult to get higher by smoking more. If one stops at this point, the most noticeable thing would be a calm and unapprehensive state. We take particular note of this diminishing of apprehensions since we are always apprehensive before we smoke DMT so its diminution or absence is very noticeable.

Curiously, although various field researchers estimate beta-carboline dosage in native brews to range between 300 to 500 mg, in our dosage we only needed dosages in the 50 mg range. As noted above, increasing the dosage did not increase the high but only aggravated the physical symptoms. Even when tryptamines were taken later in addition, increasing the dosage past this point did not significantly alter the combined trip. It was as if there was some "switch" in the brain which, with sufficient beta-carbolines, was set from "off" to "on" and no further action would take place. We do not rule out the possibility of a second "switch" at the 300 - 500 mg range that we might have missed…

We potentiated the mushrooms by each smoking about 750 grams(!) of passion flower (reduced as described above) starting about 30 minutes after eating the mushrooms…

Note the dosage and the timings, they smoked/vaped beta-carbolines 30 minutes after eating the fungi for potentiation, if the potentiation was due to MAOI activity it would make sense that the MAO enzymes involved would need to be inhibited prior to ingestion to facilitate potentiation. I believe that the symptoms they report indicate that the potentiation effect involves more than MAO inhibition and relates to the SSRI properties.
MAOI again, having been shown to weaken the effects of tryptamine psychedelics, not potentiate them, despite the oral activation involving such inhibition.

I have a hunch some of the betacarboline compounds are like NMT and DMT, orally inactive under most contexts, but that some compounds like THH may have pronounced psychoactive effects when combined with other beta-carbolines. I believe this is why caapi sees so much use as ayahuasca without the addition of a DMT containing admixture and Peganum typically isn't used in the same manner. Peganum use is much more reserved for combining with other things while caapi sees use in both ayahuasca and ayahuasca admixtures containing DMT.


It seems a lot of anxiety about betacarbolines exists due to prescription MAOI literature, this is unfortunate as that outdated information may be keeping some people from undergoing safe explorations with these rather magical chemicals."


http://www.erowid.org/chemicals/maois/maois_info7.shtml

Cheddar Cheese and Moclobemide
Anonymous (1996)

We had this argument about tyramine and selective MAOI-A's some time ago, and the data shows that tyramine is NOT a *large* problem with selective / reversible MAOI-As.

"No rise in bloodpressure was noted in 6 healthy subjects whore received cheddar cheese with tyramine content of 65 to 70 mg before and after treatment with moclobemide. In 3 subjects treated with tranylcypromine the cheese caused a pronounced and sustained rise in blood pressure." A. Korn et al., J. Pharm. Pharmac. 1984 (36 - Sup 64W)

Note : tranylcypromine is also a reversible MAOi (enzyme activity recovers after 3-5 days) and that it's maoA that protects against tyramine.

There has been a lot of research on MAOI-a since the release of moclobemide and these findings should replace the previous stupid list of danger foods entirely. That old list is a relic from the days when there were no selective MAOIs.

I just looked up the tyramine content of cheddar cheese, which is approximately 15mg per 100g. Hypertension from tyramine administered just after MAO-a inhibition required 150mg of tyramine to induce a 30mmHG rise in bp.
So the lesson is to not eat a kilo of cheddar while tripping on ayahuasca.

But even at that dosage the rise is only 30mmHG which would be barely noticable unless you already have excessively high bp."

posted by Tregar:
"Posted: Mon Feb 19, 2007 11:17 pm Post subject: I agree with this thread...coming to the same conclusions myself after taking sessions with just pure harmine vs. a caapi session (which was way more visual) due perhaps to the THH found in the caapi brew.

The harmine seems to be allowing the DMT to survive the rigors of the gut intact, then when it makes it to the brain, the THH is inhibiting serotonin reuptake...and when this happens, the DMT's half-life is being extended and perhaps potentiated--may explain why typical ayahuasca doses are from 29 to 68 mg or so--with an average of 35mg.

Quote:It seems that serotonine inhibition potentiates the effect of injected DMT....the finding that an MAO-inhibitor decreased the activity of injected DMT may be important in ayahuasca pharmacology.
Ott 'ayahuasca analogues' pg 67.

