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] 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] 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. Also documents the longer trends: heroin-involved deaths peaked at about 15,500 in 2016 and fell to roughly 4,000 by 2023 (about 80% of remaining heroin deaths also involve illicitly manufactured fentanyl), deaths involving prescription opioids rose from about 3,400 in 1999 to a peak near 17,000 in 2017 before declining, and methadone continues to contribute thousands of overdose deaths each year.
[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] 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] 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] 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] 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] 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] 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] 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] 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] 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] 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] 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] 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] 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] 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] 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] 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] 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] 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] 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.
[24] Centers for Disease Control and Prevention (CDC), National Center for Health Statistics (2024). Current Cigarette Smoking Among Adults in the United States. National Health Interview Survey, 2024 (National Center for Health Statistics). Read the source →
Supports: In 2024, about 9.9% of U.S. adults, roughly 25 million people, currently smoked cigarettes. It was the first year the adult smoking rate fell below 10% since national surveillance began, down from 10.8% in 2023.
[25] Glick SD, Maisonneuve IM, Kitchen BA, Fleck MW (2002). Antagonism of alpha 3 beta 4 nicotinic receptors as a strategy to reduce opioid and stimulant self-administration. European Journal of Pharmacology, 438(1–2), 99–105. Read the source →
Supports: Ibogaine and its analogs act as antagonists at α3β4 nicotinic acetylcholine receptors, and ibogaine is a more potent antagonist at α3β4 than at NMDA, 5-HT3, or α4β2 receptors. The paper proposes α3β4 antagonism as a strategy to reduce self-administration of several drugs of abuse.
[26] Chang Q, Hanania T, Mash DC, Maillet EL (2015). Noribogaine reduces nicotine self-administration in rats. Journal of Psychopharmacology, 29(6), 704–711. Read the source →
Supports: Noribogaine, ibogaine's long-acting metabolite, dose-dependently reduced nicotine self-administration in rats, with an efficacy comparable to varenicline, an approved smoking-cessation medication. Preclinical (animal) evidence.
[27] Maisonneuve IM, Mann GL, Deibel CR, Glick SD (1997). Ibogaine and the dopaminergic response to nicotine. Psychopharmacology, 129(3), 249–256. Read the source →
Supports: Pretreatment with ibogaine attenuated the rise in extracellular dopamine produced by nicotine in rats, suggesting ibogaine can blunt nicotine's rewarding signal. Ibogaine's behavioral effects on nicotine in other studies were mixed. Preclinical.
[28] Substance Abuse and Mental Health Services Administration (2021). Treatment for Stimulant Use Disorders (Treatment Improvement Protocol 33). SAMHSA Publication No. PEP21-02-01-004, Rockville, MD. Read the source →
Supports: There are no FDA-approved pharmacologic treatments for stimulant use disorders, including cocaine. Behavioral approaches, principally contingency management and cognitive behavioral therapy, remain the front-line treatment.
[29] Magnano AR, Talathoti NB, Hallur R, Jurus DT, Dizon J, Holleran S, Bloomfield DM (2006). Effect of acute cocaine administration on the QTc interval of habitual users. The American Journal of Cardiology, 97(8), 1244–1246. Read the source →
Supports: In habitual cocaine users given cocaine under controlled conditions, electrocardiograms showed significant prolongation of the QTc interval after administration (p < 0.001).
[30] Levin KH, Copersino ML, Epstein D, Boyd SJ, Gorelick DA (2008). Longitudinal ECG changes in cocaine users during extended abstinence. Drug and Alcohol Dependence, 95(1–2), 160–163. Read the source →
Supports: Weekly ECGs from 25 chronic cocaine users during up to three months of monitored abstinence on a closed ward. QTc shortened significantly (about 10.5 ms) during the first week of abstinence, with no further significant change afterward, and baseline QTc correlated with how much cocaine had been used beforehand. The authors conclude that cocaine-associated QTc prolongation returns toward normal within roughly the first week off cocaine.
[31] Ferreira S, Crumb WJ Jr, Carlton CG, Clarkson CW (2001). Effects of cocaine and its major metabolites on the HERG-encoded potassium channel. Journal of Pharmacology and Experimental Therapeutics, 299(1), 220–226. Read the source →
Supports: Cocaine and several of its metabolites block the HERG-encoded potassium channel, which governs cardiac repolarization. This is the same channel ibogaine inhibits, and it is the mechanism behind cocaine-associated QT prolongation.
[32] Cappendijk SLT, Dzoljic MR (1993). Inhibitory effects of ibogaine on cocaine self-administration in rats. European Journal of Pharmacology, 241(2–3), 261–265. Read the source →
Supports: A single dose of ibogaine reduced cocaine self-administration in cocaine-dependent rats for more than 48 hours, and weekly dosing across three weeks produced a more pronounced and durable reduction than daily dosing. Preclinical (animal) evidence.
[33] Binienda Z, Beaudoin MA, Thorn BT, Sadovova N, Skinner RD, Slikker W Jr, Ali SF (2000). Application of electrophysiological method to study interactions between ibogaine and cocaine. Annals of the New York Academy of Sciences, 914(1), 387–393. Read the source →
Supports: Electrocorticographic recordings in rats given high-dose ibogaine before cocaine. The combination altered brain electrical activity and dopamine levels in ways that have been read as a possible lowering of the seizure threshold. Preclinical (animal) evidence at doses far above human treatment levels.
[34] Schenberg EE, de Castro Comis MA, Chaves BR, da Silveira DX (2014). Treating drug dependence with the aid of ibogaine: a retrospective study. Journal of Psychopharmacology, 28(11), 993–1000. Read the source →
Supports: Retrospective review of 75 people treated with ibogaine in Brazil for dependence on alcohol, cannabis, cocaine and crack, 72% of them polysubstance users, under physician supervision and combined with psychotherapy. 61% were abstinent at follow-up. Median abstinence was 5.5 months after a single treatment and 8.4 months where treatment was repeated, both significantly longer than the abstinence achieved before ibogaine (p < 0.001). No fatalities and no serious adverse reactions were observed. Retrospective and uncontrolled, with self-reported abstinence, so it is real-world outcome data rather than trial evidence.
[35] Sulzer D, Sonders MS, Poulsen NW, Galli A (2005). Mechanisms of neurotransmitter release by amphetamines: a review. Progress in Neurobiology, 75(6), 406–433. Read the source →
Supports: Amphetamines, including methamphetamine, are the only widely used class of drugs that release dopamine directly rather than blocking its reuptake: they enter the neuron through the dopamine transporter, displace dopamine from its storage vesicles, and drive it back out through the transporter in reverse.
[36] Volkow ND, Chang L, Wang GJ, Fowler JS, Franceschi D, Sedler M, Gatley SJ, Miller E, Hitzemann R, Ding YS, Logan J (2001). Loss of dopamine transporters in methamphetamine abusers recovers with protracted abstinence. The Journal of Neuroscience, 21(23), 9414–9418. Read the source →
Supports: PET imaging of five methamphetamine users scanned in early abstinence (about 3 months) and again after protracted abstinence (about 14 months on average). Striatal dopamine transporter levels, which are significantly reduced in methamphetamine users, recovered substantially with sustained abstinence. Performance on motor and memory tests did not show comparable recovery over the same interval. A small sample, so a signal rather than a verdict.
[37] Zorick T, Nestor L, Miotto K, Sugar C, Hellemann G, Scanlon G, Rawson R, London ED (2010). Withdrawal symptoms in abstinent methamphetamine-dependent subjects. Addiction, 105(10), 1809–1818. Read the source →
Supports: Prospective observation of methamphetamine-dependent adults through monitored abstinence. Withdrawal symptoms were most intense during the first week, depressive symptoms did not approach healthy-control levels until about four weeks in, and craving did not decrease significantly until the second week, persisting at reduced levels through at least week five.
