Calabash
StarLagenaria siceraria
Synonyms: Lagenaria leucantha var. depressa, Lagenaria leucantha var. makinoi, Lagenaria leucantha var. microcarpa, Lagenaria siceraria var. depressa, Cucurbita ciceraria, Pepo lagenarius, Lagenaria microcarpa, Lagenaria siceraria var. laevisperma, Lagenaria idolatrica, Lagenaria hispida, Lagenaria vulgaris var. clavata, Cucurbita lagenaria, Lagenaria vulgaris var. viscosa, Lagenaria siceraria var. gourda, Cucurbita leucantha, Cucumis bicirrha, Cucurbita longa, Cucurbita lagenaria var. villosa, Cucurbita lagenaria var. oblonga, Cucurbita idololatrica, Lagenaria vulgaris var. gourda, Cucumis lagenaria, Adenopus abyssinicus var. somaliensis, Lagenaria siceraria f. depressa, Lagenaria siceraria f. microcarpa, Lagenaria vulgaris var. pyriformis, Lagenaria vulgaris var. microcarpa, Cucurbita vittata, Trochomeria rehmannii, Lagenaria vulgaris, Lagenaria bicornuta, Lagenaria vittata, Lagenaria vulgaris subsp. asiatica, Lagenaria vulgaris var. depressa, Lagenaria siceraria var. microcarpa, Lagenaria vulgaris subsp. afrikana, Cucurbita pyriformis, Lagenaria siceraria subsp. asiatica, Lagenaria virginalis, Lagenaria lagenaria, Lagenaria vulgaris var. elongata, Lagenaria cochinchinensis, Lagenaria leucantha, Cucumis mairei, Lagenaria verrucosa, Cucurbita siceraria
Safety at a glance
No rule in our tables for this herb: pregnancy, breastfeeding, incompatible pairs (十八反 / 十九畏), herb–drug, dose ceiling. This is not a safety clearance.
Not graded — No toxicity grade is recorded. Most herbs in the catalogue carry none.
Traditionally used for
- Headaches
- Urinary & fluids
- Pain & joints
- Skin
Cautions & contraindications
- Bleeding disorders
- Seizure disorders
- Toxic — professional use only
Western Herbalism Properties
Traditional Uses
The calabash gourd has an exceptionally broad ethnographic footprint among Indigenous peoples of North America, where the great majority of recorded uses are non-medicinal. The Cherokee dried the gourds for use as ladles, dippers, water bottles, and ceremonial rattles (Hamel & Chiltoskey, 1975). The Hopi, Tewa, Zuni, and Acoma cultivated the species and fashioned the shells into rattles, masks, ceremonial containers, and storage vessels (Whiting, 1939; Robbins, Harrington & Freire-Marreco, 1916; Stevenson, 1915; Castetter, 1935). The Iroquois and Meskwaki used the gourds as utility vessels and rattles, and the Seminole and Houma carried water in calabashes (Waugh, 1916; Smith, 1928; Speck, 1941). Documented medicinal use is limited: the Cherokee employed the flesh as a poultice for headache (analgesic) and skin complaints (dermatological), while a small number of records report analgesic and psychological applications. Some southwestern groups consumed the seeds and immature fruits as a minor food (Hamel & Chiltoskey, 1975; Castetter, 1935).
Gallery
Botanical Description
Lagenaria siceraria, the calabash or bottle gourd, is an annual monoecious vine of the Cucurbitaceae, one of the earliest domesticated plants, with archaeobotanical records spanning Africa, Asia, and the Americas dating to at least 10,000 BP. The plant produces a stout, ridged, hairy climbing or trailing stem 5-15 m long, anchored by branched tendrils. The alternate leaves are large, broadly cordate to reniform, soft-pubescent on both faces, and emit a musky scent when crushed. Flowers are solitary, white, and open at dusk, pollinated by night-flying insects; staminate flowers are long-pedicelled, while the pistillate flowers sit on shorter stalks bearing an inferior ovary that develops into the characteristic gourd. Fruits are extraordinarily variable in shape — bottle, dipper, club, snake, basin — with a thin epicarp that hardens at maturity into a tough, waterproof shell enclosing a spongy white pulp and many flat, white-margined seeds. Mature dried gourds have served globally as containers, ladles, musical instruments, floats, and ritual objects, while immature fruits are eaten as a vegetable across Asia, Africa, and Latin America.
