LSD
lysergic acid diethylamide
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LSD (lysergic acid diethylamide) — acid, tabs, blotter, Lucy — is a semi-synthetic psychedelic of the lysergamide class. It is derived from ergot, a fungus that grows on grain. It activates serotonin receptors in the brain, disrupting the brain's normal filtering of sensory and cognitive input.[1]
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Albert Hofmann discovered LSD in 1943 when he accidentally absorbed a trace amount during synthesis, then deliberately dosed himself three days later. It became one of the most studied psychoactive compounds in psychiatric history[2] before prohibition halted research for nearly four decades. Clinical trials have resumed since 2014, and LSD remains Schedule I in the United States.
Subjective effects include geometric visual patterns, intensified colors, time alteration, accelerated thought, and ego dissolution — the sense that the self's boundaries have dissolved. The experience is slow-building and all-encompassing, with a stimulating, electric quality that distinguishes it from psilocybin mushrooms.[3] Thought loops, anxious fixation, and difficulty sleeping through the long tail are common unwanted effects.
LSD produces no physical dependence and has no confirmed lethal dose in humans.[2] The primary risks are psychological — high doses can produce panic, paranoid thinking, and dangerous behavior, and combining LSD with lithium causes seizures in roughly half of documented cases. LSD is well-studied over eight decades, though the long-term effects of frequent use and cardiac safety of regular microdosing remain unclear.
History[edit]
Discovery
Albert Hofmann synthesized LSD on November 16, 1938 at Sandoz Laboratories in Basel, as the twenty-fifth in a series of ergot-derived compounds.[4][2] Initial animal testing showed nothing of interest, and the compound was shelved. Five years later, Hofmann accidentally absorbed a trace quantity during a re-synthesis and experienced unusual perceptual effects; three days later he deliberately took a dose — the first intentional psychedelic self-experiment on record.[2][5]
Prohibition and modern research
LSD spread into broader cultural use in the early 1960s, prompting Sandoz to stop supply in 1965–1966 and the United States to classify it Schedule I in 1970. Research halted worldwide for three decades. The first controlled modern study of LSD's acute effects ran in 2015,[6] and multiple Phase 2 trials are now active for depression, anxiety, alcohol use disorder, and cluster headache.
Clinical and institutional history
Between 1950 and 1965, an estimated 40,000 patients received LSD-assisted psychotherapy and over 1,000 clinical papers were published.[2] Simultaneously, the CIA's Project MKUltra used LSD in non-consensual experiments on civilians and military personnel — one of the worst ethical violations in the history of psychopharmacological research.
The name "LSD" comes from the German Lysergsäure-diäthylamid, abbreviated LSD-25. Street names include "acid," "tabs," "blotter," and "Lucy." April 19 is informally commemorated as "Bicycle Day" — marking Hofmann's bicycle ride home during his first intentional experience, which has become a founding myth of psychedelic culture.
Chemistry[edit]
Structural class
LSD belongs to the ergoline family — a class of compounds derived from ergot fungus (Claviceps purpurea). Its molecular formula is C₂₀H₂₅N₃O. The molecule's rigid ring structure holds it in a fixed shape that fits receptor binding sites exceptionally well — which is why LSD is 100 to 1,000 times more potent by weight than simpler psychedelics like psilocybin or DMT.[7]
Pharmacology[edit]
Mechanism of action
LSD works primarily by activating serotonin receptors on cortical neurons.[2] A drug that blocks serotonin receptors completely abolished LSD's psychedelic effects in controlled trials — confirming this is the primary mechanism.[1]
After binding to a serotonin receptor, a protein loop folds over the binding site and traps LSD inside — like a lid closing on a box.[8][9] The receptor stays activated long after LSD has cleared the bloodstream. This explains why effects last 8–12 hours despite a blood half-life of only about 3.5 hours.
