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Nutraceutical Intervention for Treatment of Alcoholism and Drinking Problems
Published in Raj K. Keservani, Anil K. Sharma, Rajesh K. Kesharwani, Nutraceuticals and Dietary Supplements, 2020
Hence, a successive study proved that both the intraperitoneal and subcutaneous administration of noribogaine, a primary metabolite of ibogaine, considerably inhibited liquor intake in liquor preferring rats (Carai et al., 2000). It has been theorized that ibogaine may exert its reducing effects on voluntary ethanol consumption by interacting with the brain systems involved in the mediation of the reinforcing effects of liquor (Carai et al., 2000).
Substrates of Human CYP2D6
Published in Shufeng Zhou, Cytochrome P450 2D6, 2018
CYP2D6 is largely responsible for the metabolism of ibogaine to its O-desmethyl active metabolite 12-hydroxyibogamine (noribogaine) (Figure 3.111) (Obach et al. 1998), a psychoactive alkaloid isolated from the root of Tabernanthe iboga, a rainforest shrub native to Africa. Ibogaine is used by indigenous peoples in low doses to combat fatigue, hunger, and thirst, and in higher doses as a sacrament in religious rituals. Ibogaine represents a potentially useful therapeutic agent in the treatment of opiate and psychostimulant addiction and opiate withdrawal (Alper et al. 1999, 2000; Frances et al. 1992; Glick et al. 1992; Popik et al. 1995). 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 (Mash et al. 2000). Ibogaine and noribogaine interacted with 5-HT transporters (SERT/SLC6A4) to inhibit 5-HT uptake (Baumann et al. 2001; Mash et al. 1995).
Changes in Withdrawal and Craving Scores in Participants Undergoing Opioid Detoxification Utilizing Ibogaine
Published in Journal of Psychoactive Drugs, 2018
Benjamin J. Malcolm, Martin Polanco, Joseph P. Barsuglia
Noribogaine (12-OH-ibogaine) is an active metabolite with many overlapping receptor affinities with its parent compound, although it has notably higher affinity for κ and μ opioid receptors (Litjens and Brunt 2016). While noribogaine binds to the μ opioid receptor with high affinity and was originally reported to have full agonist activity, it lacked agonist effects such as pupillary constriction or respiratory depression in doses up to 60 mg in healthy volunteers and is currently thought to be a partial agonist or antagonist (Antonio et al. 2013; Glue et al. 2015a; Pablo and Mash 1998). Noribogaine is lipophilic and has a large volume of distribution in the body. Additionally, it has a much longer elimination half-life than ibogaine and was found to be 28–49 hours in a dose escalation study in healthy volunteers (Glue et al. 2015a). Due to persisting effects from slow elimination and modulation of the opioid system, it has been hypothesized that noribogaine may be playing a pivotal role in blocking opiate withdrawal symptoms or cravings and may provide a “self-tapering” effect to those undergoing opioid detoxification.
Ibogaine treatment outcomes for opioid dependence from a twelve-month follow-up observational study
Published in The American Journal of Drug and Alcohol Abuse, 2018
Geoffrey E. Noller, Chris M. Frampton, Berra Yazar-Klosinski
Putative anti-addiction properties of ibogaine led to extensive studies of acute effects in dependent human volunteers with hazardous opioid use to explore the risk/benefit profile, summarized in Table 1. These studies support reproducible indications of effectiveness and an acceptable risk/benefit profile of ibogaine in the treatment of opioid dependence and withdrawal, as opioid dependence has a pooled relative mortality risk (RR) of 2.38 (95% CI: 1.79–3.17) even while in treatment. Out of treatment mortality risk was much greater (14). Ibogaine and its active metabolite noribogaine were found to have numerous direct and indirect functional targets with complex pharmacology in studies aiming to elucidate mechanism of action (15). Most recently, noribogaine was found to be the principal active moeity responsible for interrupting psychological and physiological effects of opiate dependence in rats, with profound implications for effects in humans (16).
Breaking the cycle of opioid use disorder with Ibogaine
Published in The American Journal of Drug and Alcohol Abuse, 2018
In the New Zealand study, participants described their ibogaine experience in positive terms, but one person tragically died during the treatment. Ibogaine’s legal availability in New Zealand may have offered improved outcomes because legislation allowed ibogaine treatment providers to work closely with licensed physicians. Despite the legislated approval of ibogaine at the time of this study, the death (1 in 14 patients) occurred under the care of a medical practitioner that was adjudged to have failed in their duty of care (9). This death underscores the persistent problem associated with the use of ibogaine in unregulated, nonmedical settings by unqualified persons. Ibogaine has complicated pharmacokinetics that contribute to concerns for careful dosing, potential drug interactions, and issues of cardiovascular safety (11). Ibogaine is rapidly metabolized in the liver to an active metabolite, noribogaine (12), which has a long half-life in blood (10,11). Reports of ibogaine deaths often lack any toxicologic information on the levels of ibogaine or noribogaine in blood at autopsy (13). “Staggered” doses of ibogaine will increase the area under the concentration curve for noribogaine, leading to very high levels of this active metabolite in blood. Both of the new studies reportedly used test doses and some booster doses of ibogaine (8,9), which are not a standardized dose regimen supported by pharmacokinetic studies currently available in the scientific literature.