Psychedelics and Consciousness-Altering Agents: A Comprehensive Overview

A high-level examination of psilocybin, LSD, mescaline, DMT, 5-MeO-DMT, MDMA, ketamine, ibogaine, and related agents — their receptors, likely mechanisms, therapeutic promise, and problems

What These Drugs Are, and What Unites (and Divides) Them

"Psychedelics" is a loose popular category covering a pharmacologically heterogeneous set of drugs whose only universal common feature is that they profoundly alter consciousness — perception, cognition, emotion, the sense of self and time. They do not share a mechanism. A rigorous account must therefore begin by sorting them, because lumping a 5-HT2A agonist (LSD), a serotonin releaser (MDMA), an NMDA antagonist (ketamine), and a kappa-opioid agonist (salvia) under one heading obscures more than it reveals.

What does increasingly unite most of them, and what justifies treating them as a family for psychiatric purposes, is a deeper shared property emerging from the science: rapid, dramatic induction of neural plasticity, with single or few administrations producing therapeutic effects that long outlast the drug's presence in the body. This is the opposite of the chronic-dosing, slow-accumulation model of the SSRIs (see the serotonergic document), and it connects this whole class to the plasticity reframing of psychiatric drug action that runs through this series — the idea that these agents work not by directly fixing a mood or symptom but by reopening windows of plasticity in which entrenched patterns can be reshaped by experience, which is why the psychological context ("set and setting") and the accompanying psychotherapy are treated as integral rather than incidental.

This overview covers, with proper mechanistic distinctions:

• Classic (serotonergic) psychedelics — 5-HT2A agonists: psilocybin, LSD, mescaline (peyote/San Pedro), DMT and ayahuasca, 5-MeO-DMT, and the synthetic 2C series.
• Entactogens/empathogens — MDMA, a monoamine releaser, mechanistically distinct from the classics.
• Dissociatives — NMDA antagonists: ketamine (covered pharmacologically in the glutamatergic/rapid-acting document and included here as the established clinical member of this family), with PCP and dextromethorphan as relatives.
• Atypicals — ibogaine (a complex polypharmacological anti-addiction agent) and salvinorin A (a kappa-opioid agonist), each sui generis.

The honest framing: this is the most scientifically exciting and most overhyped area in all of psychiatry — a field of genuine therapeutic promise and genuine paradigm-shifting neuroscience, freighted with serious psychological and physical risks, profound methodological problems (blinding above all), commercial and ideological fervor running well ahead of evidence, real boundary and conduct hazards in the therapy-assisted model, unresolved legal status, and a 2024 regulatory rejection (MDMA) that served as a reality check for the entire enterprise.

The Serotonergic Mechanism and the Plasticity Story

For the classic psychedelics, the proximate mechanism is well established: agonism at the 5-HT2A serotonin receptor. The evidence is decisive — 5-HT2A antagonists (like ketanserin) block the subjective and most of the neural effects of psilocybin and LSD, establishing this receptor as the necessary gateway. 5-HT2A receptors are densely expressed on cortical pyramidal neurons, particularly in higher-association cortex, and their agonism produces a cascade of downstream effects:

Acute neural effects. 5-HT2A agonism increases cortical excitability and glutamate release, disrupting normal patterns of cortical activity and connectivity. Functional imaging (Carhart-Harris and colleagues) shows psychedelics desynchronizing and disintegrating the default mode network — the self-referential, introspective network whose overactivity and rigidity are associated with depression and rumination — while increasing global connectivity between normally segregated networks. This is the neural basis of the entropic brain / REBUS hypothesis (Relaxed Beliefs Under Psychedelics): psychedelics increase the entropy (flexibility, disorder) of brain activity and relax the brain's high-level priors — the rigid, overweighted predictions and self-models that, in depression and addiction, trap a person in fixed negative patterns. Loosening these priors allows the system to be revised by new input, which dovetails with the therapeutic model (the drug loosens the rigid framework; the therapy supplies the revision).

