
Compare
Iboga Compared
Ibogaine set beside the treatments people actually weigh it against, and the evidence each one has. The asymmetry is the finding.
In this section
9 pages
- Iboga vs Ibogaine: The Difference
- Ibogaine vs Ayahuasca
- Ibogaine vs Bufo
- Is Ibogaine Like DMT?
- Ibogaine vs Kambo
- Ibogaine vs Ketamine
- Ibogaine vs Methadone
- Ibogaine vs Psilocybin
- Ibogaine vs Rapid Detox
No page in this section matches both filters.
Scientific review by Kathryn A. Cunningham, PhD ·
Ibogaine has never been compared with any of its alternatives in a human study. What can be compared is the evidence each one carries, and there the gap is wide: methadone and buprenorphine have mortality data on hundreds of thousands of people, while ibogaine has case series and two randomised trials that finished in 2024 and never reported.
People arrive at this comparison for one of two reasons. Either nothing else has worked, or what is working is something they want to stop. Both are reasonable positions, and both deserve the real numbers rather than a verdict.
The first thing to say is the thing least often said.
No study has compared ibogaine with methadone, buprenorphine, ketamine or psilocybin in humans. Not a trial, not a cohort, and no registered study that sets one against the other. We checked the literature and the trial registry four different ways.
The only head-to-head in existence anywhere is a 2026 study comparing psilocybin and ibogaine in rats, and even its title qualifies the result.
Every row below therefore sets one body of research beside another. Different populations, different endpoints, different follow-up. That is a weaker kind of comparison than a trial, and it is the only kind available.
The table
| Ibogaine | Methadone | Buprenorphine | Ketamine | Psilocybin | |
|---|---|---|---|---|---|
| Approved for addiction | Nowhere | Yes, detox and maintenance | Yes, opioid dependence | No | Nowhere |
| Best study design available | Uncontrolled case series, largest prospective follow-up 30 people | Trials plus cohorts of 122,885 to 749,634 | 32 trials, 5,808 people, plus cohorts | Phase 2 trials | Phase 3 trials, none published |
| Effect on death rate | Never measured | All-cause less than half during treatment | Same, slightly larger | Not measured for addiction | Not measured |
| Randomised trials reporting drug use | None | Standard of care | Standard of care | 15 trials, 798 people | None for opioids |
| Signature serious harm | QT prolongation, torsade, cardiac arrest | Respiratory depression, QT prolongation | Precipitated withdrawal, diversion | Dissociation, bladder damage, dependence | Prolonged psychological difficulty |
The number that matters most
If you take one figure from this page, it is not about ibogaine.
Pooling 36 cohort studies covering 749,634 people, a 2021 analysis found that all-cause mortality during opioid agonist treatment was around half what it was out of treatment, at a rate ratio of 0.47 with a confidence interval from 0.42 to 0.53. The same held for suicide, drug-related death, alcohol-related death, cardiovascular death and cancer.
Then it measured what happens when people stop.
| Period | All-cause mortality, relative to time in treatment |
|---|---|
| First four weeks after stopping | 6.01 times higher |
| The rest of the time off treatment | 1.81 times higher |
Six times, in the first month. That is the window any detoxification opens, whatever the method used to open it, and it is why leaving an agonist to try something unproven is a different kind of decision from adding something to an existing regimen.
The effect is not a historical artefact of a gentler drug supply. A cohort of 55,347 people in British Columbia found that as fentanyl saturated the supply, the relative risk of dying while off treatment rose from 2.1 to 3.4 times. The cost of a gap in treatment is higher now than when the older studies were assembled.
These are observational cohorts, not randomised trials, and the authors say so. People who stay in treatment differ from people who leave, in ways no statistical adjustment fully removes.
The randomised evidence on mortality specifically is thin: a Cochrane review found four trials and a result too imprecise to conclude anything, with a confidence interval running from a large benefit to a large harm.
