709 replies to this topic

[JustAMan]

To both MissJess and socialpirahna: Did you use a total alkaloid (TA) extraction, or the HCL salt (ibogaine HCL)? Also, how did you arrange your mental state and environment (set and setting) prior to your flood doses?

[KieranA001]

Can you explain how ibogaine is different to other psychedelics? If that's possible. It seems quite interesting, and I'm sure all the bad effects will go away over time. Your brain has to adjust itself back to normal. It might take a year to a couple of years maybe ? I don't know.

Also, thanks for removing the extra purchase from the list! Much appreciated.

[Missjess]

I used TA from ibogaworld...my set was perfect I had bwiti music playing in the background and I did everything safely and even had a nurse watching me and checking me every hour....mind u I was feeling suicidal during the week before I did iboga however I was ok on the night of the experience and I felt I was ready to die and give up I had the mindset if this is my last shot at trying to cure myself of dp or I will kill myself

Honestly I think the dose was just a little too much for my body to handle

[formergenius]

My Iboga trip was a bad trip; thought I was gonna die of bradychardia. I mean I was fine with dying and all, but it was bad timing. I'd rather die another day, under different circumstances.
Then I ate some onion cake and felt a bit better. Food tastes strange on Iboga.

I was an idiot with set and setting; it was in a location I dislike and very thin walls.. I would've preferred a sound-proof room. Plus someone walked in on me just as the trip started to come up, and got mad at me for tripping. I had 15 minutes of good experience before that, but after that things went downhill. I'm pretty sure if my set and setting had been different, that I would have had a much smoother experience. I would've preferred to have done it in solitude, but was unexpectedly accompanied; this really didn't go well with me. Setting greatly influenced my set.

Missjess your dose sounds like it was pretty high. I aimed for threshold full-trip. Yours was more than enough to accomplish that. Mind you; I wish I had tried half or even a quarter of that dose before doing the full trip.

Iboga is not something to hurry with, regardless of the urgency of necessity for relief you may have.

[formergenius]

Can you explain how ibogaine is different to other psychedelics? If that's possible. It seems quite interesting, and I'm sure all the bad effects will go away over time. Your brain has to adjust itself back to normal. It might take a year to a couple of years maybe ? I don't know.

Also, thanks for removing the extra purchase from the list! Much appreciated.

Iboga is a very complicated entheogen with many different alkaloids; the most well studied of which are Ibogaine and Nor-Ibogaine.
Ibogaine is a NMDAR antagonist and a KOR agonist; a perfect potion for dissociation. This is primarily what sets Iboga apart; classic psychedelics are 5HT2a/c agonists, sometimes 5HT releasers. Nor-Ibogaine is a KOR antagonist and a MOR agonist, as well as a pretty potent SRI.

For these reasons an Iboga flood usually sucks a lot and then leaves you with an afterglow of sorts. Though mind you, I didn't have the latter myself.
Thus the question is; who's up for trying Nor-Ibogaine on its own?

Edited by formergenius, 25 January 2014 - 06:32 PM.

[socialpiranha]

To both MissJess and socialpirahna: Did you use a total alkaloid (TA) extraction, or the HCL salt (ibogaine HCL)? Also, how did you arrange your mental state and environment (set and setting) prior to your flood doses?

Yeah i used a TA from cerberus extract. My setting could have been better and the fact that i was in the throws of opiate withdrawal obviously isn't optimal. It is extremely powerful compared to other psychedelics when a wave hits you your gone there is absolutely no chance of enacting your will. It's very hard to describe the difference in effect but it is just a whole different ballgame. It honestly felt like i was in a machine i have no words to describe it.

[Missjess]

Yes well apparently my dose was a normal full flood dose, I was going for the full brain reset.
I think there shud be more information on the possible dangers and complications of iboga it stretches far more then just heart failure and seizure. I have observed the following; bad memory & cognitive skills, zero motivation, zero social interest, blank mind, neuro/brain chemistry damage or changes, I am unable to concentrate or plan a task and I cannot work like this I tried to work 4 months after my flood and I couldn't do it!!