Plasticity effects. Like ketamine, psychedelics promote rapid structural plasticity — increased dendritic spine density and synaptogenesis in prefrontal cortex (David Olson's "psychoplastogen" concept), via glutamate, BDNF, and mTOR signaling — reaching the same plasticity endpoint as both ketamine and (slowly) the SSRIs, through the 5-HT2A door. And Gül Dölen's work suggests psychedelics reopen developmental critical periods for learning, returning the adult brain to a juvenile-like state of heightened, experience-dependent plasticity. This is the strongest unifying theory: psychedelics, ketamine, and antidepressants converge on plasticity induction, differing in speed, route, and the intensity of the accompanying subjective experience.

The subjective-experience question. A genuinely unresolved and important debate: is the dramatic subjective experience (the "trip," the mystical or peak experience) necessary for the therapeutic effect, or merely a side effect of the plasticity-inducing mechanism? Some trial data find that the intensity and quality of the subjective/mystical experience predicts and mediates clinical outcome (suggesting the experience matters), while a parallel line of drug development pursues non-hallucinogenic psychoplastogens — engineered 5-HT2A-pathway drugs that induce the plasticity without the trip, on the bet that the experience is dispensable. The answer is not known, and it is the field's deepest mechanistic and practical question: if the experience is necessary, psychedelic therapy will always require the elaborate, expensive, therapy-embedded model; if not, the plasticity could be delivered as an ordinary pill. This exactly parallels the dissociation-and-response question for ketamine (glutamatergic document).

The Classic Serotonergic Psychedelics

Psilocybin

The prodrug found in "magic mushrooms," rapidly converted to psilocin (the active 5-HT2A agonist). Psilocybin has become the lead agent of the psychiatric renaissance for practical reasons — moderate duration (4–6 hours), favorable safety, and a strong research base. It carries FDA Breakthrough Therapy designation for depression, and trials report substantial, rapid, and durable improvements in treatment-resistant and major depression (including a head-to-head trial against escitalopram that found psilocybin at least comparable on several measures), end-of-life and cancer-related existential distress (among the most striking findings — single high-dose sessions producing sustained reductions in death anxiety and demoralization, connecting to this series' existential and meaning-centered documents), and addictions (promising early data in alcohol and tobacco use disorders). It is not yet an approved medicine, though regulated, non-medical access has begun in some jurisdictions (Oregon and Colorado established supervised psilocybin-services frameworks). Among the classic psychedelics, psilocybin is the one closest to clinical approval.

LSD (lysergic acid diethylamide)

Hofmann's 1938 synthesis and 1943 accidental discovery launched the original wave of psychedelic research (extensive 1950s–60s investigation in alcoholism, anxiety, and end-of-life distress) before prohibition (Schedule I, 1970) shut the field down for decades. Pharmacologically a 5-HT2A agonist (with broad additional receptor activity and an unusually long duration, 8–12 hours, owing to its prolonged receptor binding — recently visualized crystallographically as the receptor "closing a lid" over the bound drug). Renewed trials investigate LSD in anxiety and cluster headache; its long duration makes it less practical than psilocybin for therapy, but its history and potency keep it central to the field.

Mescaline (peyote and San Pedro)

The oldest psychedelic in documented human use — the active compound of the peyote cactus, sacramental for millennia in Indigenous American traditions and central to the Native American Church (which holds a specific religious exemption for peyote in the U.S.). A phenethylamine 5-HT2A agonist with a very long duration (10–12 hours). Two issues are distinctive: conservation (peyote is slow-growing and threatened by overharvesting, raising serious sustainability and Indigenous-rights concerns, with the San Pedro cactus and synthetic mescaline as alternatives that avoid pressuring the sacred plant) and cultural appropriation (the tension between Indigenous sacramental use and the wellness/research appropriation of these traditions). Mescaline has attracted less modern clinical research than psilocybin or LSD, partly for these reasons and partly for its long duration.

