LSA
lysergic acid amide
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LSA (lysergic acid amide) — also known as ergine — is a naturally-occurring psychedelic of the lysergamide class. It is the simplest chemical relative of LSD, roughly 10–25× less potent.[1] It activates serotonin receptors in the brain, producing perceptual shifts with an unusually strong sedative component compared to other classical psychedelics.[2]
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Albert Hofmann isolated LSA from ololiuqui seeds in 1960, identifying the chemical behind centuries of Mesoamerican ritual use.[3] In the 2000s, Hawaiian baby woodrose and morning glory seeds became widely marketed online as legal alternatives to LSD.[4] Today the compound is controlled in many countries, but the seeds that naturally contain it often are not.
Subjective effects include euphoria, visual hallucinations, dreamlike sedation, time alteration, introspective thought, and muscle weakness.[5] The experience is heavier and more inward-turning than LSD — a weighted, dreamlike state with less visual elaboration.[2] Nausea is nearly universal with seed preparations, and vasoconstriction discomfort adds to a demanding body load.[2]
LSA does not produce physical dependence, and no lethal dose has been established.[5] The primary physical danger is vasoconstriction — it caused one documented brain pressure crisis with seizures,[6] compounded by seed alkaloid content that varies up to 8.6-fold between products.[7] No controlled human study has been conducted; all evidence comes from case reports and structural comparison to LSD.[5]
History[edit]
Discovery
Albert Hofmann isolated LSA from ololiuqui (Turbina corymbosa) seeds in 1960, showing for the first time that ergot alkaloids occurred in flowering plants.[3] This resolved the chemical basis of centuries of Mesoamerican ritual use for healing and prophecy. Hofmann also self-experimented with the compound, confirming psychotomimetic properties at low milligram doses.[8]
Cultural and scientific significance
The ergot alkaloids in morning glory plants are not made by the plants themselves — they are produced by Periglandula, a fungus living inside the plant in obligate symbiosis.[9] In 2026, experimental work provided chemical support for the long-held hypothesis that the kykeon of ancient Greece's Eleusinian Mysteries was psychoactive through ergot-derived LSA.[10]
Modern era
LSA gained visibility in the 2000s as a "legal high," with Hawaiian baby woodrose and morning glory seeds sold through online vendors.[4] Adverse events including hospitalizations were recorded by pharmacovigilance systems,[4] and a fatal case prompted forensic investigation.[11] Survey data also identified LSA among psychedelics self-used by cluster headache patients for prevention,[12] though no clinical trial has ever been registered.[5]
Ololiuqui (Turbina corymbosa) and tlitlitzin (Ipomoea violacea) occupy a central place in Mesoamerican ethnobotany. Aztec and Mazatec practitioners used these seeds in ritual contexts for healing, prophecy, and communication with the spirit world, documented by Spanish colonial sources including Inquisition records.[3]
The name ergine derives from "ergot," reflecting the compound's origin in the Claviceps purpurea fungal alkaloid family. Ololiuqui is the Nahuatl term for the Turbina corymbosa vine whose seeds were the primary ritual source. LSA straddles ancient ceremonial use and contemporary grey-market commerce — an unusual position among psychedelics.
Chemistry[edit]
Structural class
LSA belongs to the ergoline chemical family — the same family as LSD and ergotamine. It is the simplest amide of lysergic acid: where LSD carries a diethylamide group, LSA carries a plain, unsubstituted amide.[13] That structural difference accounts for LSA's roughly 10–25× lower potency at serotonin receptors.[1]
Molecular properties
| Molecular formula | C₁₆H₁₇N₃O |
| Molecular weight | 267.33 g/mol |
Natural occurrence
LSA is not made by host plants — it is synthesized by Periglandula, a fungus living in obligate symbiosis inside Convolvulaceae species.[9] Principal LSA-containing species include:
- Turbina corymbosa (ololiuqui) — seeds used in Mesoamerican ritual
- Ipomoea violacea (morning glory)
- Argyreia nervosa (Hawaiian baby woodrose) — the most commonly consumed commercial source
Seeds also contain co-alkaloids including ergometrine, a potent uterotonic and vasoconstrictor.[7]
Pharmacology[edit]
Mechanism of action
LSA activates serotonin receptors in the brain — the same pathway engaged by LSD, psilocin, and DMT.[13][1] It has a relatively stronger pull toward a second serotonin receptor type that produces inhibitory effects,[1] likely explaining why the experience is heavier and more sedating than LSD. It also engages dopamine receptors, which is the likely source of its prominent nausea.[2][14]
Pharmacokinetics
No human pharmacokinetic study has been published for LSA. What is known comes from one forensic case and structural comparison to LSD.[5] Onset from seed ingestion spans 30–180 minutes depending on stomach contents and seed preparation.[5] Total effects last 4–10 hours, with residual effects possible up to 24 hours.[5]
A hydroxylated metabolite of LSA was identified in urine from the forensic case,[11] closely paralleling a known LSD metabolite produced by liver enzymes,[15] suggesting similar metabolic pathways.inferred
Neuroscience[edit]
Where it acts
As a serotonin receptor activator, LSA is expected to disrupt the same brain networks documented for LSD and psilocybin: reduced filtering of sensory information, increased connectivity across brain regions, and elevated neural activity.[13] No brain imaging study has been published for LSA — these patterns are inferred from shared mechanism.inferred
Why it matters
LSA's stronger affinity for the inhibitory serotonin receptor type may partially counteract the perceptual amplification typical of classical psychedelics,[16] explaining the heavier and less visually elaborate experience. Dopamine receptor engagement likely contributes to the sedation and nausea.[14][2]
Whether LSA promotes new neural connections — as more potent psychedelics may — is unknown. Its partial agonist profile raises the question of whether it triggers the same downstream processes.