Pharmacokinetics
LSD is well-absorbed by mouth — about 80% reaches the bloodstream.[10] The liver enzyme CYP2D6 breaks it down; people who process this enzyme's substrates slowly experience roughly 75% higher drug exposure and more intense effects.[11] The terminal half-life is approximately 2.7–3.6 hours.[12][13][3]
Neuroscience[edit]
Where it acts
LSD disrupts the default mode network — the brain system that maintains the sense of self.[14] As this network loses coherence, the self's boundaries soften or disappear entirely — the subjective experience of ego dissolution. The visual cortex simultaneously forms new connections with regions not normally involved in vision, producing the vivid hallucinations.[14]
Why it matters
One influential model proposes that LSD pushes brain activity into a higher-entropy, less constrained state — weakening habitual thought patterns and making the mind more sensitive to both internal and external experience.[15]
LSD also promotes the growth of new synaptic connections in the prefrontal cortex, through a pathway linked to antidepressant effects that operates independently of the hallucinogenic mechanism.[16][17]
LSD-assisted therapy produces mood improvements lasting months after a single session,[18] but whether this durability comes from physical synaptic remodeling, cognitive flexibility, or psychological processing is not yet known. Pre-drug personality, anxiety levels, and prior experience predict response direction,[19] but no validated model exists to predict individual outcomes in clinical settings.
Subjective Effects[edit]
LSD builds slowly into a total alteration of perception, thought, and feeling. The characteristic quality is a stimulating, outward-facing electricity — the mind stays alert and engaged with the world rather than being drawn inward. Colors sharpen, thinking accelerates, and the familiar boundaries between inside and outside begin to blur.
Compared to psilocybin, LSD runs longer and carries more physical energy.[3][20] Where psilocybin tends toward introspective, emotionally saturated states, LSD maintains clarity and outward curiosity. The contrast is often described as being drawn inward versus being pushed outward.
Effect Grid
At common doses (75–150 µg oral), the full psychedelic experience emerges: pronounced open and closed-eye visuals including geometric patterns overlaying surfaces, colour shifting, drifting and morphing of objects, and tracers behind moving objects. Time distortion becomes significant — minutes may feel like hours. Thought connectivity increases dramatically, often producing novel associations, personal insights, and enhanced emotional empathy. Ego dissolution may occur, particularly at the upper end of this range. Music, art, and nature can feel profoundly meaningful.
Physically, jaw tension, temperature dysregulation, peripheral vasoconstriction (cold extremities), and occasional nausea are common. Pupil dilation is pronounced. Heart rate and blood pressure increase moderately. Effects at 100 µg last approximately 8 hours on average, with the positive subjective experience reaching a ceiling — higher doses within this range do not increase pleasant effects but extend duration.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Music enhancement · Visual morphing · Color alteration · Tracers · Light sensitivity · Auditory enhancement · Touch enhancement · Brightness alteration · Depth perception distortion · Environmental patterning · After-images · Holotropic state · Sound sensitivity · Visual haze / noise · Perspective distortion · Symmetrical texture repetition · Visual melting · Auditory distortion · Peripheral vision distortion · Proprioceptive distortion · Visual acuity enhancement · Visual diffraction · Auditory misinterpretation · Spatial disorientation · Visual processing acceleration · Synesthesia · Peripheral misidentification · Vestibular distortion · Taste enhancement · Olfactory enhancement · Ganzfeld effect · Visual magnification · Object transformations · Internal hallucinations · Flashbacks · Object activation · Visual recursion · Visual flipping · External hallucinations · Perspective hallucinations · Environmental orbism / cubism · Visual scenery slicing · Auditory hallucinations · Persisting hallucinations · Shadow people
Light sensitivity · Auditory enhancement · Touch enhancement · Brightness alteration · Depth perception distortion · Environmental patterning · After-images · Holotropic state · Sound sensitivity · Visual haze / noise · Perspective distortion · Symmetrical texture repetition · Visual melting · Auditory distortion · Peripheral vision distortion · Proprioceptive distortion · Visual acuity enhancement · Visual diffraction · Auditory misinterpretation · Spatial disorientation · Visual processing acceleration · Synesthesia · Peripheral misidentification · Vestibular distortion · Taste enhancement · Olfactory enhancement · Ganzfeld effect · Visual magnification · Object transformations · Internal hallucinations · Flashbacks · Object activation · Visual recursion · Visual flipping · External hallucinations · Perspective hallucinations · Environmental orbism / cubism · Visual scenery slicing · Auditory hallucinations · Persisting hallucinations · Shadow people