DMT and ayahuasca

DMT (N,N-dimethyltryptamine) is a 5-HT2A agonist remarkable for its brevity and intensity when smoked/injected — a 10–20 minute, overwhelmingly immersive experience (the "breakthrough"). Orally, DMT is inactive (degraded by monoamine oxidase) unless combined with an MAO inhibitor — which is precisely the pharmacological genius of ayahuasca, the Amazonian sacramental brew combining a DMT-containing plant with a β-carboline MAOI-containing plant (harmine/harmaline), rendering the DMT orally active for a prolonged (4–6 hour) experience. Ayahuasca has deep Indigenous and syncretic religious traditions and growing research interest (depression, addiction); its MAOI content creates real interaction dangers (serotonin syndrome with SSRIs and other serotonergic drugs; tyramine and other MAOI interactions), a genuine safety concern in the ceremonial-tourism context. Continuous intravenous DMT and a long-acting DMT program are in clinical development as a controllable, short-session psychedelic.

5-MeO-DMT

A distinct tryptamine (found in the secretions of the Bufo alvarius toad and synthesized) notable for being 5-HT1A-weighted relative to other classics (strong 5-HT1A plus 5-HT2A activity), producing an extremely intense, short (15–30 minute) experience often described as complete ego dissolution or a "white-out" rather than the visionary, content-rich experience of psilocybin or DMT. It is under investigation for depression and addiction with early signals of rapid effect, and its brevity is attractive for therapy. Distinctive concerns: the toad-secretion source raises serious conservation and animal-welfare issues (synthetic 5-MeO-DMT is the responsible alternative), the intensity carries real psychological risk, and the abrupt, total nature of the experience demands skilled support.

The 2C series and other synthetics

A large family of synthetic phenethylamine psychedelics (2C-B, 2C-E, and many others, largely from Alexander Shulgin's work) act as 5-HT2A agonists with varying profiles; they figure in recreational use and harm-reduction discussions more than in clinical research, and the broader proliferation of "novel psychoactive substances" (research chemicals) raises distinct safety concerns owing to unknown pharmacology and dosing.

MDMA: The Entactogen

MDMA (3,4-methylenedioxymethamphetamine) is mechanistically not a classic psychedelic and should not be conflated with them. It is an entactogen (or empathogen) — its primary action is to cause massive release of serotonin (and dopamine and norepinephrine) by reversing the monoamine transporters (an amphetamine-class mechanism), with downstream effects including oxytocin release. The subjective result is distinctive: not primarily perceptual/visionary but emotional and interpersonal — euphoria, emotional openness, reduced fear and defensiveness, increased empathy, trust, and capacity to approach painful material without being overwhelmed.

This profile is precisely why MDMA was developed for PTSD: it appears to allow trauma survivors to engage and reprocess traumatic memories within a window of reduced fear and increased trust and self-compassion — a pharmacologically-opened state for trauma-focused psychotherapy (the drug enabling the therapy, the clearest instance of the "drug + therapy as one intervention" model). The MAPS/Lykos Phase 3 trials (MAPP1, MAPP2) reported large effects on severe PTSD, generating enormous expectation.

Then came the field's defining reality check: in 2024 the FDA rejected MDMA-assisted therapy for PTSD (a complete response letter), requesting an additional trial amid concerns about functional unblinding (subjects and therapists could obviously tell who received MDMA, inflating apparent effects), trial-design and data-integrity questions, and serious therapist-conduct/boundary issues documented in the trial program (including a notorious case of misconduct toward a vulnerable participant). The rejection was a watershed — a demonstration that enthusiasm, breakthrough designation, and striking effect sizes do not substitute for methodologically sound, conduct-clean evidence, and a sobering lesson for the whole psychedelic-therapy enterprise about the unusual difficulty of rigorously evaluating drugs whose unmistakable subjective effects defeat blinding and whose therapy-embedded delivery creates profound participant vulnerability.