Iboga also damaged my thigh muscles, literally the muscle had shrunk once I got out of the hospital and I have been doing my best to tone them up and build them up again ever since

[socialpiranha]

Can you explain how ibogaine is different to other psychedelics? If that's possible. It seems quite interesting, and I'm sure all the bad effects will go away over time. Your brain has to adjust itself back to normal. It might take a year to a couple of years maybe ? I don't know.

Also, thanks for removing the extra purchase from the list! Much appreciated.

. Nor-Ibogaine is a KOR antagonist and a MOR agonist, as well as a pretty potent SRI.

KOR agonist isn't it?

Thus the question is; who's up for trying Nor-Ibogaine on its own?

[KieranA001]

Can you explain how ibogaine is different to other psychedelics? If that's possible. It seems quite interesting, and I'm sure all the bad effects will go away over time. Your brain has to adjust itself back to normal. It might take a year to a couple of years maybe ? I don't know.

Also, thanks for removing the extra purchase from the list! Much appreciated.

. Nor-Ibogaine is a KOR antagonist and a MOR agonist, as well as a pretty potent SRI.

KOR agonist isn't it?

Thus the question is; who's up for trying Nor-Ibogaine on its own?

I will try Nor-Ibogaine on its own. :D what are the effects ? All I know is that when I took Salvia, I didn't really trip. Although, I did think I was someone else. I just remember thinking that I was Mr Miyagi from Karate kid, and I was arguing with some dog poop in the back of my garden. It's very weird, and don't know what came over me. lol. Another reason why I'm not going to do Salvia again lol it's like I thought the poop had
emotions.

Is Nor-Ibogaine just a SRI ?

Edited by KieranA001, 25 January 2014 - 07:13 PM.

[socialpiranha]

I think picasso must have tried salvia

[formergenius]

Kieran; Incorrect, Ibogaine is a KOR agonist. Nor-Ibogaine is KOR antagonist.

Edited by formergenius, 25 January 2014 - 07:32 PM.

[socialpiranha]

are you sure nor-ibogaine is a kor antagonist?

[KieranA001]

Kieran; Incorrect, Ibogaine is a KOR agonist. Nor-Ibogaine is KOR antagonist.

Oh, so why are you guys taking Ibogaine. If I've got this correct, Salvia is a KOR agonist as well, and if Ibogaine is a KOR agonist then how does it get rid of the DP/DR? Salvia causes Psychosis to an extent, shouldn't Ibogaine do the same? Unless they have different ways in which they work that gives gifferent effects. :/

Nor-Ibogaine looks quite good, all I know from Google is that it's used to treat addiction like Ibogaine without some of the bad side-effects. If it works on the dopamine, apparently this stuff is neurotrophic on dopamine neurons plus others, so I guess that's how it helps with DP/DR/deression ? Maybe.

[formergenius]

are you sure nor-ibogaine is a kor antagonist?

No, I'm being a wiki-slut. I just did a !gsc search and found this:

The findings suggest that the metabolite noribogaine may be devoid of NMDA antagonist and κ-opioid agonist discriminative effects and that it may play a major role in mediating the discriminative stimulus effect of ibogaine.

But it does bind to the KOR nonetheless; hence suggesting it is an antagonist (unless there is something as a neutral ligand??).

Oh, so why are you guys taking Ibogaine. If I've got this correct, Salvia is a KOR agonist as well, and if Ibogaine is a KOR agonist then how does it get rid of the DP/DR? Salvia causes Psychosis to an extent, shouldn't Ibogaine do the same? Unless they have different ways in which they work that gives gifferent effects. :/

Nor-Ibogaine looks quite good, all I know from Google is that it's used to treat addiction like Ibogaine without some of the bad side-effects. If it works on the dopamine, apparently this stuff is neurotrophic on dopamine neurons plus others, so I guess that's how it helps with DP/DR/deression ? Maybe.

