Hallucinogen May Cure Drug Addiction

BAY AREA (KRON) ^ | February 20, 2004 | NA

[neverdem]

Say a prayer for reproducible results. Too bad no numbers were given.

[TADSLOS]

"I was hooked," she says.

and now she's a pusher.

[Destro]

LSD -- before the Hippie craze was such a wonder drug. It probably is a wonder drug but abuse of it made the Feds ban its use. Or so the official line goes.

[dogbyte12]

Come on... If the effect of this drug is to kill off the detox symptoms, it can't be all bad.

Even druggies who want to quit, are afraid to do so, because of the DT's, tremors, sweats, pain, etc.

She even cautions that this has to be a part of a full regimen of therapy etc.

Anything to get people off drugs, even if it is through the use of a single dosage of one drug, is something that should be studied for efficacy. Isn't the whole point to stop the usage?

[martin_fierro]

Hallucinogen May Cure Drug Addiction

So tell me something I don't already know.

[Joe 6-pack]

In a related announcement, the American Dental Association has discovered a new treatment for toothaches...

[templar]

Is Ibogaine physically additive in itself? (I think most of those type drugs aren't physically addictive)

[martin_fierro]

AH PITY TH' FOO' WHUT PUT HALLUCINOGENS IN MAH DRUGZ!

[45Auto]

Oh, not the old Ibogaine con game again! Dr. Mash has a vested interest in the Great Ibogaine Con because she is working off NSF grants. The idea of using psychedelics to treat addiction is not new; Tim Leary conducted research on the use of LSD and psilocybin in the treatment of alcoholics about 40 years ago. Freud experimented with the use of cocaine in the treatment of his friend's morphine addiction over a hundred years ago. His experiments ended in near disaster and after that, Freud swore off praising the benefits of cocaine (and he used it by injection).The whole idea of using one abusable substance to treat the addiction to another abusable substance is insane.

[Fedora]

When informed of this discovery, Onion correspondent Jim Anchower replied, "Dude! That's what I've been saying for years!"

[45Auto]

Ibogaine induces glial activation in parasagittal zones of the cerebellum.

O'Hearn, Elizabeth; Long, David B.; Molliver, Mark E. Sch. Med., Johns Hopkins Univ., Baltimore, MD, USA.

NeuroReport (1993), 4(3), 299-302.

Abstract

Ibogaine, an indole alkaloid, has been proposed for treatment of drug addiction, yet its mechanism, site of action, and possible neurotoxicity have not been detd. Since neuronal injury is known to activate neuroglial cells, the authors investigated potential neurotoxic effects of this drug in rats by examg. expression of specific glial markers. After treatment with ibogaine (100 mg kg-1 i.p.; 1-3 doses), the authors obsd. increased cytochem. markers in both microglia (OX-6, OX-42, W3/25) and astrocytes (GFAP), assocd. with striking morphol. changes in these cells. Activated glial cells were restricted to longitudinally oriented, parasagittal stripes within the vermis of cerebellar cortex. The ibogaine-induced activation of cerebellar glial cells is highly suggestive of neuronal degeneration, most likely of Purkinje cells.

[45Auto]

A dose-response study of ibogaine-induced neuropathology in the rat cerebellum.

Xu, Zengjun; Chang, Louis W.; Slikker, William, Jr.; Ali, Syed F.; Rountree, Robert L.; Scallet, Andrew C. Department of Pathology, University of Arkansas for Medical Sciences, Little Rock, AR, USA.

Toxicological Sciences (2000), 57(1), 95-101.

Abstract

Ibogaine (IBO) is an indole alkaloid from the West African shrub, Tabernanthe iboga. It is structurally related to harmaline, and both these compds. are rigid analogs of melatonin. IBO has both psychoactive and stimulant properties. In single-blind trials with humans, it ameliorated withdrawal symptoms and interrupted the addiction process. However, IBO also produced neurodegeneration of Purkinje cells and gliosis of Bergmann astrocytes in the cerebella of rats given even a single dose (100 mg/kg, i.p.).

