H.B. Woodrose

What separates Hawaiian baby woodrose from morning glory is not a molecule, it is a unit of account. Here three to ten seeds are swallowed where morning glory is swallowed by the hundred. The chemistry is nonetheless the same on both sides, ergot alkaloids of which the main one is LSA, or ergine, and the clinical corpus on LSA is made almost entirely of Argyreia nervosa cases: when you read a human figure on ergine, it most often comes from this plant. And the entire literature fits inside one prospective human study on four volunteers, which was halted for serious adverse effects.

What is in the seed, and does not come from the plant

The ergot alkaloids of the Convolvulaceae are not made by the plant: they come from symbiotic fungi of the genus Periglandula, transmitted vertically through the seed. A survey of eight species, this one among them, found them in all eight, at concentrations of 15.8 to 3223 µg/g, but the value specific to A. nervosa could never be obtained (Beaulieu 2015).

The composition measured on two products actually on sale gives LSA and its isomers at 83 to 84% of the ergot alkaloids, ergometrine and ergometrinine at 10 to 17%. The remainder, at less than 6.1%, appears only in the capsule product: in the collection of five seeds, only LSA and ergometrine were detected (Paulke 2014). On better-quality material the inventory lengthens, and two names there deserve to be read slowly, methylergometrine and methysergide (Paulke 2015). These are the active principles of drugs with uterine and vascular action, not chemical curiosities.

The central fact of this page is here. Between the least loaded and the most loaded seed in a single packet of five, LSA goes from 3 to about 15 µg, a factor of 5 inside one packet; between the two products, the total load varies by a factor of 8.6. The authors' literal conclusion: for a consumer, the quality of the seeds is unpredictable (Paulke 2015). To which a market fact is added: capsules sold as containing LSA have often turned out to contain none, the symptoms then coming from adulterants (Castro 2025).

This is not LSD, and that is not the same as saying it is weak

Two peer-reviewed sources have looked at the question directly and both reject the natural LSD reputation. Receptor profiling gives, in measured binding, 5-HT1A pKi 7.99, 5-HT2 pKi 7.56, alpha-2 pKi 7.21, and 6.05 to 6.85 for the dopaminergic subtypes and alpha-1: affinities lower than those of LSD for every subtype tested, and the authors conclude that LSA should not be regarded as an LSD-type psychedelic (Paulke 2013). The other writes that neither the substances nor the mixture produce LSD-type perceptual changes, and describes effects dominated by autonomic disturbances, rather sedative and uncomfortable, which it compares with those of scopolamine (Borsutzky 2002). That comparison is a clinical impression, not a claim about mechanism: the muscarinic affinity of LSA has never been measured, the question remains open.

What that study did not do has to be said. It measures binding, not function, and does not say whether LSA is an agonist, a partial agonist or an antagonist at 5-HT2A. Yet it is functional efficacy, not affinity, that decides the psychedelic effect. The method exists and is applied routinely to other lysergamides, a Gq calcium assay plus head-twitch in the mouse. Nobody has done it on LSA. Whether this molecule is a weak psychedelic or a non-psychedelic depends entirely on an answer that has never been produced.

Correcting the myth must not manufacture a second one. In the only prospective human study, four volunteers at weight-normalised doses, the study was stopped: cardiovascular disturbance in two subjects, a psychotic-type state in one, complete recovery within 9 hours for all, and reactions that differed greatly from one individual to another, in kind as in intensity, at equal dose. The authors conclude that this use is far more dangerous than is commonly believed (Kremer 2011). There is moreover no functional imaging of LSA: the only published imaging is pathological, that of the hypertensive encephalopathy case dealt with below, and it is indexed under the name of the molecule and not under that of a plant.

