I thought I'll share this: Currently used high doses (500 mg) of Ibogaine may not be necessary for anti-addiction effect according to this new study out of New Zealand.
Doses as low as 50 times lower(0.87mg/Kg) than currently used (20-40mg/Kg) good enough to treat BOTH opioid WD and long term abstinence in rats. Making Ibogaine pretty safe. way more safer than caffeine as far as cardiac arrhythmia issue is concerned since at this doses probably wotn see QT problem. Certainly way safer than cocaine. This is very interesting finding imho since at this doses there wont be any significant 5HT and/or kappa activation and induced hallucinations. Nor any significant NMDA antagonism or nicotinic modulation either! Ki is in the 10uM in almost all these (in invitro binding assay!) Which beg the question: what exactly is the mechanism of Ibogaine anti-addiction effect?
Doses as low as 50 times lower(0.87mg/Kg) than currently used (20-40mg/Kg) good enough to treat BOTH opioid WD and long term abstinence in rats. Making Ibogaine pretty safe. way more safer than caffeine as far as cardiac arrhythmia issue is concerned since at this doses probably wotn see QT problem. Certainly way safer than cocaine. This is very interesting finding imho since at this doses there wont be any significant 5HT and/or kappa activation and induced hallucinations. Nor any significant NMDA antagonism or nicotinic modulation either! Ki is in the 10uM in almost all these (in invitro binding assay!) Which beg the question: what exactly is the mechanism of Ibogaine anti-addiction effect?
The indole alkaloid ibogaine, present in the root bark of the West African rain forest shrub Tabernanthe iboga, has been adopted in the West as a treatment for drug dependence. Treatment of patients requires large doses of the alkaloid to cause hallucinations, an alleged integral part of the patient's treatment regime. However, case reports and case series continue to describe evidences of ataxia, gastrointestinal distress, ventricular arrhythmias and sudden and unexplained deaths of patients undergoing treatment for drug dependence. High doses of ibogaine act on several classes of neurological receptors and transporters to achieve pharmacological responses associated with drug aversion; limited toxicology research suggests that intraperitoneal doses used to successfully treat rodents, for example, have also been shown to cause neuronal injury (purkinje cells) in the rat cerebellum. Limited research suggests lethality in rodents by the oral route can be achieved at approximately 263mg/kg body weight. To consider an appropriate and safe initial dose for humans, necessary safety factors need to be applied to the animal data; these would include factors such as intra- and inter-species variability and for susceptible people in a population (such as drug users). A calculated initial dose to treat patients could be approximated at 0.87mg/kg body weight, substantially lower than those presently being administered to treat drug users. Morbidities and mortalities will continue to occur unless practitioners reconsider doses being administered to their susceptible patients. https://www.ncbi.nlm.nih.gov/pubmed/27426011
