Sustained abstinence in severe ketamine use disorder following ibogaine treatment case report.

Abstract

Substance use disorders (SUD) involving ketamine, cocaine, and alcohol present significant clinical challenges, often characterized by high relapse rates and limited pharmacological options. This case report details a 30-year-old male with a five-year history of severe polysubstance dependence, including daily intranasal ketamine use (2-3 g/day), cocaine, and alcohol, comorbid with recurrent depressive disorder. Despite conventional psychiatric treatment, the patient experienced severe cravings and sought ibogaine-assisted treatment. The patient underwent a structured 13-day residential program in Mexico, receiving an 800 mg ibogaine HCl flood dose (10.1 mg/kg), followed by two supplementary booster doses of 300 mg (3.8 mg/kg) under continuous medical and ECG monitoring. Following treatment, the patient reported an immediate cessation of cravings for all substances. Over approximately 17 months of follow-up including a medically supervised fractionated ibogaine intervention approximately 11 months after the initial treatment, serial toxicology and psychometric assessments were consistent with continued abstinence from ketamine, cocaine, alcohol and other previously misused substances, and significant improvements in depression (PHQ-9: 0-3), anxiety, and quality of life (WHOQOL-BREF: 55 to 71). This report represents the first longitudinally documented case of sustained abstinence in severe ketamine use disorder following ibogaine treatment, supported by serial toxicology and standardized psychometric outcomes. It adds objective, time-resolved evidence to a literature that has largely focused on ibogaine for opioid use disorder, and it highlights ketamine use disorder as a specific target for future controlled trials. The therapeutic outcome is hypothesized to arise from ibogaine's unique polypharmacology. This includes acute NMDA antagonism, which may disrupt compulsive circuits, as well as noribogaine's (the principal long-acting metabolite of ibogaine, with an elimination half-life of approximately 28-49 hours) kappa opioid receptor agonism and serotonin transporter inhibition, which stabilize reward pathways. Additionally, enhanced neuroplasticity via GDNF/BDNF expression may facilitate long-term behavioral changes. This case provides rare, rigorously documented evidence for ibogaine's potential in treating chronic ketamine dependence and highlights the urgent need for controlled clinical trials within regulated frameworks to further investigate its safety and efficacy.

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