- Does LSA's stronger inhibitory serotonin component produce measurably different brain network disruption compared to LSD?
- Does LSA promote new neural connections, or does its partial agonist profile fail to trigger the necessary downstream signaling?
- Does the shorter duration reflect faster receptor dissociation, faster metabolism, or both?
Subjective Effects[edit]
LSA's defining quality is a tension between psychedelic perception and deep sedation. Visual distortions and altered thought patterns arrive inside a heavy, dreamlike state that other classical psychedelics don't produce. The experience is inward-turning and somatic — less visual spectacle, more bodily weight and introspective pull.[2]
Compared to LSD, it occupies a lower-energy space — heavier, shorter, and less visually active. Compared to psilocin, it shares a similar duration but introduces a more demanding body load and more prominent nausea, trading psilocin's relative physical gentleness for a heavier somatic footprint.[2]
Effect Grid
At common doses, the full psychedelic experience develops: pronounced visual distortions including color enhancement, pattern recognition, drifting and morphing of surfaces, and closed-eye imagery. Thought connectivity increases significantly, producing novel associations and introspective insights. Emotional intensification is characteristic, with music and nature taking on heightened significance. Time distortion becomes marked.
The body load is substantial compared to tryptamine psychedelics — nausea, muscle weakness, physical sedation, and vasoconstriction (cold extremities, tingling) are prominent. Tremors and elevated blood pressure may occur. The overall character is "heavier" and more physically demanding than equivalent doses of LSD.
Functional impairment is significant. Sleep is unlikely for 6–8 hours after ingestion. The experience demands a committed setting with no obligations.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Light sensitivity · Depth perception distortion · Visual drifting · Auditory enhancement · Brightness alteration · Color enhancement · Geometry · Perspective distortion · Tracers · Symmetrical texture repetition · Peripheral misidentification · Auditory distortion · After-images · Auditory misinterpretation · Dreaming enhancement · Environmental patterning · Peripheral vision distortion · Proprioceptive distortion · Sound sensitivity · Spatial disorientation · Touch enhancement · Vestibular distortion · Visual haze / noise · Visual morphing · Visual processing acceleration · Visual diffraction · Visual melting · Visual acuity enhancement · Synesthesia · Visual acuity suppression · Taste enhancement · Flashbacks · Object transformations · Internal hallucinations · Visual scenery slicing · External hallucinations · Auditory hallucinations · Environmental orbism / cubism · Object activation · Perspective hallucinations · Visual processing suppression · Visual recursion · Persisting hallucinations
Brightness alteration · Color enhancement · Geometry · Perspective distortion · Tracers · Symmetrical texture repetition · Peripheral misidentification · Auditory distortion · After-images · Auditory misinterpretation · Dreaming enhancement · Environmental patterning · Peripheral vision distortion · Proprioceptive distortion · Sound sensitivity · Spatial disorientation · Touch enhancement · Vestibular distortion · Visual haze / noise · Visual morphing · Visual processing acceleration · Visual diffraction · Visual melting · Visual acuity enhancement · Synesthesia · Visual acuity suppression · Taste enhancement · Flashbacks · Object transformations · Internal hallucinations · Visual scenery slicing · External hallucinations · Auditory hallucinations · Environmental orbism / cubism · Object activation · Perspective hallucinations · Visual processing suppression · Visual recursion · Persisting hallucinations
