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Ibogaine: Neurotoxicity?

bigzip44

bigzip44

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I am quite anxious to know about ibogaine's potential for neurotoxicity - does it have any neurotoxic aspects or traits? Is there any good information that I might find useful to answering this question available online? Does anyone with an advanced understanding of ibogaine's mechanisms and/or psychopharmacological elements have any information they would be willing to divulge in order to help me understand better the potential existence of neurotoxic side effects or components to this drug.

In short, I have taken ibogaine twice and the first time it was quite effective until I drank - which definitely changed the entire "afterglow" due to the alcohol interrupting the noribogaine that was flowing through my brain at the time and I underwent a second treatment with another provider with a significantly different product and protocol and found that, indeed it did prove useful in almost totally eliminating my withdrawal symptoms but did not, however, leave me with any "afterglow" effect.

So, I have come to a place where I am considering using ibogaine once more and this would mean I would be using ibogaine three times within a relatively short period and I'm wondering what kind of toxicity I am possibly exposing myself to, specifically neurotoxicity but anything else I may encounter in terms of toxicity related to this drug.

I can say now that I appreciate any and all that have read this and, further, anyone that is willing to share any information they may have on these issues I have brought up concerning ibogaine.

Thank You
 
One thing that derailed development of ibogaine is that it was found to produce degeneration of purkinje cells in the cerebellum of rats. It is not known if this occurs in humans but the ataxia that ibogaine produces is consistant with an effect on the cerebellum. However, many people believe ibogaine is probably not neurotoxic to humans if taken infrequently at reasonable doses.
 
Don't all NMDA antagonists / kappa opioid agonists produce ataxia at high enough doses? It seems it's reversible cerebellar toxicity. Rodents have different metabolism, that's why Olney's lesions are still controversial. As a side note I've seen a chinese study of ketamine addicts and they found several lesions, but we can't rule out polydrug use.
 
i dislike NMDA antagonists personally
i read (i think on Erowid) that high-dose DXM is neurotoxic, and there actually was an entire episode of House dedicated to the neurotoxicity of DXM abuse
 
Trying2Iso said:
i dislike NMDA antagonists personally
i read (i think on Erowid) that high-dose DXM is neurotoxic, and there actually was an entire episode of House dedicated to the neurotoxicity of DXM abuse
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Luckily Dr. House doesn't need to provide references for the claims made on his show.
 
serotonin2A said:
Neither link includes any evidence that DXM is neurotoxic. The CT scan in the second link showed no abnormalities (although I wouldn't expect a CT scan would be able to detect the abnormalities that are induced by NMDA antagonists).
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read the first case report again
he never showed signs of psychosis, had no history or family history of psychiatric illness, passed a psyche exam, and coincidentally had just finished a long dxm binge and was experiencing cognitive decline, irritability, and insomnia, among other symptoms. No other substances except DXM were detected in tox screen
 
Chronic ketamine (ab)use resulted in similar problems for me and I was not surprised at all. NMDA antagonists mess with your glutamatergic system which is pretty implicated in cognitive function. Acutely the dissociation involves loss of proper use of concepts, language, orientation in place and time, etc. So it is no surprise to me that disturbing these functions chronically can also cause chronic issues with planning, orientation, speech, memory / attention, etc. I experienced that first hand, for me it was reversible and recovery time as often correlated with the extent of abuse.
Just as with compounds like noopept it seems unclear whether irritability is a direct result of frustration experienced because of other symptoms.

MXE is also said to produce acute cerebellar toxicity, but again this is reversible and seems to just mean what I have just said: that some brain function is temporarily impaired since some function relies on proper glutamatergic transmission.

Perhaps unsurprisingly racetams and other nootropics with similar effect profiles are the go-to treatment for acute or chronic issues related to dissociative use. Also I understand that CoQ10 and B12 supplemented when dissociative use / abuse is taking its toll.

I don't think ibogaine is meant to be used casually and frequently, and when it is used the therapeutic benefits likely overshadow any transient cognitive issues. Now if it were significantly neurotoxic that'd be a concern, but otherwise... put this in perspective.
 
Trying2Iso said:
read the first case report again
he never showed signs of psychosis, had no history or family history of psychiatric illness, passed a psyche exam, and coincidentally had just finished a long dxm binge and was experiencing cognitive decline, irritability, and insomnia, among other symptoms. No other substances except DXM were detected in tox screen
Click to expand...
Sure, but the fact that he showed cognitive decline doesn't necessarily mean that there were neurotoxic brain changes. NMDA receptors are involved on learning and memory and some users may experience deficits as a consequence of chronic disruption of those functions. That doesn't necessarily mean that degeneration occured. A single case report, which is entirely circumstantial, does not really prove anything. How do you know that the symptoms were caused by DXM? Some people experience those events spontaneously.
 
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i was wondering, tianeptine has NMDA antagonism no? it feels a bit dissociative in high doses. do you think it can be as neurotoxic as DXM? in high doses i mean. come to think of it, it has impaired memory quite a bit.
 
Tianeptine doesn't bind to NMDA receptors, but

For example, MOR activation in dentate granule cells is known to decrease protein kinase A activity, which results in a decrease of NMDA receptor phosphorylation and activity.
source
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Anything as hard on the mind and body as ibogaine can't be good for you. The only reason it helps opioid addicts is that ibogaine is, itself, an opiate with an extremely long half life. When the ibogaine wears off in a few weeks, most addicts go right back to shooting heroin or whatnot. It's just substituting one drug for another of the same class.
 
What do you guys think about claims of ibogaine as a therapeutic aid for PTSD/depression/bipolar/etc?
 
The only reason it helps opioid addicts is that ibogaine is, itself, an opiate with an extremely long half life. When the ibogaine wears off in a few weeks, most addicts go right back to shooting heroin or whatnot. It's just substituting one drug for another of the same class.
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Actually, no. Ibogaine has affinity for opioid receptors but is actually an antagonist at them! Ibogaine and its metabolites don't actually activate opioid receptors.

Ibogaine also has a long half life, but the effects don't last for weeks: otherwise we'd see drugs like methadone working with doses every 3-5 days rather than every day.

In rat thalamic membranes ibogaine, noribogaine and 18-MC were MOR antagonists with functional Ke values ranging from 3 uM (ibogaine) to 13 uM (noribogaine and 18MC). Noribogaine and 18-MC did not stimulate [35S]GTPγS binding in Chinese hamster ovary cells expressing human or rat MORs, and had only limited partial agonist effects in human embryonic kidney cells expressing mouse MORs. Ibogaine did not did not stimulate [35S]GTPγS binding in any MOR expressing cells. Noribogaine did not stimulate [35S]GTPγS binding in brain slices using autoradiography. An MOR agonist action does not appear to account for the effect of these iboga alkaloids on opioid withdrawal. Taken together with existing evidence that their mechanism of action also differs from that of other non-opioids with clinical effects on opioid tolerance and withdrawal, these findings suggest a novel mechanism of action, and further justify the search for alternative targets of iboga alkaloids.
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[ref]

What do you guys think about claims of ibogaine as a therapeutic aid for PTSD/depression/bipolar/etc?
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I don't see why it couldn't be tried.
 
wezface said:
What do you guys think about claims of ibogaine as a therapeutic aid for PTSD/depression/bipolar/etc?
Click to expand...

TBH I never understood it but I wouldn't doubt it would help.

But like if someone is mentally unstable with said disorders, how can it ever be a good idea to have them take Hallucinogens? Those have had me talking to myself and shit. Like unless there's a guide like on a Ayahuasca treatment then I can't see it being a good idea to send someone home with some Ibogaine.
 
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