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References & Citations

Claims on this site that depend on published research are footnoted (¹, ², …). The numbered list below is the source for each footnote. We update this page whenever we add a new citable claim.

  1. [1] Davis AK, Barsuglia JP, Windham-Herman AM, Lynch M, Polanco M (2017). Subjective effectiveness of ibogaine treatment for problematic opioid consumption: Short- and long-term outcomes and current psychological functioning. Journal of Psychedelic Studies, 1(2), 65–73. Read the source →

    Supports: Survey of 88 people who received ibogaine for opioid use disorder. 80% indicated ibogaine eliminated or drastically reduced withdrawal symptoms; 30% reported never using opioids again; 54% of those abstainers had been abstinent for at least one year.

  2. [2] National Institute on Drug Abuse (NIDA), based on CDC WONDER data (2024). Drug Overdose Death Rates. National Institutes of Health, citing CDC, National Center for Health Statistics, Multiple Cause of Death data. Read the source →

    Supports: About 73,838 U.S. overdose deaths in 2022 involved synthetic opioids other than methadone (primarily fentanyl) — roughly two-thirds of the approximately 107,900 total drug overdose deaths that year.

  3. [3] Centers for Disease Control and Prevention (CDC) (2025). Understanding the Opioid Overdose Epidemic. U.S. Centers for Disease Control and Prevention, Overdose Prevention. Read the source →

    Supports: Describes the U.S. opioid overdose epidemic in three waves: prescription opioids (rising since the 1990s), heroin (from 2010), and synthetic opioids such as illicitly manufactured fentanyl (from 2013). Source of the three-waves overdose-death chart.

  4. [4] U.S. Food and Drug Administration (FDA) (2024). FDA and Kratom. U.S. Food and Drug Administration, Public Health Focus. Read the source →

    Supports: States that an estimated 1.7 million Americans aged 12 and older used kratom in 2021, per the Substance Abuse and Mental Health Services Administration (SAMHSA) National Survey on Drug Use and Health.

  5. [5] U.S. Food and Drug Administration (FDA) (2025). FDA Takes Steps to Restrict 7-OH Opioid Products Threatening American Consumers. U.S. Food and Drug Administration, Press Announcements (July 29, 2025). Read the source →

    Supports: FDA recommended a scheduling action for concentrated 7-hydroxymitragynine (7-OH) products and described 7-OH as "an opioid that can be more potent than morphine," while distinguishing concentrated 7-OH from natural leaf kratom.

  6. [6] U.S. Department of Health and Human Services (HHS) and U.S. Food and Drug Administration (FDA) (2026). HHS, FDA Commend DEA Action Against Dangerous Enhanced 7-OH Products. U.S. Department of Health and Human Services, Press Room (July 1, 2026). Read the source →

    Supports: On July 1, 2026 the DEA issued two Notices of Intent to temporarily place 7-OH (above a threshold) and its synthetic derivatives — including dihydro-7-hydroxymitragynine (MGM-15) — into Schedule I. Federal officials compared their abuse potential to heroin, morphine, and fentanyl, and noted a roughly $1 million seizure of illegal 7-OH products in December 2025.

  7. [7] World Health Organization, Expert Committee on Drug Dependence (ECDD) (2021). Kratom (Mitragyna speciosa), mitragynine and 7-hydroxymitragynine: Critical Review Report. World Health Organization, 44th ECDD. Read the source →

    Supports: Concludes that mitragynine and 7-hydroxymitragynine act as partial agonists at the mu-opioid receptor, with 7-OH binding the receptor several times more strongly than mitragynine.

  8. [8] Alsbrook S, et al. (2025). From kratom to 7-hydroxymitragynine: evolution of a natural remedy into a public-health threat. Pharmaceutical Biology, 63(1), 896–911. Read the source →

    Supports: Peer-reviewed review of 7-OH pharmacology (far higher mu-opioid receptor affinity than mitragynine) and the 2024–2025 emergence of concentrated 7-OH and semi-synthetic derivatives such as MGM-15 in consumer products.

  9. [9] Mash DC, Duque L, Page B, Allen-Ferdinand K (2018). Ibogaine Detoxification Transitions Opioid and Cocaine Abusers Between Dependence and Abstinence: Clinical Observations and Treatment Outcomes. Frontiers in Pharmacology, 9, 529. Read the source →

    Supports: Open-label study reporting that ibogaine therapy in a safe dose range diminished opioid withdrawal symptoms and reduced drug cravings, transitioning opioid- and cocaine-dependent patients toward abstinence.

  10. [10] Guy GP Jr, Jones CM, Rikard M, Strahan AE, Zhang K, Olsen Y (2025). Individuals Dispensed Buprenorphine in the United States Before and After Federal Policy Changes Aimed at Increasing Access. Journal of Addiction Medicine, 19(5), 615–621. Read the source →

    Supports: National dispensing analysis reporting that the number of individuals dispensed buprenorphine from U.S. retail pharmacies rose from about 1.2 million in 2018 to about 1.5 million in 2023.

  11. [11] Shulman M, Wai JM, Nunes EV (2019). Buprenorphine Treatment for Opioid Use Disorder: An Overview. CNS Drugs, 33(6), 567–580. Read the source →

    Supports: Overview of medications for opioid use disorder. Describes buprenorphine as a partial mu-opioid agonist with very high receptor affinity and a long duration of action, and extended-release naltrexone (Vivitrol) as a mu-opioid antagonist that blocks the receptor.