Appetite suppression · Stimulation · Body scan awareness · Body high · Spontaneous body sensations · Bruxism · Muscle tension · Laughter fits · Physical fatigue · Tingling / electric sensations · Heart rate perception changes · Tactile euphoria · Nausea · Vibrations / buzzing · Restlessness · Body schema distortion · Yawning · Excessive sweating · Bodily lightness · Bodily pressures · Motor control impairment · Increased urination · Pain suppression · Respiratory stimulation · Trembling · Dizziness · Nystagmus (eye wobbles) · Watery eyes · Abnormal heartbeat · Breathing alteration · Sexual arousal enhancement · Dry mouth · Bodily heaviness · Dehydration sensation · Kundalini-like energy · Sexual arousal suppression · Headache · Involuntary body movements · Vomiting · Bodily dissociation · Tactile hallucination · Seizure threshold reduction
Body high · Spontaneous body sensations · Bruxism · Muscle tension · Laughter fits · Physical fatigue · Tingling / electric sensations · Heart rate perception changes · Tactile euphoria · Nausea · Vibrations / buzzing · Restlessness · Body schema distortion · Yawning · Excessive sweating · Bodily lightness · Bodily pressures · Increased urination · Pain suppression · Respiratory stimulation · Trembling · Dizziness · Nystagmus (eye wobbles) · Watery eyes · Abnormal heartbeat · Breathing alteration · Sexual arousal enhancement · Dry mouth · Bodily heaviness · Dehydration sensation · Kundalini-like energy · Sexual arousal suppression · Headache · Involuntary body movements · Vomiting · Bodily dissociation · Tactile hallucination · Seizure threshold reduction
Novelty enhancement · Aesthetic enhancement · Thought acceleration · Cognitive euphoria · Openness enhancement · Pattern recognition enhancement · Immersion enhancement · Cognitive flexibility · Creativity enhancement · Multiple thought streams · Increased nature relatedness · Focus suppression · Cognitive fatigue · Analysis enhancement · Thought loops · Thought disorganization · Humor enhancement · Language suppression · Confusion · Information processing enhancement · Cognitive impairment · Memory suppression · Synchronicity · Memory replays · Information processing suppression · Cognitive dysphoria · Memory fragmentation · Language enhancement · Motivation enhancement · Analysis suppression · Motivation suppression · Thought organization · Focus enhancement · Memory enhancement · Delusions of sobriety · Delusions · Amnesia · Delirium
Cognitive euphoria · Openness enhancement · Pattern recognition enhancement · Immersion enhancement · Cognitive flexibility · Creativity enhancement · Multiple thought streams · Increased nature relatedness · Focus suppression · Cognitive fatigue · Analysis enhancement · Thought loops · Thought disorganization · Humor enhancement · Language suppression · Confusion · Information processing enhancement · Cognitive impairment · Memory suppression · Synchronicity · Memory replays · Information processing suppression · Cognitive dysphoria · Memory fragmentation · Language enhancement · Motivation enhancement · Analysis suppression · Motivation suppression · Thought organization · Focus enhancement · Memory enhancement · Delusions · Amnesia · Delirium
Anxiety · Empathy enhancement · Simultaneous emotions · Catharsis · Anxiety suppression · Irritability · Dysphoria · Mania
Catharsis · Anxiety suppression · Irritability · Dysphoria
Sociability enhancement · Communication enhancement · Depersonalization · Communication suppression · Disinhibition · Automaticity · Compulsive behavior reduction · Flow state · Ego inflation · Sociability suppression · Social disconnection · Self-control enhancement · Ego dissolution · Boundary dissolution · Identity alteration · Cognitive disconnection · Telepathic feelings
Disinhibition · Automaticity · Compulsive behavior reduction · Flow state · Ego inflation · Sociability suppression · Social disconnection · Self-control enhancement · Ego dissolution · Boundary dissolution · Identity alteration · Cognitive disconnection · Telepathic feelings
Time cessation
Transpersonal visions · Death-rebirth sequence · Entity contact · Non-dual awareness · Voidness · Cessation · Near-death experience
Voidness · Cessation · Near-death experience
Mindfulness enhancement · Lucidity enhancement · Anticipatory response · Applied attention (vitakka) · Cognitive dissonance · Recursive awareness
Cognitive dissonance · Recursive awareness
Timeline
First alerts emerge 20–45 minutes after ingestion: a subtle shift in bodily awareness, slight brightening of colours, and a growing sense that something is changing. The stomach may feel unsettled.
Effects build steadily over 30–60 minutes. Visual field begins to shimmer, colours intensify, and thought patterns accelerate. Mild anxiety or excitement is common as the experience gathers momentum.