[38] Haning W, Goebert D (2007). Electrocardiographic abnormalities in methamphetamine abusers. Addiction, 102(Suppl 1), 70–75. Read the source →
Supports: Electrocardiograms from 158 adults with methamphetamine dependence across five US sites. 27.2% had a QTc interval longer than 440 ms, the first demonstration of clinically significant QTc prolongation in a methamphetamine-using population. Relevant to ibogaine screening because ibogaine also prolongs the QT interval.
[39] Glick SD, Gallagher CA, Hough LB, Rossman KL, Maisonneuve IM (1992). Differential effects of ibogaine pretreatment on brain levels of morphine and (+)-amphetamine. Brain Research, 588(1), 173–176. Read the source →
Supports: In rats, ibogaine given 19 hours before amphetamine significantly increased brain concentrations of amphetamine, suggesting ibogaine inhibits an amphetamine-metabolizing enzyme. Preclinical (animal) evidence, and a direct reason to keep ibogaine and methamphetamine far apart in time.
[40] Maisonneuve IM, Keller RW Jr, Glick SD (1992). Interactions of ibogaine and D-amphetamine: in vivo microdialysis and motor behavior in rats. Brain Research, 579(1), 87–92. Read the source →
Supports: In rats, ibogaine pretreatment potentiated amphetamine-induced increases in extracellular dopamine in the nucleus accumbens and striatum and enhanced amphetamine-induced motor activity. Preclinical (animal) evidence that the two compounds amplify each other rather than cancel out.
[41] Szumlinski KK, Haskew RE, Balogun MY, Maisonneuve IM, Glick SD (2001). Iboga compounds reverse the behavioural disinhibiting and corticosterone effects of acute methamphetamine: implications for their antiaddictive properties. Pharmacology Biochemistry and Behavior, 69(3–4), 485–491. Read the source →
Supports: In rats, ibogaine pretreatment blocked the behavioural disinhibition and the stress-hormone (corticosterone) surge produced by acute methamphetamine. Preclinical (animal) evidence consistent with an anti-addictive effect, from the same literature that also contains cautionary interaction findings.
[42] Cherian K, Keynan J, Anker L, Faerman A, Brown R, Shamma A, Keynan O, Coetzee J, Batail JM, Phillips A, Bassano N, Sahlem G, Inzunza J, Millar T, Dickinson J, Rolle C, Keller J, Adamson M, Kratter I, Williams N (2024). Magnesium-ibogaine therapy in veterans with traumatic brain injuries. Nature Medicine, 30, 373–381. Read the source →
Supports: The MISTIC trial. 30 male US Special Operations Forces veterans with predominantly mild traumatic brain injury received intravenous magnesium plus oral ibogaine (mean 12.1 mg/kg); 23 met criteria for PTSD at baseline. One month after treatment the group had moved from mild-to-moderate disability to no disability on the WHODAS-2.0 (30.2 to 5.1, d = 2.20), the study primary outcome. PTSD symptoms fell 88% on average, with a 100% response rate and 86% remission (d = 2.54); depression fell 87% (83% remission) and anxiety 81% (83% remission). Suicidal ideation fell from 47% at baseline to 7% at one month. Participants also gained in processing speed, executive function, verbal fluency and verbal learning, with no cognitive decline on any measure, and there were no serious or unexpected treatment-emergent adverse events. Open-label and uncontrolled, in a highly selected cohort, with magnesium co-administered, so the effect cannot be attributed to ibogaine alone.
[43] Adamson M (2025). Changes in Brain Structure and Age in Veterans With TBI After Treatment With Magnesium-Ibogaine. Archives of Physical Medicine and Rehabilitation, 106(4), e162–e163. Read the source →
Supports: The first in-human structural MRI evidence of brain change after ibogaine. In the same 30 MISTIC veterans, cortical thickness increased significantly in 11 of 13 regions of interest at roughly 7 days post-treatment and was sustained at one month, and predicted brain age fell by 1.60 years at one month (d = 1.035, p = 0.0082). The authors describe the findings as consistent with a proposed neurotrophic mechanism, not as confirmation of one.
[44] Lissemore JI, Chaiken A, Cherian KN, Buchanan D, Espil F, Keynan JN, Sridhar M, Rolle CE, Saggar M, Keller CJ, Williams NR (2025). Magnesium-ibogaine therapy effects on cortical oscillations and neural complexity in veterans with traumatic brain injury. Nature Mental Health, 3(8), 918–931. Read the source →
Supports: The first reported in-human evidence that ibogaine alters cortical oscillations in a clinically meaningful way. After treatment, slower theta-alpha rhythms gained power while faster beta-gamma activity lost it, raising the theta/beta ratio in a way that correlated with improved cognitive inhibition. Peak alpha frequency and neural complexity were lower, and the changes persisted at one-month follow-up.
[45] Shinozuka K, Rosso M, Chaiken A, Lissemore JI, Jones R, Descalco N, Subramani V, Belgers M, Cherian KN, Arns M, Momi D, Airan RD, Bonetti L, Schellekens A, Adamson MM, Keller CJ, Rolle C (2026). Ibogaine is associated with reorganization of high-beta brain networks in veterans with post-traumatic stress disorder. Neuroscience. Read the source →
Supports: EEG network analysis of the MISTIC cohort found a posterior shift in high-beta (24–25 Hz) network activation present at 3–4 days and one month after treatment, correlating with PTSD symptom improvement on the CAPS-5 (r = -0.66 immediately post, r = -0.53 at one month). Modelling attributed the shift to a roughly 15% reduction in cortico-cortical gain. Notably, the finding replicated in an independent EEG dataset of 11 opioid use disorder patients treated with ibogaine alone, without magnesium.
[46] Davis AK, Xin Y, Sepeda N, Averill LA (2023). Open-label study of consecutive ibogaine and 5-MeO-DMT assisted-therapy for trauma-exposed male Special Operations Forces Veterans: Prospective data from a clinical program in Mexico. The American Journal of Drug and Alcohol Abuse, 49(5), 587–596. Read the source →
Supports: A prospective open-label cohort of 86 trauma-exposed Special Operations Forces veterans reported large improvements in PTSD, depression, anxiety, insomnia, post-concussive symptoms and cognitive functioning, with preliminary signals of durability to six months. Because ibogaine was given alongside 5-MeO-DMT and psychotherapeutic support, the therapeutic effect cannot be attributed to ibogaine alone.
[47] Rolle C, Williams N, Faerman A, Lissemore J, Geoly A, Cherian K, Sridhar M, Kim B, Coetzee J, Anker L, Shamma A, Keynan NJ, Brown R, Phillips A, Jester A, Bassano N, Espil F, Kratter I (2025). Is ibogaine treatment durable? 12-month follow-up of magnesium-ibogaine therapy (MISTIC) in Special Operations Veterans with traumatic brain injuries. Preprint, in review. Read the source →
Supports: Twelve-month follow-up of the MISTIC cohort, reporting that the reductions in suicidal ideation seen immediately after treatment were sustained at one year. This is a preprint and has not yet completed peer review.
[48] Fox News (reporting statements by Conor McGregor) (2025). Conor McGregor says Ibogaine treatment saved his life and his family. Fox News Sports. Read the source →
Supports: Conor McGregor stated publicly that he travelled abroad and underwent ibogaine treatment, describing it as arranged with doctors from Stanford University to address trauma, and calling the experience life-saving. A public figure account, not clinical evidence.
[49] Yahoo Sports (reporting statements by Brett Favre) (2025). NFL and UFC athletes try 'game-changing' psychedelic to treat brain injury. Yahoo Sports. Read the source →
Supports: Brett Favre, who attributes his Parkinson's diagnosis to head impacts sustained across a 20-year NFL career, described travelling abroad for ibogaine and reported a shift in sleep and energy. A public figure account, not clinical evidence, and ibogaine is not an established treatment for Parkinson's.
[50] Chen DQ, et al. (2025). Neurorestorative effects of ibogaine in multiple sclerosis: serial MRI findings in two patients. Frontiers in Immunology. Read the source →
Supports: The first published neuroimaging data on ibogaine in multiple sclerosis. Two patients underwent serial MRI. One, a 41-year-old man with relapsing-remitting MS, showed a 70% reduction in lesion volume (1,609.8 to 480.5 mm3) at three months, with diffusion changes consistent with remyelination and reduced inflammation. The second, a 44-year-old woman with secondary progressive MS, showed cortical and subcortical changes. Two patients, one clinic, unblinded and uncontrolled: a first signal, not a result.
