Psilocybin mushrooms
4-phosphoryloxy-N,N-dimethyltryptamine
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Psilocybin mushrooms (Psilocybe spp., Hymenogastraceae) — magic mushrooms, shrooms — are psychoactive fungi comprising roughly 165 species found on every continent except Antarctica.[1] The dominant alkaloid, psilocybin, is converted by the body into psilocin, the compound responsible for the psychedelic state. Psilocin activates serotonin receptors in the cortex, disrupting the brain's default resting network and generating the characteristic psychedelic experience.[2]
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Ceremonial use in Mesoamerica dates to at least 1000 BCE; Albert Hofmann isolated psilocybin in 1958.[3] Prohibition under the 1971 UN Convention halted research for decades. Clinical trials in depression[4][5] and addiction[6] reignited scientific interest; Australia authorized therapeutic use in 2023, and Oregon and Colorado now operate regulated access frameworks.[7]
Subjective effects include brightened colors, geometric visual patterns, emotional enhancement, and — at higher doses — ego dissolution, where the sense of a separate self temporarily collapses.[8] The experience is shaped decisively by dose, psychological state, and environment; alkaloid content varies up to 11-fold within a single species.[9] Nausea during onset is common, and challenging experiences — panic, paranoia, thought loops — scale with dose.[10]
Psilocybin produces no physical dependence and no withdrawal;[11] acute physical toxicity at documented human doses is negligible.[12] The primary danger is psychological — difficult experiences at high doses — with lithium and MAOI co-administration posing the most serious drug interaction risks.[13] Wild-harvested specimens carry serious misidentification risk with lethal species such as Galerina marginata.[14]
History[edit]
Traditional and historical use
Archaeological evidence places ceremonial mushroom use in Mesoamerica at least as far back as 1000 BCE — stone effigies from highland Guatemala suggest organized ritual veneration.[15] The Aztecs called them teonanácatl ("flesh of the gods") and consumed them for healing, divination, and spiritual ceremony. R. Gordon Wasson attended a Mazatec velada in Oaxaca in 1955 and published his account in Life magazine in 1957, catalyzing Western interest while disrupting Mazatec communities.[16]
Research era and prohibition
Roger Heim described Psilocybe mexicana taxonomically in 1957, and Albert Hofmann at Sandoz isolated psilocybin and psilocin the following year.[3] Psychiatric research continued through the 1960s before psilocybin was placed in Schedule I under the US Controlled Substances Act in 1970 and the 1971 UN Convention.[7] The mushroom itself was not explicitly named in the 1971 convention — a legal ambiguity later exploited in several jurisdictions.[17]
Modern research revival
The Heffter Research Institute, founded in 1993, provided early infrastructure for renewed clinical work.[18] Griffiths and colleagues published a landmark 2006 study on psilocybin-occasioned mystical experiences,[8] followed by Phase 2 trials in treatment-resistant depression[4][5] and addiction.[6] Australia authorized therapeutic use in 2023; Oregon and Colorado established regulated access frameworks.[7] No Phase 3 trial is complete as of May 2026.
The Mazatec people of Oaxaca maintained continuous ceremonial mushroom use into the modern era through the velada — an all-night healing ceremony led by a curandera or curandero. Mushrooms were consumed as a sacrament within structured frameworks of preparation, intention, and community.[16] These practices represent documented historical and cultural tradition with specific therapeutic and spiritual parameters distinct from recreational consumption.
Botanical Overview[edit]
Taxonomy and classification
Psilocybe is a genus of small fungi in the family Hymenogastraceae, comprising roughly 165 recognized species.[1] The most widely cultivated species is Psilocybe cubensis, available in many named cultivars such as 'Golden Teacher' and 'Penis Envy'. P. semilanceata (the liberty cap) is the most common wild species in temperate Europe and North America.
Habitat and distribution
P. cubensis grows on bovine dung and enriched soils in tropical and subtropical regions. P. semilanceata inhabits acidic, sheep-grazed grasslands across the British Isles, Scandinavia, and the Pacific Northwest. P. cyanescens (wavy cap) colonizes wood-chip mulch in urban and suburban gardens.
Identification
Psilocybin-containing species share several field features: small fruiting bodies, a cap that shifts color as moisture changes (hygrophanous), dark purple-brown spore prints, and blue bruising where tissue is damaged. Galerina marginata — a lethal species — grows on the same wood-chip substrates as P. cyanescens and can look similar to inexperienced foragers.[14] Spore print color is the key distinction: Galerina prints rusty brown; Psilocybe prints dark purple-brown.
