Psychedelic research timeline
Substance Use Disorders (SUD): the psychedelic research timeline
Substance-use research spans almost the full modern history of psychedelics. The record is broad but fragmented: different compounds target alcohol, opioids and nicotine through very different treatment models.
Milestones are editorially selected from Blossom’s research catalogue. Future markers are limited to important trials with dated public guidance and are shown as planned, not promised.
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The first treatment era
1962 to 1992LSD alcoholism studies and the ibogaine observation create two very different traditions.1962
Lotsof observes opioid withdrawal interrupted
Howard Lotsof, then a heroin user in his teens, takes ibogaine recreationally and finds his withdrawal symptoms gone.
The founding observation of the entire anti-addiction case for ibogaine came from someone taking it for fun and noticing that something else had happened. He was not withdrawing, and he did not want the drug. Lotsof spent the next four decades trying to turn that into a medicine.
It is an unusually honest origin story, and it sets the pattern for what follows. The signal here has always been strong enough to keep people interested and never been produced under conditions that would satisfy a regulator. Fifty-one years pass between this moment and the first ibogaine trial in our database.
What would it take to test a claim like this properly? A randomised comparison against the current standard of care in opioid use disorder, powered for relapse rather than for withdrawal scores. That study has still not been run.
1966-01
Controlled LSD studies for alcoholism
Randomised studies test high-dose LSD as an adjunct to alcoholism treatment, creating the first substantial psychedelic indication literature.
Formalising the evidence
1993 to 2019Re-analyses, safety work and small pilots move anecdote towards clinical research.1993-07
Neuropharmacology
Cocaine self-administration falls in rats
Preclinical work shows ibogaine reducing cocaine self-administration, the result that put public money behind the compound.
Preclinical means animal and cell work, before any human trial. Rats given ibogaine pressed the lever for cocaine less often, and the effect outlasted the drug in the bloodstream. That combination is what made the field take the anti-addiction claim seriously, because it suggested something was being changed rather than merely blocked.
This is still one of the most cited papers in our ibogaine set. It also anchors a pattern worth naming early: the strongest evidence for ibogaine is preclinical and observational, and the strongest evidence against it is clinical.
1998-01
Ketamine psychotherapy for heroin dependence
A double-blind dose-comparison trial in Leningrad, running in parallel with the first depression work.
Two-year follow-up data from a randomised trial in a treatment population Western research would not reach for another two decades. It ran at the same time as Berman’s Yale study, with no contact between the two.
Addiction and depression separated into different research lineages here and stayed separate. The addiction line goes quiet for years and only resurfaces in the 2020s with the UK alcohol programme further along this canvas.
2007-08
The medical subculture is documented
A paper counts the people being treated with ibogaine outside conventional medicine, and finds the great majority of them there.
Alper, Lotsof and Kaplan did something the field badly needed: they counted. Their survey of the ibogaine treatment scene established that a substantial and growing population was receiving ibogaine, overwhelmingly in private clinics, guesthouses and lay settings rather than in hospitals or trials.
Blossom currently lists more than thirty ibogaine providers as organisations, in Mexico, Costa Rica, South Africa, Portugal, Bali and elsewhere. Nine registered trials sit against that. If you want one number that explains ibogaine, it is that ratio.
This is not a story of brave outsiders versus timid regulators, and it is not a story of reckless cowboys either. It is what happens when demand for a treatment is real, the evidence to authorise it does not exist, and nobody with the money to generate that evidence has a reason to.
2008-09
A psilocybin smoking-cessation pilot opens
Johns Hopkins begins a pilot combining psilocybin sessions with structured smoking-cessation treatment.
2012-01
J Psychopharmacology
The 1960s alcoholism data, re-analysed
A meta-analysis pools six randomised trials from 1966 to 1970 and finds a significant effect of a single dose on alcohol misuse.
A useful demonstration that some of the first-era work was better than its reputation. Six randomised controlled trials existed, had never been pooled, and when they were, the effect on alcohol misuse was statistically significant at short follow-up.
Two cautions come with it. The effect faded over twelve months, and re-analysing forty-year-old trials cannot fix problems in how they were run. What the paper really established was that the question had been abandoned rather than answered, which is a different and more damning claim.
2014-11
Radboud University
Radboud opioid pilot runs for six years
An open-label, single-fixed-dose pilot in opioid-dependent patients takes six and a half years to complete.
Open-label means everyone knows who is getting the drug, so expectation cannot be separated from effect. Single fixed dose means no titration. It is a modest design, and it still took six and a half years to finish.
That duration is the point. Recruiting opioid-dependent participants into an inpatient study of a cardiotoxic Schedule I compound, in an academic centre with no commercial sponsor, is close to the hardest thing to do in this field. Meanwhile the clinics on the lane above were treating people continuously throughout.
The pharmacokinetic and pharmacodynamic results reached print in 2024, a decade after the trial opened.
2015-01
Frontiers in Pharmacology
ended earlyThe heart problem is named
A review sets out ibogaine’s effect on cardiac conduction, and the field acquires a mechanism for the deaths it already knew about.
