Psychedelic research timeline
Schizophrenia: the psychedelic research timeline
Schizophrenia is not a psychedelic treatment programme. The historical record uses LSD, psilocybin and DMT to model psychosis; later work questions that analogy and examines risk, exclusion and adverse outcomes.
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 psychedelic psychosis model
1952 to 1997LSD and DMT are used to imitate or probe schizophrenia-like states.1952-01
First clinical study on record
The earliest LSD study indexed in Blossom, running two years and published in 1954. The clinical era starts fourteen years after synthesis.
Compare this with the compound the first version of this canvas covered. 5-MeO-DMT waited eighty-three years between synthesis and its first registered trial. LSD waited fourteen, because in 1952 there was no scheduling regime to wait for and the manufacturer was actively handing the drug out.
The design would not pass review today. These were open observational series without randomisation, blinding or a control group, in an era before informed consent had a settled meaning. That is the caveat attached to every record on this lane until 2008.
1965
DMT is reported in human blood and urine
Analytical work detects DMT in human body fluids, and an enzyme capable of making it is described. The compound becomes a candidate cause of psychosis.
If the body makes its own psychedelic, perhaps psychosis is a manufacturing fault. That hypothesis, usually called the transmethylation hypothesis, drove a substantial share of DMT research through the 1960s and 1970s and was the reason public money was available for it at all.
The evidence has never settled. A critical review covering 1955 to 2010 found that most positive detections came from assays that could not reliably distinguish DMT from related compounds, and that concentrations, where measured properly, were very low. Later work has confirmed the presence of DMT and of the enzyme INMT in mammalian tissue without establishing that either does anything at physiological levels.
It is a live argument sixty years on, and worth flagging because the popular version of it, that DMT floods the brain at death, is not something the papers in this database support. The near-death comparison rests on the resemblance between the two experiences, not on any measured surge.
1976-02
American Journal of Psychiatry
ended earlyThe psychosis model is assessed and found wanting
A review in the American Journal of Psychiatry examines DMT as a model of schizophrenia and concludes the resemblance does not hold.
This paper closes the era that Szára opened. Having spent twenty years treating DMT as a chemical stand-in for schizophrenia, the field concluded that the two states differ in ways that matter: the DMT experience is predominantly visual, brief, and retains insight, while schizophrenia is none of those things.
The model failing is part of why DMT went quiet rather than merely underground. Its main scientific justification had evaporated, its legal status made new work expensive, and no therapeutic hypothesis had yet replaced the psychotomimetic one. There was nothing left to fund.
Testing the model’s limits
1998 onwardsReceptor studies and safety reviews separate acute psychedelic states from a chronic disorder.1998-12
University of Zurich
A receptor mechanism in humans
Zurich work shows psilocybin acting through the serotonin 5-HT2A receptor, giving the field a testable mechanism.
Franz Vollenweider’s group in Zurich shows that psilocybin’s effects in humans depend on the serotonin 5-HT2A receptor, demonstrated by blocking the receptor and watching the effects disappear. This is the point at which psilocybin stops being a curiosity and becomes a pharmacological tool with a named target.
The framing of that early work is telling. It was pitched as a model of psychosis rather than a treatment for depression, because in 1998 a psychosis model was fundable and an antidepressant claim was not. The compound did not change. The question researchers were allowed to ask about it did.
2024-03
Risk for worsened mental health is examined
A study examines psychiatric predictors of worsened mental health after psychedelic use, relevant to populations routinely excluded from trials.
2024-12
JAMA Psychiatry
Adverse events, pooled
A systematic review in JAMA Psychiatry pools adverse events across classic psychedelic trials, alongside a re-examination of psychosis risk.
Individual psychedelic trials are too small to detect rare harms. Pooling them is the only way to see signals that no single study could catch, and a JAMA Psychiatry systematic review does exactly that across the classic psychedelics. A separate 2024 overview re-examined the long-standing claim that psychedelics trigger psychosis, and found the evidence weaker than the received wisdom suggests.
Safety evidence is evidence, and it belongs on the same canvas as the deals. Two things are true at once here: the acute risk profile in supervised trial settings looks better than the compound’s reputation implies, and trial populations are heavily screened, so what happens in a state-licensed service or an authorised prescriber’s clinic is a different question that these reviews cannot answer.
Schizophrenia
Psychedelics as a psychosis model, and the limits of that analogy
Research Landscape
What the registered trials connected to Schizophrenia look like when you line them up. Counts come from Blossom’s trial records as of August 2026.
What's live right now, and what stopped?
SourcedRegistry status of all 9 Schizophrenia trials Blossom tracks. Orange marks trials recruiting or opening.
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.
Publication Landscape
How the 205 papers Blossom links to Schizophrenia 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 Schizophrenia research grown?
SourcedTracked papers by publication year; 39 earlier papers published before 2012. Click a year for the running total.
Don't read as total output: only the 205 of 205 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 Schizophrenia?
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 Schizophrenia 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.