Rapid intensification toward the peak over 45–90 minutes. Open-eye visuals emerge — geometric overlays, drifting surfaces, colour shifting. Emotional amplification and time distortion become unmistakable.
Maximum intensity sustained for 2–3 hours. Full visual, cognitive, and emotional effects: geometric hallucinations, ego dissolution at higher doses, profound alterations in meaning and connectedness. Music and sensory experiences feel deeply significant.
Gradual easing from peak intensity over 1. 5–3 hours. Visuals soften but persist.
Steady return toward baseline over 1. 5–3 hours. Residual visual enhancement (colour saturation, mild drifting) and emotional sensitivity persist but thinking normalises progressively.
A period of 6–48 hours following resolution characterised by elevated mood, enhanced emotional openness, increased aesthetic sensitivity, and a sense of psychological clarity. Some users report mild residual visual enhancement. Fatigue from the extended experience is common.
Safety[edit]
- Acute toxicity
- Negligible
- Chronic toxicity
- Low
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 14 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- psilo · mesc · DMT
Toxicity
Acute toxicity
LSD has an exceptionally wide safety margin — the estimated lethal dose is roughly 1,000 times the standard active dose.safety citation needed No confirmed human death from LSD's direct pharmacological effects has been documented.[2]
Deaths recorded in forensic cases typically involve other drugs, misidentified substances such as 25x-NBOMe compounds, or accidental falls at standard doses.
Heart and circulation
LSD produces moderate, temporary increases in blood pressure (~10–20 mmHg) and heart rate (~10–20 bpm) at clinical doses.[21][6] No significant heart rhythm abnormalities have been documented at doses up to 200 µg, including during co-administration with SSRIs.[22]
5-HT₂B and heart valve concern
LSD is chemically related to ergot drugs known to cause heart valve damage through repeated receptor stimulation.[23] This concern applies mainly to regular microdosing regimens — several doses per week over months.
No clinical cases of LSD-induced valve damage have been reported, and one echocardiographic study at 8 weeks of microdosing found no abnormalities.[23] The risk is mechanistically plausible but clinically unconfirmed.
Controlled study safety
Across multiple controlled studies at doses up to 200 µg, no serious adverse events have occurred.[21] Side effects are mild to moderate: nausea, headache, and anxiety.[21]
Psychological Risks
Hallucinogen persisting perception disorder (HPPD)
HPPD involves persistent visual disturbances after psychedelic use that interfere with daily functioning. Two forms exist: Type I — brief, intermittent flashbacks that are generally harmless and self-limiting — and Type II, chronic distressing perceptual changes that persist long-term.[24]
LSD is the substance most commonly linked to HPPD in clinical reports, and it can occur after a single exposure.[25][24] Risk factors include personal or family history of anxiety disorders, pre-existing psychiatric conditions, cannabis use, and frequent high-dose use.[24] Treatments with reported benefit include benzodiazepines, levetiracetam, and clonidine.[26][25] Risperidone is contraindicated — it has been documented to worsen HPPD symptoms.[26]
Psychosis
LSD carries significant psychosis risk for people with pre-existing psychotic disorders.[27] Personal or family history of schizophrenia or bipolar disorder type I is an exclusion criterion across all modern LSD clinical trials.[6]
Tolerance & Dependence
Near-complete tolerance to psychedelic effects develops within 3–4 days of consecutive use, driven by serotonin downregulation.[2] Full reset takes 10–14 days. This rapid tolerance functionally prevents compulsive daily use.
Cross-tolerance is complete and bidirectional with all other classical serotonin-acting psychedelics — psilocybin, mescaline, DMT, and 2C-x compounds.[2] LSD produces no physical dependence and no withdrawal.[2] Psychological dependence is negligible — LSD does not activate reward circuitry in patterns associated with addictive drugs.[2]
Drug Interactions
Lithium is the most dangerous documented interaction. Seizures have been reported within 30 minutes of LSD ingestion in people taking lithium — even at blood levels below the therapeutic range.[28] About half of documented combined cases resulted in seizures.[29] This combination is absolutely contraindicated.