Ibogaine blocks a potassium channel in heart muscle called hERG. That lengthens the QT interval, the window during which the heart’s electrical system resets, and a long enough QT interval can tip into torsades de pointes, an arrhythmia that kills. This is not a rare idiosyncratic reaction. It is a dose-dependent pharmacological property of the compound.
Ibogaine is also usually given to people with several of the things that make QT prolongation more dangerous: opioid dependence, methadone (itself QT-prolonging), electrolyte disturbance from vomiting, dehydration, poor cardiac health, and sometimes slow CYP2D6 metabolism. The risks stack.
Two companion papers in 2016 asked the practical questions that follow: how toxic is ibogaine, and what dose is safe? Neither could give a clean answer, and the honest reading is that the therapeutic window is narrow enough that dosing without cardiac monitoring, electrolyte correction and resuscitation capability is indefensible. Some clinics do all of that. Not all of them do.
2017-11
The Global Ayahuasca Survey opens
A large international online survey begins collecting data from ayahuasca drinkers, eventually running to tens of thousands of responses across dozens of countries.
This is how the ayahuasca literature grew to 250 papers without 250 trials. A self-selecting online cohort cannot demonstrate that ayahuasca causes anything, but it can do things no trial can afford: describe who drinks and why, map settings from indigenous ceremony to European neo-shamanic circle, and count events too rare for a trial of thirty people to see.
Successive analyses from it have reported associations with lower problematic alcohol use, differences in outcome by context and setting, and long-term wellbeing measures in people who continue drinking. Read every one of those as a description of a population, not as an effect of a drug. People who feel a practice is helping them are the ones who keep doing it and the ones who answer surveys about it.
The survey has been most valuable where trials are weakest, which is on harms. That is the next marker.
Modern indication trials
2020 onwardsAlcohol, opioid and nicotine programmes begin using contemporary trial designs.2020-10
University of Exeter
The first registered DMT trial
UNITy tests whether DMT changes drinking behaviour in alcohol use disorder, and studies the neuroplasticity that might explain it. Eighty-nine years after the synthesis.
The clinical record for DMT starts here, in October 2020, and it starts with a hard indication rather than an easy one. Alcohol use disorder is a condition where the standard of care is weak, relapse is the norm and the placebo response is large, which makes it a demanding place to look for a signal.
The design pairs the behavioural question with a mechanistic one, asking not only whether drinking falls but whether markers of neuroplasticity move with it. That is the hypothesis underneath most of the modern psychedelic field: that a brief pharmacological event opens a window in which learning is easier, and that the therapy rather than the drug does the work inside it.
It is also the longest-running study on this canvas, listed to complete at the end of 2027. Seven years for a single academic trial is a fair measure of how difficult this work remains even after the compound has become fashionable.
2021-10
Federal University of São Paulo (UNIFESP)
The randomised placebo-controlled trial
A Brazilian Phase II in alcohol use disorder is the only randomised, double-blind, placebo-controlled ibogaine trial in the database.
One trial. Out of nine, across sixty-four years, this is the single study in Blossom’s ibogaine record that randomises participants, blinds them and includes a placebo arm, and it is in alcohol use disorder rather than in the opioid indication the compound is famous for.
It also uses an escalating-dose design, which is a serious attempt to find the point where benefit and cardiac risk trade off rather than assuming a single dose is right for everyone. Run by a public university in São Paulo, completing at the end of 2024.
Set this against the 5-MeO-DMT canvas, where a randomised readout arrived seven years after the first trial and a $2.8bn acquisition followed. Ibogaine has had six decades and one randomised trial. The question that raises is not whether ibogaine works. It is why nobody with money has been willing to find out.
2022-10
JAMA Psychiatry
Alcohol use disorder result in JAMA Psychiatry
A randomised trial reports a large reduction in heavy drinking days, opening a second serious indication.
Michael Bogenschutz and colleagues at NYU report that psilocybin-assisted psychotherapy substantially reduced the percentage of heavy drinking days compared with an active placebo. It is the strongest randomised evidence for psilocybin outside depression.
Alcohol use disorder matters here for a reason beyond the numbers. It is enormous, poorly served by existing medication, and it gives the field a second commercial story to tell if depression proves crowded. Several programmes on this canvas, including Clairvoyant’s 154-patient Phase 2b and a planned Ceruvia Phase 2b, exist because of this result.
A phase 2 relapse-prevention trial published in 2025 was more equivocal. One strong randomised result is a starting point, not a conclusion.
2023-02
Nature
Analogues disrupt opioid use without the cardiac signal
A new class of iboga alkaloids reproduces the anti-addiction effect in animals while dropping the hERG activity that makes ibogaine dangerous.
This is the most important scientific development on the canvas, and it is easy to under-read. Chemists rebuilt the molecule to keep the kappa-opioid and neuroplasticity effects while removing the potassium-channel block responsible for the QT prolongation. In animals, the anti-addiction behaviour survives the surgery.