  12. [12] Cherian K, Shinozuka K, Tabaac BJ, et al. (2024). Psychedelic Therapy: A Primer for Primary Care Clinicians—Ibogaine. American Journal of Therapeutics, 31(2), e133–e140. Read the source →

    Supports: Peer-reviewed clinical primer noting that patients receiving ibogaine for opioid use disorder must withdraw from long-acting opioids first, ensuring they are no longer present in plasma, with clinicians recommending a switch to short-acting opioids up to two weeks before treatment.

  13. [13] Esser MB, Sherk A, Liu Y, Naimi TS (2024). Deaths from Excessive Alcohol Use — United States, 2016–2021. MMWR Morbidity and Mortality Weekly Report, 73(8), 154–161. Read the source →

    Supports: CDC surveillance report estimating an average of 178,307 deaths per year from excessive alcohol use in the United States during 2020–2021, roughly 488 deaths a day, and a 29% increase over the 2016–2017 average.

  14. [14] McPheeters M, O’Connor EA, Riley S, et al. (2023). Pharmacotherapy for Alcohol Use Disorder: A Systematic Review and Meta-Analysis. JAMA, 330(17), 1653–1665. Read the source →

    Supports: Meta-analysis of 118 trials and 20,976 participants. Acamprosate showed a number needed to treat of 11 and oral naltrexone 18 to prevent one person returning to any drinking. Injectable naltrexone showed no significant effect on return to any drinking, and disulfiram did not outperform placebo.

  15. [15] He DY, McGough NN, Ravindranathan A, Jeanblanc J, Logrip ML, Phamluong K, Janak PH, Ron D (2005). Glial Cell Line-Derived Neurotrophic Factor Mediates the Desirable Actions of the Anti-Addiction Drug Ibogaine against Alcohol Consumption. The Journal of Neuroscience, 25(3), 619–628. Read the source →

    Supports: Rodent study identifying GDNF signalling in the ventral tegmental area as the mechanism through which ibogaine reduces alcohol intake, including in a relapse model. Ibogaine injected directly into the VTA produced dose-dependent reductions in ethanol self-administration.

  16. [16] Rezvani AH, Overstreet DH, Perfumi M, Massi M (2003). Plant derivatives in the treatment of alcohol dependency. Pharmacology Biochemistry and Behavior, 75(3), 593–606. Read the source →

    Supports: Review reporting that ibogaine suppresses alcohol intake in a dose-dependent way in rat strains selectively bred for heavy drinking and relapse-like ethanol consumption.

  17. [17] Marton S, González B, Rodríguez-Bottero S, et al. (2019). Ibogaine Administration Modifies GDNF and BDNF Expression in Brain Regions Involved in Mesocorticolimbic and Nigral Dopaminergic Circuits. Frontiers in Pharmacology, 10, 193. Read the source →

    Supports: Rodent study showing that a single dose of ibogaine raises BDNF expression in the nucleus accumbens, substantia nigra, and prefrontal cortex, and selectively raises GDNF in the ventral tegmental area at the dose range effective in self-administration models.

  18. [18] Henriques GM, Anjos-Santos A, Rodrigues IR, et al. (2021). Ibogaine Blocks Cue- and Drug-Induced Reinstatement of Conditioned Place Preference to Ethanol in Male Mice. Frontiers in Pharmacology, 12, 739012. Read the source →

    Supports: Rodent study reporting that oral ibogaine blocked both drug-primed and cue-induced reinstatement of ethanol conditioned place preference, at doses that produced no rewarding effect on their own.

  19. [19] Barsuglia JP, Polanco M, Palmer R, Malcolm BJ, Kelmendi B, Calvey T (2018). A case report SPECT study and theoretical rationale for the sequential administration of ibogaine and 5-MeO-DMT in the treatment of alcohol use disorder. Progress in Brain Research, 242, 121–158. Read the source →

    Supports: Single case report of a man with moderate alcohol use disorder treated with ibogaine followed by 5-MeO-DMT. He reported improved mood, cessation of drinking, and reduced cravings at five days and one month, with a partial return to mild drinking by two months. Because two compounds were given, ibogaine cannot be isolated as the cause.

  20. [20] Koenig X, Hilber K (2015). The Anti-Addiction Drug Ibogaine and the Heart: A Delicate Relation. Molecules, 20(2), 2208–2228. Read the source →

    Supports: Review of ibogaine cardiac risk, including QT prolongation and arrhythmia. Documents a fatality in a 52-year-old man with a 20-year history of alcohol use disorder in whom postmortem examination found hepatic cirrhosis and steatosis alongside coronary artery sclerosis, supporting pre-existing liver disease as a significant risk factor and pre-treatment liver function testing as essential screening.

  21. [21] Brown TK, Noller GE, Denenberg JO (2019). Ibogaine and Subjective Experience: Transformative States and Psychopharmacotherapy in the Treatment of Opioid Use Disorder. Journal of Psychoactive Drugs, 51(2), 155–165. Read the source →

    Supports: Observational study of 44 people undergoing ibogaine treatment for opioid dependence, in which 43% met criteria for a complete mystical experience on the Altered States of Consciousness questionnaire. The cohort was opioid-dependent, not alcohol-dependent.

  22. [22] Alper KR, Lotsof HS, Frenken GM, Luciano DJ, Bastiaans J (1999). Treatment of acute opioid withdrawal with ibogaine. The American Journal on Addictions, 8(3), 234–242. Read the source →

    Supports: Open-label case series of 33 heroin-dependent patients treated with a single dose of ibogaine. 25 of the 33 (about 73%) showed no objective signs of opioid withdrawal and no drug-seeking behavior during the 72-hour observation window. One death occurred, possibly involving surreptitious heroin use. Uncontrolled and unblinded.