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Acetylcholine systemHyoscyamus niger
Black henbane (Hyoscyamus niger L., Solanaceae) is a toxic herbaceous plant whose preparations act as anticholinergic deliriants. Its dominant psychoactive alkaloids are scopolamine (hyoscine) and hyoscyamine, both of which block muscarinic acetylcholine receptors throughout the nervous system.[1] Scopolamine drives the central effects — sedation, amnesia, and delirium — by suppressing cholinergic signaling across the brain.[2]
Black henbane (Hyoscyamus niger L., Solanaceae) is a toxic herbaceous plant whose crude preparations function as anticholinergic deliriants. Its principal psychoactive alkaloids, scopolamine and hyoscyamine, are competitive muscarinic acetylcholine receptor antagonists.[1] Scopolamine drives the central nervous system effects — sedation, amnesia, and delirium — by blocking muscarinic signaling across cortical and subcortical brain regions.[2]
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Acetylcholine systemArchaeological evidence places deliberate human use of H. niger at least as far back as 4,000 BC.[3] Greek priests used it at oracular sites, medieval Europeans added it to beer and flying ointments, and its alkaloids were eventually isolated and developed into modern pharmaceuticals. The plant remains unscheduled under international drug treaties, though some jurisdictions impose restrictions.[4]
Subjective effects include delirium, visual and auditory hallucinations, amnesia, and severe cognitive disorientation. The defining quality is anticholinergic delirium — a non-lucid, agitated state in which the person cannot distinguish hallucination from reality and has no awareness of being intoxicated.[5] Peripheral effects — dilated pupils, rapid heart rate, dry mouth, and urinary retention — accompany every psychoactive dose.
No dependence or withdrawal has been documented; the aversive nature of anticholinergic delirium strongly limits voluntary repeat use.[6] The margin between a psychoactive dose and a dangerous one is narrow and unpredictable — alkaloid content varies enormously across strains, plant parts, and growing conditions.[5] No clinical trials have tested crude preparations, and how the alkaloids behave in the body after plant ingestion remains uncharacterized.[7]
History[edit]
Traditional and historical use
Formally described by Carl Linnaeus in 1753,[8] H. niger has documented human use stretching back at least 4,000 years.[3] In Greek antiquity it was known as Herba Apollinaris and used by oracular priests at Delphi to induce trance states; Dioscorides documented it as a sedative and analgesic.[3] Seeds recovered from a Viking grave at Fyrkat, Denmark have prompted speculation about its role in the berserker states described in Norse sagas — though this remains unconfirmed.[3]
Medieval and early modern use
In medieval Europe, henbane was added to beer before hops became standard; the Bavarian Purity Law of 1516 effectively ended the practice.[3] It also appeared in transdermal "flying ointments" associated with witchcraft — the anticholinergic delirium those preparations produced, including vivid sensations of flight, likely gave rise to broomstick-riding folklore.[3] Teodorico Borgognoni incorporated narcotic plants including henbane in medieval surgical anesthetics,[9] and contemporary ethnobotanical surveys document continued traditional medicinal use among Tashelhit-speaking communities in Morocco.[10]
Pharmaceutical development
The isolation of hyoscyamine and scopolamine in the 19th and 20th centuries transformed henbane from a folk remedy into a pharmaceutical source. Scopolamine became one of the first medications delivered via a transdermal patch — for motion sickness prevention.[2] Both alkaloids now appear on the WHO List of Essential Medicines, though commercial production has shifted to hybrid Duboisia crops cultivated in Australia.[11]
Henbane's common names reflect its history: "stinking nightshade" references its foetid smell; "henbane" derives from the Anglo-Saxon hennebana ("hen-killer"), reflecting its known toxicity to poultry. Its association with witchcraft, poison, and oracular prophecy recurs across classical, medieval, and early modern literature — from Dioscorides to Shakespeare. Plants with cholinergic antagonist properties — including henbane — were recorded for amnesia-inducing effects long before the cholinergic hypothesis of Alzheimer's disease was established.[12]
Botanical Overview[edit]
Hyoscyamus niger L. belongs to the family Solanaceae — the nightshades — sharing this family with Atropa belladonna, Datura stramonium, tobacco, and tomato. The genus Hyoscyamus contains approximately 20 species distributed across the Mediterranean, Middle East, and central Asia. H. niger is the species most widely documented for both medicinal and psychoactive use.
The plant is native to the Mediterranean basin and western Asia but has naturalized across much of Europe, northern Africa, and temperate North America. Several US states and Canadian provinces classify it as a noxious weed.[13] It favours disturbed ground, roadsides, and waste areas with well-drained, nitrogen-rich soil.
H. niger grows as an annual or biennial herb, reaching 30–100 cm tall. Its leaves are large, coarsely toothed, and covered in sticky glandular hairs that produce a strong unpleasant odour — hence "stinking nightshade." Flowers are funnel-shaped and pale yellow with dark purple veining. The seeds are small and kidney-shaped, easily mistaken for poppy or mustard seedscitation needed — the plant part most often involved in accidental poisonings. All parts contain tropane alkaloids, with seeds and roots carrying the highest concentrations.[5][1]
Alkaloid Profile[edit]
The psychoactive and toxic properties of H. niger are driven by two tropane alkaloids: scopolamine (hyoscine) and hyoscyamine. Both block muscarinic acetylcholine receptors throughout the nervous system.[1] Scopolamine crosses the blood-brain barrier more readily and is responsible for the sedation, amnesia, and delirium that characterize henbane intoxication.
Hyoscyamine — whose racemic mixture form is the pharmaceutical atropine — exerts predominantly peripheral effects at lower doses, with central effects appearing only at higher concentrations.[1][5] Minor alkaloids including atroscine and cuscohygrine are present but contribute minimally to the overall pharmacological profile.citation needed
Alkaloid content varies dramatically across plant parts, geographic strains, and growing conditions — more than 10-fold between European and Egyptian populations.[5] This variability is the main reason dose prediction from crude plant material is clinically unreliable. The European Food Safety Authority set a group Acute Reference Dose of 0.016 µg/kg body weight for the combined alkaloids[14] — a threshold so low that trace food contamination can exceed it, particularly for young children.[14]
Neuroscience[edit]
Where it acts
Scopolamine and hyoscyamine block muscarinic acetylcholine receptors across the central and peripheral nervous system.[1] In the body's periphery, this produces dilated pupils, rapid heart rate, dry skin, and suppressed gut motility. In the brain — particularly the cortex and hippocampus — it disrupts cholinergic circuits, producing the sedation, amnesia, and delirium that define the H. niger experience.[2]
What it changes
Scopolamine's disruption of hippocampal signaling causes profound anterograde amnesia — users typically retain no memory of events during intoxication. At toxic doses, the state shifts from sedation to excited delirium with fully formed visual, auditory, and tactile hallucinations. Scopolamine is broken down in the liver and crosses both the blood-brain barrier and the placenta.[2]
No neuroimaging studies of H. niger intoxication have been published. How the alkaloids behave in the body after ingestion of crude plant material — oral tea, seed ingestion, smoked preparations — remains entirely uncharacterized. The scopolamine-to-hyoscyamine ratio varies across wild populations, but no systematic study has quantified this variation for predicting psychoactive potency or toxicity risk.
