Areca catechu · PhytoNexus

01 Identity and provenance

Accepted binomial: Areca catechu
Common names: Areca Nut
Family (APG IV): Arecaceae
Part used: Seed
Verification tier: Tier 2 · Verified Clinical columns reviewed and a source is on record.
Reviewer note (2026 audit): Gupta PC & Ray CS. Areca nut use and cancer in India | PMC11414337 (OSMF prevalence) | VERIFIED 2026 - synthetic analogue, application, interactions, side effects and references populated from retrieved primary/regulatory sources (see References). Interaction entries are labelled CLINICAL (case reports or trials in humans) vs THEORETICAL (in-vitro or animal only). Marketed-formulation column intentionally left blank. | REGULATORY

02 Constituent chemistry

Chemical class	Marker compound	Synthetic analogue in use
Pyridine alkaloids	Arecoline Seed	Pilocarpine (FUNCTIONAL - arecoline is a muscarinic agonist).

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: NO RECOMMENDED THERAPEUTIC USE. Historically an anthelmintic and masticatory. Listed here as a major public-health hazard, not as a therapy.
Reported adverse effects: IARC GROUP 1 CARCINOGEN (areca nut, with and without tobacco). Causes oral submucous fibrosis - irreversible, progressive trismus and dysphagia that persists after cessation; malignant transformation reported at 3-6%. Also leukoplakia, and cancer of oral cavity, pharynx and oesophagus. OSMF prevalence 12.9% in one Indian areca-user cohort. Associated with liver injury. Dependence-forming.

04 Interaction matrix

Source column, verbatim: CLINICAL: additive cholinergic effect; antagonism of anticholinergic drugs. Chewing with slaked lime hydrolyses arecoline to arecaidine, increasing carcinogenicity. Concurrent tobacco greatly amplifies risk.
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 ▾
Chemistry of this pair. These alkaloids inhibit acetylcholinesterase or agonise muscarinic receptors, raising synaptic acetylcholine. 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
Cholinesterase inhibitors and cholinergic drugs Autonomic	4Contraindicated	PD-additive	predicted D	Cholinergic crisis: bradycardia, bronchorrhoea, bronchospasm, miosis, sei…	why ▾
Chemistry of this pair. These alkaloids inhibit acetylcholinesterase or agonise muscarinic receptors, raising synaptic acetylcholine. Class mechanism. Physostigmine-, galantamine- and arecoline-type constituents inhibit acetylcholinesterase or agonise muscarinic receptors, adding to donepezil, rivastigmine, neostigmine or pyridostigmine. Expected Cholinergic crisis: bradycardia, bronchorrhoea, bronchospasm, miosis, seizures, weakness that mimics myasthenic crisis. Management Avoid. In suspected crisis distinguish cholinergic from myasthenic weakness before giving further anticholinesterase. Onset rapid 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. Alkaloidal bases have pH-dependent absorption and commonly interact with hepatic CYP isoenzymes and efflux transporters. 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
Antacids, PPIs and H2 blockers Gastrointestinal	3Major	PK-absorption	predicted D	Reduced or erratic absorption of alkaloids; heartburn and reflux from pre…	why ▾
Chemistry of this pair. Alkaloidal bases have pH-dependent absorption and commonly interact with hepatic CYP isoenzymes and efflux transporters. Class mechanism. Gastric pH elevation alters the dissolution and ionisation of alkaloidal and enteric-coated botanical products; menthol- and peppermint-oil products lose their enteric protection at high pH and can be released prematurely. Expected Reduced or erratic absorption of alkaloids; heartburn and reflux from premature release of volatile-oil preparations. Management Separate administration by 2 hours. Avoid non-enteric peppermint oil in reflux disease. Onset unspecified Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism

05 Hazard register

carcinogen classification - IARC Group 1; oral submucous fibrosi

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
Physostigma venenosum Calabar Bean	Fabaceae	4	0.50
Duboisia myoporoides Corkwood	Solanaceae	4	0.67
Galanthus nivalis Snowdrop	Amaryllidaceae	4	0.80
Huperzia serrata Chinese Club Moss	Lycopodiaceae	4	0.80
Atropa belladonna Belladonna	Solanaceae	3	0.50
Hyoscyamus niger Henbane	Solanaceae	3	0.50

10 References and notes

Source column: IARC Monographs Vol 85: Betel-quid and Areca-nut Chewing

IARC Monographs Vol 85: Betel-quid and Areca-nut Chewing

Official monograph manual

BibTeX for all 1 records

@article{anon,
  title = {IARC Monographs Vol 85: Betel-quid and Areca-nut Chewing},
}

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