[51] Acuña A, Billeri F, Totaro V, Carrera I, Mesa JM, Pizzorusso T, Rossi FM (2025). Ibogaine induces juvenile-like plasticity and modulates functional and structural regulators of plasticity in the adult mouse visual cortex. Preprint, in review (Research Square). Read the source →
Supports: Mouse study reporting that a single dose of ibogaine (40 mg/kg) restored a juvenile-like plasticity response in the adult visual cortex: four days of covering one eye then shifted visual acuity and reduced dendritic spine density, which normally only happens during the developmental critical period. Ibogaine also reduced perineuronal net staining intensity and density by roughly 30%, lowered the share of parvalbumin interneurons wrapped in those nets, and reduced inhibitory vGAT puncta, all consistent with the cortex being disinhibited. Vehicle-treated controls showed none of it. A preprint that has not completed peer review, in mice, at a dose that does not translate directly to humans.
[52] Ivan VE, Tomàs-Cuesta DP, Esteves IM, Curic D, Mohajerani M, McNaughton BL, Davidsen J, Gruber AJ (2024). The Nonclassic Psychedelic Ibogaine Disrupts Cognitive Maps. Biological Psychiatry Global Open Science, 4(1), 275–283. Read the source →
Supports: Two-photon calcium imaging in mice showed that ibogaine destabilised the brain internal map of space. Position-related firing in retrosplenial cortex neurons lost reliability, error in decoding the animal location from population activity rose roughly threefold, and functional connectivity reorganised toward greater independence between neurons, while responses to actual sensory cues were preserved. Offered by the authors as a candidate mechanism for how ibogaine loosens rigid learned patterns. Animal study.
[53] Ly C, Greb AC, Cameron LP, Wong JM, Barragan EV, Wilson PC, Burbach KF, et al. (2018). Psychedelics Promote Structural and Functional Neural Plasticity. Cell Reports, 23(11), 3170–3182. Read the source →
Supports: Cell and rodent study showing that psychedelics, including the iboga alkaloid noribogaine, increase dendritic branching, dendritic spine density and synapse number in cortical neurons, through TrkB, mTOR and AMPA receptor signalling. Establishes that the structural remodelling is a shared property of the class rather than something specific to one compound. Preclinical.
[54] Esperança MP, Gomes NG, Campos MG (2026). Ibogaine: Therapeutic Potential, Cardiac Safety, and Translational Perspectives in the Treatment of Substance Use Disorders. A Scoping Review. Molecules, 31(3), 545. Read the source →
Supports: Scoping review establishing the current tier of human evidence for ibogaine: no randomized, placebo-controlled trial has yet evaluated its efficacy in substance use disorders, and every human efficacy finding to date comes from open-label observational studies, retrospective analyses and case reports. Also covers the cardiac safety profile and the translational work now moving ibogaine into regulated clinical development.
[55] Nardou R, Sawyer E, Song YJ, Wilkinson M, Padovan-Hernandez Y, de Deus JL, Wright N, Lama C, Faltin S, Goff LA, Stein-O'Brien GL, Dölen G (2023). Psychedelics reopen the social reward learning critical period. Nature, 618(7966), 790–798. Read the source →
Supports: Mouse study from Gül Dölen's lab testing five psychedelics (ketamine, psilocybin, MDMA, LSD and ibogaine) and finding that each reopens a critical period for social reward learning that adult animals have normally lost. The length of the reopened window tracked the duration of the acute subjective effects reported in humans: roughly 48 hours for ketamine, about two weeks for psilocybin and MDMA, about three weeks for LSD, and about four weeks for ibogaine, the longest of the five. Preclinical. The open state was measured behaviourally in mice, not by any direct readout of plasticity in a person.
[56] Calvey T, Govender D, Owen GR, Tumba N, Lang D, Lerer B, Stein DJ, Shoptaw S (2026). Neurorestorative properties of ibogaine: Linking multi-receptor affinities to remyelination and metabolic restoration. Acta Neuropsychiatrica, 38, e26. Read the source →
Supports: Argues from ibogaine's binding profile that it is unusually well placed among psychedelic compounds to support white matter repair, ranking its affinities at kappa-opioid, NMDA and sigma-2 receptors as the ones most relevant to oligodendrocyte maturation, protection against excitotoxic damage, and axonal repair. A mechanistic argument built on binding data, not a demonstration that any of it happens in a person with demyelinating disease.
[57] Whone A, Luz M, Boca M, Woolley M, Mooney L, Dharia S, Broadfoot J, Cronin D, Schroers C, Barua NU, Longpre L, Barclay CL, Boiko C, Johnson GA, Fibiger HC, Harrison R, Lewis O, Pritchard G, Howell M, Irving C, Johnson D, Kinch S, Marshall C, Lawrence AD, Blinder S, Sossi V, Stoessl AJ, Skinner P, Mohr E, Gill SS (2019). Randomized trial of intermittent intraputamenal glial cell line-derived neurotrophic factor in Parkinson's disease. Brain, 142(3), 512–525. Read the source →
Supports: Placebo-controlled trial that delivered GDNF, the growth factor ibogaine is proposed to raise, directly into the putamen of people with Parkinson's disease every four weeks for nine months. Imaging showed the drug was reaching and engaging the tissue, with an increase in putamen 18F-DOPA uptake, but the primary clinical endpoint was not met: motor scores in the treated group did not differ significantly from placebo. The clearest available evidence that raising GDNF in a human brain is not the same as reversing a neurodegenerative disease.
[58] Beerepoot P, Lam VM, Salahpour A (2016). Pharmacological Chaperones of the Dopamine Transporter Rescue Dopamine Transporter Deficiency Syndrome Mutations in Heterologous Cells. Journal of Biological Chemistry, 291(42), 22053–22062. Read the source →
Supports: Cell study showing that ibogaine can act as a molecular chaperone for the dopamine transporter, helping misfolded copies of the protein fold correctly and reach the cell surface. Rescue was demonstrated for two mutations that cause dopamine transporter deficiency syndrome, a rare inherited condition that produces dystonia and parkinsonism in children. That is a protein-folding disorder, not idiopathic Parkinson's disease, and the work is in cells.
[59] National Council on Problem Gambling (2024). NGAGE 3.0 National Survey: Key Findings. National Council on Problem Gambling, survey fielded by Ipsos, January–March 2024. Read the source →
Supports: US national survey finding that roughly 8% of American adults, about 20 million people, showed at least one indicator of problematic gambling in 2024. NCPG separately estimates that about 1% of US adults meet criteria for a severe gambling problem. "One indicator of risk" is a much broader net than a clinical diagnosis, and the survey is self-report.
[60] Wardle H, Degenhardt L, Marionneau V, Reith G, Livingstone C, et al. (2024). The Lancet Public Health Commission on gambling. The Lancet Public Health, 9(11), e950–e994. Read the source →
Supports: Global commission estimating that around 80 million adults worldwide have gambling disorder or problematic gambling, with roughly 450 million experiencing at least some risk of gambling harm. Modeled from heterogeneous national surveys, with wide uncertainty intervals the Commission itself flags.
[61] American Gaming Association (2025). Commercial Gaming Revenue Tracker, CY2024. American Gaming Association, February 2025. Read the source →
Supports: Industry figures showing US legal sportsbooks took nearly $150 billion in bets in 2024, generating a record $13.7 billion in revenue, up from roughly $13 billion in total handle in 2019, the first full year after the Supreme Court cleared states to legalize sports betting. Covers legal commercial wagering only; illegal and offshore betting sits on top of it.