Subjective Effects[edit]
The experience produced by H. niger is fundamentally unlike the visionary or introspective states associated with serotonergic psychedelics or dissociatives. Anticholinergic delirium is a non-lucid condition: the person loses all insight into being intoxicated, interacts with phantom people and objects, and cannot distinguish hallucination from reality. Set and setting exert minimal moderating influence — the delirious state overrides environmental awareness entirely. Alkaloid variability across geographic strains and plant parts is the dominant unpredictable modifier of intensity.
Among anticholinergic deliriants, H. niger is most comparable to Datura stramonium and Atropa belladonna, sharing the same tropane alkaloid pharmacology and clinical presentation. Henbane's relatively high scopolamine-to-hyoscyamine ratio produces a more sedative and amnestic profile than atropine-dominant species — though all three plants produce the same core anticholinergic syndrome at toxic doses.[15] Reported hallucinations commonly include conversations with absent persons, interaction with non-existent objects, and phantom activities such as cigarette smoking.[15]
Archaeological evidence places deliberate human use of H. niger at least as far back as 4,000 BC in southern and central Europe.[3] The plant served as a sedative, ritual intoxicant, and brewing additive through the classical and medieval periods before its alkaloids were isolated and developed into modern pharmaceuticals. It remains unscheduled under international drug treaties, though individual jurisdictions impose restrictions.[4]
Subjective effects include delirium, visual and auditory hallucinations, amnesia, sedation, and severe cognitive disorientation. The defining quality is anticholinergic delirium — a non-lucid, agitated state in which the user cannot distinguish hallucination from reality and has no awareness of intoxication.[5] Peripheral effects — pupil dilation, tachycardia, dry mouth, and urinary retention — accompany all psychoactive doses.
No tolerance, dependence, or withdrawal data exist for H. niger; the aversive nature of anticholinergic delirium strongly limits voluntary repeat use.[6] The margin between psychoactive and life-threatening doses is narrow and clinically unreliable, driven by extreme alkaloid variability across strains, plant parts, and growing conditions.[5] No clinical trials have been conducted using crude H. niger preparations, and pharmacokinetics of plant-derived alkaloid ingestion remain uncharacterized.[7]
History[edit]
Traditional and historical use
Hyoscyamus niger was formally described by Carl Linnaeus in Species Plantarum (1753),[8] though archaeological evidence documents deliberate human use dating to at least 4,000 BC.[3] Seeds have been recovered from 65 of 83 Roman-period archaeological sites in the Netherlands, and a hollowed bone containing over 1,000 seeds — dated to approximately AD 70–100 — suggests deliberate medicinal or ritual storage.[3]
In Greek antiquity the plant was known as Herba Apollinaris and used by oracular priests and priestesses — including at Delphi — to induce trance states.[3] Dioscorides documented it as a sedative and analgesic in De Materia Medica, while Pliny the Elder described it as "of the nature of wine and therefore offensive to the understanding".[3] Seeds recovered from a Viking grave at Fyrkat, Denmark have prompted speculation that anticholinergic intoxication may have contributed to the berserker states described in Norse sagas, though this remains unconfirmed.[3]
Medieval and early modern use
In medieval Europe, H. niger became a documented ingredient in transdermal "flying ointments" associated with witchcraft — the anticholinergic delirium they produced, including sensations of flight, likely gave rise to broomstick-riding folklore.[3] The plant also served as a beer additive in the herbal mixture called gruit before hops became standard; the Bavarian Purity Law of 1516 (Reinheitsgebot) effectively ended its use in brewing.[3]
Teodorico Borgognoni (1205–1296) included narcotic plants — likely including henbane — in his surgical anesthetic preparations.[9] Shakespeare referenced henbane in Hamlet as the poison used to murder Hamlet's father, reflecting its established reputation in Elizabethan England. Ibn Sina (Avicenna, 980–1037 AD) described H. niger in the Canon of Medicine for pain suppression, including toothache and joint pain,citation needed and contemporary ethnobotanical surveys document its continued traditional medicinal use among High Atlas Tashelhit-speaking communities in Morocco.[10]
Pharmaceutical development
The isolation of hyoscyamine and scopolamine in the 19th and 20th centuries transformed H. niger from a folk remedy into a source of clinical-grade pharmaceutical agents. Scopolamine became one of the first drugs delivered via a transdermal patch system for motion sickness prevention.[2] Both alkaloids now appear on the WHO List of Essential Medicines, though commercial-scale production has shifted from H. niger to hybrid Duboisia myoporoides × D. leichhardtii crops cultivated in Australia.[11]
Henbane's long entanglement with European folk culture is preserved in its common names: "stinking nightshade" references its foetid smell; "henbane" derives from the Anglo-Saxon hennebana ("hen-killer"), reflecting its known toxicity to poultry. The plant's association with witchcraft, poison, and oracular prophecy recurs across classical, medieval, and early modern literature — from Dioscorides to Shakespeare — making it one of the most culturally embedded toxic plants in Western history. Plants containing cholinergic antagonists, including henbane, were recorded historically for amnesia-inducing properties long before the cholinergic hypothesis of Alzheimer's disease was established.[12]
Botanical Overview[edit]
Hyoscyamus niger L. belongs to the family Solanaceae (nightshades), sharing its family with Atropa belladonna, Datura stramonium, tobacco, and tomato. The genus Hyoscyamus contains approximately 20 species distributed across the Mediterranean, Middle East, and central Asia; H. niger is the most widely documented species for both medicinal and psychoactive use.
