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LSD
lysergic acid diethylamide
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]
LSD (lysergic acid diethylamide) is a semi-synthetic psychedelic of the lysergamide class. It is structurally derived from ergot alkaloids, compounds produced by grain fungi. LSD is a 5-HT₂A receptor agonist, producing its effects by disrupting the brain's default 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.
LSD was discovered in 1943 when Albert Hofmann inadvertently absorbed a dose during synthesis at Sandoz Laboratories in Basel. It became the most studied psychoactive compound in postwar psychiatry — over 1,000 papers and 40,000 patients receiving LSD-assisted therapy — before international scheduling halted research for nearly four decades.[2] It remains Schedule I in the United States, though controlled clinical trials have resumed since 2014.
Subjective effects include geometric visual patterns, color enhancement, time alteration, thought acceleration, and ego dissolution. The experience is defined by its scope — a slow-building, all-encompassing alteration of perception, cognition, and emotion with a stimulating somatic electricity that distinguishes it from tryptamine psychedelics.[3] Thought loops, anxious fixation, and difficulty sleeping through the extended tail are common unsought effects.
LSD produces no physical dependence and has no established lethal dose in humans — rapid tolerance after consecutive doses makes compulsive redosing self-limiting.[2] The primary risk is psychological: high-dose experiences can produce acute panic, paranoid ideation, and dangerous behavior, scaling with dose and predisposition. LSD is well-characterized across eight decades of research, though long-term effects of repeated use and cardiac safety of chronic microdosing remain understudied.
History[edit]
Discovery
Albert Hofmann synthesized LSD on November 16, 1938 at Sandoz Laboratories in Basel, Switzerland, as the twenty-fifth compound in a series of lysergic acid derivatives.[4][2] Initial animal testing revealed nothing remarkable, and the compound was shelved for five years. On April 16, 1943, Hofmann inadvertently absorbed a trace quantity and experienced unusual perceptual disturbances; three days later he deliberately ingested 250 µg — several times the effective dose — in the first intentional psychedelic self-experiment under documented conditions.[2][5] Werner Stoll published the first clinical paper in 1947, and Sandoz subsequently marketed LSD as Delysid for psychiatric research.[6][2]
Prohibition and modern research
By the early 1960s, LSD had diffused beyond clinical settings into broader cultural use, catalyzed by figures including Timothy Leary and Ken Kesey. Regulatory backlash followed: Sandoz discontinued supply in 1965–1966, and the United States Controlled Substances Act of 1970 classified LSD as Schedule I. Clinical research effectively ceased worldwide for three decades. Systematic reinvestigation began with the first fully controlled modern study of LSD's acute effects at the University of Basel in 2015.[7] The Basel program, led by Matthias Liechti, has since produced the definitive modern pharmacological characterization of LSD, with multiple Phase 2 trials 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, making LSD one of the most intensively studied psychoactive compounds in history.[2] Therapeutic approaches ranged from psycholytic therapy (low-dose repeated sessions) to psychedelic therapy (single high-dose sessions) for conditions including alcoholism and treatment-resistant depression. Parallel to legitimate research, the CIA's Project MKUltra (1953 onward) investigated LSD as an interrogation tool, involving non-consensual administration to civilians and military personnel — one of the most significant ethical violations in the history of psychopharmacological research.
The name "LSD" derives from the German Lysergsäure-diäthylamid, abbreviated LSD-25 for the twenty-fifth compound in Hofmann's amide series. Common street names include "acid," "tabs," "blotter," and "Lucy." April 19 is informally commemorated as "Bicycle Day" — referencing Hofmann's bicycle ride home during his first intentional self-experiment, which has become the closest thing psychedelic culture has to a founding myth.