[62] Karlsson A, Håkansson A (2018). Gambling disorder, increased mortality, suicidality, and associated comorbidity: A longitudinal nationwide register study. Journal of Behavioral Addictions, 7(4), 1091–1099. Read the source →
Supports: Swedish national register study of 2,099 people treated for gambling disorder, finding a suicide mortality rate 15 times that of the general population; suicide accounted for 31% of all deaths in the cohort. A treatment-seeking clinical population in one country, representing the severe end of the spectrum rather than everyone who gambles problematically.
[63] Fiedler I, Kairouz S, Costes JM, Weißmüller KS (2019). Gambling spending and its concentration on problem gamblers. Journal of Business Research, 98, 82–91. Read the source →
Supports: Multi-country analysis finding that problem and pathological gamblers account for roughly a third of all gambling spending (31.6% in Québec, 40.2% in France, 32% in Germany) despite being a small minority of gamblers. Survey-based spending estimates; the share varies widely by gambling product and jurisdiction.
[64] Kraus SW, Krueger RB, Briken P, First MB, Stein DJ, Kaplan MS, Voon V, Abdo CHN, Grant JE, Atalla E, Reed GM (2018). Compulsive sexual behaviour disorder in the ICD-11. World Psychiatry, 17(1), 109–110. Read the source →
Supports: Documents the World Health Organization adding compulsive sexual behaviour disorder to ICD-11 under code 6C72. Worth being precise about: ICD-11 classifies it as an impulse-control disorder, not formally as an addiction, and DSM-5 does not include it at all.
[65] Dickenson JA, Gleason N, Coleman E, Miner MH (2018). Prevalence of Distress Associated With Difficulty Controlling Sexual Urges, Feelings, and Behaviors in the United States. JAMA Network Open, 1(7), e184468. Read the source →
Supports: US nationally representative survey finding 8.6% of adults (10.3% of men, 7.0% of women) reported clinically relevant distress or impairment tied to difficulty controlling sexual feelings, urges, and behaviors. This measures distress, not a diagnosis; true diagnostic prevalence is lower.
[66] Bőthe B, Koós M, Nagy L, Kraus SW, Demetrovics Z, Potenza MN, et al. (2023). Compulsive sexual behavior disorder in 42 countries: Insights from the International Sex Survey and introduction of standardized assessment tools. Journal of Behavioral Addictions, 12(2), 393–407. Read the source →
Supports: Survey of 82,243 people across 42 countries in which 4.8% scored in the high-risk range for compulsive sexual behaviour disorder, and only 14% of that high-risk group had ever sought treatment for it. A non-probability online sample, and a screening scale rather than a clinical diagnosis.
[67] Robb MB, Mann S (2023). Teens and Pornography. Common Sense Media, survey of 1,358 US teens aged 13–17, fielded September 2022. Read the source →
Supports: US teen survey finding the average age of first seeing online pornography is 12, with 15% first exposed at age 10 or younger and 73% of teens 13 to 17 having watched porn online. Self-report and recall-based. The widely circulated claim that average first exposure is age 8 has no credible primary source; this is the citable figure.
[68] Deloitte Access Economics (2020). The Social and Economic Cost of Eating Disorders in the United States of America. Report commissioned by STRIPED (Harvard T.H. Chan School of Public Health) and the Academy for Eating Disorders. Read the source →
Supports: Modeled estimate that 9% of the US population, about 28.8 million Americans, will have an eating disorder in their lifetime. Includes subclinical presentations; strict DSM-5 survey prevalence runs lower, so cite as an estimate rather than a count.
[69] Udo T, Grilo CM (2018). Prevalence and Correlates of DSM-5-Defined Eating Disorders in a Nationally Representative Sample of U.S. Adults. Biological Psychiatry, 84(5), 345–354. Read the source →
Supports: The largest DSM-5 national survey of eating disorders (36,306 US adults), finding binge eating disorder the most common eating disorder in American adults, ahead of anorexia nervosa and bulimia nervosa. Absolute prevalence figures vary several-fold between surveys, but binge eating disorder ranking first holds across them.
[70] Arcelus J, Mitchell AJ, Wales J, Nielsen S (2011). Mortality rates in patients with anorexia nervosa and other eating disorders: a meta-analysis of 36 studies. Archives of General Psychiatry, 68(7), 724–731. Read the source →
Supports: Meta-analysis finding people with anorexia nervosa die at 5.86 times the expected rate, among the highest mortality of any psychiatric illness, with about one in five of those deaths by suicide. "Among the highest" is the defensible phrasing: mortality in some substance use disorders is of comparable magnitude.
[71] Juul F, Parekh N, Martinez-Steele E, Monteiro CA, Chang VW (2022). Ultra-processed food consumption among US adults from 2001 to 2018. American Journal of Clinical Nutrition, 115(1), 211–221. Read the source →
Supports: NHANES analysis showing ultra-processed foods supply about 57% of the calories US adults eat, up from roughly 54% two decades earlier. Based on 24-hour dietary recall and the NOVA classification, which some nutrition researchers contest.
[72] Gearhardt AN, Bueno NB, DiFeliceantonio AG, Roberto CA, Jiménez-Murcia S, Fernandez-Aranda F (2023). Social, clinical, and policy implications of ultra-processed food addiction. BMJ, 383, e075354. Read the source →
Supports: Analysis drawing on pooled Yale Food Addiction Scale data estimating that 14% of adults meet criteria for addiction to ultra-processed foods, comparable to prevalence rates for alcohol and tobacco. "Food addiction" is not a recognized diagnosis in DSM-5 or ICD-11; the scale applies substance-use criteria by analogy, and the construct is actively debated.
[74] Meng SQ, Cheng JL, Li YY, Yang XQ, Zheng JW, Chang XW, Shi Y, Chen Y, Lu L, Sun Y, Bao YP, Shi J (2022). Global prevalence of digital addiction in general population: A systematic review and meta-analysis. Clinical Psychology Review, 92, 102128. Read the source →
Supports: Meta-analysis across 504 studies and 2.1 million people estimating 26.99% of the general population screens positive for smartphone addiction and 17.42% for social media addiction. Almost certainly overestimates of anything clinically meaningful: low screening thresholds, enormous heterogeneity, and "smartphone addiction" is not a recognized diagnosis. Read as "screens positive," not "is addicted."
[75] Twenge JM (2020). Increases in Depression, Self-Harm, and Suicide Among U.S. Adolescents After 2012 and Links to Technology Use. Psychiatric Research and Clinical Practice, 2(1), 19–25. Read the source →
Supports: Documents the sharp rise in US adolescent depression after 2012, including a roughly 52% increase in past-year major depressive episodes among teens between 2005 and 2017, and argues the timing tracks the spread of smartphones and social media. The rise itself is well documented; the causal role of social media is genuinely contested.
[76] Orben A, Przybylski AK (2019). The association between adolescent well-being and digital technology use. Nature Human Behaviour, 3(2), 173–182. Read the source →
Supports: Large-scale analysis finding the association between digital technology use and adolescent well-being is real but small, explaining at most a tiny fraction of the variance. The standard counterweight to strong causal claims about screens and the teen mental health decline; we cite it so the debate stays visible.
[77] Grant JE, Potenza MN, Weinstein A, Gorelick DA (2010). Introduction to Behavioral Addictions. American Journal of Drug and Alcohol Abuse, 36(5), 233–241. Read the source →
Supports: The standard review showing behavioral addictions produce the same core clinical picture as substance addictions (craving, escalation, loss of control, continued use despite harm) and engage overlapping brain reward circuitry, including altered dopamine signaling in the mesolimbic pathway. The neuroimaging evidence is strongest for gambling; for newer candidates like porn and social media it is suggestive, not conclusive.
[78] Sussman S, Lisha N, Griffiths M (2011). Prevalence of the addictions: a problem of the majority or the minority?. Evaluation & the Health Professions, 34(1), 3–56. Read the source →
Supports: A provocative and widely cited review arguing that, counting both substances and behaviors, around 47% of US adults show signs of at least one addictive disorder in a 12-month period. A loose synthesis using generous definitions; we cite it as one review's argument, not an established prevalence figure.