What makes the case strong is not any single study. It is that every large estimate points the same way, across countries and decades, with a dose-response in how long people stay.
Detoxification, as a category, has been measured
This is the finding most directly relevant to what an ibogaine clinic sells, and it does not concern ibogaine at all.
A study of 40,885 people compared six real-world treatment pathways. Only buprenorphine and methadone reduced overdose, cutting it to roughly a quarter of baseline risk at three months and 41 per cent at twelve.
Inpatient detoxification and residential treatment showed no such reduction.
Ibogaine is not those things and the study did not test it. But the structure of what is being sold, an intensive supervised episode ending in abstinence, is the structure that did not reduce overdose in this data. That is worth knowing before paying for one.
Note also who funded it: six of the eight authors declare employment or funding from the insurer whose claims data this is, and a seventh is affiliated to it. It is disclosed in the paper.
Where the comparison is fairer than people expect
Two honesty points cut the other way.
Methadone is also cardiotoxic. Its US label carries a boxed warning naming QT prolongation and torsade de pointes, the same mechanism that kills people on ibogaine, and noting that cases have occurred at ordinary maintenance doses. The difference is not that one drug affects the heart and the other does not. It is that methadone’s risk is characterised, dose-known, monitored under a regulatory framework, and outweighed by a measured mortality benefit across three quarters of a million people. Ibogaine’s is characterised too, and there is nothing on the other side of the scale yet.
Starting methadone carries its own spike. Mortality in the first four weeks of methadone runs about twice that of the rest of treatment. Buprenorphine does not show that pattern. Neither fact is usually mentioned by people advocating for agonist treatment, and both belong here.
Methadone retains people better than buprenorphine. Across 32 randomised trials covering 5,808 people and 69 observational studies, retention at six months favoured methadone consistently. On most other outcomes the two differ little, and the authors’ own recommendation is that the choice follow the patient’s preference.
The other two comparisons
Ketamine and psilocybin come up constantly, and the honest position on both is narrower than their reputations.
Neither is approved for any substance use disorder, anywhere. Esketamine’s approval covers treatment-resistant depression and depression with acute suicidality, and every intravenous ketamine clinic treating addiction is operating off-label. Psilocybin has no marketing approval in any jurisdiction, and no phase 3 trial has published a result for any indication.
The single meta-analysis of ketamine for substance use disorder found the benefit at under a month and not at one to six months. Ibogaine and ketamine sets out that record. Ibogaine and psilocybin does the same for the other.
What to do with all this
The comparison does not resolve into a recommendation, and this site does not make treatment recommendations. Three things follow from the evidence.
The treatments with the strongest mortality evidence are the ones people are often trying to leave. That tension is real and it is not resolved by pretending the evidence is weaker than it is.
The gap in the ibogaine column is a gap in knowledge, not a proof of failure. Nobody can give you the odds, and what the trials found explains why.
And the highest-risk moment in this whole picture is not the dosing session. It is the weeks afterwards, when tolerance has fallen. When it does not work covers what happened to the people who were followed.
Common questions
Sources
5 sources · How we source
- Association of Opioid Agonist Treatment With All-Cause Mortality and Specific Causes of Death Among People With Opioid Dependence
Primary source · JAMA Psychiatry, 2021 · accessed 25 Aug 2026
- Mortality risk during and after opioid substitution treatment: systematic review and meta-analysis of cohort studies
Primary source · BMJ, 2017 · accessed 25 Aug 2026
- Comparative Effectiveness of Different Treatment Pathways for Opioid Use Disorder
Primary source · JAMA Network Open, 2020 · accessed 25 Aug 2026
- Opioid agonist treatment and risk of mortality during opioid overdose public health emergency: population based retrospective cohort study
Primary source · BMJ, 2020 · accessed 25 Aug 2026
- Buprenorphine versus methadone for the treatment of opioid dependence: a systematic review and meta-analysis of randomised and observational studies
Primary source · Lancet Psychiatry, 2023 · accessed 25 Aug 2026