Chemistry[edit]
Structural class
LSD belongs to the ergoline family — tetracyclic alkaloids sharing an indole ring fused to a partially saturated quinoline system. The parent scaffold is lysergic acid, a naturally occurring compound produced by the ergot fungus (Claviceps purpurea). LSD is formed by bonding diethylamine to the carboxylic acid at C-8 of lysergic acid.[8]
The ergoline scaffold's rigid, pre-organized shape is the source of LSD's extraordinary potency — it locks the molecule into an optimal orientation for receptor binding, making LSD 100 to 1,000 times more potent by weight than simpler psychedelics such as psilocybin, DMT, or mescaline.[9]
Molecular identity
| Molecular formula | C₂₀H₂₅N₃O |
| Molecular weight | 323.4 g/mol |
The molecule contains four fused rings with three nitrogen atoms. No freely rotatable bonds exist within the core ring system, giving LSD high conformational rigidity — it arrives at the receptor already shaped to fit.[9]
Stereochemistry
LSD has two chirality centers, producing four possible stereoisomers. Only the (6aR,9R) form — d-LSD or (+)-LSD — is psychoactive. The mirror-image l-LSD is inactive at 5-HT₂A receptors.[2] iso-LSD, a common degradation product formed under heat, acid, or ultraviolet light, is also inactive.
Stability
LSD degrades readily under ultraviolet light, heat, and oxidative conditions, producing inactive breakdown products. Storage in amber glass at freezer temperatures under inert gas preserves potency.citation needed Clinical formulations have used tartrate oral solutions and ethanolic base solutions; the two are bioequivalent.[10]
Pharmacology[edit]
Mechanism of action
LSD produces its psychedelic effects primarily through partial agonism at 5-HT₂A serotonin receptors on cortical neurons.[2] This was confirmed definitively when the selective 5-HT₂A blocker ketanserin completely abolished all psychedelic effects of LSD at doses up to 200 µg in a controlled crossover study.[1]
Beyond 5-HT₂A, LSD activates a broad range of serotonin, dopamine, and adrenergic receptors.[2][8][11][9] Its dopamine receptor activity does not engage the brain's reward circuitry in the pattern associated with addictive drugs, consistent with LSD's negligible abuse potential.[2]
A defining structural feature explains LSD's unusually long duration: after LSD binds to the 5-HT₂A receptor, a protein loop (extracellular loop 2) folds over the binding pocket like a lid, trapping the molecule inside.[8][11] This produces exceptionally slow unbinding, meaning the receptor remains activated long after LSD has been cleared from the bloodstream — explaining why effects persist 8–12 hours despite a plasma half-life of only ~3.5 hours.
LSD also binds directly to TrkB, the brain's primary receptor for the growth factor BDNF, with affinity roughly 1,000-fold higher than conventional antidepressants.[12] This drives structural changes in neurons — new dendritic spines and synaptic connections — through a pathway independent of 5-HT₂A activation.[12][13] The dissociation is significant: TrkB engagement may underlie antidepressant effects while 5-HT₂A activation produces the hallucinogenic experience.
Pharmacokinetics
Oral bioavailability is approximately 80%, with LSD base and tartrate formulations confirmed bioequivalent.[10] Peak plasma concentration is reached within 1.1–1.4 hours at standard doses,[14] and plasma levels scale linearly across the 5–200 µg range.[15]
Intravenous administration produces stronger peak effects — including greater ego dissolution and anxiety — than oral dosing at equivalent amounts, consistent with faster receptor engagement.[10]
LSD is primarily broken down by the liver enzyme CYP2D6.[16][17] Individuals who metabolize CYP2D6 substrates poorly experience approximately 75% higher drug exposure, longer elimination, and more intense effects.[16] The terminal plasma half-life is approximately 2.7–3.6 hours.[14][15][3]
The hallmark pharmacological feature of LSD is the disconnect between plasma levels and effect duration: subjective effects outlast measurable blood concentrations by 4–8 hours.[8] This is explained by the lid mechanism described above, not by active metabolites or redistribution into tissues.