The plant is native to the Mediterranean basin and western Asia but has naturalized across much of Europe, northern Africa, and temperate North America, where several US states and Canadian provinces classify it as a noxious weed.[13] It favours disturbed ground, roadsides, field margins, and waste areas with well-drained, nitrogen-rich soil.
H. niger grows as an annual or biennial herb, reaching 30–100 cm in height. Its leaves are large, ovate, and coarsely toothed with a sticky, glandular-hairy surface that produces a distinctive unpleasant odour — hence the common name "stinking nightshade." Flowers are funnel-shaped, pale yellow with prominent dark purple veining, and arranged in one-sided terminal clusters. The fruit is a capsule (pyxis) enclosed in the persistent calyx, containing numerous small, kidney-shaped seeds — the plant part most frequently implicated in accidental poisonings due to their resemblance to poppy or mustard seeds.citation needed
All parts of the plant contain tropane alkaloids, but concentration varies significantly by tissue: seeds and roots typically carry the highest alkaloid loads, while leaves and flowers contain lower but still pharmacologically active quantities.[5][1] Potency also varies substantially across geographic populations — alkaloid content can differ more than 10-fold between European and Egyptian strains.[5]
Alkaloid Profile[edit]
The psychoactive and toxic properties of H. niger are driven by two tropane alkaloids: scopolamine (hyoscine) and hyoscyamine. Both are muscarinic acetylcholine receptor antagonists, but they differ sharply in their central-to-peripheral effect balance.[1] Scopolamine crosses the blood-brain barrier more readily and is responsible for the sedation, amnesia, and delirium that characterize henbane intoxication. Hyoscyamine — whose racemic mixture form is the pharmaceutical agent atropine — exerts predominantly peripheral effects at lower doses, with central effects emerging only at higher concentrations.[1][5]
The ratio of scopolamine to hyoscyamine in H. niger varies substantially with plant part, geographic origin, and growing conditions. Alkaloid content can differ more than 10-fold between European and Egyptian populations,[5] making this variability the single most important factor rendering dose prediction from crude plant material clinically unreliable. Seeds and roots generally carry the highest alkaloid concentrations, while leaves and flowers contain lower but pharmacologically active quantities.
Minor tropane alkaloids present in H. niger include atroscine and cuscohygrine, though these contribute minimally to the overall pharmacological profile relative to the two dominant alkaloids. The pharmacological significance of these minor constituents in crude preparations has not been systematically studied.citation needed
The European Food Safety Authority established a group Acute Reference Dose of 0.016 µg/kg body weight for the sum of hyoscyamine and scopolamine.[14] This threshold is so low that even trace contamination of food products with H. niger seeds can exceed safe exposure limits — particularly for toddlers, where dietary exposure exceeded the ARfD on 11–18% of consumption days in limited EU data.[14]
Neuroscience[edit]
Where it acts
Scopolamine and hyoscyamine block muscarinic acetylcholine receptors (M1, M2, M3) across both the central and peripheral nervous system.[1] Peripheral blockade produces the physical signs of anticholinergic toxidrome: dilated pupils, tachycardia, dry skin, and suppressed gut motility. Central blockade — driven primarily by scopolamine — disrupts cholinergic circuits in the cortex and hippocampus, producing the sedation, amnesia, and delirium that define the H. niger experience.[2]
What it changes
Scopolamine's disruption of hippocampal cholinergic signaling produces profound anterograde amnesia — users frequently retain no memory of events during intoxication. At toxic doses, the balance shifts from sedation to excited delirium with fully formed visual, auditory, and tactile hallucinations. Scopolamine is metabolized primarily via glucuronide conjugation and CYP3A4-mediated oxidative demethylation, and crosses both the blood-brain barrier and the placenta.[2]
No neuroimaging studies of H. niger intoxication have been published. The pharmacokinetics of alkaloids consumed via crude plant material — oral tea, seed ingestion, smoked preparations — remain entirely uncharacterized. The scopolamine-to-hyoscyamine ratio varies across wild populations, but no comprehensive study has quantified this variability for predicting psychoactive potency or toxicity risk.
Subjective Effects[edit]
The experience produced by H. niger is fundamentally unlike the visionary or introspective states associated with serotonergic psychedelics or dissociatives. Anticholinergic delirium is a non-lucid condition: the user loses all insight into being intoxicated, interacts with phantom persons and objects, and cannot distinguish hallucination from reality. Set and setting exert minimal moderating influence because the delirious state overrides environmental awareness. Preparation type modulates onset and duration but not the fundamental character; the extreme variability in alkaloid content across geographic strains and plant parts is the dominant unpredictable modifier of intensity.
Among anticholinergic deliriants, H. niger is most closely comparable to Datura stramonium and Atropa belladonna, sharing the same tropane alkaloid pharmacology and clinical presentation. Its relatively high scopolamine-to-hyoscyamine ratio produces a more sedative and amnestic profile compared with atropine-dominant species, though all three plants produce the same core anticholinergic syndrome at toxic doses. Reported hallucinations commonly include conversations with absent persons, interaction with non-existent objects, and phantom activities such as cigarette smoking.[15]
Effect Grid
There is no common recreational dose for Hyoscyamus niger. All documented psychoactive exposures in published literature are poisoning cases — either accidental ingestion or deliberate consumption resulting in anticholinergic toxidrome. The concept of a common dose implies a dose range used with some regularity and predictability, neither of which applies here.
Alkaloid content varies more than 10-fold between geographic strains. The same mass of plant material from different origins can produce effects ranging from barely perceptible to life-threatening. This variability makes any common dose range clinically meaningless.