Alkaloid Profile[edit]
Dominant alkaloid: psilocybin and psilocin
Psilocybin is the dominant alkaloid in Psilocybe mushrooms, functioning as a prodrug. The body converts it to psilocin — the compound that produces psychedelic effects by activating serotonin receptors in the cortex.[19] In dried P. cubensis, psilocybin content typically ranges from about 0.14% to 1.86% by dry weight.[20]
Minor alkaloids
Several minor alkaloids co-occur with psilocybin in most Psilocybe species. Baeocystin, norbaeocystin, and aeruginascin have been identified across various strains — aeruginascin has been linked anecdotally to differences in subjective character in some P. cubensis strains. No controlled human studies have isolated the contributions of any minor alkaloid; their role in shaping the experience remains unresolved.
Variability
Alkaloid concentrations vary dramatically across species, cultivars, and individual specimens — up to 11-fold within a single P. cubensis population.[9] Named cultivar reputations (e.g., 'Penis Envy' for high potency) carry some weight among cultivators, but standardized analytical data remain limited.[20] This variability is the central challenge for consistent dosing with whole-mushroom preparations.
Neuroscience[edit]
Where it acts
Psilocin binds primarily to serotonin receptors on cortical neurons.[19][21] Brain imaging confirms that the intensity of the psychedelic experience correlates directly with how much of those receptors psilocin occupies.[2] The disruption of the brain's default resting network — the circuit active during self-referential thought — produces ego dissolution and the characteristic sense of boundary loss.
What it changes
A 2024 study showed that a single 25 mg psilocybin dose produces massive desynchronization across brain networks — connectivity changes more than three times those from methylphenidate.[22] Psilocybin also promotes the growth of new neural connections,[23] and these connectivity changes can persist for weeks, linked to antidepressant effects.[22] Tolerance builds within 24 hours through serotonin downregulation[21] and resets fully after approximately 7 days.
- Whether tea, lemon-acidified, or edible preparations produce meaningfully different psilocin exposure profiles remains uncharacterized in published studies.
- The functional contributions of minor alkaloids (baeocystin, norbaeocystin, aeruginascin) to the subjective experience have not been studied in controlled human trials.
- Whether CYP2D6 genetic variation should inform clinical dosing decisions has not been prospectively investigated.
Subjective Effects[edit]
The psilocybin mushroom experience unfolds in layers. At lower doses, colors intensify, surfaces appear to breathe with subtle movement, and mood lifts into an open, wondering state.[8] As dose increases, effects deepen into vivid visual phenomena, emotional catharsis, and — at the upper range — ego dissolution, where the boundary between self and environment collapses. Set and setting exert outsized influence; the same dose can produce radically different outcomes depending on mental state and environment.[24]
Among serotonergic psychedelics, psilocybin mushrooms occupy a middle position. The experience is shorter than LSD (4–8 hours versus 8–12) and more prolonged and perceptually elaborate than vaporized DMT. Tea preparations produce faster onset and shorter total duration than dried whole fruiting bodies. The pronounced nausea of whole dried mushrooms distinguishes them from the synthetic psilocybin capsules used in clinical settings.
Effect Grid
A full psychedelic experience. Geometry — structured visual patterns, lattices, and mandalas — becomes prominent with eyes open or closed. Color alteration transforms the visual field; depth perception distortion and visual morphing reshape spatial relationships. Internal hallucinations develop as vivid closed-eye imagery. Environmental patterning overlays surfaces with repeating motifs.
Emotional enhancement intensifies significantly in both positive and challenging directions. Thought connectivity links disparate concepts; pattern recognition enhancement and conceptual thinking produce novel associations. Personal insight and introspection enhancement deepen. Ego boundaries begin to soften, introducing early identity alteration. Confusion and thought loops may emerge intermittently. Time alteration is pronounced — minutes feel stretched.
Nausea is common at onset, particularly with whole dried mushroom material (less with tea). Pupil dilation is marked. Bodily heaviness or body schema distortion may occur. Motor control impairment makes navigation clumsy. Functional capacity is substantially reduced — plan for 4–6 hours of commitment with dried fruiting bodies. Drug dose is the single most important predictor of all acute response variables (Studerus 2012).