Neuroscience[edit]
Where it acts
LSD's most prominent neural effect is the dissolution of the default mode network (default mode network), the brain system responsible for self-referential thought and narrative identity. Under LSD, the DMN loses internal coherence and decouples from memory-related structures; the degree of this decoupling correlates directly with the subjective experience of ego dissolution.[18]
Simultaneously, the visual cortex receives increased blood flow while its normal regulatory rhythms weaken, forming novel connections with brain regions not typically involved in visual processing — accounting for the vivid hallucinations and the sense that imagination bleeds into perception.[18] Across the whole brain, LSD breaks down the modular boundaries between functional networks, producing a state of heightened global integration whose intensity tracks with ego dissolution scores and maps onto the cortical distribution of 5-HT₂A receptors.[5]
Why it matters
The entropic brain hypothesis proposes that LSD pushes brain activity past a critical threshold into a less constrained, higher-entropy state — weakening the ego, loosening habitual thought patterns, and increasing sensitivity to both internal and external stimuli.[19] The REBUS model extends this: psychedelics are thought to relax the brain's top-down predictions, allowing raw sensory and emotional information to reshape rigid beliefs — a mechanism that may explain therapeutic effects in depression and addiction.citation needed
Independently, LSD promotes structural neuroplasticity — the growth of new dendritic spines and synaptic connections in prefrontal cortex — via TrkB receptor binding at affinities far exceeding conventional antidepressants.[12][13] This positions LSD within the broader psychoplastogen hypothesis: the proposal that rapid-acting antidepressants work by physically rebuilding synaptic connections eroded by depression.
Several fundamental questions remain unresolved. LSD-assisted therapy produces sustained mood improvements lasting months after a single session,[20] but whether this durability reflects physical synaptic remodeling, enhanced cognitive flexibility, or psychological integration is unknown.
Subjective Effects[edit]
LSD produces a slow-onset, all-encompassing shift in perception, cognition, and emotion that unfolds in waves over its extended duration. At lower doses, effects center on sensory enhancement — intensified colors, sharpened music perception, mild geometric patterning — while the cognitive architecture remains largely intact. At higher doses, the experience becomes increasingly immersive: ego boundaries soften, thought takes on symbolic or recursive qualities, and the distinction between self and environment can dissolve entirely. Set and setting exert unusually powerful influence — pre-existing mood, physical environment, and social context shape the trajectory as strongly as any variable except dose itself.[21]
Compared to psilocybin at equivalent subjective intensity, LSD produces a longer and more analytically-toned experience with greater physical stimulation and cardiovascular activation.[3][22] Where psilocybin tends toward introspective, emotionally saturated states, LSD carries a characteristic lucidity and outward-directed curiosity — a distinction often described as the difference between being pulled inward and 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.
Auditory enhancement · Visual drifting · Visual morphing · Tracers · Touch enhancement · After-images · Light sensitivity · Color alteration · Brightness alteration · Holotropic state · Sound sensitivity · Visual haze / noise · Visual melting · Visual acuity enhancement · Environmental patterning · Peripheral vision distortion · Proprioceptive distortion · Visual diffraction · Depth perception distortion · Perspective distortion · Auditory misinterpretation · Spatial disorientation · Visual magnification · Peripheral misidentification · Vestibular distortion · Taste enhancement · Olfactory enhancement · Ganzfeld effect · Visual processing acceleration · Auditory distortion · Synesthesia · Symmetrical texture repetition · Flashbacks · Object activation · Internal hallucinations · Object transformations · Visual flipping · Perspective hallucinations · Environmental orbism / cubism · Visual recursion · Visual scenery slicing · External hallucinations · Auditory hallucinations · Persisting hallucinations · Shadow people