Published clinical series describe the full anticholinergic syndrome — delirium, amnesia, external hallucinations, tachycardia, mydriasis — as the typical presentation, not a dose-dependent spectrum.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Sleep-transition hallucinations · Depth perception distortion · Peripheral misidentification · Vestibular distortion · Visual haze / noise · Auditory distortion · Auditory misinterpretation · Peripheral vision distortion · Dreaming enhancement · Proprioceptive distortion · External hallucinations · Auditory hallucinations · Shadow people · Visual processing suppression · Object activation · Internal hallucinations · Object transformations
Visual haze / noise · Auditory distortion · Auditory misinterpretation · Peripheral vision distortion · Dreaming enhancement · Proprioceptive distortion · External hallucinations · Auditory hallucinations · Shadow people · Visual processing suppression · Object activation · Internal hallucinations · Object transformations
Temperature dysregulation · Dehydration sensation · Dizziness · Heart rate perception changes · Restlessness · Breathing alteration · Physical fatigue · Sedation · Insomnia · Muscle relaxation · Nausea · Nausea suppression · Stimulation · Wakefulness · Body schema distortion · Involuntary body movements · Nystagmus (eye wobbles) · Pain suppression · Trembling · Vomiting · Tactile hallucination · Bodily dissociation
Restlessness · Breathing alteration · Physical fatigue · Sedation · Insomnia · Muscle relaxation · Nausea · Nausea suppression · Stimulation · Wakefulness · Body schema distortion · Involuntary body movements · Nystagmus (eye wobbles) · Pain suppression · Trembling · Vomiting · Tactile hallucination · Bodily dissociation
Memory fragmentation · Analysis suppression · Information processing suppression · Memory suppression · Thought disorganization · Cognitive dysphoria · Cognitive fatigue · Language suppression · Suggestibility enhancement · Motivation suppression · Thought deceleration · Amnesia · Delirium · Delusions
Memory suppression · Thought disorganization · Cognitive dysphoria · Cognitive fatigue · Language suppression · Motivation suppression · Thought deceleration · Amnesia · Delirium · Delusions
Anxiety suppression · Euphoria
Derealization · Emotional susceptibility · Depersonalization · Cognitive disconnection · Boundary dissolution · Identity alteration
Boundary dissolution · Identity alteration
Timeline · by preparation
Preparations[edit]
H. niger has been consumed historically as seeds, leaves, flowers, root material, smoked preparations, and transdermal ointments. No preparation has an established safe dose. All dose information below derives from historical case reports and ethnobotanical accounts, not controlled studies. Alkaloid content varies enormously by plant part, geographic strain, and growing conditions.[5]
Seeds (oral)
Seeds carry the highest alkaloid concentrations of any plant tissue and are easily mistaken for poppy or mustard seeds.[14] Historical reports indicate as few as 10–20 seeds have caused clinical anticholinergic syndrome in adults, though the threshold varies widely with strain.safety citation needed Onset is typically 30–60 minutes after ingestion; effects last 12–24 hours or longer.[5] Seeds have entered the food supply via contamination of cereal grains, herbal teas, and linseed during harvest and processing.[16]
Leaf and flower (oral)
Leaves and flowers contain lower alkaloid concentrations than seeds but remain pharmacologically active. In children, as few as 4 flowers have caused clinical poisoning.[5]safety citation needed Historical use includes direct chewing of fresh material, dried leaf infusions, and incorporation into food. A 1976 Australian case report documented deliberate chewing of henbane flowers.[17] Onset and duration are comparable to seed ingestion when consumed orally.
Smoked (leaf or flower)
Smoking dried H. niger leaf or flower produces faster onset — within minutes — and shorter duration than oral preparations, though clinical data are sparse.citation needed This route was documented historically for toothache relief, with smoke directed into the oral cavity. Dose titration is somewhat easier due to the shorter onset window, but alkaloid variability between batches still makes predictable dosing impossible.
Transdermal ointment
Transdermal ointments are the preparation most associated with medieval European witchcraft. Henbane was combined with other Solanaceae in fat-based preparations applied to thin-skinned areas.[3] Transdermal absorption produces slower, more gradual onset than oral ingestion. No quantitative dose or pharmacokinetic data exist for this preparation form.
Per-preparation dose tiers, timelines, and bioavailability data — where available — are in the Dose · by preparation card on this page.
Safety[edit]
- Acute toxicity
- Critical
- Chronic toxicity
- High
- Withdrawal
- None
- Tolerance buildup
- —
- Tolerance reset
- —
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- atropine · scopolamine (pharmaceutical) · other muscarinic antagonists
○ not assessed: TOL
Toxicity
H. niger is a highly toxic plant — every part contains pharmacologically active tropane alkaloids.[5][1] The European Food Safety Authority's Acute Reference Dose for these alkaloids is 0.016 µg/kg body weight[14] — so low that trace food contamination can exceed it.
Acute poisoning presents as full anticholinergic syndrome. In published clinical series: pupil dilation in 94.8% of cases, restlessness in 89.5%, and hallucinations in 89.5%.[5] Additional features include tachycardia, dry mouth, warm flushed skin, hyperthermia, urinary retention, and confusion. Severe cases progress to arrhythmia, convulsions, and coma.[5]
All psychoactive effects occur at doses that overlap with the toxic range. No sub-toxic psychoactive threshold has been established.[5]
Contaminant and food safety risk: Seeds enter cereal grains, herbal teas, and linseed during harvest and processing.[16] Toddler dietary exposure could exceed the group ARfD on 11–18% of consumption days in EU data.[14] For deliberately obtained plant material, intra-batch alkaloid variability — driven by geographic origin, growing conditions, and plant part — is the primary safety variable. No ISO/IEC-accredited lab testing exists for H. niger sold in commerce.
Vulnerable populations:
- Children: Substantially more sensitive to anticholinergic effects; as few as 4 flowers may cause clinical poisoning[5]safety citation needed
- Elderly: Heightened anticholinergic sensitivity; long-term exposure associated with increased dementia risk[18]
- Pregnant individuals: scopolamine crosses the placenta; use without clinical supervision is contraindicated[2]
- Hepatic impairment: May reduce alkaloid metabolism; no H. niger-specific data available
Psychological Risks
The primary psychoactive effect at any dose achievable from plant material is delirium — an agitated, non-lucid state with hallucinations and confusion that cannot be voluntarily controlled.[5] This is pharmacologically and experientially distinct from the hallucinatory states produced by serotonergic psychedelics.
Reality testing is severely impaired. A person in anticholinergic delirium may act on hallucinations with risk of self-harm, falls, or injury from spatial disorientation. Reported hallucinations commonly include conversations with absent persons and interaction with non-existent objects.[15]
Anticholinergic delirium may precipitate or worsen psychotic episodes in psychiatrically predisposed individuals.citation needed
Tolerance & Dependence
Published data on tolerance, dependence, or withdrawal specific to H. niger — outside pharmaceutical contexts — are absent from the literature. Scopolamine is classified as non-addictive in pharmaceutical use and is not scheduled for abuse potential in most jurisdictions. The aversive nature of anticholinergic delirium strongly limits voluntary repeat use.[6]
Drug Interactions
CYP3A4 inhibitors slow scopolamine breakdown, increasing its concentration in the body. Grapefruit juice alone raised scopolamine blood levels to approximately 142% of control values.[2] Drugs including ketoconazole, erythromycin, and HIV protease inhibitors would produce a similar or stronger effect.