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Auditory enhancement · Geometry · Visual breathing · Tracers · After-images · Symmetrical texture repetition · Perspective distortion · Depth perception distortion · Brightness alteration · Environmental patterning · Visual morphing · Touch enhancement · Visual haze / noise · Visual diffraction · Auditory distortion · Sound sensitivity · Visual melting · Peripheral vision distortion · Spatial disorientation · Vestibular distortion · Synesthesia · Light sensitivity · Auditory misinterpretation · Peripheral misidentification · Proprioceptive distortion · Visual acuity enhancement · Dreaming enhancement · Visual magnification · Taste enhancement · Internal hallucinations · Visual recursion · Object transformations · External hallucinations · Flashbacks · Environmental orbism / cubism · Object activation · Visual scenery slicing · Perspective hallucinations · Auditory hallucinations · Olfactory hallucination · Persisting hallucinations
After-images · Symmetrical texture repetition · Perspective distortion · Depth perception distortion · Brightness alteration · Environmental patterning · Visual morphing · Touch enhancement · Visual haze / noise · Visual diffraction · Auditory distortion · Sound sensitivity · Visual melting · Peripheral vision distortion · Spatial disorientation · Vestibular distortion · Synesthesia · Light sensitivity · Auditory misinterpretation · Peripheral misidentification · Proprioceptive distortion · Visual acuity enhancement · Dreaming enhancement · Visual magnification · Taste enhancement · Internal hallucinations · Visual recursion · Object transformations · External hallucinations · Flashbacks · Environmental orbism / cubism · Object activation · Visual scenery slicing · Perspective hallucinations · Auditory hallucinations · Olfactory hallucination · Persisting hallucinations
Nausea · Body high · Body schema distortion · Stimulation · Appetite suppression · Laughter fits · Physical fatigue · Tingling / electric sensations · Bodily heaviness · Muscle tension · Bodily lightness · Tactile euphoria · Vibrations / buzzing · Breathing alteration · Dizziness · Excessive sweating · Heart rate perception changes · Insomnia · Wakefulness · Sedation · Pain suppression · Bodily pressures · Dry mouth · Muscle relaxation · Restlessness · Headache · Trembling · Watery eyes · Nasal congestion · Salivation · Involuntary body movements · Diarrhea · Nystagmus (eye wobbles) · Vomiting · Yawning · Increased urination · Brain zaps · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Stimulation · Appetite suppression · Laughter fits · Physical fatigue · Tingling / electric sensations · Bodily heaviness · Muscle tension · Bodily lightness · Tactile euphoria · Vibrations / buzzing · Breathing alteration · Dizziness · Excessive sweating · Heart rate perception changes · Insomnia · Wakefulness · Sedation · Pain suppression · Bodily pressures · Dry mouth · Muscle relaxation · Restlessness · Headache · Trembling · Watery eyes · Nasal congestion · Salivation · Involuntary body movements · Diarrhea · Nystagmus (eye wobbles) · Vomiting · Yawning · Increased urination · Brain zaps · Bodily dissociation · Tactile hallucination
Introspection enhancement · Openness enhancement · Cognitive flexibility · Pattern recognition enhancement · Conceptual thinking · Novelty enhancement · Increased nature relatedness · Cognitive euphoria · Confusion · Memory suppression · Focus suppression · Multiple thought streams · Cognitive impairment · Creativity enhancement · Humor enhancement · Language suppression · Thought deceleration · Thought loops · Cognitive fatigue · Memory fragmentation · Memory replays · Motivation suppression · Synchronicity · Analysis suppression · Information processing suppression · Thought disorganization · Analysis enhancement · Thought organization · Information processing enhancement · Thought acceleration · Cognitive dysphoria · Memory enhancement · Focus enhancement · Delusions · Delirium
Pattern recognition enhancement · Conceptual thinking · Novelty enhancement · Increased nature relatedness · Cognitive euphoria · Confusion · Memory suppression · Focus suppression · Multiple thought streams · Cognitive impairment · Creativity enhancement · Humor enhancement · Language suppression · Thought deceleration · Thought loops · Cognitive fatigue · Memory fragmentation · Memory replays · Motivation suppression · Synchronicity · Analysis suppression · Information processing suppression · Thought disorganization · Analysis enhancement · Thought organization · Information processing enhancement · Thought acceleration · Cognitive dysphoria · Memory enhancement · Focus enhancement · Delirium