Bodily heaviness · Muscle tension · Appetite suppression · Physical fatigue · Body scan awareness · Spontaneous body sensations · Dizziness · Body high · Temperature dysregulation · Dehydration sensation · Headache · Excessive sweating · Dry mouth · Heart rate perception changes · Tingling / electric sensations · Yawning · Tactile euphoria · Abnormal heartbeat · Involuntary body movements · Sexual arousal suppression · Increased urination · Stimulation · Wakefulness · Bodily pressures · Body schema distortion · Insomnia · Restlessness · Vibrations / buzzing · Breathing alteration · Diarrhea · Laughter fits · Nystagmus (eye wobbles) · Trembling · Vomiting · Watery eyes · Bodily dissociation · Tactile hallucination
Physical fatigue · Body scan awareness · Spontaneous body sensations · Dizziness · Body high · Dehydration sensation · Headache · Excessive sweating · Dry mouth · Heart rate perception changes · Tingling / electric sensations · Yawning · Tactile euphoria · Abnormal heartbeat · Involuntary body movements · Sexual arousal suppression · Increased urination · Stimulation · Wakefulness · Bodily pressures · Body schema distortion · Insomnia · Restlessness · Vibrations / buzzing · Breathing alteration · Diarrhea · Laughter fits · Nystagmus (eye wobbles) · Trembling · Vomiting · Watery eyes · Bodily dissociation · Tactile hallucination
Novelty enhancement · Thought connectivity · Thought loops · Immersion enhancement · Cognitive impairment · Cognitive euphoria · Language suppression · Memory suppression · Thought acceleration · Aesthetic enhancement · Cognitive fatigue · Cognitive flexibility · Confusion · Focus suppression · Multiple thought streams · Openness enhancement · Increased nature relatedness · Thought disorganization · Humor enhancement · Analysis enhancement · Creativity enhancement · Analysis suppression · Information processing suppression · Memory fragmentation · Memory replays · Motivation suppression · Thought deceleration · Cognitive dysphoria · Synchronicity · Delusions · Delirium
Immersion enhancement · Cognitive impairment · Cognitive euphoria · Language suppression · Memory suppression · Thought acceleration · Aesthetic enhancement · Cognitive fatigue · Cognitive flexibility · Confusion · Focus suppression · Multiple thought streams · Openness enhancement · Increased nature relatedness · Thought disorganization · Humor enhancement · Analysis enhancement · Creativity enhancement · Analysis suppression · Information processing suppression · Memory fragmentation · Memory replays · Motivation suppression · Thought deceleration · Cognitive dysphoria · Synchronicity · Delirium
Euphoria · Simultaneous emotions · Empathy enhancement · Catharsis · Dysphoria · Irritability
Dysphoria · Irritability
Communication suppression · Disinhibition · Sociability suppression · Automaticity · Flow state · Ego inflation · Boundary dissolution · Cognitive disconnection · Identity alteration · Ego dissolution · Telepathic feelings
Flow state · Ego inflation · Boundary dissolution · Cognitive disconnection · Identity alteration · Ego dissolution · Telepathic feelings
Time cessation
Entity contact · Non-dual awareness · Transpersonal memory access · Death-rebirth sequence · Voidness · Near-death experience
Voidness · Near-death experience
Recursive awareness
Timeline
First alerts emerge as mild somatic awareness — abdominal unease, slight heaviness, and faint mood shift. Nausea frequently appears before any psychoactive effects, reflecting early D2 receptor engagement.
Psychoactive effects build gradually: visual brightening, color enhancement, increasing body load, and growing nausea. The sedating character becomes apparent, distinguishing the trajectory from LSD or psilocybin come-ups.
Maximum intensity of visual distortion, thought alteration, emotional amplification, and ego softening. Nausea typically subsides during peak but body load — muscle weakness, heaviness, vasoconstriction — persists. The experience is more introspective and sedating than stimulating.
Effects stabilize at reduced intensity. Visual and cognitive alterations remain present but manageable. Physical sedation and muscle weakness may dominate.
Gradual return toward baseline cognition and perception. Residual visual brightening and mild thought alteration persist. Physical fatigue and muscle weakness may intensify as psychoactive effects recede.
Residual mood changes, mild fatigue, and subtle perceptual shifts may persist for 6–24 hours. Physical recovery from vasoconstriction and muscle weakness continues. Some users report lingering introspective clarity.