Here, we treated rats (n = 6 per group) with either a single i.p. injection of saline or with 25 mg/kg, 50 mg/kg, 75 mg/kg, or 100 mg/kg of IBO. As biomarkers of cerebellar neurotoxicity, we specifically labeled degenerating neurons and axons with silver, astrocytes with antisera to glial fibrillary acidic protein (GFAP), and Purkinje neurons with antisera to calbindin.

All rats of the 100-mg/kg group showed the same pattern of cerebellar damage previously described: multiple bands of degenerating Purkinje neurons.

All rats of the 75-mg/ kg group had neurodegeneration similar to the 100-mg/kg group, but the bands appeared to be narrower. Only 2 of 6 rats that received 50 mg/kg were affected; despite few degenerating neuronal perikarya, cerebella from these rats did contain patches of astrocytosis similar to those obsd. with 75 or 100 mg/kg IBO. These observations affirm the usefulness of GFAP immunohistochem. as a sensitive biomarker of neurotoxicity. None of the sections from the 25-mg/kg rats, however stained, were distinguishable from saline controls, indicating that this dose level may be considered as a no-observable-adverse-effect level (NOAEL).

[45Auto]

Here's a more "neutral" paper:

Ibogaine neurotoxicity assessment: electrophysiological, neurochemical, and neurohistological methods.

Binienda, Zbigniew K.; Scallet, Andrew C.; Schmued, Larry C.; Ali, Syed F. Division of Neurotoxicology, FDA/National Center for Toxicological Research, Jefferson, AR, USA.

Alkaloids (Academic Press) (2001), 56(Ibogaine), 193-210.

Abstract

A review discusses the interactions of ibogaine with various neurotransmitter systems. Electrophysiol., neurochem., and neurohistol. tools were used to evaluate ibogaine neurotoxicity. Electrophysiol. studies indicated that ibogaine stimulates monoaminergic neurons and may lower the threshold for cocaine induced electrog. seizures. Ibogaine interacts with several neurotransmitter-binding sites, produces significant alterations in neurotransmitter concns. in different regions of the brain, and also induces immediate early genes. Neuropathol. investigations showed that ibogaine administered at high doses produces selective neuronal degeneration. Thus, ibogaine might have potential use for the treatment of drug addiction, but may also be neurotoxic at high doses.

[StriperSniper]

[neverdem]

Is Ibogaine physically additive in itself? (I think most of those type drugs aren't physically addictive)

I'm not aware of hallucinogens being physically addictive.

[neverdem]

LOL

[tacticalogic]

The whole idea of using one abusable substance to treat the addiction to another abusable substance is insane.

Like methadone?

[45Auto]

The upshot is, that while ibogaine is an interesting substance and possibly useful in basic studies in pharmacology and brain chemistry, it doesn't hold much promise as a "magic bullet" to render the addict "cured". Its side effect profile suggests that it might indeed be somewhat neurotoxic at certain dose levels or with certain levels of repeated treatment. There are much better (and safer) drugs in current use to curtail some of the withdrawal problems associated with the opiates. And there is no substitute, I repeat, no substitute for massive and continued group therapy for addicts, including twelve step organizations. There's no easy way; those who think there might be are seriously deluded, at least by current medical scientific knowledge.

[neverdem]

The whole idea of using one abusable substance to treat the addiction to another abusable substance is insane.

The war on drugs is insane too, reminding me of a dog chasing its tail, but that's another story.

A single dose of ibogaine in a controlled clinical setting is certainly not abuse and definitely worth investigating in a time of AIDS with all the innocent people threatened from the sexual behavior of injecting drug users.

The story doesn't say how funding was obtained. Hopefully, the announcement of the FDA findings will be simultaneous with publication. Thanks for the abstracts. Did you find them at PubMed?

[45Auto]

Methadone might be useful in the early stages of treating opiate addiction; it is, in my opinion, not too useful over the long term precisely because it simply substitutes one drug for another. The addict still has to remain "in the cycle" of drug using behavior, even though methadone is somewhat less "disrupting" to one's daily behavior. Current medical philosophy and that of addiction treatment is that there is no "easier, softer way" to beat an addiction whether to alcohol or other drug. There is more to addiction then merely weaning the addict from a preferred substance. Long-term counseling including twelve step programs like AA, have a fair success rate, although one could argue about the details. No treatment will work if the addict refuses to see that once started, he/she cannot control the level, outcome , or repetition of drug use.