Emotional lability · Catharsis · Simultaneous emotions · Anxiety suppression · Anxiety · Dysphoria
Anxiety · Dysphoria
Communication suppression · Depersonalization · Disinhibition · Sociability enhancement · Compulsive behavior reduction · Sociability suppression · Communication enhancement · Flow state · Social disconnection · Ego inflation · Boundary dissolution · Identity alteration · Cognitive disconnection · Ego dissolution · Telepathic feelings
Compulsive behavior reduction · Sociability suppression · Communication enhancement · Flow state · Social disconnection · Ego inflation · Boundary dissolution · Identity alteration · Cognitive disconnection · Ego dissolution · Telepathic feelings
Time cessation
Entity contact · Transpersonal visions · Cessation · Transpersonal memory access · Voidness · Death-rebirth sequence · Near-death experience
Voidness · Death-rebirth sequence · Near-death experience
Recursive awareness
Timeline · by preparation
Safety[edit]
- Acute toxicity
- Negligible
- Chronic toxicity
- Negligible
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 7 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- LSD · mesc · DMT
Toxicity
No lethal dose has been established for psilocybin.[12] Clinical data across 598 participants showed nausea, headache, and transient anxiety as the most common adverse events — no serious adverse events were attributable to psilocybin.[25] A 2023 clinical trial found higher overall adverse event rates at 25 mg versus placebo, but no serious treatment-emergent events.[5]
Transient blood pressure and heart rate increases occur during the acute experience. A case series of Psilocybe keralensis poisonings documented myocardial injury with cardiovascular complications — findings not replicated with P. cubensis or other commonly consumed species.[26]
Commercial edibles carry the highest adulteration risk, with inconsistent formulations and unlisted ingredients documented in NPDS data.[27] Wild-harvested specimens risk misidentification with lethal species (see Botanical Overview). Ehrlich reagent (purple/violet reaction) confirms indole tryptamine presence but cannot determine dose.
Psychological Risks
Challenging experiences are common at higher doses — particularly with negative mindset or unsupportive setting. Dose is the single most important predictor of acute response.[24] In a US survey, 8.9% of lifetime psychedelic users reported impairment lasting more than a day from their most difficult experience, and 2.6% sought medical or psychiatric help.[10]
Psilocybin is contraindicated in people with personal or family history of psychotic spectrum disorders — clinical trials uniformly exclude these populations,[17][5] as psilocybin may trigger or worsen psychotic episodes in vulnerable individuals.[17]safety citation needed Persistent perceptual disturbances (HPPD) are rare but documented.[28][29]
Tolerance & Dependence
Tolerance builds virtually completely within 24 hours via serotonin downregulation[21] and resets fully after approximately 7 days. Cross-tolerance occurs with LSD and other serotonergic hallucinogens but not with non-serotonergic substances.[19]
Psilocybin produces no physical dependence and no withdrawal.[11][6] Psychological dependence liability is very low — no compulsive use patterns comparable to classical drugs of abuse have been documented.[27] The rapid tolerance mechanism makes daily use pharmacologically self-limiting.
Drug Interactions
Lithium — dangerous. Co-use with lithium is the strongest predictor of serious harm from psilocybin in population data.[10] Lithium lowers the seizure threshold; combined with serotonergic stimulation, this creates seizure risk.safety citation needed
MAOIs — dangerous. MAOIs block psilocin breakdown and simultaneously raise serotonin levels, creating risk of hypertensive emergency.[13]
Tramadol — dangerous (pharmacological plausibility). Tramadol's serotonergic activity creates theoretical serotonin syndrome risk in combination with psilocybin.safety citation needed No peer-reviewed case reports of this specific combination have been identified.
Cannabis — unknown. One case of persistent perceptual disturbance followed combined psilocybin and cannabis use.[28] Cannabis may amplify subjective intensity; no controlled interaction studies exist.
SSRIs. Chronic SSRI use generally blunts psilocybin's effects through serotonin receptor downregulation.[30] The combination does not appear dangerous at standard doses but significantly reduces therapeutic efficacy.
Contraindications
Psychotic spectrum disorders (schizophrenia, schizoaffective disorder, bipolar disorder with psychotic features) — personal or family history. All clinical trials exclude these populations.[17][5] Absolute contraindication.