Safety[edit]
- Acute toxicity
- Low
- 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 · psilo · mesc
Toxicity
No lethal dose has been established for LSA in humans or animals.[5]
Vasoconstriction and blood pressure
LSA narrows blood vessels — a property of the ergoline chemical family — and raises blood pressure.[5][6]
One case saw this escalate into a brain pressure crisis with concurrent seizures — Posterior Reversible Encephalopathy Syndrome (PRES) — when blood pressure rose faster than the brain's circulation could compensate.[6] This is the only published case of LSA-induced PRES.
Dose unpredictability
Alkaloid content in Argyreia nervosa products ranges from 3–15 µg per raw seed to ~34 µg per commercial capsule, with 8.6-fold variability between products.[7] Seeds also contain ergometrine — a potent uterotonic and vasoconstrictor — adding unpredictable effects beyond LSA itself.
Fatal case
One death has been attributed to behavioral consequences of LSA intoxication: an individual fell from a building during a psychotomimetic state.[11] Cannabis and alcohol were also present. The fatality resulted from disinhibited behavior, not direct pharmacological toxicity.
Psychological risks
Acute panic, hallucinations, and impaired reality testing are documented.[11][4] French pharmacovigilance data recorded 4 cases of unintended psychological effects, with 2 requiring hospitalization.[4]
Post-use suicidal thoughts and psychosis-like states requiring hospitalization have been reported.[2] Pre-existing mental health conditions and polysubstance use complicate these cases; no controlled data exist.
Tolerance & dependence
LSA produces rapid tolerance through serotonin downregulation — significant decreases in receptor availability within days, with recovery in roughly 96 hours.[17][18] This tolerance is shared across classical psychedelics: prior LSD or psilocybin use reduces LSA's effects, and vice versa.[18]
No dependence syndrome, compulsive use pattern, or withdrawal has been identified. The rapid tolerance mechanism itself acts as a biological deterrent to frequent dosing.
Drug interactions
Combining LSA with serotonin-active drugs — MAOIs, SSRIs, SNRIs, tramadol — adds serotonergic load that can trigger a dangerous overheating and seizure response.safety citation needed The ergoline scaffold adds a second risk: combining with triptans, ergotamine derivatives, or stimulants compounds vasoconstriction, raising the risk of blood pressure crisis or brain injury such as PRES.[6]
Lithium combined with classical psychedelics has been associated with seizures and prolonged psychotic states in case reports.safety citation needed No published drug interaction study exists for LSA with any co-administered substance.
Contraindications
Absolute:
- Pregnancy and breastfeeding: Seeds contain ergometrine, a uterine stimulant with abortifacient risk. This applies specifically to seed-based preparations; purified LSA's reproductive toxicity is unevaluated.safety citation needed
Relative:
- High blood pressure and heart disease: Ergoline-class vasoconstriction is documented via case reports.[6]
- Cerebrovascular disease: PRES is a direct documented complication from LSA's vasoconstrictive mechanism.[6]
- Personal or family history of psychotic disorders: Psychosis-like states documented post-LSA use.[2]
- Seizure disorders: The PRES case involved seizures, suggesting threshold lowering is possible.[6]
- Concurrent serotonergic medication: serotonin syndrome risk from combined serotonergic activity.
Harm Reduction[edit]
Forms & Identification
LSA reaches users almost exclusively through plant seeds rather than as a purified compound. Alkaloid content varies several-fold between individual seeds, batches, and species — seed-count dosing is an approximation at best.
Commercial "standardized" capsules offer no reliable consistency guarantee. Seeds treated with pesticides, fungicides, or anti-germination coatings carry ingestion risks unrelated to LSA itself.
Guidelines
- Test any seed product with appropriate reagent kits before ingestion.
- Start with a fraction of any reported dose — alkaloid content varies dramatically between seeds and batches.
- Avoid eating for 2–3 hours before ingestion to reduce nausea.
- Keep a basin, water, and electrolytes within reach; nausea and vomiting are expected.
- Choose a physically safe environment — no heights, no access to balconies or rooftops, no driving.
- Have a sober sitter present who knows what has been taken and when.
- Avoid redosing during the experience; effects may still be building at 2–3 hours.
- Clear all obligations for 24 hours — residual effects can persist well beyond the primary experience.
Set & Setting
LSA's heavy sedation and body load make physical comfort a priority. A familiar, quiet indoor space with bathroom access reduces both physical and psychological risk. The 4–10 hour duration, with residual effects up to 24 hours, requires clearing a full day.
A sober sitter is strongly recommended, given documented impaired judgment and risk of dangerous behavior during intense experiences.