Touch enhancement · After-images · Light sensitivity · Color alteration · Brightness alteration · Holotropic state · Sound sensitivity · Visual haze / noise · Visual melting · Visual acuity enhancement · Environmental patterning · Peripheral vision distortion · Proprioceptive distortion · Visual diffraction · Depth perception distortion · Perspective distortion · Auditory misinterpretation · Spatial disorientation · Visual magnification · Peripheral misidentification · Vestibular distortion · Taste enhancement · Olfactory enhancement · Ganzfeld effect · Visual processing acceleration · Auditory distortion · Synesthesia · Symmetrical texture repetition · Flashbacks · Object activation · Internal hallucinations · Object transformations · Visual flipping · Perspective hallucinations · Environmental orbism / cubism · Visual recursion · Visual scenery slicing · External hallucinations · Auditory hallucinations · Persisting hallucinations · Shadow people
Stimulation · Body scan awareness · Body high · Appetite suppression · Spontaneous body sensations · Laughter fits · Physical fatigue · Tingling / electric sensations · Heart rate perception changes · Muscle tension · Vibrations / buzzing · Restlessness · Bodily lightness · Dehydration sensation · Tactile euphoria · Bodily pressures · Respiratory stimulation · Excessive sweating · Increased urination · Abnormal heartbeat · Body schema distortion · Nausea · Trembling · Dizziness · Nystagmus (eye wobbles) · Watery eyes · Breathing alteration · Pain suppression · Sexual arousal enhancement · Dry mouth · Bodily heaviness · Kundalini-like energy · Sexual arousal suppression · Vasoconstriction · Bruxism · Yawning · Headache · Involuntary body movements · Vomiting · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Appetite suppression · Spontaneous body sensations · Laughter fits · Physical fatigue · Tingling / electric sensations · Heart rate perception changes · Muscle tension · Vibrations / buzzing · Restlessness · Bodily lightness · Dehydration sensation · Tactile euphoria · Bodily pressures · Respiratory stimulation · Excessive sweating · Increased urination · Body schema distortion · Nausea · Trembling · Dizziness · Nystagmus (eye wobbles) · Watery eyes · Breathing alteration · Pain suppression · Sexual arousal enhancement · Dry mouth · Bodily heaviness · Kundalini-like energy · Sexual arousal suppression · Vasoconstriction · Bruxism · Yawning · Headache · Involuntary body movements · Vomiting · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Conceptual thinking · Novelty enhancement · Aesthetic enhancement · Introspection enhancement · Cognitive flexibility · Openness enhancement · Immersion enhancement · Creativity enhancement · Cognitive euphoria · Multiple thought streams · Increased nature relatedness · Focus suppression · Cognitive fatigue · Analysis enhancement · Humor enhancement · Language suppression · Confusion · Information processing enhancement · Memory fragmentation · Cognitive impairment · Memory suppression · Synchronicity · Memory replays · Information processing suppression · Cognitive dysphoria · Language enhancement · Motivation enhancement · Motivation suppression · Thought disorganization · Analysis suppression · Focus enhancement · Memory enhancement · Thought loops · Thought organization · Delusions of sobriety · Delusions · Amnesia · Delirium
Introspection enhancement · Cognitive flexibility · Openness enhancement · Immersion enhancement · Creativity enhancement · Cognitive euphoria · Multiple thought streams · Increased nature relatedness · Focus suppression · Cognitive fatigue · Analysis enhancement · Humor enhancement · Language suppression · Confusion · Information processing enhancement · Memory fragmentation · Cognitive impairment · Memory suppression · Synchronicity · Memory replays · Information processing suppression · Cognitive dysphoria · Language enhancement · Motivation enhancement · Motivation suppression · Thought disorganization · Analysis suppression · Focus enhancement · Memory enhancement · Thought loops · Thought organization · Delusions · Amnesia · Delirium
Emotional lability · Simultaneous emotions · Catharsis · Anxiety suppression · Irritability · Anxiety · Dysphoria · Paranoia
Anxiety suppression · Irritability · Anxiety · Dysphoria
Sociability enhancement · Communication suppression · Disinhibition · Automaticity · Compulsive behavior reduction · Derealization · Flow state · Ego inflation · Sociability suppression · Social disconnection · Depersonalization · Self-control enhancement · Boundary dissolution · Cognitive disconnection · Telepathic feelings · Ego dissolution · Identity alteration
Compulsive behavior reduction · Derealization · Flow state · Ego inflation · Sociability suppression · Social disconnection · Depersonalization · Self-control enhancement · Boundary dissolution · Cognitive disconnection · Telepathic feelings · Ego dissolution · Identity alteration
Time cessation
Transpersonal visions · Cessation · Near-death experience · Death-rebirth sequence · Entity contact · Non-dual awareness · Voidness
Entity contact · Non-dual awareness · Voidness
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
7 knownPersonal 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.