Counting seeds is not dosing

Two families of figures circulate, and the contradiction has to be shown rather than settled. Direct per-seed measurements give 3 to 15 µg of LSA, up to about 34 µg in a capsule (Paulke 2014). The figure that circulates everywhere, 2 to 5 mg for 5 to 10 seeds, implies 200 to 1000 µg per seed, a gap of a factor of 13 to more than 300; it comes from Juszczak and Swiergiel 2013, whose full text has not been read and whose upstream source has never been traced back. The two families are not necessarily incompatible: scaled to a seed of about 125 mg, the range in Beaulieu 2015 covers 2 to 403 µg per seed and overlaps both. A reservation not to be left unsaid, that mass comes from a vendor, no academic source gives the mass of an A. nervosa seed, and two products analysed in a single laboratory are not the population of seeds.

⚠️ Do not read this section backwards. That the milligram figure does not hold does not mean the seeds are weak, and it is that reading which does the harm. The only prospective human study administered 5.88 mg/kg of seed preparation, that is about 400 mg in a 70 kg adult, of the order of three to four seeds. It was at that dose that 3 subjects out of 4 had severe adverse effects. And a peer-reviewed source, specific to this plant, writes that the psychiatric and somatic adverse effects are not related to the dose of LSA (Sobanski 2021). Severity does not follow dose: that is the best argument against any titration strategy, and it is worth more than any arithmetic on micrograms.

Compared with morning glory, for which this wiki keeps a separate page, the difference is not the one people assume. The per-seed values overlap, about 4 to 23 µg of ergine for Ipomoea, a range calculated from the published contents and not read as such in the authors' own text, against 3 to 15 µg measured here, but these are different laboratories and different methods, never a direct comparison. What really separates the two plants is the unit of intake, a handful against several hundred seeds.

Duration and tolerance

The only upper bound observed under controlled conditions is the complete recovery within 9 hours in Kremer 2011. Serum LSA was measured between 0.66 and 3.15 ng/mL about 2 hours after ingestion, and it remains detectable in urine from 1 to 24 hours, no longer at all at 48 hours (Paulke 2012). That is all: none of the parameters one would need in order to derive a duration has ever been published, no Tmax, no bioavailability, no half-life, no effect-time curve, under a reservation not to be left unsaid, the full text of Klinke 2010 has not been read and that article is indexed under the term half-life. The 6 to 8 hour range that circulates everywhere comes from user wikis and sales sites, at least one of them in manifest conflict of interest, and it is merely compatible with the 9 hour bound. The onset time is not sourced either: the figure that circulated was attributed to a poison centre series whose text does not contain it, and it is not taken up here.

On tolerance, nothing. No repeated-dosing study, and LSA does not appear in the literature on tolerance to 5-HT2A agonists. The only indirect element runs against intuition: the adolescent in the induced psychosis case had already taken the same seeds once without incident (Sobanski 2021). A previous uneventful experience protects against nothing.

Harm reduction

Pregnancy: a contraindication, and it is the best-founded point on this page. A clinical paper explicitly devotes a part to foetal distress linked to the ergometrine contained in the seeds, and it is indexed under the terms foetal distress, pregnancy, risk factors (Borsutzky 2002). Ergometrine accounts for 10 to 17% of the measured alkaloids, and methylergometrine has been detected: these are the active principles of the uterotonics used in obstetrics to make the uterus contract. A pregnant person who takes these seeds takes an unmeasured dose of uterotonic. This point is absent from most general-audience pages, which talk about nausea.

The vascular side is the best-supported mechanistic thread, and it is not the one people talk about. Four sources of very different kinds converge: LSA is by itself a vasoconstrictor, comparable to ergonovine and ergotamine, in bovine vessel (Oliver 1993, ex vivo, never replicated on human tissue); cardiovascular disturbance affects 2 volunteers out of 4 (Kremer 2011); a rise in blood pressure is among the severe autonomic effects correlated with serum levels (Paulke 2012); and the only picture that required intensive care in this corpus is a hypertensive encephalopathy with status epilepticus (Legriel 2008, a case indexed under LSA, with no plant named, see the reservation on the seizure threshold). Populations to exclude first: hypertension, coronary artery disease, peripheral arterial disease, a history of stroke, migraine treated with triptans or with ergot derivatives. What must not be implied, on the other hand: no case of ergotism, gangrene or limb ischaemia attributed to these seeds is published. The risk is established at the blood pressure level, not at the tissue level.