Because there's a lot of spiritual marketing round it (also claims of a "brain-reset" etc. that for someone who's just starting to get in to pharmacology can sound very attractive).
And theoretically the agonism could cause long-term down-regulation I suppose with a flood dose.
Ibogaine also has other effects, also its metabolite nor-iboagine has KOR antagonistic properties, so they interact.
It also hasn't been studied completely and other MOA's may yet to be uncovered.

Nor-Ibogaine vs. Ibogaine would indeed be more easy on the mind probably.

EDIT: Can we please remain on topic w.r.t. JDTic? We can open a new topic for Iboga discussion.

Edited by formergenius, 25 January 2014 - 08:03 PM.

[addx]

The study mentioned above ignores the fact that k-opioid agonists do not cause addiction and are generally disphoric and thus repulsive and as such rats will not self-administer them even if they were introduced to ibogaine. This does not prove noribogaine is not a k-opioid agonist.

Infact, I know I have seen a study about this, comparing required molar values of both ibogaine and noribogaine to activate a range of receptors they suspected. IIRC noribogaine is stronger at k-opioid receptors than ibogaine and they are both agonists and both mu and kappa.

I do believe the mechanism by which noribogaine "cures" removes tolerance is "emulating" fear extinction by flooding pretty much the correct receptors to do it. Agonism of kappa opioid receptors causes fear memory schema recall into "working memory" only to have the fear component extincted by my opioid agonist which may also require ibogaine serotonin activity(ibogaine is active at 5ht2a site by itself AFAIK)

The lasting effects of inability to think, motivate and depersonalization I believe come from the lasting kappa opioid agonism of the lingering metabolite noribogaine. It stays active for months.


There is no natural kappa opioid antagonist to the best of my knowledge.

Edited by addx, 27 January 2014 - 07:58 AM.

[addx]

Ah, found a nice post to confirm what I wrote with heaps of info about both ibogaine and noribogaine that should resolve this

[socialpiranha]

I've definitely seen conflicting data all i can say is i know how high doses of buprenorphine feels and i know how salvia feels and ibogaine feels a lot more like salvia. suboxone is the hardest drug to get off with ibogaine because there is some conflict with the kappa receptor, I would guess it's because an agonist in iboga has a higher affinity for the receptor. Switching abruptly from chronic antagonism to strong agonism would explain the difference in difficulty between methadone and suboxone.

[addx]

[url="http://www.ncbi.nlm.nih.gov/pubmed/7796150"]http://www.ncbi.nlm.nih.gov/pubmed/7796150[/url]

Radioligand-binding studies were performed to ascertain the actions of noribogaine, a suspected metabolite of ibogaine, on opioid receptors. Consistent with previous results, ibogaine showed highest affinity for kappa opioid receptors (Ki = 3.77 +/- 0.81 microM), less affinity for mu receptors (Ki = 11.04 +/- 0.66 microM) and no affinity for delta receptors (Ki > 100 microM). Noribogaine showed a higher affinity than ibogaine for all of the opioid receptors: kappa Ki = 0.96 +/- 0.08 microM, mu Ki = 2.66 +/- 0.62 microM and delta Ki = 24.72 +/- 2.26 microM. These data suggest that noribogaine is active in vivo and that it may contribute to ibogaine's pharmacological effects.

[url="http://www.ncbi.nlm.nih.gov/pubmed/9106462"]http://www.ncbi.nlm.nih.gov/pubmed/9106462[/url]

