Camellia sinensis · PhytoNexus

01 Identity and provenance

Accepted binomial: Camellia sinensis
Common names: Green Tea
Family (APG IV): Theaceae
Part used: Leaf
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
Catechins (flavan-3-ols), flavonoids, methylxanthines, phenolic acids, amino acids	Epigallocatechin gallate (EGCG), Epicatechin gallate (ECG), Epicatechin (EC), Epigallocatechin (EGC), Caffeine, Theanine Leaf	Dexmethylphenidate, Modafinil (stimulant properties); Rosuvastatin, Atorvastatin (functional cardioprotective similarity); Probucol (antioxidant similarity)

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: Antioxidant, weight management, cardiovascular health, cognitive enhancement, anti-inflammatory, anticancer (adjunct research), metabolic syndrome
Marketed in: Green tea capsules, tea bags, ready-to-drink beverages, nutraceutical tablets, antioxidant supplements, cosmetic creams, topical gels
Reported adverse effects: Insomnia, anxiety, palpitations, gastrointestinal irritation, nausea, caffeine-related effects, rare hepatotoxicity (high-dose extracts)

04 Interaction matrix

Source column, verbatim: Anticoagulants (warfarin), antiplatelets, stimulants, antihypertensives, antidiabetic drugs, iron supplements, CYP-metabolized drugs, bortezomib
Normalised onto 8 canonical drug classes below.

