Myristica fragrans · PhytoNexus

01 Identity and provenance

Accepted binomial: Myristica fragrans
Common names: Nutmeg
Family (APG IV): Myristicaceae
Part used: Seed, Aril
Verification tier: Tier 2 · Verified Clinical columns reviewed and a source is on record.
Reviewer note (2026 audit): Demetriades AK et al. Emerg Med J 2005 | PMC11571034 (nutmeg poisoning with electrolyte abnormalities) | PMC11754422 (mace poisoning, reversible coma in a child) | INCHEM PIM 355 | VERIFIED 2026 (batch 6) - synthetic analogue, application, interactions, side effects and references populated from retrieved primary/regulatory sources. Interactions labelled CLINICAL vs THEORETICAL. Marketed-formulation column intentionally blank. | DOSE

02 Constituent chemistry

Chemical class	Marker compound	Synthetic analogue in use
Volatile oil, phenylpropanoids	Myristicin Seed, Aril	No therapeutic analogue. Myristicin is metabolised to 3-methoxy-4,5-methylenedioxyamphetamine (MMDA), which accounts for the psychedelic effect; it also weakly inhibits monoamine oxidase.

The analogue column is what makes the interaction reasoning tractable: where a constituent has a marketed structural counterpart, the counterpart's interaction profile is the starting hypothesis for the plant.

Looking up structures and physicochemical properties from PubChem…

03 Stated application

Reported activity: Culinary spice (seed = nutmeg, aril = mace). Traditional carminative. NO CLINICAL TRIALS SUPPORT ANY THERAPEUTIC DOSE.
Reported adverse effects: THE CULINARY AND TOXIC DOSES ARE UNCOMFORTABLY CLOSE. Around 5 g of ground nutmeg (1-2 mg myristicin) is a recognised toxic dose; 2-3 teaspoons produce an anticholinergic-like picture and 2 tablespoons or more can cause severe psychosis and dehydration. Onset 3-6 h, effects up to 72 h. Features: hallucinations, delirium, a characteristic sense of impending doom, tachycardia, flushing, dry mouth, mydriasis, nausea. DIAGNOSTIC TRAP: laboratory tests are typically normal and the toxidrome is CONTRADICTORY - mydriasis WITH a preserved light reflex, mixing anticholinergic and sympathomimetic features - so it fits no standard textbook pattern and is easily missed. Anticholinergic dry mouth can drive excessive water intake to the point of hyponatraemia. Paediatric accidental ingestion is well described, including a 6-year-old in reversible coma after eating six pieces of mace. Recreational misuse concentrates in ages 13-20. Deaths are rare but reported.

04 Interaction matrix

Source column, verbatim: CLINICAL: MAO-inhibitory activity means caution with serotonergic and sympathomimetic drugs. Additive sedation - combined diazepam and nutmeg oil produced respiratory depression in mice. Anticholinergic burden adds to other antimuscarinics.
Normalised onto 1 canonical drug class below.

Curated from the reviewed source

Drug class	Severity	Mechanism type	Provenance	Expected effect
Anticholinergics Autonomic	4Contraindicated	PD-additive	curated A	Anticholinergic toxidrome: dry mouth, urinary retention, blurred vision, …	why ▾
Class mechanism. Tropane alkaloids (atropine, hyoscine, hyoscyamine) are competitive muscarinic antagonists; added to prescribed anticholinergics, antihistamines or tricyclics the burden summates. Expected Anticholinergic toxidrome: dry mouth, urinary retention, blurred vision, tachycardia, delirium, hyperthermia. Management Calculate total anticholinergic burden. Avoid in older adults, prostatism and narrow-angle glaucoma. Onset rapid Evidence A - human data with a cited source Matched on “anticholinergic” Find evidence for this pair Map this mechanism

Predicted from constituent chemistry

These edges are not clinical findings. Each one is a rule inference: a constituent class in this plant is known to act on a target that the drug class also acts on. They are shown because a blank cell reads as “safe”, and for a Tier 1 entry a blank cell only means “not yet looked at”. Treat them as a literature-search agenda, not as a warning.