Ibogaine, an alkaloid isolated from the bark of the African shrub, Tabernanthe iboga, has been claimed to decrease the self-administration of drugs of abuse like morphine, cocaine and alcohol. To determine whether these effects are mediated via opioid receptor systems, the effects of ibogaine and its metabolite, noribogaine on the antinociceptive actions of morphine, U-50,488H and [D-Pen2,D-Pen5]enkephalin (DPDPE) which are mu- kappa- and delta-opioid receptor agonists, respectively, were determined in male Swiss-Webster mice. Administration of morphine (7 or 10 mg/kg, s.c.), U-50,488H (15 or 25 mg/kg, i.p.) or DPDPE (10 microg/mouse, i.c.v.) produced antinociception in mice as measured by the tail-flick test. Ibogaine (10, 20 or 40 mg/kg, i.p.) by itself did not alter the tail-flick latency. The same doses of ibogaine injected 10 min before the opioid drugs did not modify the antinociceptive actions of morphine, U-50,488H or DPDPE. Ibogaine administered 4 h or 24 h prior to morphine injection did not modify the antinociceptive action of the latter. A dose of 40 mg/kg (i.p.) of noribogaine enhanced the antinociceptive activity of morphine (10 mg/kg, s.c.). Similarly, the doses of 40 and 80 mg/kg of noribogaine enhanced the antinociception produced by a smaller dose of morphine (5 mg/kg, s.c.). However, antinociception induced by U-50,488H and DPDPE was not modified by noribogaine (10-40 mg/kg). It is concluded that ibogaine, which has been suggested to decrease the self-administration of cocaine and opiates like heroin in humans, does not produce such an action by interacting directly with multiple opioid receptors. However, the metabolite of ibogaine enhances the antinociception of morphine but not of U-50,488H or DPDPE. Thus, in vivo evidence has been provided for the possible interaction of ibogaine with mu-opioid receptor following its metabolism to noribogaine.

These guys came to a weak conclusion. It seems noribogaine is able to enhance morphine analgesia through it's activity with delta opioid receptor which is lacking in ibogaine. It is well known that delta opioids can do this mostly thanks to forming heterodimers(pairs) with mu opioid receptors - which require then both opioids at the receptor to activate it. So flooding delta with mu opioids unlocks some extra analgesia locked up in mu-delta heterodimers, I've seen this trick played in studies trying to beat ever increasing opioid tolerance for pain. I don't think I've seen the reason why some people have more heterodimers than others, it also seems to be some adaptation that happens but the reason is yet unclear.

Delta opioids have also been involved in all this in some more covert form. They seem to facilitate a mechanism for inhibiting "initial frustration from disappointment" (successive reward downshift paradigm, giving rats 32% sucrose and then rats reject 6% sucrose afterwards unless flooded with delta opioid agonists).
As such delta, opioids seem to facilitate a response to an unlearned/unexpected but acutely frustrating situation. The next time rats are given sucrose kappa opioids play part of managing the "frustration"(because it was expected and thus anticipated by the fear system) and delta opioids do not "rescue" the frustration at all - because now this is a learned fear, not an unlearned situation.

Delta opioids are involved in response to alcohol with delta opioid receptor knock out rats being insanely responsive to alcohol. Interestingly enough it can be said that alcohol also "rescues frustration of disappointment" in some ways.

Delta opioids have been involved or implicated in mechanisms for developing tolerance. If tolerance really is what I think it is, a kappa opioid "overgrowth"(or prodynorphin gene expression increase), then it might be feasible that this overgrowth can be retarded by delta opioid agonism - reducing the frustration of disappointment with everything new you do leads to learning less fear of frustration - less kappa opioid receptors - less tolerance. Fear(tolerance or kappa opioid receptor density) causes avoidance(of life without drugs that make it rewarding). Still, this would only help novel, unexpected situations that have not had a fear component learned about them. Which is why I still focus on kappa opioids, but I wouldn't be suprised if "true wellbeing" required something that worked on both or even better for example: JDTic for initial fear reduction via kappa opioid receptor destruction and a lifetime chronic supplement inhibiting enkephalinase, perhaps even one inhibiting FAAH which seems healthy for other reasons but in my book for keeping anandamide levels higher.

[formergenius]

I thought this may be of interest to others as well.
A Kappa Opioid Model of Atypical Altered Consciousness and Psychosis: U50488, DOI, AC90179 Effects on Prepulse Inhibition and Locomotion in Mice.

[addx]

It is of interest, thanks!

It spawned a clue for my next inspiration.

Kappa opioids are in charge of facilitating the fear resposne. This requires them to associate to memories containing a fear component. But fear memories are also usually repressed/unavailable, especially those that have reinforced to the level of learned helplessness.