Quote:There is some evidence, that THH, the second most abundant B-carboline in the beverage, acts as a weak 5-HT uptake inhibitor and MAOI. Thus, THH may prolong the half-life of DMT by blocking its intaneuronal uptake, and hence, its inactivation by MAO, localized in mitochondria within the neuron.

On the other hand, THH may block serotonin uptake into the neuron, resulting in higher levels of 5HT in the synaptic cleft; this 5-HT, in turn, may attenuate the subjective effects of orally ingested dmt by competion with it at post-synaptic receptor sites.
Callaway, 1997.

Quote:This selectivity of B-carbolines for MAO-A over MAO-B, combined with their relatively low affinity for liver MAO compared to brain MAO, may explain why reports of hypertensive crises following the ingestion of ayahuasca have not been documented.

On the other hand, Suzuki et al. (1981) has reported that DMT is primarily oxidized by MAO-B; it is possible, therefore, that high concentrations of B-carbolines, partially inhibit MAO-B as well as MAO-A; but the greater affinity of tyramine for MAO-B enables it to compete for binding to the enzyme and displace any residual B-carbolines.

This mechanism would explain the lack of any reports of peripheral autonomic stimulation associated with the ingestion of ayahuasca in combination with foods containing tyramine.
Callaway 1997.

Since caapi is hallucinogenic on its own--I know I've taken large doses of caapi brew all by itself and had fantastic closed eye visuals in dark greens and blues--like silohuettes just not bright--the 3 tricyclic indole compounds found in caapi working together synergistically are fascinating all on their own.

130 to 193 mg THH found in an average caapi brew along with 204 to 306 mg of harmine and 24 to 36mg harmaline.

Archaea said:
Quote:I have a hunch some of the betacarboline compounds are like NMT and DMT, orally inactive under most contexts, but that some compounds like THH may have pronounced psychoactive effects when combined with other beta-carbolines. I believe this is why caapi sees so much use as ayahuasca without the addition of a DMT containing admixture and Peganum typically isn't used in the same manner. Peganum use is much more reserved for combining with other things while caapi sees use in both ayahuasca and ayahuasca admixtures containing DMT.
My thoughts exactly.

Quote:While ayahasca MAO-inhibitors enable DMT to survive the rigors of the gut and thus rendered active orally, they may exert an anti-DMT effect in the brain, which explains why oral DMT is much less active than DMT smoked.
Ott, 'Ayahuasca Analogues' pg 67.

Quote:However, subjects who took Sansert, a serotonine antagonist, reported a "strong potentiating effect" on injected DMT.
Ott, 'Ayahuasca Analogues' pg 67.

THH in caapi may be exerting the same strong serotonin reuptake inhibition in the brain -- rendering the oral DMT that reached the brain to be potentiated and extended."

Reputation Comments on this post:

	interesting info
	Wow, good info.

[Paracelsus]

Originally Posted by Enfinity

However, subjects who took Sansert, a serotonine antagonist, reported a "strong potentiating effect" on injected DMT.

That isn't surprising. Sansert (by the way related to LSD) is hallucinogenic on it's own (10-20mg).

[psyche]

The betacarboline potentiation of tryptamines is due to their SSRI properties. MAOI's attenuate the effects of tryptamines while SSRI's potentiate them. Because the betacarbolines have both MAOI and SSRI actions, among others, they can allow oral activation of DMT and potentiate it.

I think I'm a bit mixed here as I remember reading from someone that MAOI's and SSRI's make DMT weaker because there is more serotonine to compete with DMT for receptors.(Might've been Strassmann) Too bad I don't know where I read it... That doesn't seem to be a common opinion about the subject. SSRI's take almost all of the ecstacys magic out but I guess that's a different story because of MDMA's role on reuptake pump which SSRI's block. If that would be the case with MAOI's then all other psychedelics would be also tamed by peganum and potentiated only by it's psychoactive effects alone. Could someone offer an answer?

Very good read, enfintity, really.

Edit: Sorry, didn't read the whole post. I just spotted this and my internet connection went down for some time:

Quote:While ayahasca MAO-inhibitors enable DMT to survive the rigors of the gut and thus rendered active orally, they may exert an anti-DMT effect in the brain, which explains why oral DMT is much less active than DMT smoked.
Ott, 'Ayahuasca Analogues' pg 67.

Right, it was Ott who I remembered wrote something like that, not Strassman.