The documented lethal risk is behavioural, not toxicological. The only published death for this plant is a fall from a building, in a subject whose account mentioned the wish to jump out of the window, with 4.9 µg/L of LSA in the blood against 1.8 in a surviving comparison subject. The picture is confounded, THC at 22 µg/L and ethanol at 0.71 g/L, and it must not be attributed to LSA alone (Klinke 2010). To be set beside suicidal ideas reported by two users in the corpus (Juszczak 2013) and the most recent systematic review, 17 studies and 219 patients, which finds among the severe cases a suicide following agitation and psychosis, and no fatal overdose on record (Castro 2025). A sober person and a place one cannot fall from are the first protection. They are not the only ones: 12.3% of those 219 patients required medical care, and the only poison centre series available, 29 exposures in Texas over eighteen years, reports 7% major effect, 28% intravenous fluids and 21% benzodiazepines (Forrester 2019). The sober third party does not replace blood pressure monitoring.

Combinations, naming what is elsewhere in this wiki.

• Serotonergics. No case of serotonin syndrome is published for A. nervosa or for LSA in particular, and the search was run again. But an absence of cases in a literature this thin proves nothing, and class evidence points towards risk: ergot alkaloids are serotonin agonists, and dihydroergotamine given to human beings can cause serotonin syndrome (Eadie 2003). The seed contains, as measured, methysergide and methylergometrine, that is to say precisely serotonergic ergolines. Do not be reassured.
• Syrian rue. The usual caution about MAOIs comes from the analogy with simple tryptamines, which are MAO substrates. LSA is an ergoline, not a simple tryptamine, and no study establishes that it is an MAO substrate. The question is genuinely open and it stays open. What is not open is the class evidence above: an unanswered question does not read as a green light.
• CYP3A4. Ergot alkaloids are, as a class, CYP3A4 substrates, and potent inhibitors (macrolides, azole antifungals, HIV protease inhibitors) can precipitate vasospasm. Nothing establishes that LSA itself is that substrate. The warning appears here because the molecules for which it was written, ergometrine, methylergometrine, methysergide, are actually present in the seed, measured and not presumed. A two-stage inference, and both stages are named. The only CYP3A4 inhibitor in this batch is Syrian rue, and its inhibition is in vitro.
• Other vasoconstrictors. Triptans, other ergot derivatives, stimulants, cocaine: the effects run in the same direction. Class reasoning, no case reported for this plant. The question is complicated by the fact that some users take these seeds for the same indication as triptans, cluster headache.
• Dextromethorphan. The only co-use in this batch actually encountered in the user corpus, along with cannabis and hashish, and no clinical outcome is attached to it (Juszczak 2013). It is therefore not a documented danger. What is documented elsewhere is that DXM is sedative and as potent a SERT inhibitor as fluoxetine at recreational concentrations: on that count it falls on the serotonergic axis above and on the vomiting axis below.
• Vomiting under a sedative. Vomiting is the rule with these seeds. This chain is anchored on one case, elsewhere in this corpus: the only published death from DPT is a deep aspiration of gastric contents, and the order there is collapse, convulsion, then vomiting, so in a person already unconscious. Monitoring must not wait for the first vomit before it starts. The sedatives in this batch are DXM, diphenhydramine and nitrous oxide, and alcohol was present in the only published death for this plant. Vomiting being a foregone conclusion here, the countermeasure is prepared before the dose and is not administered: someone who stays sober, and who knows how to put a person in the recovery position.
• Seizure threshold. The only intensive care picture published in this corpus, the PRES of Legriel 2008, includes status epilepticus, but it does not belong to this plant in its own right: the article is indexed under the molecule, LSA was not assayed in it and no species is named there. This seed is therefore one of the wiki's four substances, out of fourteen, carrying no convulsive signal of its own, and that is a rare position which above all does not amount to protection: the other ten carry one, six on counted human cases and four on weaker material, an animal signal, an isolated case or an unquantified clinical mention, and combining two of them very often comes down to adding two lowerings of the threshold.