Aftercare & integration. LSA's physical demands can leave users feeling drained. Prioritize sleep, hydration, and light food in the 24 hours following. Physical symptoms — muscle weakness, residual nausea — typically resolve within a day.
LSA's introspective character can surface emotionally intense material. Journaling or discussing the experience with a trusted person within the first few days helps consolidate insights and process difficult content. If distressing thoughts, perceptual disturbances, or mood instability persist beyond a week, consult a mental health professional — ideally one familiar with psychedelic experiences.
Recovery & Support
LSA does not produce physical dependence, and compulsive use patterns are not documented. If LSA use has become a recurring coping mechanism or is causing distress, support is available through psychedelic integration therapists, harm reduction organizations such as the Fireside Project (62-FIRESIDE), and general substance use support services including SAMHSA's helpline (1-800-662-4357).
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Discomfort, nausea, and anxiety are common and not emergencies. Seek immediate help for: severe headache with vision changes (possible blood pressure crisis), seizures, chest pain, complete disconnection from reality with self-harm risk, or loss of consciousness.
- Call emergency services immediately if any of the above are present.
- Keep the person in a safe, open area away from heights and sharp objects. Do not restrain unless there is immediate danger of self-harm.
- If unconscious and breathing, place in the recovery position (on their side, airway clear).
- Do not induce vomiting.
- Monitor breathing and responsiveness continuously while waiting for help.
What to tell the dispatcher: Name the substance (LSA, from the specific seed type if known), approximate amount and time of ingestion, current symptoms, and any other substances consumed. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
Legal Status[edit]
The legal status of LSA varies sharply by jurisdiction — in many countries the pure compound is controlled while the seeds that contain it remain legal, a gap that has facilitated the "legal high" market.[4]
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule III (Controlled Substances Act) | Listed as a depressant despite psychedelic mechanism; pure compound controlled; seeds containing LSA are legal to possess[19] |
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Controlled as LSD precursor; maximum penalties equivalent to other Class A substances[19] |
| Netherlands | Controlled substance | Possession, distribution, and production without license prohibited[19] |
| Sweden | Controlled substance | Listed since May 2007[19] |
| Canada | Not scheduled (CDSA) | Plants and seeds uncontrolled; selling as human drug likely prohibited under the Food and Drugs Act[19] |
| New Zealand | Controlled (chemical) | Pure compound controlled; plants and seeds legal to possess, cultivate, and distribute[19] |
| Australia | State-level prohibition | Most states prohibit consumption of LSA-containing plant materials[19] |
| Hungary | Not classified | Legal per available sources[19] |
The US classification of LSA as a Schedule III "depressant" is a historical artifact predating pharmacological characterisation of its mechanism; the compound is pharmacologically a serotonergic psychedelic, not a CNS depressant.[19]
Legal status data for Germany and most EU member states outside the Netherlands and Sweden could not be confirmed from official government or peer-reviewed sources.citation needed
Legal status changes frequently and varies within jurisdictions. This information may be outdated. Nothing here constitutes legal advice.
references
- [1] ^abcdPaulke A, Kremer C, Wunder C, Achenbach J, Djahanschiri B, Elias A, Schwed JS, Hubner H, Gmeiner P, Proschak E, Toennes SW, Stark H (2013) Argyreia nervosa (Burm. f.): receptor profiling of lysergic acid amide and other potential psychedelic LSD-like compounds by computational and binding assay approaches — Journal of Ethnopharmacology doi:10.1016/j.jep.2013.04.044
- [2]
- [3] ^abcHofmann A, Tscherter H (1960) Isolation of lysergic acid alkaloids from the Mexican drug ololiuqui (Rivea corymbosa (L.) Hall.f.) — Experientia PMID:13715089
- [4]
- [5] ^abcdefghiCastro PSCC, Leopoldo K, Pedro MOP, Takitane J, Bombana HS, Negrao AB, Scholz JR, Castaldelli-Maia JM (2025) Lysergic Acid Amide (LSA), an LSD Analog: Systematic Review of Pharmacological Effects, Adverse Outcomes, and Therapeutic Potentials — Pharmacy (Basel, Switzerland) doi:10.3390/pharmacy13040098
- [6] ^abcdefgLegriel S, Bruneel F, Spreux-Varoquaux O, Birenbaum A, Chadenat ML, Mignon F, Abbosh N, Henry-Lagarrigue M, Revault D'Allonnes L, Guezennec P, Troche G, Bedos JP (2008) Lysergic Acid Amide-Induced Posterior Reversible Encephalopathy Syndrome with Status Epilepticus — Neurocritical Care doi:10.1007/s12028-008-9096-5