Kappa opioids inhibit dopamine but it is normally serotonin that modulates dopamine - satiety of results(serotonin) inhibits urge towards producing them(dopamine).

Dopaminergic systems themselves serve for tracking objects into target positions. They facilitate feedback control loops that enable guiding objects according to eye sight and other senses. They also facilitate higher order guiding - social objects into a social position etc. So, dopaminergic neurons pretty much position themselves between "imagination" and "reality" providing distance/tracking/giuding.

My idea is that a dopaminergic system develops for tracking and guiding feared objects as well. This then feeds into the fear response, providing a measure of inevitability. This must exist in the brain and AFAIK only dopaminergic networks provide such tracking services.

However, if this were to be conscious then you wouldn't have obsessive or compulsive behavior which is fear driven, you also wouldnt have people depressed/anhedonic and not knowing the reason why - which is also fear driven.

It is my idea that this dopaminergic system of tracking fears is modulated by the unconscious serotonin networks - 5ht 2a receptors - the psychedelic ones. Meaning that a reinforcement of the fear(the anticipated stress coming true) results in more dopaminergic tracking(more urge). Serotonin normally inhibits but 5ht 2a are excitatory meaning a reinforcement of the fear(satiey) would cause the dopaminergic tracking system of it to grow further in importance/urgentness which seems evolutionary sound. Now I only need to find studies that link this all up nicely.

It also explains the PDF you posted, the involvement of REM sleep and serotonin levels in depression the fact that SSRI suicide victims have more 5ht 2a receptors etc.

Edited by addx, 27 January 2014 - 09:38 PM.

[socialpiranha]

There's a lot of speculation there, but it's a nice idea.

I thought this may be of interest to others as well.
A Kappa Opioid Model of Atypical Altered Consciousness and Psychosis: U50488, DOI, AC90179 Effects on Prepulse Inhibition and Locomotion in Mice.

very interesting study

[celebes]

Just to add my experience with iboga: I started taking root powder micro/mini-doses after it came up on this thread. During the 'trips' I did have my emotions and vitality substantially come back, letting me feel like 'myself' albeit with visual distortions/hallucinations going on. Afterwards though, much like Missjess, it left me increasingly numb, empty, blank, with serious avolition, worsened cognition, and physically weaker. Conversely, it did improve my vision a lot, with everything more vivid and widescreen. Yet too numb to enjoy or even register much from visual stimulation.

The afterglow being the precise opposite of the trip chimes with receptor re-regulation going on... but apparently the wrong ones, at least for trauma/DP/DR/schizoid symptoms. Maybe addiction isn't as similar biochemically as we've somewhat assumed? If my experience is representative, the afterglow is virtually the opposite of Salvia's which gave me my feelings back for a year with one trip.

Even writing this much has taken me 4 times longer than it would have a couple months ago.

Edited by celebes, 28 January 2014 - 06:11 AM.

[Missjess]

I will never touch iboga again, I literally cannot function at all anymore, I cannot work and I cannot think my cognitive skills are shocking. I always have a low mood and I just feel like there's a bubble around my head constantly

[celebes]

Although I persisted with it longer than I should have, I'm grateful I never took a flood dose. I'm very sorry to hear everything you're going through. Hopefully one or other of the substances we're looking at will prove to be some help.

Edited by celebes, 28 January 2014 - 06:08 AM.

[Missjess]

Yeah I really hope I can find some help or I will have to go on disability

[Spruslope]

I'm interested but from Finland, too.

[Remon]

I'm interested as well.

I live in the EU though and don't know about costums.
Plus I've got some issues with my paypal right now.

[formergenius]

Depending on where you live in the EU, it might not be a problem.. I know where I live I've never had issues with customs.

[Remon]

Oh, I live in the Netherlands just like you, so that's a real comfort, thanks!

[formergenius]

Oh, I live in the Netherlands just like you, so that's a real comfort, thanks!

Deduced as much from the name, haha. You're welcome.