[80] The White House (2026). Fact sheet: President Donald J. Trump is accelerating medical treatments for serious mental illness. whitehouse.gov, 18 April 2026. Read the source →
Supports: The April 2026 executive order directing the FDA to prioritise review of psychedelic medicines, naming ibogaine, easing DEA research restrictions, and funding the effort with $50 million.
[81] He DY, Ron D (2006). Autoregulation of glial cell line-derived neurotrophic factor expression: implications for the long-lasting actions of ibogaine. The FASEB Journal, 20(13), 2420–2422. Read the source →
Supports: Shows ibogaine triggers a sustained, self-sustaining upregulation of GDNF in reward-related brain regions — a mechanism for effects that outlast the drug itself.
[82] Brown TK, Alper K (2017). Treatment of opioid use disorder with ibogaine: detoxification and drug use outcomes. The American Journal of Drug and Alcohol Abuse, 44(1), 24–36. Read the source →
Supports: Prospective study of 30 people treated with ibogaine for opioid use disorder in Mexico, followed for twelve months; documents substantial detoxification effects and month-by-month drug-use trajectories afterwards.
[83] Noller GE, Frampton CM, Yazar-Klosinski B (2018). Ibogaine treatment outcomes for opioid dependence from a twelve-month follow-up observational study. The American Journal of Drug and Alcohol Abuse, 44(1), 37–46. Read the source →
Supports: Twelve-month observational follow-up of 14 people receiving legal ibogaine treatment in New Zealand; documents reduced opioid use and depression over the follow-up year.
[84] Meinhofer A, Williams AR, Johnson P, Schackman BR, Bao Y (2019). Prescribing decisions at buprenorphine treatment initiation: do they matter for treatment discontinuation and adverse opioid overdose outcomes?. Journal of Substance Abuse Treatment, 105, 37–43. Read the source →
Supports: Large claims-data study of buprenorphine treatment showing how commonly treatment is discontinued and how discontinuation relates to overdose outcomes.
[85] Arns M, Shinozuka K, Barsuglia J (2026). Indication-stratified mortality risk of ibogaine treatment under contemporary safety protocols: a multisite analysis of 19,071 patients and updated systematic review of fatalities. Research Square preprint (posted 17 June 2026; not yet peer reviewed). Read the source →
Supports: The largest ibogaine safety analysis to date: 19,071 patients treated under the 2016 safety guidelines at 11 international clinics. Six deaths occurred within 72 hours of dosing (0.03%), all among the 10,382 opioid use disorder patients; there were none among 8,689 non-SUD patients. An updated systematic review found 41 of 44 fatalities with a known indication involved substance use disorder, predominantly opioid detox. The authors describe the 0.03% as a lower bound rather than the true rate, since clinic participation was voluntary and deaths were not independently adjudicated. A preprint that has not completed peer review; one author holds equity in ibogaine companies and was firewalled from the data analysis.
[86] World Health Organization (2025). Mental disorders (fact sheet, updated 30 September 2025). World Health Organization. Read the source →
Supports: An estimated 1.1 billion people worldwide, nearly 1 in 7, were living with a mental disorder in 2021, with anxiety and depressive disorders the most common. Also documents the treatment gap: even in high-income countries only about a third of people with depression receive formal care. Modelled Global Burden of Disease estimates, not diagnosed cases.
[87] World Health Organization (2022). Mental health and COVID-19: early evidence of the pandemic's impact (scientific brief). World Health Organization, 2 March 2022. Read the source →
Supports: Global prevalence of anxiety and depression rose an estimated 25% in the first year of the COVID-19 pandemic. A modelled estimate for the first pandemic year; prevalence has since receded toward baseline.
[88] World Health Organization (2025). Suicide (fact sheet, updated 25 March 2025). World Health Organization. Read the source →
Supports: More than 720,000 people die by suicide every year (727,000 in 2021), and suicide is the third leading cause of death among 15 to 29 year olds. Suicide is under-registered in many countries, so these are WHO-modelled estimates.
[89] National Institute of Mental Health, reporting CDC WISQARS/NVSS data (2025). Suicide (statistics page, data year 2023). National Institute of Mental Health. Read the source →
Supports: Over 49,300 people died by suicide in the United States in 2023, making it the 11th leading cause of death overall and the second leading cause among people aged 10 to 34. Death-certificate data republished from the CDC.
[90] National Institute of Mental Health, from the SAMHSA 2022 NSDUH (2024). Mental Illness (statistics page, data year 2022). National Institute of Mental Health. Read the source →
Supports: 23.1% of US adults, 59.3 million people, lived with a mental illness in 2022, and only about half of them (50.6%) received mental health treatment that year. Household survey data based on self-report.
[91] Chisholm D, Sweeny K, Sheehan P, Rasmussen B, Smit F, Cuijpers P, Saxena S (2016). Scaling-up treatment of depression and anxiety: a global return on investment analysis. The Lancet Psychiatry, 3(5), 415–424. Read the source →
Supports: Depression and anxiety cost the global economy an estimated US$1 trillion each year in lost productivity, about 12 billion working days. The same model found every $1 invested in scaled-up treatment returns roughly $4 in better health and productivity. A 2016 economic model.
[92] World Health Organization (2025). Depressive disorder (depression) (fact sheet, updated 29 August 2025). World Health Organization. Read the source →
Supports: An estimated 332 million people worldwide, 5.7% of adults, were living with depression in 2021; it is about 1.5 times more common in women than men. Modelled Global Burden of Disease estimates.
[93] National Institute of Mental Health, from the SAMHSA 2021 NSDUH (2023). Major Depression (statistics page, data year 2021). National Institute of Mental Health. Read the source →
Supports: 21.0 million US adults (8.3%) had at least one major depressive episode in 2021, and 39% of them received no treatment for it. Among adolescents aged 12 to 17 the rate was 20.1% (5.0 million), of whom about 59% went untreated. Self-reported survey screen.
[95] Rush AJ, Trivedi MH, Wisniewski SR, et al. (2006). Acute and longer-term outcomes in depressed outpatients requiring one or several treatment steps: a STAR*D report. The American Journal of Psychiatry, 163(11), 1905–1917. Read the source →
Supports: In the largest real-world antidepressant trial run, remission rates fell from 36.8% on the first medication to 13.0% by the fourth attempt; roughly one in three patients did not remit even after four sequential treatments, and relapse was more likely the more steps it took. Open-label, 2006.
[96] GBD 2021 Diseases and Injuries Collaborators (Ferrari AJ, et al.) (2024). Global incidence, prevalence, years lived with disability (YLDs), disability-adjusted life-years (DALYs), and healthy life expectancy (HALE) for 371 diseases and injuries in 204 countries and territories: a systematic analysis for the Global Burden of Disease Study 2021. The Lancet, 403(10440), 2133–2161. Read the source →
Supports: Depressive disorders were the second leading cause of years lived with disability worldwide in 2021.
[97] World Health Organization (2025). Anxiety disorders (fact sheet, updated 8 September 2025). World Health Organization. Read the source →
Supports: An estimated 359 million people worldwide were living with an anxiety disorder in 2021, the most common of all mental disorders, and only about 1 in 4 people who need treatment for one (27.6%) receive any. Modelled estimates.
[98] National Institute of Mental Health, from the Harvard National Comorbidity Survey Replication (2017). Any Anxiety Disorder (statistics page). National Institute of Mental Health. Read the source →
Supports: An estimated 31.1% of US adults experience an anxiety disorder at some point in their lives, and 19.1% had one in the past year (women 23.4% vs men 14.3%). Survey data collected 2001–2003; still the standing NIMH figure.
[99] Wang PS, Berglund P, Olfson M, Pincus HA, Wells KB, Kessler RC (2005). Failure and delay in initial treatment contact after first onset of mental disorders in the National Comorbidity Survey Replication. Archives of General Psychiatry, 62(6), 603–613. Read the source →
Supports: The median delay between the onset of an anxiety disorder and first treatment contact in the US is 9 to 23 years, against 6 to 8 years for mood disorders. Retrospective self-report.