The most clinically dangerous interaction class is additive anticholinergic burden[19]:
- Tricyclic antidepressants (amitriptyline, imipramine): strong additive risk for delirium, urinary retention, and hyperthermia
- First-generation antihistamines (diphenhydramine, hydroxyzine): additive anticholinergic effects
- Antipsychotics (phenothiazines, clozapine): additional anticholinergic burden
- Benzodiazepines and alcohol: additive CNS sedation with scopolamine
Physostigmine reverses severe anticholinergic delirium. A randomized trial found it superior to lorazepam for antimuscarinic toxidrome,[20] a prospective poison-center study confirmed its superiority over non-antidote therapy,[21] and a retrospective analysis of 815 patients found it associated with lower intubation rates (1.9% vs 8.4%).[22]
Contraindications
Absolute contraindications:
- Concurrent anticholinergic medication: Tricyclic antidepressants, first-generation antihistamines, and antipsychotics with anticholinergic properties create additive burden that substantially lowers the toxicity threshold
- Pregnancy: Scopolamine crosses the placenta; any exposure requires clinical supervision[2]
- Children: Substantially heightened sensitivity to anticholinergic effects[5]
Relative contraindications:
- Cardiac conditions: Anticholinergic-induced tachycardia and arrhythmia pose elevated risk in pre-existing cardiac disease
- Urinary retention or prostatic hypertrophy: Muscarinic blockade worsens urinary retention
- Angle-closure glaucoma: Mydriasis may trigger acute angle-closure crisis
- Hepatic impairment: Slower scopolamine clearance prolongs and intensifies effects
- Psychiatric history (psychotic spectrum): Anticholinergic delirium may precipitate or worsen psychotic episodescitation needed
- Elderly: Age-related anticholinergic sensitivity; long-term exposure associated with dementia risk[18]
Detection
Standard immunoassay drug panels do not detect scopolamine or hyoscyamine.[23] LC-MS/MS can detect both in serum and urine but requires a specific request for tropane alkaloid screening. In a documented drug-facilitated assault case, scopolamine was detected in urine at 41 µg/L at 18 hours post-exposure and in hair at 5 weeks post-exposure; blood was negative at 18 hours.[24]
Poison Control Center (US): 1-800-222-1222
Harm Reduction[edit]
Forms & Identification
H. niger preparations are not sold through regulated markets in any jurisdiction. Plant material obtained in the wild or through informal channels carries no quality controls, no standardized alkaloid content, and no third-party testing. No Certificate of Analysis infrastructure or ISO-accredited lab testing program exists for henbane products.
Alkaloid concentration varies enormously: seeds carry the highest concentrations, leaves lower — and populations differ by up to 10-fold between geographic strains. A prior dose that produced a given effect from one batch is not a reliable guide for a subsequent batch from different plant material.
Guidelines
- This plant has no established safe dose for any preparation. The margin between psychoactive and life-threatening effects is narrow and unpredictable. Psychedex does not recommend intentional consumption of H. niger in any form.
- If exposure occurs despite this warning: never use alone. A sober, informed sitter is not optional — it is the minimum threshold for survivable use.
- Do not combine H. niger with any anticholinergic medication (tricyclic antidepressants, diphenhydramine, hydroxyzine, antipsychotics), benzodiazepines, or alcohol.
- Do not consume material from an unfamiliar plant batch without first testing a much smaller amount and waiting at least 2 hours to assess response. Even this does not guarantee safety due to intra-batch alkaloid variation.
- Inform a trusted person outside the space of what has been consumed, the approximate amount, and the time. Provide the Poison Control number: 1-800-222-1222 (US).
- Hydrate actively. Anticholinergic effects suppress sweating and increase hyperthermia risk.
- Keep ambient temperature cool. Monitor for flushed, dry skin — an early sign of anticholinergic toxidrome.
Set & Setting
Anticholinergic delirium overrides environmental awareness entirely. Set and setting exert far less moderating influence than with serotonergic psychedelics or cannabis — the non-lucid, agitated state means rational decision-making is impossible during intoxication.
If exposure occurs, the single most important environmental factor is a sober, physically capable sitter prepared to prevent self-harm and call emergency services. An indoor space with locked doors and no access to heights, roadways, or water is essential. Remove sharp objects, medications, and car keys from the space.
Aftercare & integration. Anticholinergic delirium typically resolves within 24 hours, with approximately 85% of alkaloids excreted in that period. Post-experience effects may include persistent dry mouth, visual acuity suppression, urinary difficulty, cognitive fog, and fatigue lasting 24–48 hours.
Rehydrate aggressively — anticholinergic effects suppress normal fluid regulation. Eat bland, easily digested food when appetite returns. Rest in a low-stimulation environment.
Anterograde amnesia is expected: the person may have no memory of events during intoxication. A sitter's account of what occurred can help process the experience. If persistent confusion, visual disturbances, or psychological distress continue beyond 48 hours, seek medical evaluation.
Recovery & Support
Compulsive repeat use of H. niger is rare due to the aversive nature of anticholinergic delirium. No formal tolerance, dependence, or withdrawal data exist, and no substance-specific cessation protocols have been developed.
If persistent psychological distress, flashbacks, or anxiety follow a henbane experience, standard trauma-informed counselling and psychiatric evaluation are appropriate.
Crisis and support resources:
- SAMHSA National Helpline (US): 1-800-662-4357 (free, confidential, 24/7)
- Poison Control (US): 1-800-222-1222
- Crisis Text Line (US): Text HOME to 741741
- Samaritans (UK): 116 123
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency:
- Severely dilated pupils unresponsive to light
- Hot, dry, flushed skin with absence of sweating
- Heart rate above 120 bpm or irregular heartbeat
- Agitated delirium: confusion, combativeness, inability to recognize surroundings or people
- Seizures, loss of consciousness, or inability to be roused
- Urinary retention or complete inability to urinate
Immediate steps:
- 1. Call emergency services (911 in US, 112 in EU, 000 in Australia).
- 2. Do not leave the person alone. Prevent self-injury — restrain gently if necessary.
- 3. Move to a cool environment. Apply cool, wet cloths to skin if hyperthermia is suspected.
- 4. Do not induce vomiting. Do not administer ipecac.
- 5. If the person is unconscious, place in the recovery position to protect the airway.