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 in humans (~100 mg oral) is roughly 1,000 times the standard active dose of 100 µg.safety citation needed No confirmed human death attributable solely to LSD's direct pharmacological effects has been documented in the medical literature.[2]
Deaths associated with LSD in forensic records typically involve polydrug ingestion, misidentified substances (particularly 25x-NBOMe compounds, which carry far greater toxicity), or behavioral causes such as 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.[23][7] No significant heart rhythm abnormalities have been documented at doses up to 200 µg, including during co-administration with the SSRI paroxetine.[17]
5-HT₂B and heart valve concern
LSD is structurally related to ergot drugs (pergolide, methysergide) known to cause heart valve damage through chronic stimulation of serotonin₂B receptors.[24] This concern applies primarily to repeated 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.[24] The risk is mechanistically plausible but clinically unconfirmed.
Controlled study safety
Across multiple controlled studies at the University of Basel, no serious adverse events have occurred at doses up to 200 µg.[23] Reported side effects are mild to moderate: nausea, headache, and anxiety — the latter mainly at the 200 µg dose.[23]
Psychological Risks
Hallucinogen persisting perception disorder (HPPD)
HPPD involves persistent visual disturbances after psychedelic use that cause functional impairment. Two forms are recognized: Type I (brief, intermittent flashbacks — generally harmless and self-limiting) and Type II (chronic, distressing perceptual changes with significant impact on daily life).[25]
LSD is the substance most commonly linked to HPPD in clinical reports.[26][25] It can occur after a single exposure. Risk factors include personal or family history of anxiety disorders, pre-existing psychiatric conditions, cannabis use, high doses, and frequent use.[25]
Flashbacks have been documented even in supervised clinical trial settings, with LSD more commonly associated with the phenomenon than psilocybin.[27]
Treatment options with reported benefit include benzodiazepines, levetiracetam, and clonidine.[28][26] Risperidone is contraindicated — it has been documented to worsen HPPD symptoms.[28]
Psychosis
A meta-analysis by Sabé et al. (2025) identified significant psychosis risk in persons with pre-existing psychotic disorders.[29] Personal or family history of schizophrenia or bipolar disorder type I is a standard exclusion criterion across all modern LSD clinical trials.
LSD at 200 µg impairs sensorimotor gating — a deficit that serves as a surrogate marker for psychosis vulnerability.[7]
Tolerance & Dependence
Tolerance: Near-complete tolerance to psychedelic effects develops within 3–4 days of consecutive dosing, driven by 5-HT₂A downregulation and desensitization.[2] Full reset occurs within 10–14 days. This rapid tolerance functionally prevents compulsive daily use.
Cross-tolerance: Complete and bidirectional between LSD and all other classical 5-HT₂A psychedelics (psilocybin, mescaline, DMT, 2C-x compounds).[2]
Physical dependence: None. LSD produces no withdrawal.[2]
Psychological dependence: Negligible. LSD does not sustain self-administration in animal models and 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 persons taking lithium — even at blood levels below the therapeutic range.[30] A retrospective analysis found seizures in roughly 47–49% of combined LSD+lithium reports (27 of 55 cases), with multiple requiring intensive care; no seizures occurred in LSD+lamotrigine reports (0 of 43).[31] This combination is absolutely contraindicated.
Tramadol carries serotonin syndrome risk through overlapping serotonergic activity — tramadol blocks serotonin reuptake while LSD directly stimulates serotonin receptors. Severe presentations can include dangerously high body temperature, muscle rigidity, and seizures.citation needed
SSRIs interact through two pathways: a metabolic component (certain SSRIs slow LSD breakdown via CYP2D6 inhibition) and a receptor component (chronic SSRI use reduces 5-HT₂A sensitivity). Paroxetine co-administration increased LSD blood levels by 40–50% at 100 µg without worsening subjective effects — paroxetine actually reduced anxiety and nausea.[17] Add-on LSD to SSRI therapy appears well-tolerated at 100 µg based on current data.[17]
MDMA presents theoretical serotonin syndrome risk from combined receptor stimulation and serotonin release, plus additive cardiovascular strain. No controlled data or case series exist for this combination.citation needed
MAOIs carry theoretical serotonin syndrome risk through impaired serotonin breakdown combined with direct receptor stimulation. Adequate washout from irreversible MAOIs is recommended before LSD use.citation needed
Contraindications
7 knownPersonal or family history of schizophrenia or psychotic disorder — absolute contraindication. LSD may trigger or worsen psychotic episodes in predisposed individuals; this is a standard exclusion in all modern clinical trials.[29][7]
Bipolar disorder type I — absolute contraindication (relative for bipolar II with careful assessment). Risk of triggering manic episodes.[29]
Current lithium therapy — absolute contraindication. Seizures documented even at below-therapeutic lithium levels.[30][31]
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.[23]
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
The critical testing concern for LSD is that blotter paper, the most common distribution form, cannot be visually distinguished from paper dosed with 25x-NBOMe compounds — substances with substantially greater toxicity and a documented fatality record at recreational doses. Ehrlich's reagent is the primary identification tool: LSD produces a purple/violet reaction, while NBOMe compounds produce none. A positive Ehrlich result confirms the presence of an indole-containing compound but does not confirm purity, dose, or the absence of additional substances.