[100] US Department of Veterans Affairs, National Center for PTSD (2024). How Common is PTSD in Adults?. US Department of Veterans Affairs. Read the source →
Supports: About 6% of US adults will have PTSD at some point in their lives (8% of women, 4% of men), and about 5%, roughly 13 million adults in 2020, have it in a given year.
[101] US Department of Veterans Affairs, National Center for PTSD (2024). How Common is PTSD in Veterans?. US Department of Veterans Affairs. Read the source →
Supports: 29% of veterans of the post-9/11 wars will have PTSD at some point in their lives, against 21% for Gulf War veterans, 10% for Vietnam veterans, and 7% of veterans overall.
[102] Kessler RC, Sonnega A, Bromet E, Hughes M, Nelson CB (1995). Posttraumatic stress disorder in the National Comorbidity Survey. Archives of General Psychiatry, 52(12), 1048–1060. Read the source →
Supports: Among people reporting rape, 45% of women and 65% of men met criteria for PTSD, the highest conditional risk of any trauma studied. DSM-IV-era national survey data.
[103] US Department of Veterans Affairs (2026). 2025 National Veteran Suicide Prevention Annual Report (data through 2023). US Department of Veterans Affairs, Office of Mental Health. Read the source →
Supports: An average of 17.5 US veterans died by suicide each day in 2023, 6,398 over the year: 44 fewer than in 2022, and lower than in 14 of the prior 15 years.
[104] National Institute of Mental Health, from the Harvard National Comorbidity Survey Replication (2017). Obsessive-Compulsive Disorder (OCD) (statistics page). National Institute of Mental Health. Read the source →
Supports: An estimated 2.3% of US adults experience OCD at some point in their lives and 1.2% had it in the past year (women 1.8%, men 0.5%). Half of past-year cases (50.6%) were classified as causing serious impairment. Survey data collected 2001–2003.
[105] Pellegrini L, Giobelli S, Burato S, di Salvo G, Maina G, Albert U (2025). Meta-analysis of age at help-seeking and duration of untreated illness (DUI) in obsessive-compulsive disorder (OCD). Journal of Affective Disorders, 380, 212–225. Read the source →
Supports: Across 31 studies, people with OCD waited a pooled average of about 7 years from onset before seeking help, and lived with untreated illness for about 6.7 years on average.
[106] World Health Organization (2019). Burn-out an "occupational phenomenon": International Classification of Diseases. World Health Organization, 28 May 2019. Read the source →
Supports: The WHO classifies burnout in ICD-11 as an occupational phenomenon, not a medical condition: a syndrome resulting from chronic workplace stress that has not been successfully managed, with three dimensions (exhaustion, cynicism or mental distance, and reduced efficacy).
[107] Gallup (2026). State of the Global Workplace: 2026 Report (global data summary). Gallup. Read the source →
Supports: 40% of employees worldwide said they experienced a lot of stress the previous day, and only 20% were engaged at work. Single-item self-report survey.
[108] Gallup (2026). How to Prevent Employee Burnout. Gallup (Q4 2025 survey data). Read the source →
Supports: 31% of US working women and 23% of working men say they very often or always feel burned out at work. Gallup updates this page periodically, so figures may shift on refresh.
[109] Shanafelt TD, West CP, Sinsky C, Trockel M, et al. (2025). Changes in burnout and satisfaction with work-life integration in physicians and the general US working population between 2011 and 2023. Mayo Clinic Proceedings, 100(3). Read the source →
Supports: 45.2% of US physicians reported at least one symptom of burnout in 2023, down from a peak of 62.8% in 2021 but still elevated against the general working population. Triennial AMA/Mayo/Stanford survey.
[110] Benwell ME, Holtom PE, Moran RJ, Balfour DJ (1996). Neurochemical and behavioural interactions between ibogaine and nicotine in the rat. British Journal of Pharmacology, 117(4), 743–749. Read the source →
Supports: Counter-evidence carried honestly: male rats given 40 mg/kg ibogaine made fewer entries into open runways for about 22 hours afterwards, a response the authors read as anxiety-like and long-lasting. An animal study; recovering animals may avoid open spaces for reasons other than anxiety, but the finding warrants stating on any anxiety page.
[111] Mash DC (2023). IUPHAR invited review — Ibogaine: A legacy within the current renaissance of psychedelic therapy. Pharmacological Research, 190, 106620. Read the source →
Supports: Mechanism synthesis: ibogaine inhibits the serotonin transporter noncompetitively, its long-lived metabolite noribogaine slows serotonin reuptake and acts as a G-protein-biased kappa-opioid agonist, and rapid antidepressant-like effects are thought to involve ketamine-like NMDA receptor blockade. All framed as proposed mechanisms under investigation, not demonstrated clinical effects.
[112] Nicolas M (2025). Ibogaine's potential role in supporting reward system recovery across diagnostic boundaries. Frontiers in Pharmacology, 16, 1744383. Read the source →
Supports: A theoretical proposal that ibogaine's growth-factor induction, glutamatergic modulation, dopaminergic recalibration and reopening of neuroplasticity could amount to one mechanism for restoring reward-system function across substance use disorder, PTSD, OCD and eating disorders. A hypothesis paper: it is the only place OCD appears in the research literature summarised by the MAPS Investigator's Brochure, and it contains no OCD patient data.
[113] Heink A, Katsikas S, Lange-Altman T (2017). Examination of the phenomenology of the ibogaine treatment experience: role of altered states of consciousness and psychedelic experiences. Journal of Psychoactive Drugs, 49(3), 201–208. Read the source →
Supports: Survey of 27 people who underwent ibogaine treatment: all reported insights about their personal past, 97% experienced visions, 77% saw content drawn from their own childhood, and 85% reported subjective relief from guilt. Large majorities reported insights about the meaning of life, death, and creation. A small, self-selected online survey, reported as phenomenology rather than outcome evidence.
[114] 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: In 44 opioid-dependent people undergoing ibogaine treatment, 43% met criteria for a complete mystical experience. Participants described cyclic visual content leading to confronting realisations involving remorse and regret toward others, subjective release from guilt and worthlessness, and many compared the significance of the experience to a spiritual transformation.
[115] Camlin TJ, Eulert D, Horvath AT, Bucky SF, Barsuglia J, Polanco M (2018). A phenomenological investigation into the lived experience of ibogaine and its potential to treat opioid use disorders. Journal of Psychedelic Studies, 2(1), 24–35. Read the source →
Supports: Qualitative study of 10 people treated with ibogaine in Mexico: 80% described the experience as physically draining, one comparing it to having survived cancer. The source for stating honestly that the treatment night is often demanding or harrowing rather than pleasant, which also helps explain ibogaine's low abuse potential.
[116] Olash C, Buchanan DM, Brown R, Faerman A, Cherian K, Lin G, Spiegel D, Gross JJ, Williams N (2026). Accelerated recovery using magnesium ibogaine: characterizing the subjective experience of its rapid healing from neuropsychiatric disorders. npj Mental Health Research, 5(1), 8. Read the source →
Supports: Qualitative analysis of the Stanford MISTIC veterans' accounts, characterising the ibogaine experience as a compressed form of therapeutic processing within a single treatment: trauma-related content surfacing, shifts in self-experience, emotional resolution, and perceived neurobiological change.
[117] Staley BS, Robinson LR, Claussen AH, et al. (CDC) (2024). Attention-deficit/hyperactivity disorder diagnosis, treatment, and telehealth use in adults — National Center for Health Statistics Rapid Surveys System, United States, October–November 2023. MMWR Morbidity and Mortality Weekly Report, 73(40), 890–895. Read the source →
Supports: An estimated 6.0% of US adults, about 15.5 million people, had a current ADHD diagnosis in late 2023; over half (55.9%) were not diagnosed until adulthood, and 71.5% of adults taking stimulant medication reported difficulty getting a prescription filled in the past year because it was unavailable. Self-reported survey data, not clinical assessment.