Curated from the reviewed source

Drug class	Severity	Mechanism type	Provenance	Expected effect
Antihypertensives Cardiovascular	4Contraindicated	PD-additive	curated B	Orthostatic hypotension, dizziness, syncope and falls; or loss of blood-p…	why ▾
Chemistry of this pair. Phenethylamine and methylxanthine constituents release noradrenaline and block adenosine receptors, producing direct sympathomimetic drive. Class mechanism. Vasodilator, diuretic, ACE-inhibitory and calcium-antagonist activity in botanical extracts adds to prescribed blood-pressure lowering. A minority (ephedrine-, glycyrrhizin- and caffeine-bearing) act in the opposite direction and antagonise control. Expected Orthostatic hypotension, dizziness, syncope and falls; or loss of blood-pressure control with pressor botanicals. Management Home BP log for 2 weeks after any change. Warn about postural symptoms; review in the elderly and in those on multiple agents. Onset rapid Evidence B - reviewed clinical column, source pending Matched on “antihypertensives” Find evidence for this pair Map this mechanism
CNS stimulants and sympathomimetics CNS	4Contraindicated	PD-additive	curated B	Tachycardia, hypertension, arrhythmia, insomnia, anxiety, stroke and myoc…	why ▾
Chemistry of this pair. Phenethylamine and methylxanthine constituents release noradrenaline and block adenosine receptors, producing direct sympathomimetic drive. Class mechanism. Ephedrine, pseudoephedrine, caffeine, synephrine and cathine-type constituents add to prescribed stimulant and decongestant sympathomimetic drive. Expected Tachycardia, hypertension, arrhythmia, insomnia, anxiety, stroke and myocardial infarction in susceptible people. Management Avoid in cardiovascular disease, hyperthyroidism and pregnancy. Ask about weight-loss and sports supplements by brand. Onset rapid Evidence B - reviewed clinical column, source pending Matched on “stimulants” Find evidence for this pair Map this mechanism
Cytotoxic and targeted anticancer drugs Oncology	4Contraindicated	PK-CYP3A4/UGT + PD-antagonistic	curated B	Neutropenic sepsis and severe diarrhoea from over-exposure, or reduced an…	why ▾
Chemistry of this pair. Flavonoids inhibit CYP3A4, CYP1A2, OATP1B1 and UGT to a variable extent and have measurable antiplatelet activity. Class mechanism. Botanical CYP3A4 and UGT1A1 modulation alters exposure to irinotecan, taxanes, vinca alkaloids and kinase inhibitors. High-dose antioxidant botanicals may also oppose the oxidative mechanism of some cytotoxics and of proteasome inhibitors. Expected Neutropenic sepsis and severe diarrhoea from over-exposure, or reduced antitumour effect; boronic-acid proteasome inhibitors are directly antagonised by polyphenols. Management No botanical should be taken during active cytotoxic therapy without oncology sign-off. Record all supplements in the chemotherapy chart. Onset unspecified Evidence B - reviewed clinical column, source pending Matched on “bortezomib” Find evidence for this pair Map this mechanism
Narrow-therapeutic-index CYP3A4 substrates Pharmacokinetic	4Contraindicated	PK-CYP3A4	curated B	Toxic accumulation or subtherapeutic failure of the co-prescribed drug, s…	why ▾
Chemistry of this pair. Flavonoids inhibit CYP3A4, CYP1A2, OATP1B1 and UGT to a variable extent and have measurable antiplatelet activity. 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 B - reviewed clinical column, source pending Matched on “cyp-metabolized drugs” Find evidence for this pair Map this mechanism
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
Antidiabetic drugs (insulin, sulfonylureas, biguanides, GLP-1, SGLT2) Endocrine	3Major	PD-additive	curated B	Symptomatic hypoglycaemia, sweating, tremor, confusion; severe events rep…	why ▾
Class mechanism. Hypoglycaemic botanicals act through insulin secretagogue, insulin-sensitising, alpha-glucosidase-inhibiting or glucose-transport routes. Added to a titrated pharmacological regimen the effects summate rather than plateau. Expected Symptomatic hypoglycaemia, sweating, tremor, confusion; severe events reported with insulin and sulfonylureas. Management Increase self-monitoring frequency for 2 weeks after starting or stopping. Anticipate a downward dose adjustment of insulin or sulfonylurea. Onset rapid Evidence B - reviewed clinical column, source pending Matched on “antidiabetic drugs” Find evidence for this pair Map this mechanism
Antiplatelet agents Haemostasis	3Major	PD-additive	curated B	Prolonged bleeding time, surgical and post-procedural bleeding, bruising,…	why ▾
Chemistry of this pair. Flavonoids inhibit CYP3A4, CYP1A2, OATP1B1 and UGT to a variable extent and have measurable antiplatelet activity. 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 B - reviewed clinical column, source pending Matched on “antiplatelets” Find evidence for this pair Map this mechanism
Iron, calcium and mineral supplements Nutrition	2Moderate	PK-chelation	curated B	Failure of iron-deficiency correction, unexplained non-response to oral i…	why ▾
Class mechanism. Tannins, phytates, oxalates and mucilage form insoluble complexes with divalent and trivalent cations in the gut lumen, reducing absorption of both the mineral and any co-administered chelating drug. Expected Failure of iron-deficiency correction, unexplained non-response to oral iron or calcium. Management Separate mineral doses from tannin- and fibre-rich botanicals by at least 2 hours; take iron with ascorbate instead. Onset unspecified Evidence B - reviewed clinical column, source pending Matched on “iron supplements” 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
Antiarrhythmics Cardiovascular	4Contraindicated	PD-additive + electrolyte-mediated	predicted D	Proarrhythmia, QT prolongation, torsade de pointes, ventricular arrhythmi…	why ▾
Chemistry of this pair. Phenethylamine and methylxanthine constituents release noradrenaline and block adenosine receptors, producing direct sympathomimetic drive. Class mechanism. Botanicals that shift potassium or magnesium, block sodium or potassium channels, or prolong repolarisation add to class I and class III antiarrhythmic effects on an already unstable myocardium. Expected Proarrhythmia, QT prolongation, torsade de pointes, ventricular arrhythmia. Management Avoid. If unavoidable, baseline and follow-up ECG with QTc measurement plus potassium and magnesium correction. Onset rapid Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
Cardiotoxic drugs Organ toxicity	4Contraindicated	Organ-toxicity additive	predicted D	Arrhythmia, reduced ejection fraction, myocarditis-like presentation.	why ▾
Chemistry of this pair. Phenethylamine and methylxanthine constituents release noradrenaline and block adenosine receptors, producing direct sympathomimetic drive. Class mechanism. Aconitine-type alkaloids, cardenolides and high-dose ephedrine add to anthracycline, trastuzumab and antiarrhythmic myocardial toxicity. Expected Arrhythmia, reduced ejection fraction, myocarditis-like presentation. Management Avoid during cardiotoxic chemotherapy. Baseline and follow-up echocardiography where exposure has occurred. Onset unspecified Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
Statins and lipid-lowering drugs Cardiovascular	2Moderate	PK-CYP3A4/OATP	predicted D	Myalgia, raised creatine kinase, rhabdomyolysis, hepatic transaminase ele…	why ▾
Chemistry of this pair. Flavonoids inhibit CYP3A4, CYP1A2, OATP1B1 and UGT to a variable extent and have measurable antiplatelet activity. Class mechanism. CYP3A4 and OATP1B1 inhibition by furanocoumarin- and flavonoid-rich botanicals raises simvastatin, atorvastatin and lovastatin exposure. Some botanicals themselves contain monacolin K, which is chemically lovastatin. Expected Myalgia, raised creatine kinase, rhabdomyolysis, hepatic transaminase elevation. Management Ask specifically about red-yeast-rice type products. Check CK and ALT if muscle symptoms appear; prefer a non-3A4 statin. Onset unspecified 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.

Gaultheria fragrantissima

Wintergreen

Ericaceae

Shares the common name "green"

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
Phyllanthus amarus Bhui Amla	Phyllanthaceae	8	0.53
Vaccinium macrocarpon Cranberry	Ericaceae	7	0.64
Vaccinium myrtillus Bilberry	Ericaceae	7	0.54
Cyperus rotundus Nagarmotha	Cyperaceae	7	0.54
Garcinia indica Kokum	Clusiaceae	7	0.58
Citrus aurantium Bitter Orange	Rutaceae	5	0.38

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.

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