Tramadol carries serotonin syndrome risk. Tramadol blocks serotonin reuptake while LSD directly stimulates serotonin receptors — together they push serotonin activity to dangerous levels. Severe presentations can include dangerously high body temperature, muscle rigidity, and seizures.citation needed
SSRIs interact through two pathways: certain SSRIs slow LSD breakdown, raising blood levels; and chronic SSRI use reduces serotonin receptor sensitivity. Paroxetine increased LSD blood levels by 40–50% at 100 µg but actually reduced anxiety and nausea.[22] LSD at 100 µg added to SSRI therapy appears well-tolerated based on current data.[22]
MDMA presents theoretical serotonin syndrome risk from combined receptor stimulation and serotonin release, plus additive cardiovascular strain. No controlled data exist for this combination.citation needed
MAOIs slow serotonin breakdown while LSD directly stimulates serotonin receptors — a combination that risks dangerous serotonin overload. An adequate washout period from irreversible MAOIs is recommended before LSD use.citation needed
Contraindications
Personal or family history of schizophrenia or psychotic disorder — absolute contraindication. LSD may trigger or worsen psychotic episodes in predisposed individuals.[27][6]
Bipolar disorder type I — absolute contraindication (relative for bipolar II with careful assessment). Risk of triggering manic episodes.[27]
Current lithium therapy — absolute contraindication. Seizures documented even at below-therapeutic lithium levels.[28][29]
Seizure disorder — absolute contraindication. The lithium interaction data and pharmacological profile suggest independent seizure risk in vulnerable individuals.safety citation needed
Significant heart condition — relative contraindication. Blood pressure and heart rate increases are moderate and temporary in healthy individuals but may pose risk for those with high blood pressure, coronary artery disease, or irregular heart rhythm.[21]
Current MAOI therapy — relative contraindication. Theoretical serotonin syndrome risk; adequate washout period required.citation needed
Pregnancy and breastfeeding — absolute contraindication. No reproductive safety data exist; the ergoline structure raises theoretical concerns about effects on uterine contractions.safety citation needed
Harm Reduction[edit]
Forms & Identification
Blotter paper is the most common form. The critical concern is that LSD blotter looks identical to paper dosed with 25x-NBOMe compounds — substances far more toxic than LSD with a documented fatality record at recreational doses.
Ehrlich's reagent is the primary test: LSD produces a purple/violet reaction; NBOMe compounds produce none. A negative result means the substance is not LSD. A positive result confirms an indole-containing compound but does not confirm purity, dose, or the absence of additional substances.
Dose precision on unregulated blotter is inherently limited. Distribution across the paper is uneven, and stated doses from unregulated sources are unreliable.
Guidelines
- Test every dose with Ehrlich's reagent before ingestion — a negative result means the substance is not LSD
- Start with a low dose if inexperienced; individual sensitivity varies substantially, and there is no way to reduce a dose once taken
- Clear the schedule — block 12–16 hours with no driving, work, or social obligations
- Prepare the space — comfortable temperature, accessible water and light food, calming music available, minimal fall hazards
- Have a sober sitter present, especially at higher doses or for first experiences
- Avoid redosing during the experience — tolerance begins immediately, and additional doses extend duration more than they increase intensity
- Avoid cannabis co-use, which frequently intensifies effects unpredictably and is a common trigger for anxiety escalation
- Eat a light meal 2–3 hours before dosing; avoid taking LSD on an empty or very full stomach
Set & Setting
LSD's effects are unusually sensitive to psychological state and physical environment. Pre-drug anxiety and negative expectations reliably push the experience toward distress.[19] The extended duration — 8 to 12 hours plus residual stimulation — demands more planning than shorter-acting psychedelics.
A familiar, physically safe, and comfortable space with no obligations for 12–16 hours is the baseline. A trusted, sober companion significantly reduces the risk of psychological distress escalating into crisis. Unfamiliar social environments and crowds should be avoided.
Aftercare & integration. The day after an LSD experience typically involves physical fatigue, emotional sensitivity, and a residual sense of cognitive openness. Sleep may be disrupted the first night. Plan for a quiet recovery day with no demanding obligations.
Psychedelic experiences involving ego dissolution or emotionally intense content benefit from deliberate processing. Journaling within the first 24–48 hours captures insights before they fade. If distressing thoughts, perceptual disturbances, or mood changes persist beyond two weeks, consult a mental health professional with psychedelic integration experience. The Fireside Project (62-FIRESIDE / 623-473-7433) offers free peer support.
Recovery & Support
LSD does not produce physical dependence or withdrawal, but patterns of frequent use can develop — particularly when the substance is used to avoid confronting difficult emotions. If use is escalating in frequency, interfering with responsibilities, or continuing despite negative consequences, professional support is warranted.
