Posted by: Chris Maloney | November 26, 2011

Freedom of Medicine and Diet: Ibogaine-For Weight loss?

Tabernanthe iboga-14

Image by Giorgio Samorini via Flickr

In the world of drugs, Ibogaine is receiving a lot more attetion recently.  Is it cure-all as depicted by the internet?

Freedom of Medicine and Diet: What About Ibogaine- Dana Beal.

No, it isn’t harmless.  It can cause brain damage, whole body tremors, and stop your heart in extreme doses.

But we’ve got a new, patented extract 18-MC, that is in animal trials to stop us from overeating.  Look to see all the side effects of the raw material get downplayed in the pharmaceutical.

Both cause a complex interaction with multiple brain transmitters and are taken out of the body by a specific part of the liver.  If you have the necessary genetics, the stuff can work great on you.  If you lack the genetics, say hello to a whole new world of interesting side effects.

Here’s the data from medline with relevant sentences highlighted.

I would steer clear of this as a weight loss aid when it come out on the market.  Too complicated.

including the O-demethylation of ibogaine to 12-hydroxyibogamine (noribogaine). Blood concentration-time effect profiles of ibogaine and noribogaine obtained for individual subjects after single oral dose administrations demonstrate complex pharmacokinetic profiles. Ibogaine has shown preliminary efficacy for opiate detoxification and for short-term stabilization of drug-dependent persons as they prepare to enter substance abuse treatment. We report here that ibogaine significantly decreased craving for cocaine and heroin during inpatient detoxification. Self-reports of depressive symptoms were also significantly lower after ibogaine treatment and at 30 days after program discharge. Because ibogaine is cleared rapidly from the blood, the beneficial aftereffects of the drug on craving and depressed mood may be related to the effects of noribogaine on the central nervous system.

PMID: 11085338

Ann N Y Acad Sci. 2000;909:88-103.

Development of novel medications for drug addiction. The legacy of an African shrub.

Glick SD, Maisonneuve IM.

Source

Department of Pharmacology and Neuroscience, Albany Medical College, New York 12208, USA. glicks@mail.amc.edu

Abstract

Ibogaine, one of several alkaloids found in the root bark of the African shrub Tabernanthe iboga, has been claimed to be effective in treating multiple forms of drug abuse. Problems associated with side effects of ibogaine have spawned a search for more effective and safer structural derivatives. 18-Methoxycoronaridine (18-MC), a novel iboga alkaloid congener, appears to have substantial potential for broad use as an anti-addictive therapy. Like ibogaine (40 mg/kg), 18-MC (40 mg/kg) decreases the intravenous self-administration of morphine and cocaine and the oral self-administration of ethanol and nicotine in rats; unlike ibogaine, 18-MC does not affect responding for a non-drug reinforcer (water). Ibogaine and 18-MC appear to reduce the reinforcing efficacies, rather than the potencies, of drugs of abuse. Both ibogaine and 18-MC decreases extracellular levels of dopamine in the nucleus accumbens while only ibogaine increases serotonin levels in this brain region. Both ibogaine and 18-MC block morphine-induced and nicotine-induced dopamine release in the accumbens; only ibogaine enhances cocaine-induced increases in dopamine levels. Ibogaine produces whole body tremors and, at high doses (at least 100 mg/kg), cerebellar damage; 18-MC does not produce these effects. Ibogaine, but not 18-MC, causes bradycardia at high doses. Ibogaine and its metabolite noribogaine have low microM affinities for kappa and mu opioid receptors, NMDA receptors, 5HT-3 receptors, sigma-2 sites, sodium channels and the serotonin transporter. 18-MC has low microM affinities at all three opioid receptors and at 5HT-3 receptors but much lower or no affinities for NMDA and sigma-2 receptors, sodium channels, and the 5HT transporter. Both 18-MC and ibogaine are sequestered in fat and, like ibogaine, 18-MC probably has an active metabolite. 18-MC also has (+) and (-) enantiomers, both of which are active. Considered together, all of the data indicate that 18-MC should be safer than ibogaine and at least as efficacious as an anti-addictive medication.

PMID: 10911925

Psychopharmacology (Berl). 2008 Dec;201(3):339-50. Epub 2008 Aug 28.

18-methoxycoronaridine: a potential new treatment for obesity in rats?

Taraschenko OD, Rubbinaccio HY, Maisonneuve IM, Glick SD.

Source

Center for Neuropharmacology and Neuroscience MC-136, Albany Medical College, Albany, NY 12208, USA. tarasco@mail.amc.edu

Abstract

RATIONALE:

Excessive eating often leads to obesity. Although a variety of neurotransmitters and brain regions are involved in modulating food intake, a role of accumbal dopamine is thought to be critical for several aspects of this behavior. Since 18-methoxycoronaridine (18-MC), a selective antagonist of alpha3beta4 nicotinic receptors, was previously shown to alter dopamine release in the nucleus accumbens in response to chronic injections of cocaine and morphine, this drug could be a promising therapy for abnormal eating behavior.

OBJECTIVES:

Assess the effect of 18-MC on the consumption of sucrose (15%) vs. water in a self-administration paradigm and on the intake of freely available palatable fluids (i.e., 5% sucrose, 0.1% saccharin, and 0.6% saline solutions) as well as on water intake. Determine whether repeated administration of 18-MC (20 mg/kg i.p.) affects weight gain, food intake, and fat deposition in rats drinking 30% sucrose solution.

RESULTS:

Acute administration of 18-MC (10-40 mg/kg i.p.) reduced operant responding for sucrose and decreased ad libitum ingestion of sucrose, saccharin, and saline. The highest dose of 18-MC also reduced consumption of water when palatable fluids were not available. In rats having unlimited access to sucrose (30%), chronic treatment with 18-MC (20 mg/kg i.p.) prevented sucrose-induced increases in body weight, decreased fat deposition, and reduced consumption of sucrose while not altering food intake.

CONCLUSIONS:

These data suggest that antagonism of alpha3beta4 nicotinic receptors may be involved in the regulation of intake of palatable substances regardless of its caloric value and may participate in maintaining obesity.

PMID: 18751969

 

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