MDMA's specific physical risks also distinguish it: hyperthermia (the cause of most recreational MDMA deaths, especially in hot, crowded settings with exertion), hyponatremia (from excess water intake combined with SIADH-like effects — also fatal), serotonergic toxicity, cardiovascular strain, and a contested but real concern about serotonergic neurotoxicity with heavy repeated use (the clinical-dose, occasional-use therapeutic context is far lower risk than heavy recreational use, but the question is not fully settled).

Ketamine: The Dissociative

Ketamine — an NMDA-receptor antagonist (dissociative anesthetic), covered pharmacologically in the glutamatergic/rapid-acting document — belongs in this overview as the established clinical member of the consciousness-altering family and the bridge between the psychedelic frontier and conventional psychiatry. Unlike the classic psychedelics, MDMA, and ibogaine, ketamine (as esketamine) is FDA-approved (for treatment-resistant depression and depression with acute suicidality) and racemic ketamine is in wide off-label use — making it the one drug in this document that is actually, legally, a medicine. Its dissociative experience (depersonalization, perceptual changes, ego dissolution at higher doses) overlaps phenomenologically with the psychedelics despite the different mechanism, and the open question of whether its dissociation is necessary for its antidepressant effect parallels the subjective-experience debate for the classics. Ketamine's profile — rapid, robust, NMDA-mediated, with real abuse and bladder-toxicity liabilities and transient effects requiring repeated dosing — is detailed in the companion document; here it serves as the proof of concept that a consciousness-altering, plasticity-inducing agent can become a delivered psychiatric treatment, and as the most clinically mature point on the spectrum this document covers. Its relatives PCP and dextromethorphan complete the dissociative class (DXM appears in the oral NMDA antidepressant Auvelity; PCP is essentially a drug of abuse with no therapeutic role).

The Atypicals: Ibogaine and Salvinorin A

Ibogaine

Ibogaine (from the West African Tabernanthe iboga, sacramental in the Bwiti tradition) is pharmacologically unlike anything else here — a complex polypharmacological agent acting at NMDA receptors, kappa- and mu-opioid receptors, sigma receptors, nicotinic receptors, and the serotonin transporter, among others. Its remarkable and genuinely intriguing property is an apparent ability to interrupt opioid (and other) addiction — dramatically reducing withdrawal symptoms and craving after a single treatment, with anecdotal and small-study reports of patients emerging from a long ibogaine experience (which includes a lengthy oneiric/dreamlike phase) with their physical dependence and craving substantially reset. This anti-addiction signal has driven a persistent underground and offshore treatment scene and growing research interest.

Ibogaine thus embodies the field's tension in extreme form: a genuinely promising anti-addiction mechanism unlike any approved treatment, and a genuinely lethal cardiac liability, dispensed largely in an unregulated, offshore, harm-prone setting. Current research aims at cardiac-safer analogs and rigorously monitored protocols; the honest status is "remarkable promise, real and demonstrated lethality, not ready for unmonitored use."

Salvinorin A (Salvia divinorum)

Salvinorin A, the active compound of Salvia divinorum, is mechanistically distinct again — a potent, selective kappa-opioid receptor agonist (not serotonergic, not glutamatergic), producing an intense, brief (minutes), often dysphoric and profoundly dissociative/disorienting experience quite unlike the classic psychedelics. It has attracted little therapeutic traction (the kappa system is of interest in depression and addiction, but kappa agonism tends to be dysphoric, and salvinorin's experience is generally not therapeutically desirable), and it is included mainly for completeness and because its wholly different mechanism underscores the point that "psychedelic" is a phenomenological umbrella, not a pharmacological class.

What They Actually Do: The Evidence and Its Hard Problems

The promising signals are real: psilocybin for depression and end-of-life distress, MDMA for PTSD, and emerging data for psychedelics in addiction represent genuinely striking effect sizes — often larger, faster, and more durable than conventional treatments — in serious, treatment-resistant conditions. The neuroscience (plasticity, network desynchronization, critical-period reopening) is genuinely paradigm-shifting. This is not nothing, and the dismissive view underrates it.