Active suicidal ideation with intent or plan — emotional enhancement during a high-dose experience creates unacceptable risk. Absolute contraindication.
Lithium or MAOI co-administration — dangerous interactions documented above. Absolute contraindication.
Cardiovascular disease — transient hypertension and tachycardia warrant caution; a myocardial injury case series raises additional concern.[26] Relative contraindication.
Pregnancy — no peer-reviewed human safety data exist.safety citation needed Relative contraindication.
Pediatric use — no clinical safety data in individuals under 18. Contraindicated.
Preparations[edit]
Psilocybin mushrooms are consumed in several distinct preparations, each with different onset, duration, and intensity. Potency varies up to 11-fold between individual specimens within the same species,[9] making preparation-specific dosing essential.
Dried Fruiting Bodies
The most common preparation worldwide. Whole mushrooms are dried at low heat and consumed directly, ground into capsules, or mixed into food.
- Dose (dried whole): Threshold: 0.1–0.25 g. Common: 1–2.5 g. Strong: 2.5–5 g.
- Onset: 30–60 minutes.
- Duration: 4–8 hours.
- Nausea during onset is common, caused by indigestible fungal cell wall material.
Tea Infusion
Crushed dried mushrooms steeped in hot (not boiling) water for 10–20 minutes, often with ginger or lemon juice.
- Dose (tea): Same starting weight as dried fruiting bodies.
- Onset: 15–30 minutes (faster than whole dried material).
- Duration: 3–5 hours.
- Route-specific pharmacokinetic data for tea have not been published in peer-reviewed studies.
Lemon Tek
Ground dried mushrooms soaked in lemon or lime juice for 15–30 minutes before ingestion. The acidic environment is proposed to accelerate conversion of psilocybin to psilocin before consumption.
- Dose (lemon tek): Treat as more potent per gram than equivalent dried material consumed directly.
- Onset: 15–20 minutes.
- Duration: 3–4 hours, with a more compressed and intense peak.
- This mechanism has not been confirmed in published pharmacokinetic studies.
Edible Preparations (Chocolates, Gummies)
Ground mushroom material incorporated into food products. Increasingly common in unregulated markets.
Harm Reduction[edit]
Forms & Identification
Lab testing is the only reliable way to confirm psilocybin content and rule out adulterants. For whole dried mushrooms, visual identification by an experienced mycologist combined with spore-print verification provides reasonable species confidence. Commercial edibles cannot be visually assessed for content or purity — analytical testing is the only safeguard against inconsistent dosing and synthetic adulterants.[27]
Ehrlich reagent provides a basic screen: a purple/violet reaction confirms an indole tryptamine is present but cannot identify the compound or determine dose. When lab testing is unavailable, starting with a fraction of a typical dose is the most practical harm-reduction strategy.
Guidelines
Practical Guidelines
- 1. Test first. Use Ehrlich reagent at minimum. Purple/violet confirms indole presence. No reaction: do not consume.
- 2. Start low. For unfamiliar specimens or cultivars, begin with 0.5–1 g dried and assess potency before taking more. Specimen-to-specimen variability is substantial.[9]
- 3. Wait before redosing. Onset from dried mushroom material is 30–60 minutes. Do not redose during this window. Tea and lemon tek onset faster (15–30 minutes).
- 4. Prepare the environment. Choose a comfortable indoor space with soft lighting, access to water, calming music, and a sober companion.
- 5. Allow enough time. The experience lasts 6–8 hours — do not drive, operate machinery, or make consequential decisions until fully baseline.
- 6. Hydrate and eat lightly. A light meal 2–3 hours before consumption reduces nausea. Keep water accessible throughout.
- 7. Avoid dangerous combinations. Do not combine with lithium, MAOIs, or tramadol.[13]
Set & Setting
Psilocybin's effects are unusually sensitive to psychological state and physical environment. A calm, familiar, physically safe space with minimal external stimulation reduces the likelihood of a challenging experience. Avoid public settings, crowds, or situations requiring coordination or rapid decision-making.
Unresolved anxiety, acute grief, or emotional distress raises the risk of difficult experiences.[24] A trusted, sober companion who can provide calm reassurance is strongly recommended, especially at higher doses or for first experiences.
Aftercare & integration.