Harm reduction-oriented therapists and psychedelic integration specialists can help identify problematic patterns without requiring an abstinence-only approach. SMART Recovery and other non-12-step programs offer evidence-based support compatible with a harm reduction philosophy.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Most difficult LSD experiences are psychologically distressing but not medically dangerous. Recognizing the difference is critical.
Uncomfortable but manageable: anxiety, thought loops, paranoid thoughts, nausea, feeling overwhelmed. These are common and almost always resolve as the drug wears off.
Seek immediate help if:
- The person is attempting to harm themselves or others
- Complete disconnection from reality with dangerous behavior (climbing, running into traffic)
- Seizures — especially if the person takes lithium
- Signs of serotonin syndrome: high body temperature, severe muscle rigidity, rapid heart rate, confusion (relevant if other serotonergic drugs are involved)
Immediate steps:
- 1. Move the person to a quiet, safe space
- 2. Speak calmly and simply — "You took a substance, you are safe, this will end"
- 3. Do not restrain unless there is immediate danger to life
- 4. If symptoms suggest a medical emergency, call emergency services immediately
What to tell the dispatcher: the substance taken (or suspected), the amount if known, when it was taken, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
Legal Status[edit]
LSD is listed in Schedule I of the United Nations Convention on Psychotropic Substances (1971) — the international treaty framework adopted by virtually all signatory nations. No jurisdiction has rescheduled it for medical use as of April 2026, despite active clinical research programs and mounting evidence of therapeutic efficacy.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I (Controlled Substances Act, 1970) | Federally controlled since October 24, 1968; research requires DEA Schedule I researcher license and FDA IND exemption[30] |
| United Kingdom | Class A (Misuse of Drugs Act 1971), Schedule 1 | Maximum penalties: possession 7 years, supply/production life imprisonment; research requires Home Office Schedule 1 license[31] |
| Canada | Schedule III (CDSA, 1996) | Possession: up to 3 years indictable; trafficking: up to 10 years; Section 56 ministerial exemptions for research[32] |
| Australia | Schedule 9 — Prohibited Substance (SUSMP) | No therapeutic use permitted; research requires TGA permit; same schedule as heroin[33] |
| Germany | Betäubungsmittelgesetz (BtMG) — illegal | Not marketable for therapeutic use; research exemptions available |
| Netherlands | Opium Act, List I — illegal | Personal possession not prosecuted in practice (de facto decriminalization) |
| France | Schedule I equivalent — illegal | No therapeutic use provisions |
| Switzerland | Controlled narcotic | Compassionate use authorization granted since ~2014; active Phase 2/3 clinical trials at University Hospital Basel |
Legal status changes frequently and varies by jurisdiction. This information is not legal advice.
references
- [1] ^abHolze F, Vizeli P, Müller F, Ley L, Duerig R, Varghese N, Zizzari P, Liechti ME (2021) Acute dose-dependent effects of lysergic acid diethylamide in a double-blind placebo-controlled study in healthy subjects — Neuropsychopharmacology doi:10.1038/s41386-020-00883-6
- [2]
- [3] ^abcLey L, Holze F, Arikci D, Becker AM, Straumann I, Klaiber A, Coviello F, Dierbach S, Thomann J, Duthaler U, Luethi D, Varghese N, Eckert A, Liechti ME (2023) Comparative acute effects of mescaline, lysergic acid diethylamide, and psilocybin in a randomized, double-blind, placebo-controlled cross-over study in healthy participants — Neuropsychopharmacology doi:10.1038/s41386-023-01607-2
- [4]
- [5] ^Tagliazucchi E, Roseman L, Kaelen M, Orban C, Muthukumaraswamy SD, Murphy K, Laufs H, Leech R, McGonigle J, Crossley N, Bullmore E, Williams T, Bolstridge M, Feilding A, Nutt DJ, Carhart-Harris R (2016) Increased Global Functional Connectivity Correlates with LSD-Induced Ego Dissolution — Current Biology doi:10.1016/j.cub.2016.02.010
- [6] ^abcdSchmid Y, Enzler F, Gasser P, Grouzmann E, Preller KH, Vollenweider FX, Brenneisen R, Müller F, Borgwardt S, Liechti ME (2015) Acute Effects of Lysergic Acid Diethylamide in Healthy Subjects — Biological Psychiatry doi:10.1016/j.biopsych.2014.11.015