But the methodological problems are severe and specific:

• The blinding crisis. Psychedelics produce unmistakable effects; participants and raters almost always know who got the drug. This functional unblinding inflates apparent effects through expectancy — and expectancy is especially potent in a field with intense belief, self-selected enthusiastic participants, and elaborate therapeutic ritual. This is not a minor caveat; it is a fundamental threat to the validity of the entire trial literature, and it was central to the MDMA rejection.
• The therapy confound. Psychedelic treatment is delivered embedded in substantial psychotherapy; the "drug effect" cannot be cleanly separated from the therapy, the preparation, and the integration sessions — which is theoretically coherent (plasticity needs input) but makes attributing the benefit to the drug, and standardizing/regulating it, genuinely difficult.
• Small samples, short follow-up, allegiance, and publication enthusiasm — the trials are mostly small, conducted by committed advocates, with the field's strong ideological priors a real source of bias.
• The expectancy-and-hype ecosystem surrounding psychedelics is unusually intense, and the gap between public/commercial enthusiasm and regulatory-grade evidence is wide — the MDMA rejection being the clearest demonstration.

The honest synthesis: genuine promise, genuinely paradigm-shifting neuroscience, and a trial literature with fundamental methodological vulnerabilities that the field is only beginning to address honestly — with the MDMA rejection marking the moment the regulatory standard collided with the enthusiasm.

Problems With Their Use

Psychological risks. Acute: overwhelming anxiety, panic, and frightening experiences ("bad trips"), and the risk of dangerous behavior during altered states (the reason for supervised settings). Persistent: hallucinogen persisting perception disorder (HPPD) — lasting perceptual disturbances (visual snow, trails) after psychedelic use, uncommon but real and sometimes distressing; and prolonged psychological destabilization in vulnerable individuals.

Precipitating psychosis or mania. The hardest contraindication: psychedelics (and the plasticity/destabilization they induce) can precipitate or worsen psychosis and mania, and a personal or family history of psychotic or bipolar disorder is a firm contraindication for the classic psychedelics. This is non-negotiable and central to screening.

Physical risks, agent-specific: MDMA's hyperthermia, hyponatremia, and serotonergic/cardiovascular toxicity; ibogaine's lethal cardiac (QT/torsades) risk; ayahuasca's MAOI interactions (serotonin syndrome with serotonergic drugs — a real danger given how many people take SSRIs); ketamine's bladder toxicity and abuse liability. The serotonergic-interaction danger is especially important in a population often already on antidepressants.

The therapist-conduct and boundary hazard. The psychedelic-therapy model places patients in states of extreme suggestibility, vulnerability, and openness, with a therapist present throughout — creating real risk of boundary violations and abuse, made concrete by documented misconduct in the MDMA trial program. This is a structural vulnerability of the therapy-embedded model, demanding rigorous safeguards (dyad therapists, recording, oversight) that the field is still developing.

The blinding and evidence problems (above) are themselves a "problem with their use" in the sense that they mean the actual magnitude and reliability of benefit are less certain than the headlines suggest.

Commercialization, hype, and access. A gold-rush commercial environment (psychedelic startups, clinics, intellectual-property races), intense ideological advocacy, and a wide gap between promise and proof create real risk of premature, profit-driven, or poorly-controlled deployment — the same deployment-problem theme that recurs across this series, in an unusually heated form.

Legal, regulatory, and cultural issues. Most remain Schedule I (research and limited regulated-access exceptions aside); the legal landscape is shifting and uneven; and the appropriation of Indigenous sacramental traditions and plants (peyote, ayahuasca) — and the conservation pressures on peyote and the Bufo toad — raise serious ethical issues distinct from the pharmacology.