What to tell the dispatcher: "Possible henbane / anticholinergic plant poisoning. Tropane alkaloid exposure — scopolamine and hyoscyamine." State the preparation consumed (seeds, leaves, tea), estimated amount, time of ingestion, and current symptoms.
Reversal agent: Physostigmine is the specific antidote for severe anticholinergic toxidrome, administered only by medical professionals in a monitored setting. It is not available over the counter.
Good Samaritan laws exist in many US states and other jurisdictions, providing legal protection for individuals who call emergency services to report a drug-related medical emergency.
Legal Status[edit]
H. niger is not controlled under any of the three major UN drug control treaties (1961, 1971, 1988). Its primary alkaloids — scopolamine and hyoscyamine — are established pharmaceutical compounds on the WHO List of Essential Medicines, not internationally scheduled substances. Where domestic regulation exists, it typically targets the plant as a poison or agricultural pest rather than as a controlled drug.[4]
In the United States, henbane is not a controlled substance under federal law but must carry poison labeling with sales records maintained.[4] Louisiana prohibits it when intended for human consumption.[4] Multiple states designate it a noxious weed for agricultural purposes — including Washington, California, Colorado, Idaho, New Mexico, Nevada, South Dakota, and Wyoming.[13] Canada does not schedule it federally, though Alberta lists it as a noxious weed.[13] In the United Kingdom, the plant is not scheduled under the Misuse of Drugs Act 1971, though pharmaceutical scopolamine and hyoscyamine products are prescription-only medicines.citation needed Germany is reported to impose additional restrictions on cultivation and possession, though specific legislation is unconfirmed.citation needed Australia does not appear to schedule the plant specifically, though pharmaceutical forms are regulated.citation needed
Analog and treaty considerations
H. niger occupies an unusual regulatory position: its alkaloids are FDA-approved pharmaceutical agents with WHO Essential Medicines status, yet neither the alkaloids nor the plant are internationally controlled. Legal exposure in most jurisdictions is limited to poison-labeling requirements, intent-based consumption prohibitions, and agricultural noxious weed designations.
Legal status changes frequently. This overview reflects the status as of the article's last update and is not legal advice. Verify current law in the relevant jurisdiction before acting on this information.
Safety[edit]
- Acute toxicity
- Critical
- Chronic toxicity
- High
- Withdrawal
- None
- Tolerance buildup
- —
- Tolerance reset
- —
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- atropine · scopolamine (pharmaceutical) · other muscarinic antagonists
○ not assessed: TOL
Toxicity
H. niger is a highly toxic plant; all parts — leaves, seeds, flowers, and roots — contain pharmacologically active tropane alkaloids.[5][1] No published LD₅₀ data for whole plant material in humans exist. The EFSA group Acute Reference Dose for tropane alkaloids is 0.016 µg/kg body weight[14] — a threshold so low that trace food contamination can exceed it.
Acute poisoning presents as full anticholinergic syndrome. In published clinical series: pupil dilation in 94.8% of cases, restlessness in 89.5%, and hallucinations in 89.5%.[5] Additional features include tachycardia, dry mouth, warm flushed skin, hyperthermia, urinary retention, confusion, and combative behaviour. Severe cases progress to arrhythmia, convulsions, and coma.[5]
All psychoactive effects occur at doses that overlap with the toxic range; no sub-toxic psychoactive threshold has been established.[5]
Contaminant and food safety risk: The primary contamination vector is food supply contamination — seeds enter cereal grains, herbal teas, edible flowers, beans, and linseed during harvest and processing.[16] EFSA found that toddler dietary exposure could exceed the group ARfD on 11–18% of consumption days.[14] No regulatory maximum limits for tropane alkaloids in food had been established at the time of the 2013 EFSA opinion.[14] For deliberately obtained plant material, intra-batch alkaloid variability — driven by geographic origin, growing conditions, and plant part — is the primary safety variable. No ISO/IEC-accredited laboratory testing or Certificate of Analysis requirement exists for H. niger sold in commerce.
Vulnerable populations:
- Children: Substantially more sensitive to anticholinergic effects; as few as 4 flowers may cause clinical poisoning[5]safety citation needed
- Elderly: Heightened anticholinergic sensitivity with elevated delirium risk; long-term anticholinergic exposure is associated with increased dementia risk[17]
- Pregnant individuals: scopolamine crosses the placenta; use without clinical supervision is contraindicated[2]
- Hepatic impairment: May reduce alkaloid metabolism via CYP3A4; no H. niger-specific data available
Psychological Risks
The primary psychoactive effect of H. niger at doses achievable from plant material is delirium — an agitated, non-lucid state with hallucinations and confusion that is not voluntarily controllable.[5] This is pharmacologically and experientially distinct from the hallucinatory states produced by serotonergic psychedelics.
Reality testing is severely impaired. Individuals may act on delusions with risk of self-harm, falls, or injury from spatial disorientation. Reported hallucinations commonly include conversations with absent persons, interaction with non-existent objects, and phantom activities.[15]
Anticholinergic delirium may precipitate or exacerbate psychotic episodes in psychiatrically predisposed individuals.citation needed
Tolerance & Dependence
Published data on tolerance, dependence, or withdrawal specific to H. niger or its alkaloids in a non-pharmaceutical context are absent from the literature. No tolerance studies for chronic scopolamine or hyoscyamine consumption outside pharmaceutical contexts have been published. No abuse liability studies exist, and no withdrawal syndrome has been documented.
Scopolamine is classified as a non-addictive agent in pharmaceutical use and is not scheduled based on abuse potential in most jurisdictions. The unpleasant and often terrifying nature of anticholinergic delirium strongly limits voluntary repeat use.[6]
Drug Interactions
CYP3A4 inhibitors increase scopolamine exposure. Co-administration with grapefruit juice increased scopolamine AUC₀₋₂₄ to approximately 142% of control values, and oral bioavailability rose from the 3–27% range to 6–37%.[2] Any CYP3A4 inhibitor — including ketoconazole, erythromycin, and HIV protease inhibitors — would be expected to produce a similar effect.