If it holds in humans, ibogaine’s central dilemma dissolves: you would have the effect without the arrhythmia risk, and a patentable molecule that a company can afford to develop properly. Follow-on work through 2026 extends the same approach to alcohol drinking.
The caution is the usual one, and it is not small. Animal models of addiction predict human results badly, and a compound that is safer on paper still has to prove it works. Note also what this does to the ibogaine question itself: if the analogues succeed, the parent compound may never get the trial it has been waiting sixty years for.
2023-05
AtaiBeckley
Alcohol use disorder
A single-dose open-label study widens the indication surface beyond depression.
Evidence that the sponsor treated BPL-003 as a platform rather than a single-indication asset, which is relevant to how the acquisition was valued.
Alcohol use disorder is a large market with few effective pharmacological options, so an early signal there raises the ceiling on a compound whose lead indication is crowded. The study is small and open-label, so it establishes feasibility rather than efficacy.
2025-12
Addiction
Alcohol use disorder results published
The open-label Phase 2 proof-of-concept in alcohol use disorder reports in Addiction.
The 2023 alcohol study reads out in print two years after it closed. Proof-of-concept and open-label, so it establishes feasibility rather than efficacy, but it moves the second indication from claim to published record.
Publication lag is worth noticing across this canvas. Trials finish long before anyone outside the sponsor can read the numbers, which means a valuation can move on data the field has not yet seen.
2026-03
JAMA Network Open
Smoking cessation, retested against the patch
The 2014 result that reported 80% abstinence is finally tested against nicotine replacement in a randomised pilot.
Johns Hopkins’ 2014 open-label pilot in tobacco addiction reported abstinence rates far above anything nicotine replacement achieves, and that single number has been quoted in almost every popular account of psychedelic medicine since. A randomised pilot comparing psilocybin against a nicotine patch publishes in JAMA Network Open in March 2026.
This is what replication looks like, and it took twelve years. Pilot randomised trials are designed to establish feasibility rather than to settle efficacy, so the honest reading is that the comparison has finally started, not that it has finished.
The pattern generalises across this canvas. The striking early numbers came from small, unblinded, single-site studies. Every time one has been tested against an active comparator, the gap has narrowed.
Substance Use Disorders (SUD)
From LSD for alcoholism and ibogaine detoxification to modern controlled trials
Research Landscape
What the registered trials connected to Substance Use Disorders (SUD) look like when you line them up. Counts come from Blossom’s trial records as of August 2026.
How fast is Substance Use Disorders (SUD) research growing?
SourcedRegistered trials by recorded study-start year; 18 earlier trials began before 2013. Click a year for the running total.
Don't read as total research effort: only registered trials with a recorded start date are counted (109 of 109 tracked). Recent years under-count because of registration lag; striped bars are still filling in or are planned starts.
What's live right now, and what stopped?
SourcedRegistry status of all 109 Substance Use Disorders (SUD) trials Blossom tracks. Orange marks trials recruiting or opening.
- Recruiting or opening
- 3835%
- Underway, not recruiting
- 87%
- Completed
- 5046%
- Stopped early
- 98%
- Unknown / other
- 44%
Don't read stopped trials as failures: trials end early for funding, recruitment, and strategy reasons too. Status is as last synced from the registry; some 'recruiting' trials may already have finished.
Which compounds carry the Substance Use Disorders (SUD) research?
SourcedTrials per compound. Orange marks the most-studied compound.
Don't read shares as adding to 100%: a trial testing several compounds counts once per compound, and placebo comparator arms are not shown. Trial volume signals research attention, not evidence quality.
How does Substance Use Disorders (SUD) research split by subtopic?
SourcedTrials per subtopic within the 109 Substance Use Disorders (SUD) trials on this page. Orange marks the largest subtopic.
Don't read shares as adding to 100%: a trial can name several subtopics (MDD and TRD often travel together), and 'no subtopic specified' means the trial is tagged only with this broader category. Each subtopic's own page can show a different total because it also tracks trials outside this set.
Publication Landscape
How the 572 papers Blossom links to Substance Use Disorders (SUD) line up by year, compound and journal. This is the psychedelic-relevant literature in Blossom's records as of August 2026, not the condition's full medical literature.
How has Substance Use Disorders (SUD) research grown?
SourcedTracked papers by publication year; 37 earlier papers published before 2012. Click a year for the running total.
Don't read as total output: only the 572 of 572 tracked papers with a recorded publication date are counted, and these are the psychedelic-relevant papers Blossom tracks, not a complete bibliography. The current year is still filling in.
Which compounds shape Substance Use Disorders (SUD)?
SourcedTracked papers per compound. Orange marks the largest literature.
A paper studying several compounds counts once per compound, and placebo comparator arms are not shown. These are the psychedelic-relevant papers Blossom tracks.
Where is Substance Use Disorders (SUD) research published?
SourcedTracked papers per journal. Orange marks the most-used journal.
Counts the journal recorded on each tracked paper; papers without a journal on file are omitted. Blossom tracks psychedelic-relevant papers rather than each journal's full catalogue.