Peeling the seeds is not a detoxification. No peer-reviewed source establishes the presence of cyanogenic glycosides in the seed of Argyreia nervosa, and the dedicated search returns nothing on this genus. What the literature offers instead needs no cyanide: the nausea is attributed to D2 stimulation, compatible with the measured D2 affinity and with the classic emetic mechanism of ergot alkaloids, but nobody has tested it directly. A symmetrical reservation to keep: no study describes the distribution of the alkaloids inside the seed, so neither can it be asserted that peeling changes nothing about the dose.

In the emergency department. There is no treatment recommendation for the psychiatric syndromes induced by LSA (Sobanski 2021). What was done in the published cases: intravenous fluids, benzodiazepines, and aggressive antihypertensives plus intravenous anticonvulsants in the PRES case. Signs that should prompt medical attention: a persistent rise in blood pressure, severe headache, visual disturbance, seizure, confusion or aphasia, suicidal ideas or a wish to throw oneself from a height, intractable vomiting, and any psychotic state or any effect persisting beyond about 9 to 12 hours, since the only controlled series recovered completely within 9 hours.

Nobody will be identified by a drug screen. Ergine appears in no routine assay and a negative screen rules nothing out: saying what was taken and keeping what is left, seeds, packet or capsules, materially changes the care given. Two things specific to this plant are added to that. The only published LSA concentrations come from dedicated toxicology work and not from a hospital panel (Paulke 2012, Klinke 2010), and the urinary window closes between 24 and 48 hours: there is no test to request urgently to confirm the intake. And capsules sold as containing LSA have often turned out to contain none, the symptoms then coming from adulterants (Castro 2025): the kept packaging is sometimes the only thing that points to something other than ergine.

What this page will not say, and why

The aphrodisiac reputation does indeed exist in the scientific literature, but it bears on the root and on the rat. This is not a taxonomic ambiguity, A. speciosa being a synonym of the same plant: it is a confusion of organ, the Ayurvedic Vriddhadaru being the root.

The traditional entheogenic use of these seeds is undocumented, which is not the same thing as false. The first identification of ergoline alkaloids dates from 1965 and its authors present it as provisional, Western recreational use is documented from 1983 onwards, and the Mesoamerican tradition of morning glory seeds concerns another plant, Turbina corymbosa. A 2025 systematic review nonetheless asserts in its introduction an ancient ritual use by indigenous populations, with no primary source at all: that is exactly how a reputation acquires a reference.

One point finally runs the other way and must not be erased either. LSA appears effective in cluster headache in a survey of patients, with self-rated efficacy and a modest denominator: aggregating the three available studies, Castro 2025 puts the base at about 120 patients, of whom roughly 20% report efficacy in prevention. It is the only documented benefit signal for this molecule, and it is not a therapeutic recommendation.