Aftercare & Integration
The period following a psilocybin experience often carries emotional residue — positive or challenging — that benefits from deliberate processing. Rest, adequate sleep, and good nutrition in the 24–48 hours afterward support recovery.
Journaling or conversation with a trusted person helps consolidate insights and process difficult material. For experiences that included challenging psychological content, integration work is particularly important: unprocessed difficult experiences can manifest as lingering anxiety or confusion.
Mild headache is common in the hours afterward. Hydration and over-the-counter analgesics are typically sufficient. If persistent mood disturbance, depersonalization, or perceptual changes continue beyond a few days, consult a mental health professional.
Recovery & Support
Recovery & Support
Psilocybin carries very low abuse liability, and most users do not develop problematic patterns. However, some individuals experience psychological difficulty integrating intense psychedelic experiences, or develop habitual use that interferes with daily functioning.
For persistent psychological difficulties after psychedelic use — including anxiety, depersonalization, or existential distress — specialized integration therapy is available through directories such as the Psychedelic Support Network and MAPS therapist finder.
Tolerance resets fully in approximately 7 days. Spacing sessions at least 1–2 weeks apart preserves sensitivity and reduces risk of psychological overload.
For crisis support, contact the Fireside Project psychedelic peer support line (62-FIRESIDE / 623-473-7433) or the SAMHSA National Helpline (1-800-662-4357), available 24/7.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Emergency Response
Recognizing an emergency:
- Severe panic or paranoia unresponsive to reassurance
- Dissociation so profound the person cannot communicate or recognize surroundings
- Seizure activity (especially if lithium has been co-administered)
- Signs of serotonin syndrome: hyperthermia, rigid muscles, rapid heart rate, agitation
- Chest pain or difficulty breathing
Immediate steps:
- 1. Stay with the person. Move to a quiet, safe space if possible.
- 2. Speak calmly and reassuringly. Remind them the effects are temporary and will pass.
- 3. If severely distressed and unresponsive to reassurance, call emergency services.
- 4. If seizures occur, protect the head and call emergency services immediately.
What to tell the dispatcher:
- The substance consumed (psilocybin mushrooms), approximate amount, and time of ingestion
- Current symptoms
- Any co-administered substances, particularly lithium or MAOIs
- Good Samaritan laws provide legal protection in many jurisdictions
Reversal agents: No specific pharmacological reversal agent exists for psilocybin. Benzodiazepines may be administered by medical professionals for severe anxiety or agitation.
Legal Status[edit]
Psilocybin and psilocin are listed under Schedule I of the 1971 UN Convention on Psychotropic Substances. The physical mushroom was not explicitly named in the Convention — a legal ambiguity exploited in several jurisdictions.[17] In the United States, psilocybin remains federally Schedule I; an April 2026 executive order directed fast-tracked psychedelic research review but did not alter scheduling.[7] Oregon and Colorado have established regulated access frameworks; several US cities, including Denver, Oakland, and Seattle, have enacted decriminalization ordinances. Australia became the first country to authorize therapeutic psilocybin use in 2023, under licensed psychiatrist supervision. Canada's Special Access Program permits access for serious conditions. The United Kingdom classifies psilocybin as Class A. The Netherlands prohibits fruiting bodies but permits psilocybin-containing truffles in licensed shops. Germany has opened compassionate access at two clinics, and the Czech Republic became the first EU member state with a specific medical psilocybin framework in January 2026.[7] Possession remains a serious criminal offense in most jurisdictions worldwide.
Legal status changes frequently. This overview reflects the status as of the article's last update and is not legal advice. Verify current law in the relevant jurisdiction before acting on this information.
references
- [1]
- [2] ^abMadsen MK, Fisher PM, Burmester D, et al. (2019) Psychedelic effects of psilocybin correlate with serotonin 2A receptor occupancy and plasma psilocin levels — Neuropsychopharmacology doi:10.1038/s41386-019-0324-9
- [3]
- [4] ^abGoodwin GM, Aaronson ST, Alvarez O, et al. (2022) Single-Dose Psilocybin for a Treatment-Resistant Episode of Major Depression — New England Journal of Medicine doi:10.1056/nejmoa2206443
- [5]
- [6] ^abcMeshkat S, Malik G, Zeifman RJ, et al. (2025) Efficacy and safety of psilocybin for the treatment of substance use disorders: A systematic review — Neuroscience and Biobehavioral Reviews doi:10.1016/j.neubiorev.2025.106163