Elettaria cardamomum · PhytoNexus

01 Identity and provenance

Accepted binomial: Elettaria cardamomum
Common names: Cardamom
Family (APG IV): Zingiberaceae
Part used: Fruit
Verification tier: Tier 2 · Verified Clinical columns reviewed and a source is on record.
Reviewer note (2026 audit): Reference not supplied - claim unverified against primary literature.

02 Constituent chemistry

Chemical class	Marker compound	Synthetic analogue in use
Essential oil	1,8-Cineole Fruit	Eucalyptol

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: Carminative
Marketed in: Dabur Hing Goli
Reported adverse effects: heartburn

04 Interaction matrix

Source column, verbatim: Anticoagulants
Normalised onto 1 canonical drug class below.

Curated from the reviewed source

Drug class	Severity	Mechanism type	Provenance	Expected effect
Anticoagulants (vitamin-K antagonists, DOACs) Haemostasis	3Major	PD-additive + PK-CYP2C9	curated B	INR destabilisation in either direction; ecchymosis, epistaxis, gum bleed…	why ▾
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 B - reviewed clinical column, source pending Matched on “anticoagulants” 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
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
Antiepileptics CNS	3Major	PK-CYP induction + PD-antagonistic	predicted D	Breakthrough seizures, status epilepticus, or additive sedation and ataxi…	why ▾
Chemistry of this pair. Volatile monoterpenes are GABA-A antagonists at higher exposure, lowering seizure threshold, and are metabolised to reactive intermediates. Class mechanism. Enzyme-inducing botanicals lower plasma anticonvulsant concentrations, while GABAergic constituents add sedation and a few (thujone, camphor, beta-asarone, pinene-rich oils) are directly proconvulsant and lower seizure threshold. Expected Breakthrough seizures, status epilepticus, or additive sedation and ataxia. Management Measure anticonvulsant levels before and 2-4 weeks after any change. Avoid proconvulsant essential oils entirely in epilepsy. Onset delayed Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
Hepatotoxic drugs Organ toxicity	3Major	Organ-toxicity additive	predicted D	Transaminase elevation, cholestasis, sinusoidal obstruction syndrome, acu…	why ▾
Chemistry of this pair. Volatile monoterpenes are GABA-A antagonists at higher exposure, lowering seizure threshold, and are metabolised to reactive intermediates. 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
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 monoterpenes are GABA-A antagonists at higher exposure, lowering seizure threshold, and are metabolised to reactive intermediates. 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

The audit recorded no hazard beyond the interaction profile. The controlled-vocabulary field reads not assessed, which means the assessment has not been done rather than that it came back clear.

06 Confusable material

These entries could be mistaken for this one in trade, in the herbarium, or in a prescription. Powdered material is often indistinguishable, so the check is macroscopic, microscopic and chromatographic rather than nominal.

Amomum subulatum

Black Cardamom

Zingiberaceae

Shares the common name "cardamom"

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
Achillea millefolium Yarrow	Asteraceae	5	0.42
Artemisia absinthium Wormwood	Asteraceae	5	0.71
Melaleuca alternifolia Tea Tree	Myrtaceae	4	0.80
Amomum subulatum Black Cardamom	Zingiberaceae	4	0.80
Salvia rosmarinus Rosemary	Lamiaceae	4	0.80
Salvia officinalis Sage	Lamiaceae	4	0.80

10 References and notes

No citation is on record for this entry. That is itself the finding: the audit flagged it, and it is why the entry does not carry an A evidence grade.

Curator notes

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