A Theoretical Synthesis

The deepest lesson of this class, and the one that ties it to the rest of the series, is the plasticity convergence: the classic psychedelics (via 5-HT2A → glutamate → BDNF → synaptogenesis), ketamine (via NMDA antagonism → the same downstream cascade), MDMA (via monoaminergic and oxytocinergic opening of a fear-reduced state), and even the SSRIs (slowly, via the same machinery) all appear to induce neural plasticity and reopen the brain to experience-dependent change — differing in speed, route, intensity, and the character of the accompanying subjective state. On this view, what these consciousness-altering agents fundamentally do is not "treat depression" or "treat PTSD" directly but destabilize entrenched patterns and open a window of plasticity — relaxing the rigid priors and self-models (the entropic-brain/REBUS account), reopening critical-period-like learning (Dölen), and growing new synapses (the psychoplastogen account) — within which the right therapeutic context can install lasting change. This is why "set and setting" and the embedded psychotherapy are not optional accessories but, on the theory, the mechanism's other half: the drug opens the window; the experience and the therapy determine what comes through it.

This framing also organizes the field's central unresolved question — is the subjective experience necessary? If the trip, the mystical experience, the ego dissolution is the means by which the plasticity gets therapeutically directed (and the mediation data suggesting experience-intensity predicts outcome point this way), then psychedelic therapy will always be the elaborate, experiential, therapy-embedded, expensive enterprise it currently is. If the experience is merely an epiphenomenon of the plasticity-inducing mechanism (and the non-hallucinogenic-psychoplastogen program bets this way), then the benefit could in principle be delivered as an ordinary pill without the trip. The same question shadows ketamine (is the dissociation necessary?). It is the field's deepest practical fork, and it is unresolved.

The honest state of the field: a genuine scientific revolution in understanding how the brain can be opened to therapeutic change, a small number of genuinely promising treatments for serious and treatment-resistant conditions, a trial literature with fundamental and only-now-acknowledged methodological vulnerabilities, real and sometimes lethal physical and psychological risks, a profound and unresolved set of conduct, commercial, legal, and cultural problems, and — in the MDMA rejection — a clear signal that the enthusiasm has, in places, outrun the evidence. Both the revolutionary promise and the serious cause for caution are real, and the discipline of holding them together is exactly the editorial stance this series has applied throughout.

The Clinical Bottom Line

Ketamine/esketamine is the only member of this family that is an established, approved treatment (treatment-resistant depression, acute suicidality), used as a monitored medical intervention with its specific liabilities (see the glutamatergic document) — the proof of concept that a consciousness-altering, plasticity-inducing agent can become real psychiatry.

Psilocybin is the classic psychedelic closest to approval — promising for treatment-resistant depression, end-of-life distress, and addiction, available through regulated non-medical frameworks in a few jurisdictions, and Breakthrough-designated but not yet an approved medicine; investigational, delivered only in supervised, therapy-embedded, carefully-screened protocols.

MDMA for PTSD remains investigational after the 2024 FDA rejection, with its striking effect sizes shadowed by the blinding, data-integrity, and conduct problems that rejection exposed — a cautionary case for the whole field.

LSD, mescaline, DMT/ayahuasca, and 5-MeO-DMT are investigational and/or traditional/sacramental agents with varying and mostly earlier-stage evidence, each carrying specific risks (ayahuasca's MAOI interactions especially) and, for the plant/animal sources, real conservation and cultural-appropriation concerns.

Ibogaine has a genuinely intriguing anti-addiction mechanism and a demonstrated lethal cardiac risk, dispensed largely in an unregulated and dangerous offshore setting — promising in principle, not safe for unmonitored use, awaiting cardiac-safer approaches.

Across all of them: firm contraindication in personal/family history of psychosis or bipolar disorder; serious attention to physical risks (MDMA hyperthermia/hyponatremia, ibogaine cardiac, ayahuasca/serotonergic interactions, ketamine bladder/abuse); recognition that the therapy-embedded model creates real boundary and conduct hazards requiring rigorous safeguards; sober reading of a trial literature compromised by the blinding problem; and resistance to the intense commercial and ideological hype. These agents represent the most exciting frontier in psychiatric treatment in decades and the one most in need of disciplined, honest, cautious development — genuinely promising, genuinely risky, and genuinely not yet what the enthusiasm claims.