[118] Danielson ML, Claussen AH, Bitsko RH, et al. (CDC) (2024). ADHD prevalence among U.S. children and adolescents in 2022: diagnosis, severity, co-occurring disorders, and treatment. Journal of Clinical Child & Adolescent Psychology, 53(3), 343–360. Read the source →
Supports: 11.4% of US children aged 3–17, about 1 in 9 (7.1 million), have received an ADHD diagnosis at some point, roughly a million more than in 2016. Parent-reported diagnosis from the 2022 National Survey of Children's Health, not clinical evaluation.
[119] Song P, Zha M, Yang Q, Zhang Y, Li X, Rudan I (2021). The prevalence of adult attention-deficit hyperactivity disorder: a global systematic review and meta-analysis. Journal of Global Health, 11, 04009. Read the source →
Supports: Globally, an estimated 2.58% of adults (about 140 million) have persistent ADHD carried from childhood, and 6.76% (about 366 million) meet symptom criteria regardless of documented childhood onset. The two figures answer different questions and should not be blended.
[120] Kessler RC, Adler L, Barkley R, et al. (2006). The prevalence and correlates of adult ADHD in the United States. The American Journal of Psychiatry, 163(4), 716–723. Read the source →
Supports: In the 2001–2003 national survey, 4.4% of US adults aged 18–44 had current ADHD, and only 10.9% of them had received any ADHD treatment in the prior year. Historical framing: treatment rates have risen substantially since.
[121] US Food and Drug Administration & Drug Enforcement Administration (Califf RM, Milgram A) (2023). Joint letter on prescription stimulant shortages, 1 August 2023. US Food and Drug Administration. Read the source →
Supports: US dispensing of prescription stimulants rose 45.5% between 2012 and 2021, and the shortage that began in late 2022 left roughly a billion authorized amphetamine doses unproduced in 2022. A policy statement rather than a study; shortage conditions have evolved since.
[122] Litjens RPW, Brunt TM (2016). How toxic is ibogaine?. Clinical Toxicology, 54(4), 297–302. Read the source →
Supports: Review of ibogaine's toxicity and interactions. Medications that inhibit the CYP2D6 enzyme, including SSRIs such as fluoxetine and paroxetine and the antidepressant bupropion, impair ibogaine metabolism and should be discontinued before treatment, with washout periods matched to the half-life of the drug and its active metabolites. Fluoxetine's long-lived metabolite can warrant several weeks.
[123] Knuijver T, Ter Heine R, Schellekens AFA, Heydari P, Lucas L, Westra S, Belgers M, Van Oosteren T, Verkes RJ, Kramers C (2024). The pharmacokinetics and pharmacodynamics of ibogaine in opioid use disorder patients. Journal of Psychopharmacology, 38(5), 481–488. Read the source →
Supports: PK/PD study in opioid use disorder patients: ibogaine clearance varies more than ten-fold with CYP2D6 enzyme activity, and QTc prolongation tracks drug exposure. The quantitative basis for strict cardiac screening and for clearing CYP2D6-inhibiting medications before treatment.
[124] Davis AK, Renn E, Windham-Herman AM, Polanco M, Barsuglia JP (2018). A mixed-method analysis of persisting effects associated with positive outcomes following ibogaine detoxification. Journal of Psychoactive Drugs, 50(4), 287–297. Read the source →
Supports: In a retrospective study of 73 people treated with ibogaine for opioid use disorder, roughly 23% reported difficulty integrating the experience into daily life afterwards. The evidence that ibogaine is a beginning that needs a structured program around it, not a standalone treatment.
[125] Brody DJ, Gu Q (2020). Antidepressant use among adults: United States, 2015–2018. NCHS Data Brief No. 377, CDC National Center for Health Statistics. Read the source →
Supports: In 2015–2018, 13.2% of US adults had used an antidepressant in the past 30 days: 17.7% of women and 8.4% of men, rising to 24.3% among women over 60. A self-report survey covering all antidepressant classes, some prescribed for conditions other than depression.
[126] Pratt LA, Brody DJ, Gu Q (2017). Antidepressant use among persons aged 12 and over: United States, 2011–2014. NCHS Data Brief No. 283, CDC National Center for Health Statistics. Read the source →
Supports: A quarter of past-month antidepressant users (25.3%) had been taking them for ten years or more, nearly double the share of a decade earlier, and the median duration of use exceeded five years. Self-reported survey data from 2011–2014.
[127] Henssler J, Schmidt Y, Schmidt U, Schwarzer G, Bschor T, Baethge C (2024). Incidence of antidepressant discontinuation symptoms: a systematic review and meta-analysis. The Lancet Psychiatry, 11(7), 526–535. Read the source →
Supports: The largest meta-analysis of antidepressant discontinuation to date (79 studies, 21,002 people): symptoms occurred in about 31% of people stopping an antidepressant versus 17% stopping placebo, putting the drug-attributable rate at roughly one in six to seven, with severe symptoms in about 3%. Based largely on short-duration trials, which critics argue understates withdrawal after years of use.
[128] Davies J, Read J (2019). A systematic review into the incidence, severity and duration of antidepressant withdrawal effects: are guidelines evidence-based?. Addictive Behaviors, 97, 111–121. Read the source →
Supports: Reported that 56% of people stopping antidepressants experience withdrawal symptoms, nearly half of them severe. A disputed figure: it leans on self-selected surveys of long-term users and was criticised on those grounds (Jauhar & Hayes, 2019), while the trial-based estimate is closer to one in six. The honest range runs from roughly 15% to over 50% depending on how long people have taken the drug.
[129] Eveleigh R, Muskens E, Lucassen P, Verhaak P, Spijker J, van Weel C, Oude Voshaar R, Speckens A (2018). Withdrawal of unnecessary antidepressant medication: a randomised controlled trial in primary care. BJGP Open, 2(4), bjgpopen18X101663. Read the source →
Supports: In a Dutch primary-care trial of long-term antidepressant users with no remaining medical indication, only 51% were willing to attempt tapering when advised to, and just 6% actually managed to stop. A single trial of 146 people, but the clearest measure of how hard discontinuation is without real support.
[130] Moore TJ, Mattison DR (2017). Adult utilization of psychiatric drugs and differences by sex, age, and race. JAMA Internal Medicine, 177(2), 274–275. Read the source →
Supports: One in six US adults (16.7%) filled at least one psychiatric drug prescription in 2013: 12.0% antidepressants, 8.3% anxiolytics, sedatives and hypnotics, 1.6% antipsychotics. Most use was long-term, with 84.3% of users refilling repeatedly or continuing a drug started years earlier. Prescription-fill data, which undercounts relative to surveys.
[131] Van Leeuwen E, van Driel ML, Horowitz MA, Kendrick T, Donald M, De Sutter AI, Robertson L, Christiaens T (2021). Approaches for discontinuation versus continuation of long-term antidepressant use for depressive and anxiety disorders in adults. Cochrane Database of Systematic Reviews, 4, CD013495. Read the source →
Supports: The Cochrane review of how to stop long-term antidepressants found only 33 usable trials, most tapering over four weeks or less or stopping abruptly, and could draw no firm conclusions about the safety or effectiveness of any approach. Evidence that structured support for coming off these medications has barely been studied.
[132] Maust DT, Lin LA, Blow FC (2019). Benzodiazepine use and misuse among adults in the United States. Psychiatric Services, 70(2), 97–106. Read the source →
Supports: 30.6 million US adults, 12.6%, reported benzodiazepine use in the past year (2015–2016): 10.4% as prescribed and 2.2% misuse. Roughly double what prescription records alone had suggested. Self-report survey data.
[133] US Food and Drug Administration (2020). FDA requiring Boxed Warning updated to improve safe use of benzodiazepine drug class. FDA Drug Safety Communication, 23 September 2020. Read the source →
Supports: An estimated 92 million benzodiazepine prescriptions were dispensed from US pharmacies in 2019. About half of patients dispensed oral benzodiazepines received them for two months or longer, and the FDA states that physical dependence can develop within days to weeks of steady use, even when taken exactly as prescribed.