Drug class	Severity	Mechanism type	Provenance	Expected effect
Anticoagulants (vitamin-K antagonists, DOACs) Haemostasis	4Contraindicated	PD-additive + PK-CYP2C9	predicted D	INR destabilisation in either direction; ecchymosis, epistaxis, gum bleed…	why ▾
Chemistry of this pair. Phenylpropanoids inhibit platelet aggregation and thromboxane synthesis and are direct mucosal irritants; some deplete hepatic glutathione at high dose. Class mechanism. Coumarin-, salicylate- and coumestan-bearing botanicals add to vitamin-K-antagonist effect; several also compete for CYP2C9 and CYP3A4, raising S-warfarin exposure. Botanicals rich in vitamin K1 act in the opposite direction and blunt anticoagulation. Expected INR destabilisation in either direction; ecchymosis, epistaxis, gum bleeding, GI or intracranial haemorrhage. Management Do not start or stop the botanical without INR cover. Check INR at 3-5 days and again at 2 weeks. Document the product, batch and dose in the anticoagulation record. Onset rapid Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
Antiplatelet agents Haemostasis	4Contraindicated	PD-additive	predicted D	Prolonged bleeding time, surgical and post-procedural bleeding, bruising,…	why ▾
Chemistry of this pair. Phenylpropanoids inhibit platelet aggregation and thromboxane synthesis and are direct mucosal irritants; some deplete hepatic glutathione at high dose. Class mechanism. Organosulfur compounds, gingerols, salicylates, ginkgolides and eugenol inhibit thromboxane A2 synthesis, platelet aggregation and PAF-mediated activation, duplicating the pharmacology of aspirin and P2Y12 blockers. Expected Prolonged bleeding time, surgical and post-procedural bleeding, bruising, haematuria. Management Stop the botanical 7-14 days before elective surgery or neuraxial anaesthesia. Record it on the pre-operative medicines list. Onset rapid Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
Hepatotoxic drugs Organ toxicity	4Contraindicated	Organ-toxicity additive	predicted D	Transaminase elevation, cholestasis, sinusoidal obstruction syndrome, acu…	why ▾
Chemistry of this pair. Phenylpropanoids inhibit platelet aggregation and thromboxane synthesis and are direct mucosal irritants; some deplete hepatic glutathione at high dose. Class mechanism. Pyrrolizidine alkaloids, high-dose anthraquinones, kava constituents and germander-type diterpenes cause hepatocellular or sinusoidal injury that adds to the risk from paracetamol, isoniazid, methotrexate, azoles and statins. Expected Transaminase elevation, cholestasis, sinusoidal obstruction syndrome, acute liver failure. Management Baseline and 4-weekly ALT and bilirubin. Stop the botanical at any transaminase rise above three times the upper reference limit. Onset unspecified Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
Narrow-therapeutic-index CYP3A4 substrates Pharmacokinetic	4Contraindicated	PK-CYP3A4	predicted D	Toxic accumulation or subtherapeutic failure of the co-prescribed drug, s…	why ▾
Chemistry of this pair. Volatile terpenes are lipophilic, cross membranes readily and induce or inhibit CYP2B6 and CYP3A4 depending on the constituent. Class mechanism. Furanocoumarins, bergamottin, piperine, glabridin and berberine inhibit CYP3A4; hyperforin, andrographolide and several diterpenes induce it through PXR. Because CYP3A4 handles roughly half of marketed drugs, the affected list is broad and the direction is product-specific. Expected Toxic accumulation or subtherapeutic failure of the co-prescribed drug, sometimes fatal for antiarrhythmics, immunosuppressants and oncology agents. Management Screen the full regimen for 3A4 substrates. Where the substrate has a narrow index, avoid rather than monitor. Onset unspecified Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
NSAIDs Analgesia	4Contraindicated	PD-additive	predicted D	Peptic ulceration, upper GI bleeding, acute kidney injury in volume-deple…	why ▾
Chemistry of this pair. Phenylpropanoids inhibit platelet aggregation and thromboxane synthesis and are direct mucosal irritants; some deplete hepatic glutathione at high dose. Class mechanism. Salicylate-, coumarin- and eugenol-bearing botanicals add both antiplatelet activity and direct gastric mucosal irritation to cyclo-oxygenase inhibition; several also reduce renal prostaglandin-dependent perfusion. Expected Peptic ulceration, upper GI bleeding, acute kidney injury in volume-depleted patients. Management Avoid in ulcer history. Add gastroprotection where the combination is unavoidable, and monitor renal function in the elderly. Onset rapid Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
Topical antiseptics, keratolytics and irritants Dermatology	3Major	PD-additive local	predicted D	Contact dermatitis, chemical burn, photoirritation, unexpected systemic a…	why ▾
Chemistry of this pair. Volatile terpenes are lipophilic, cross membranes readily and induce or inhibit CYP2B6 and CYP3A4 depending on the constituent. Class mechanism. Essential-oil terpenes, capsaicinoids and phorbol-type diterpenes add to the barrier disruption caused by topical antiseptics, retinoids and keratolytics, and increase percutaneous absorption of anything applied with them. Expected Contact dermatitis, chemical burn, photoirritation, unexpected systemic absorption from broken skin. Management Patch test first. Never apply undiluted essential oils to broken or freshly shaved skin, or with occlusion. Onset rapid Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism

05 Hazard register

threshold - Culinary and toxic doses are close (~5 g toxic). Als

06 Confusable material

No same-genus or shared-common-name entry in the corpus.

07 Mechanism map

Chemistry sorts to the left, pharmacology to the right. Dashed edges are predicted. Drag nodes, scroll to zoom, export at 3× for a figure.

species

chemical class

marker compound

drug class

expected effect

hazard

08 Open literature

Abstract-scoped query built from this binomial, its common names and its marker compounds, run live against Europe PMC, PubMed and OpenAlex, then ranked locally against an evidence hierarchy.

Checking openFDA spontaneous reports…

09 Isomechanistic neighbours

Species whose interaction profile overlaps this one, ranked by shared severity weight rather than by count — a shared contraindication counts for more than a shared minor signal. Practical use: these are the plants you should not stack with this one, because the mechanisms summate.

Species	Family	Shared classes	Jaccard
Ocimum tenuiflorum Tulsi	Lamiaceae	6	0.67
Thymus vulgaris Thyme	Lamiaceae	6	0.86
Origanum vulgare Oregano	Lamiaceae	6	0.86
Cinnamomum cassia Cassia Cinnamon	Lauraceae	6	0.75
Achillea millefolium Yarrow	Asteraceae	5	0.36
Artemisia absinthium Wormwood	Asteraceae	5	0.56

10 References and notes

Source column: Rahman NAA et al. Int J Adv Sci Eng Inf Technol 2015;5:212-5

Rahman NAA et al. Int J Adv Sci Eng Inf Technol 2015

Rahman NAA et al. Int J Adv Sci Eng Inf Technol 2015 manual

5:212-5

manual

BibTeX for all 2 records

@article{RahmanNAAe2015,
  title = {Rahman NAA et al. Int J Adv Sci Eng Inf Technol 2015},
  author = {Rahman NAA et al.},
  journal = {Int J Adv Sci Eng Inf Technol},
  year = {2015},
}

@article{anon,
  title = {5:212-5},
}

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