Sources

• A. Paulke et al. (2013), receptor profiling of LSA and the other compounds of Argyreia nervosa, J Ethnopharmacol (central source; binding, not function).
• A. Paulke et al. (2014), ergot alkaloid profiles in two Argyreia nervosa products, Forensic Sci Int (per-seed figures, the factor of 5 and the factor of 8.6).
• A. Paulke et al. (2015), alkaloid composition of Hawaiian baby woodrose, Forensic Sci Int (methylergometrine, methysergide, ergopeptides).
• A. Paulke et al. (2012), LSA in human serum and urine after seed ingestion, Anal Bioanal Chem.
• C. Kremer, A. Paulke, C. Wunder, S.W. Toennes (2011), variable adverse effects after ingestion of equal doses of Argyreia nervosa seeds, Forensic Sci Int (the only prospective human study, halted).
• P.S.C.C. Castro et al. (2025), LSA, an analogue of LSD: systematic review of pharmacological effects, adverse outcomes and therapeutic potential, Pharmacy (PRISMA, 17 studies, 219 patients; full text read).
• E. Sobanski et al. (2021), induced psychosis after consumption of Hawaiian baby woodrose seeds, Z Kinder Jugendpsychiatr Psychother (severity is not related to dose).
• M. Borsutzky, T. Passie, W. Paetzold, H.M. Emrich, U. Schneider (2002), psychopharmacological effects of Argyreia nervosa seeds, Der Nervenarzt (source of the pregnancy point; paper in German, English abstract alone read).
• H.B. Klinke, I.B. Muller, S. Steffenrud, R. Dahl-Sorensen (2010), two cases of lysergamide intoxication, Forensic Sci Int (the death by fall).
• S. Legriel et al. (2008), LSA-induced PRES with status epilepticus, Neurocritical Care (indexed under the molecule, not under a plant).
• J.W. Oliver, L.K. Abney, J.R. Strickland, R.D. Linnabary (1993), lysergamide-induced vasoconstriction in bovine vasculature, J Anim Sci (ex vivo, bovine).
• M.B. Forrester (2019), Argyreia nervosa exposures reported to Texas poison centres, J Addict Dis (29 cases over 2000-2018, a very small denominator).
• G.R. Juszczak and A.H. Swiergiel (2013), recreational use of D-lysergamide, J Psychoactive Drugs (user corpus; full text not read, and it is from it that the 2 to 5 mg figure comes, whose upstream source has never been traced back).
• M.J. Eadie (2003), convulsive ergotism: epidemics of the serotonin syndrome?, Lancet Neurology (class evidence).
• W.T. Beaulieu et al. (2015), diversity of Periglandula in eight new Convolvulaceae hosts, Mycologia (15.8 to 3223 µg/g across the eight species; the value specific to A. nervosa could not be obtained).
• C. Ponté and M. Lapeyre-Mestre (2017), psychoactive effects of LSA, Thérapie (Toulouse addictovigilance, 4 cases in 2016).
• E.A.D. Schindler et al. (2015), indoleamine hallucinogens in cluster headache, J Psychoactive Drugs (survey; the denominator specific to LSA is not the 496 participants).
• Erowid, Hawaiian Baby Woodrose Vault (corpus of user reports, to be read on site; its licence forbids reproduction. Page inaccessible, HTTP 403, at the time of this search).
• RIVM, Risk assessment of Argyreia nervosa, letter report 2019-0210, 2019. Not read, deliberately not opened (PDF). It is the only document dedicated to a risk and dose assessment for this plant, and the biggest hole in this page. What circulates from it comes only from search engine renderings and is not cited here.
• J.M. Chao and A.H. Der Marderosian (1973), ergoline alkaloidal constituents of Hawaiian baby woodrose, J Pharm Sci 62(4):588-591. Not read: no indexed abstract, publisher pages in HTTP 403. It is the apparent source of the figure of 0.5 to 0.9% total alkaloids, which could therefore not be verified.
• W.E. Shawcross (1983), recreational use of the ergoline alkaloids of Argyreia nervosa, J Psychoactive Drugs 15(4):251-259, and W.H. Vogel et al. (1972), physiological disposition of isoergine, Psychopharmacologia 24(2):238-242. Not read, no abstract available. The first is indexed under the term dose-response relationship and could be the upstream origin of the dose figures that circulate.
• Albert Hofmann's self-experiment with ergine, much cited, was not reached through any primary source and is therefore not taken up here.