Additive anticholinergic burden is the most clinically dangerous interaction class. The following medication categories carry anticholinergic properties that are additive with H. niger alkaloids[18]:
- Tricyclic antidepressants (amitriptyline, imipramine): strong anticholinergic properties; additive risk for delirium, urinary retention, and hyperthermia
- First-generation antihistamines (diphenhydramine, hydroxyzine): additive anticholinergic effects
- Antipsychotics (phenothiazines, clozapine): additional anticholinergic burden
- Benzodiazepines and alcohol: additive CNS depression with scopolamine's sedative effects
Physostigmine (a cholinesterase inhibitor) reverses severe anticholinergic delirium. A randomized trial found physostigmine superior to lorazepam for antimuscarinic toxidrome,[19] and a prospective poison-center study confirmed its superiority over non-antidote therapy.[20] A retrospective analysis of 815 patients found physostigmine associated with lower intubation rates (1.9% vs 8.4%).[21]
Contraindications
Absolute contraindications:
- Concurrent anticholinergic medication use: Tricyclic antidepressants, first-generation antihistamines, antipsychotics with anticholinergic properties, and antiparkinsonian anticholinergics create additive anticholinergic burden that substantially lowers the toxicity threshold
- Pregnancy: Scopolamine crosses the placenta; teratogenicity data are limited but clinical supervision is required for any exposure[2]
- Pediatric exposure: Children demonstrate substantially heightened sensitivity to anticholinergic effects[5]
Relative contraindications:
- Cardiac conditions: Anticholinergic-induced tachycardia and potential arrhythmia pose elevated risk in pre-existing cardiac disease
- Urinary retention or prostatic hypertrophy: Muscarinic blockade exacerbates urinary retention
- Angle-closure glaucoma: Mydriasis may precipitate acute angle-closure crisis
- Hepatic impairment: Reduced CYP3A4 capacity may slow scopolamine clearance, prolonging and intensifying effects
- Psychiatric history (psychotic spectrum disorders): Anticholinergic delirium may precipitate or worsen psychotic episodescitation needed
- Elderly: Age-related increase in anticholinergic sensitivity; long-term exposure associated with dementia risk[17]
Detection
Standard immunoassay drug panels do not detect scopolamine or hyoscyamine — these alkaloids are not included in routine urine drug screens.[22] LC-MS/MS can detect both in serum and urine, but requires a specific laboratory request for tropane alkaloid screening. In a drug-facilitated assault case, scopolamine was detected in urine at 41 µg/L at 18 hours post-exposure and in hair at 5 weeks post-exposure; blood was negative at 18 hours.[23]
Poison Control Center (US): 1-800-222-1222
Preparations[edit]
H. niger has been consumed historically as seeds, leaves, flowers, root material, smoked preparations, and transdermal ointments. No preparation has an established safe dose. All dose information below is derived from historical case reports and ethnobotanical accounts, not from controlled studies. Alkaloid content varies enormously by plant part, geographic strain, and growing conditions — any stated dose range carries extreme uncertainty.[5]
Seeds (oral)
Seeds are the plant part most commonly involved in both accidental and deliberate poisonings. They carry among the highest alkaloid concentrations of any tissue and are easily mistaken for poppy or mustard seeds.[14] Historical reports indicate that as few as 10–20 seeds have produced clinical anticholinergic syndrome in adults, though the threshold varies widely with strain.safety citation needed Onset is typically 30–60 minutes after ingestion, with effects lasting 12–24 hours or longer.[5] Seeds have entered the food supply via contamination of cereal grains, herbal teas, and linseed during harvest and processing.[16]
Leaf and flower (oral)
Leaves and flowers contain lower alkaloid concentrations than seeds but remain pharmacologically active. Historical consumption includes direct chewing of fresh material, dried leaf infusions, and incorporation into food. In children, as few as 4 flowers have caused clinical poisoning.[5]safety citation needed Onset and duration are comparable to seed ingestion when consumed orally. A 1976 Australian case report documented deliberate chewing of henbane flowers, noting more widespread use than clinical reports suggested.[24]
Smoked (leaf or flower)
Smoking dried H. niger leaf or flower material produces faster onset (within minutes) and shorter duration compared with oral preparations, though clinical data are sparse. This route was documented historically for toothache relief — the smoke was directed into the oral cavity — and for psychoactive use.citation needed Dose titration is somewhat easier than with oral preparations due to the shorter onset window, but alkaloid variability between batches still makes predictable dosing impossible.
Transdermal ointment
Transdermal ointments represent the preparation most associated with medieval European witchcraft practices. Henbane was combined with other Solanaceae (Atropa belladonna, Mandragora officinarum) in fat-based preparations applied to thin-skinned areas.[3] Transdermal absorption produces a slower, more gradual onset than oral ingestion. No quantitative dose or pharmacokinetic data exist for this preparation form.
Per-preparation dose tiers, timelines, and bioavailability data — where available — are in the Dose · by preparation card on this page.
Harm Reduction[edit]
Forms & Identification
H. niger preparations are not sold through regulated markets in any jurisdiction. Plant material obtained in the wild or through informal channels carries no quality controls, no standardized alkaloid content, and no third-party testing. Unlike cannabis or kratom, no Certificate of Analysis infrastructure or ISO-accredited lab testing program exists for henbane products.
Alkaloid concentration varies enormously by plant part (seeds highest, leaves lower), geographic strain (10-fold variation between populations), and growing conditions. This means that even experienced users of crude plant material cannot reliably predict potency from one batch to the next. Any prior dose that produced a given effect is not a reliable guide for subsequent use from different plant material.
Guidelines
- This plant has no established safe dose for any preparation. The margin between psychoactive and life-threatening effects is narrow and unpredictable. Psychedex does not recommend intentional consumption of H. niger in any form.
- If exposure occurs despite this warning: never use alone. A sober, informed sitter is not optional — it is the minimum threshold for survivable use.
- Do not combine H. niger with any anticholinergic medication (tricyclic antidepressants, diphenhydramine, hydroxyzine, antipsychotics), benzodiazepines, or alcohol.
- Do not consume material from an unfamiliar plant batch without first testing a much smaller amount and waiting at least 2 hours to assess response. Even this does not guarantee safety due to intra-batch alkaloid variation.
- Inform a trusted person outside the space of what has been consumed, the approximate amount, and the time. Provide the Poison Control number: 1-800-222-1222 (US).
- Hydrate actively. Anticholinergic effects suppress sweating and increase hyperthermia risk.
- Keep ambient temperature cool. Monitor for flushed, dry skin — an early sign of anticholinergic toxidrome.
Set & Setting
Anticholinergic delirium overrides environmental awareness — set and setting exert far less moderating influence than with serotonergic psychedelics or cannabis. The non-lucid, agitated state means the user cannot make rational decisions during intoxication and may act on hallucinations with risk of injury.