[134] National Institute on Drug Abuse (2025). Drug overdose deaths: facts and figures. National Institutes of Health (CDC WONDER mortality data). Read the source →
Supports: In 2023, 10,870 US overdose deaths involved benzodiazepines. The overwhelming majority also involved opioids, most recently illicit fentanyl; deaths from benzodiazepines alone are rare. "Involved" means the drug appeared on the death certificate, not that it was the sole cause.
[135] National Institute for Health and Care Excellence (2004). Guidance on the use of zaleplon, zolpidem and zopiclone for the short-term management of insomnia (TA77). NICE Technology Appraisal Guidance 77. Read the source →
Supports: UK national guidance restricts hypnotic sleep medications, both z-drugs and benzodiazepine hypnotics, to short-term use only, generally no more than two to four weeks at the lowest effective dose, because tolerance and dependence can develop within weeks. Still-current guidance; millions take these drugs far longer.
[136] Ritvo AD, Foster DE, Huff C, Finlayson AJR, Silvernail B, Martin PR (2023). Long-term consequences of benzodiazepine-induced neurological dysfunction: a survey. PLOS ONE, 18(6), e0285584. Read the source →
Supports: In the largest survey of benzodiazepine users to date (1,207 people recruited from support communities), a majority of those reporting symptoms such as anxiety, memory problems and low energy said they lasted a year or more after stopping. A self-selected sample: it documents that protracted withdrawal is real for some people, not how common it is. No reliable population prevalence exists.
[137] IQVIA (report prepared for the US Drug Enforcement Administration) (2024). Stimulant prescription trends in the United States from 2012–2023. US Drug Enforcement Administration, 13 November 2024. Read the source →
Supports: US dispensing of prescription stimulants rose 60% between 2012 and 2023. Growth was fastest in adults: up 240% among people aged 31–40, who are now the largest group receiving stimulant prescriptions. Counts prescriptions dispensed, not individual people.
[138] Staley BS, Robinson LR, Claussen AH, Katz SM, Danielson ML, Summers AD, Farr SL, Blumberg SJ, Tinker SC (2024). Attention-deficit/hyperactivity disorder diagnosis, treatment, and telehealth use in adults — United States, October–November 2023. MMWR Morbidity and Mortality Weekly Report, 73(40), 890–895. Read the source →
Supports: An estimated 6.0% of US adults, about 15.5 million people, had a current ADHD diagnosis in late 2023. Roughly one third had taken a prescription stimulant in the past year, and 71.5% of those reported difficulty getting a prescription filled during the shortage. A self-report rapid survey.
[139] Danielson ML, Claussen AH, Bitsko RH, Katz SM, Newsome K, Blumberg SJ, Kogan MD, Ghandour R (2024). ADHD prevalence among US children and adolescents in 2022. Journal of Clinical Child & Adolescent Psychology, 53(3), 343–360. Read the source →
Supports: In 2022, 11.4% of US children aged 3–17, over seven million, had ever been diagnosed with ADHD, and 53.6% of those with a current diagnosis were taking ADHD medication. Parent-report national survey data.
[140] Reuben C, Elgaddal N, Black LI (2023). Sleep medication use in adults aged 18 and over: United States, 2020. NCHS Data Brief No. 462, CDC National Center for Health Statistics. Read the source →
Supports: In 2020, 8.4% of US adults took medication for sleep every day or most days in the past month, and about 18% used it at least some days. The figure spans prescription drugs and over-the-counter sleep aids; women and older adults used them most. Self-report survey data.
[141] van Straten A, et al. (2025). The prevalence of insomnia disorder in the general population: a meta-analysis. Journal of Sleep Research, e70089. Read the source →
Supports: Pooled across general-population studies, roughly one in eight adults meets full clinical criteria for insomnia disorder (12.4% by clinician interview, 16.3% by self-reported criteria), and about three in ten report insomnia symptoms. Prevalence estimates vary with the measurement instrument used.
[142] Substance Abuse and Mental Health Services Administration (2013). Emergency department visits for adverse reactions involving the insomnia medication zolpidem. Drug Abuse Warning Network (DAWN) Report, May 2013. Read the source →
Supports: US emergency department visits for adverse reactions involving zolpidem more than tripled in five years, from 6,111 in 2005 to 19,487 in 2010; two thirds of the 2010 visits were women and half involved zolpidem combined with other drugs. Older federal surveillance data, but the canonical figure.
[143] World Health Organization (2025). Bipolar disorder (fact sheet). World Health Organization, updated September 2025. Read the source →
Supports: An estimated 1 in 200 people, about 37 million worldwide, live with bipolar disorder (2021 modelled estimates), and WHO states that treatment coverage is low. Modelled Global Burden of Disease figures, not diagnosed cases.
[144] Merikangas KR, Jin R, He JP, Kessler RC, Lee S, Sampson NA, Viana MC, Andrade LH, Hu C, Karam EG, et al. (2011). Prevalence and correlates of bipolar spectrum disorder in the World Mental Health Survey Initiative. Archives of General Psychiatry, 68(3), 241–251. Read the source →
Supports: Across 11 countries, 2.4% of people met lifetime criteria for bipolar spectrum disorder, fewer than half of those affected ever received mental health treatment, and in low-income countries only 25.2% had any contact with the mental health system.
[145] Carton L, Cottencin O, Lapeyre-Mestre M, Geoffroy PA, Favre J, Simon N, Bordet R, Rolland B (2015). Off-label prescribing of antipsychotics in adults, children and elderly individuals: a systematic review of recent prescription trends. Current Pharmaceutical Design, 21(23), 3280–3297. Read the source →
Supports: Systematic review finding that 40–75% of adult antipsychotic prescriptions are off-label, with quetiapine the most frequently prescribed off-label antipsychotic, most often for insomnia and anxiety rather than psychosis or bipolar disorder.
[146] National Institute for Health and Care Excellence (2015). Bipolar disorder in adults: quality standard QS95 (lithium monitoring). NICE Quality Standard 95, statement 5. Read the source →
Supports: UK guidance requires people taking lithium to have blood levels checked every three months in the first year, with kidney, thyroid and calcium monitoring every six months, more often for older adults or anyone on interacting medications. The monitoring burden of a drug framed as lifelong maintenance.
[147] Mojtabai R, Olfson M (2010). National trends in psychotropic medication polypharmacy in office-based psychiatry. Archives of General Psychiatry, 67(1), 26–36. Read the source →
Supports: The share of US psychiatrist visits where two or more psychotropic medications were prescribed rose from 42.6% to 59.8% in a decade, and visits with three or more medications doubled to 33.2%. Historical trend data ending in 2006, documenting the drift toward medication stacking.
[85] Daly N, Jacobs A (2026). Americans Encounter Risks at Psychedelic Clinics Abroad. The New York Times, 26 August 2026. Read the source →
Supports: Investigation into overseas psychedelic clinics. The Times counted at least 40 clinics and wellness centers in Mexico offering ibogaine, up from almost none a decade ago, and found no official tally anywhere of injuries or deaths. Patients described absent medical screening, prescription drugs given without regard to medical history, pressure to stop psychiatric medications abruptly, upselling during treatment, and sexual assault with little legal recourse. Also reports a JAMA survey of 49 retreats and clinics in which fewer than half employed a medical professional and roughly 10% employed a staff member with emergency medical training.
[86] Barsuglia JP and colleagues (2026). Indication-stratified mortality risk of ibogaine treatment under contemporary safety protocols: a multisite analysis of 19,071 patients and updated systematic review of fatalities. Research Square preprint rs-9966269 (not yet peer reviewed). Read the source →
Supports: The largest ibogaine safety dataset to date: 19,071 treatments across 11 international clinics operating under contemporary safety protocols. Six deaths occurred within 72 hours, all among patients treated for opioid use disorder (6 of 10,382); none occurred among the 8,689 patients treated for non-substance-use indications. In the accompanying review of documented fatalities, 41 of 44 with a known indication involved substance use disorder, predominantly opioid detoxification, clustering around preexisting cardiovascular disease, concurrent CNS depressants such as opioids and benzodiazepines, and absent or inadequate pretreatment cardiac screening. A preprint: it has not completed peer review.