For blotter specifically, dose precision is inherently limited — distribution across the paper is uneven, and stated doses from unregulated sources are unreliable. Liquid formulations offer marginally better dose control but still depend entirely on the accuracy of the original preparation.
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, emotional excitability, and expectations reliably predict whether the experience trends positive or negative.[21] The extended duration (8–12 hours plus residual stimulation) demands more environmental planning than shorter-acting psychedelics.
A familiar, physically safe, and comfortable space with minimal obligations for 12–16 hours is the baseline. A trusted, sober companion ("sitter") significantly reduces the risk of psychological distress escalating into crisis. Avoid unfamiliar social environments, crowds, and any setting that cannot be left safely if the experience becomes difficult.
Aftercare & integration. The day following 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 — particularly those involving ego dissolution or emotionally intense content — benefit from deliberate processing. Journaling within the first 24–48 hours captures insights before they fade. Conversation with someone familiar with psychedelic experiences can help contextualize difficult material. 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 rather than to explore them. 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 framework. SMART Recovery and other non-12-step programs offer evidence-based approaches 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 governing psychoactive substances. This classification — substances deemed to have high abuse potential and no recognized therapeutic use — has been adopted by virtually all signatory nations and forms the basis for domestic scheduling in most jurisdictions. Despite active clinical research programs and mounting evidence of therapeutic efficacy in anxiety, depression, and alcohol use disorder, no jurisdiction has rescheduled LSD for medical use as of April 2026.
| 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[32] |
| 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[33] |
| Canada | Schedule III (CDSA, 1996) | Possession: up to 3 years indictable; trafficking: up to 10 years; Section 56 ministerial exemptions for research[34] |
| Australia | Schedule 9 — Prohibited Substance (SUSMP) | No therapeutic use permitted; research requires TGA permit; same schedule as heroin[35] |
| 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 |
Switzerland occupies a distinctive regulatory position: while LSD remains a controlled substance, the Swiss regulatory framework has enabled the most productive modern LSD research program globally, with compassionate use provisions supporting clinical access in therapeutic contexts.
Frequently asked questions
What is LSD?
LSD is a semisynthetic ergoline psychedelic and 5-HT₂A partial agonist active at microgram doses, first synthesized by Albert Hofmann in 1938. Its receptor lid mechanism produces 8–12 hour effects; active Phase 2 trials target anxiety, depression, and alcohol use disorder.
How long does LSD last?
Total duration by route of administration — Oral: 7 – 12 hours. Ranges vary with dose and individual factors; see the duration table for onset, peak, and after-effect phases.
Where can I find dosage information for LSD?
Psychedex publishes a dosage table for LSD on this page covering these routes of administration: oral. Dose values are presented only in that table, always alongside their route of administration.
What are dangerous combinations with LSD?
The highest-severity documented interactions for LSD: MAOIs (Lethal), Dopamine agonists (Dangerous), GHB, Baclofen (Dangerous), GHB, GBL (Dangerous), Ibogaine (Dangerous). See the interactions section for the full list with mechanisms and severity levels.
Is LSD addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for LSD: tolerance builds rapid; full reset takes 14 days; cross-tolerance develops with psilocybin, mescaline, DMT, psilocin, 2C-B, 2C-E, 2C-I. See the article's dependence and safety sections for recorded dependence data.
external links
experience reports
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First-person accounts of subjective effects, timing, and outcomes — submitted for harm reduction.
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
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] ^abTagliazucchi 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]