If exposure occurs, the single most important environmental factor is the presence of a sober, physically capable sitter who is prepared to restrain the user from self-harm and to call emergency services. An indoor environment with locked doors and no access to heights, roadways, or water is essential. Remove sharp objects, medications, and car keys from the space.
Aftercare & integration. Anticholinergic delirium typically resolves within 24 hours, with approximately 85% of alkaloids excreted in that period. Post-experience effects may include persistent dry mouth, visual acuity suppression, urinary difficulty, cognitive fog, and fatigue lasting 24–48 hours.
Rehydrate aggressively — anticholinergic effects suppress normal fluid regulation. Eat bland, easily digested food when appetite returns. Rest in a low-stimulation environment.
Anterograde amnesia is expected: the user may have no memory of events during intoxication. A sitter's account of what occurred can help the user process the experience. If persistent confusion, visual disturbances, or psychological distress continue beyond 48 hours, seek medical evaluation.
Recovery & Support
Compulsive repeat use of H. niger is rare due to the aversive nature of anticholinergic delirium. No formal tolerance, dependence, or withdrawal data exist, and no substance-specific cessation protocols have been developed.
If persistent psychological distress, flashbacks, or anxiety follow a henbane experience, standard trauma-informed counselling and psychiatric evaluation are appropriate.
Crisis and support resources:
- SAMHSA National Helpline (US): 1-800-662-4357 (free, confidential, 24/7)
- Poison Control (US): 1-800-222-1222
- Crisis Text Line (US): Text HOME to 741741
- Samaritans (UK): 116 123
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency:
- Severely dilated pupils unresponsive to light
- Hot, dry, flushed skin with absence of sweating
- Heart rate above 120 bpm or irregular heartbeat
- Agitated delirium: confusion, combativeness, inability to recognize surroundings or people
- Seizures, loss of consciousness, or inability to be roused
- Urinary retention or complete inability to urinate
Immediate steps:
- 1. Call emergency services (911 in US, 112 in EU, 000 in Australia).
- 2. Do not leave the person alone. Prevent self-injury — restrain gently if necessary.
- 3. Move to a cool environment. Apply cool, wet cloths to skin if hyperthermia is suspected.
- 4. Do not induce vomiting. Do not administer ipecac.
- 5. If the person is unconscious, place in the recovery position to protect the airway.
What to tell the dispatcher: "Possible henbane / anticholinergic plant poisoning. Tropane alkaloid exposure — scopolamine and hyoscyamine." State the preparation consumed (seeds, leaves, tea), estimated amount, time of ingestion, and current symptoms.
Reversal agent: Physostigmine is the specific antidote for severe anticholinergic toxidrome, administered only by medical professionals in a monitored setting. It is not available over the counter.
Good Samaritan laws exist in many US states and other jurisdictions, providing legal protection for individuals who call emergency services to report a drug-related medical emergency.
Legal Status[edit]
H. niger is not controlled under any of the three major UN drug control treaties (1961, 1971, 1988). Its primary alkaloids — scopolamine and hyoscyamine — are established pharmaceutical compounds on the WHO List of Essential Medicines, not internationally scheduled substances. Where domestic regulation exists, it typically targets the plant as a poison or agricultural pest rather than as a controlled drug.[4]
| Jurisdiction | Status | Notes |
|---|---|---|
| United States (federal) | Not scheduled (CSA) | Not a controlled substance. Listed as a "poison" under 21 USC Chapter 7; products must carry poison labeling with sales records maintained[4] |
| Louisiana | Prohibited for human consumption | Act No. 159 (effective 8 August 2005) prohibits H. niger when intended for human consumption; permits possession for aesthetic, landscaping, or decorative purposes[4] |
| Tennessee | Not scheduled | A proposed ban was not enacted[4] |
| US states (agricultural) | Noxious weed | Designated noxious weed in Washington, California, Colorado, Idaho, New Mexico, Nevada, South Dakota, and Wyoming — agricultural regulation, not controlled substance classification[13] |
| Canada (federal) | Not scheduled | Not a controlled substance. Alberta designates it as a noxious weed under provincial invasive species regulation[13] |
| United Kingdom | Not specifically scheduledcitation needed | Plant not scheduled under the Misuse of Drugs Act 1971. Pharmaceutical scopolamine and hyoscyamine preparations are prescription-only medicines (POM) |
| Germany | Uncertaincitation needed | Multiple sources suggest regulation of cultivation and possession beyond other European countries; specific legislation not confirmed |
| Australia | Not believed scheduledcitation needed | Plant not specifically scheduled under TGA scheduling. Pharmaceutical scopolamine and hyoscyamine products are scheduled prescription medicines. Recreational use documented in 1976[24] |
Analog and treaty considerations
H. niger occupies an unusual regulatory position: its alkaloids are FDA-approved pharmaceutical agents with WHO Essential Medicines status, yet neither the alkaloids nor the plant are controlled under international treaties. Legal exposure in most jurisdictions is limited to poison-labeling requirements, intent-based consumption prohibitions, and agricultural noxious weed designations — reflecting the plant's low prevalence as a substance of intentional use relative to other anticholinergic Solanaceae.
Frequently asked questions
What is Hyoscyamus niger?
Hyoscyamus niger is a toxic solanaceous plant containing the tropane alkaloids scopolamine and hyoscyamine, classified as a deliriant. All psychoactive effects occur at doses overlapping with the anticholinergic toxic range; no safe dose has been established for any preparation.
What are dangerous combinations with Hyoscyamus niger?
The highest-severity documented interactions for Hyoscyamus niger: Amphetamines (Dangerous), Antihistamines (Dangerous), Antipsychotics (Dangerous), Atypical antipsychotics (Dangerous), Buprenorphine, Kratom (Dangerous). See the interactions section for the full list with mechanisms and severity levels.
experience reports
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First-person accounts of subjective effects, timing, and outcomes — submitted for harm reduction.
references
- [1]
- [2]
- [3]
- [4]
- [5]
- [6] ^abFatur K, Kreft S (2021) Nixing the nightshades: Traditional knowledge of intoxicating members of the Solanaceae among hallucinogenic plant and mushroom users in Slovenia — PLoS ONE doi:10.1371/journal.pone.0247688
references
- [1]
- [2]
- [3]
- [4]
- [5]
- [6] ^abFatur K, Kreft S (2021) Nixing the nightshades: Traditional knowledge of intoxicating members of the Solanaceae among hallucinogenic plant and mushroom users in Slovenia — PLoS ONE doi:10.1371/journal.pone.0247688