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Stay up to date with the latest research papers, clinical trials, blog posts, and site updates.
In a crossover study of 10 healthy volunteers given computer-assisted continuous infusions, subanaesthetic ketamine (50–200 ng/ml steady-state plasma concentrations) produced dose-related psychedelic effects. Subjective ratings (VAS and the Hallucinogen Rating Scale) correlated highly linearly with venous ketamine concentrations (R ≈ 0.93–0.99 for VAS; overall plasma-target correlation R = 0.997) and yielded HRS scores comparable to those seen with DMT.
This double-blind, placebo-controlled study (n=154) of ketamine (35mg/70kg) (or placebo) with (and without) positive self-regard training (automated self-association training) finds that the combination can extend the positive antidepressant (MADRS) effects of ketamine, whilst the effects of ketamine alone was not distinguishable from placebo 30 days later.
Using magnetoencephalography, the authors show that spontaneous neural signal diversity (entropy and Lempel–Ziv complexity) increases reliably under psilocybin, ketamine and LSD—most strongly for single-channel (temporal) LZ—and that these changes correlate with reported intensity of the psychedelic experience. This first application of such measures to the psychedelic state suggests that sustained psychedelic phenomenology corresponds to an elevated level of consciousness as indexed by neural signal diversity.
This commentary (2021) provides an overview of the human behavioural pharmacology of the classic psychedelic; psilocybin, LSD and DMT. Special considerations when conducting human research with psychedelics are discussed as well as the subjective, physiological, and clinical effects of these substances.
A PRISMA-guided systematic review of ergolamines, simple tryptamines and phenylethylamines (33 studies from 3,032 records) finds that classic psychedelics are active at very low doses, non‑addictive and generally only harmful at extremely high doses, with no established lethal dose for LSD or psilocybin. MDMA appears to carry the greatest apparent toxicity—likely confounded by recreational misuse—and the authors emphasise that risk is strongly modulated by set and setting.
This commentary paper (2006) traces the history of LSD as a treatment for alcoholism from 1950-1970.
This review summarises preclinical and clinical evidence that ketamine, psilocybin, LSD and MDMA have therapeutic potential for psychiatric disorders — with robust support for ketamine in depression, emerging evidence for psilocybin and LSD in treating depression and modulating functional brain connectivity, and MDMA showing efficacy in PTSD. It also delineates the pharmacology and behavioural effects of psychedelic versus non‑psychedelic hallucinogens and entactogens.
This review (2008) summarises the published research into hallucinogen-induced stimulus control in phenethylamine- and tryptamine-based hallucinogens, highlighting the receptors involved in their mechanism of action.
This book chapter (2018) describes the history, physiological response to psychedelics, and signaling pathway activated by serotonin (5-HT) 2A receptors.
This seminal review paper (2004) reviews the psychedelics literature up to this point. It specifically looks at how the psychedelics influence the brain (regions). The main conclusion is that psychedelics increase prefrontal cortical metabolism, and correlations have been developed between activity in specific brain areas and psychological elements of the psychedelic experience. The paper foreshadows the research on the practical uses of psychedelics for (mental) illnesses.
This review summarises clinical and preclinical evidence that classic serotonergic psychedelics (LSD, psilocybin, ayahuasca) can produce rapid antidepressant and anxiolytic effects in major depressive disorder. These effects are primarily attributed to 5-HT2A receptor agonism, but current human data are limited and further research is required to confirm long-term safety, efficacy and mechanisms.
This retrospective series of 13 patients and review of 24 case reports found that HPPD commonly causes visual snow, floaters, palinopsia, photophobia and nyctalopia despite normal ophthalmic and neurological investigations, producing a phenotype that overlaps substantially with Visual Snow Syndrome. The authors argue DSM‑5 diagnostic criteria should be expanded to include these symptoms, that VSS patients be screened for prior hallucinogen use, and that controlled studies compare primary and secondary VSS to clarify pathophysiology and treatment.