Selected References and Further Reading

1. Nichols, D.E. (2016). Psychedelics. Pharmacological Reviews, 68(2), 264–355.
2. Carhart-Harris, R.L., & Friston, K.J. (2019). REBUS and the anarchic brain: Toward a unified model of the brain action of psychedelics. Pharmacological Reviews, 71(3), 316–344.
3. Carhart-Harris, R.L., et al. (2014). The entropic brain: A theory of conscious states informed by neuroimaging research with psychedelic drugs. Frontiers in Human Neuroscience, 8, 20.
4. Carhart-Harris, R.L., et al. (2021). Trial of psilocybin versus escitalopram for depression. New England Journal of Medicine, 384(15), 1402–1411.
5. Goodwin, G.M., et al. (2022). Single-dose psilocybin for a treatment-resistant episode of major depression (COMPASS). New England Journal of Medicine, 387(18), 1637–1648.
6. Griffiths, R.R., et al. (2016). Psilocybin produces substantial and sustained decreases in depression and anxiety in patients with life-threatening cancer. Journal of Psychopharmacology, 30(12), 1181–1197.
7. Mitchell, J.M., et al. (2021, 2023). MDMA-assisted therapy for severe PTSD (MAPP1, MAPP2). Nature Medicine. [FDA Complete Response Letter, 2024.]
8. Olson, D.E. (2018). Psychoplastogens: A promising class of plasticity-promoting neurotherapeutics. Journal of Experimental Neuroscience, 12.
9. Ly, C., et al. (2018). Psychedelics promote structural and functional neural plasticity. Cell Reports, 23(11), 3170–3182.
10. Nardou, R., Dölen, G., et al. (2023). Psychedelics reopen the social reward learning critical period. Nature, 618(7966), 790–798.
11. dos Santos, R.G., et al. (2016). Antidepressive, anxiolytic, and antiaddictive effects of ayahuasca, psilocybin and LSD: A systematic review. Therapeutic Advances in Psychopharmacology, 6(3), 193–213.
12. Davis, A.K., et al. (2021). Effects of psilocybin-assisted therapy on major depressive disorder. JAMA Psychiatry, 78(5), 481–489.
13. Bogenschutz, M.P., et al. (2022). Percentage of heavy drinking days following psilocybin-assisted treatment for alcohol use disorder. JAMA Psychiatry, 79(10), 953–962.
14. Mash, D.C., et al. (2018). Ibogaine detoxification transitions opioid and cocaine abusers (and the cardiac safety literature: Koenig & Hilber, 2015, Molecules). Journal of Psychopharmacology.
15. Noller, G.E., Frampton, C.M., & Yazar-Klosinski, B. (2018). Ibogaine treatment outcomes for opioid dependence. American Journal of Drug and Alcohol Abuse, 44(1), 37–46.
16. Halpern, J.H., & Pope, H.G. (2003). Hallucinogen persisting perception disorder. Drug and Alcohol Dependence, 69(2), 109–119.
17. Muthukumaraswamy, S.D., Forsyth, A., & Lumley, T. (2021). Blinding and expectancy confounds in psychedelic randomized controlled trials. Expert Review of Clinical Pharmacology, 14(9), 1133–1152.
18. Schenberg, E.E. (2018). Psychedelic-assisted psychotherapy: A paradigm shift in psychiatric research and development. Frontiers in Pharmacology, 9, 733.
19. Johnson, M.W., Richards, W.A., & Griffiths, R.R. (2008). Human hallucinogen research: Guidelines for safety. Journal of Psychopharmacology, 22(6), 603–620.
20. Aday, J.S., et al. (2022). Great expectations: Recommendations for improving the methodological rigor of psychedelic clinical trials. Psychopharmacology, 239, 1989–2010.