Active Constituents
Cucurbitacin B
Tetracyclic triterpenoid (cucurbitacin)Concentration: Quantified by a molecularly imprinted polymer assay at 2.81 mg per 100 g in commercial juice, 3.37 mg per 100 g in peel and 2.39 mg per 100 g in pulp; review figures put fruit cucurbitacin content generally below 130 ppm, but bitter fruits are the outliers that cause harm
Cucurbitacin B is the compound that turns an ordinary vegetable into a poisoning. It is intensely bitter and is the direct cause of the erosive oesophagitis, gastric erosions, ulcers, duodenitis, haematemesis and hypotension recorded after drinking bitter bottle gourd juice. It is also stable to processing: in the assay study, neither gamma irradiation nor beta-glucosidase treatment significantly reduced cucurbitacin concentration, so a practitioner should not assume that any kitchen or industrial treatment makes a bitter fruit safe. Bitterness is the only practical warning sign, and the correct response to it is to discard the fruit.
Cucurbitacins D, E, G and H
Tetracyclic triterpenoids (cucurbitacins)Concentration: Minor cucurbitacins accompanying cucurbitacin B in the fruit
The remaining cucurbitacins of the fruit, sharing the bitter taste and the cytotoxic profile of cucurbitacin B. Cucurbitacin D is described as increasing capillary permeability, which is the accepted explanation for the sustained hypotension and third-space fluid loss seen in severe bottle gourd poisoning rather than the bleeding alone.
Lagenin
Type 1 ribosome-inactivating protein with ribonucleolytic activityConcentration: Isolated from the seed; a protein constituent, not quantified as a percentage of the crude drug
A ribosome-inactivating protein characterised from bottle gourd seed in 2000. Ribosome-inactivating proteins arrest protein synthesis, and their presence is a reason to treat raw seed preparations differently from cooked fruit flesh. There is no evidence that lagenin contributes to the recognised bitter-fruit poisoning syndrome, which is a cucurbitacin effect.
Seed fixed oil, rich in linoleic acid
Triglyceride fixed oil (polyunsaturated fatty acids)Concentration: Crude fat reported at 45.0 to 47.8 g per 100 g of seed
The seed is close to half oil by weight, dominated by linoleic acid, which is why bottle gourd seed oil appears as a nutritional rather than a medicinal product. It carries none of the cucurbitacin risk of the bitter fruit pulp.
Seed protein
Storage proteinsConcentration: Crude protein reported at 35.0 to 37.2 g per 100 g of seed
The seed is an unusually protein-dense cucurbit seed. This is a food-composition fact rather than a pharmacological one and is included so that seed and fruit are not conflated.
Fucosterol and campesterol
PhytosterolsConcentration: Sterols identified in the fruit
Plant sterols of the fruit, of interest mainly as the chemical basis for the lipid-lowering and cardioprotective claims made for bottle gourd juice. No human trial has shown that these claims hold at achievable dietary intakes.
Isoquercitrin, kaempferol and related flavonoids
Flavonoids and flavonoid glycosidesConcentration: Present in the edible fruit; no consistent quantitative figures across the literature
The antioxidant fraction of the fruit, on which most of the in vitro pharmacology rests. Their presence does not offset the cucurbitacin hazard of a bitter fruit, and they are not a reason to drink the juice.
⚠ Drug Interactions
Warfarin, direct oral anticoagulants, aspirin and clopidogrel
This is the most important entry for this plant and it should not be softened. Bitter bottle gourd juice produces direct chemical injury to the upper gastrointestinal tract. In a consecutive series of fifteen patients reported from India, endoscopy after ingestion showed oesophagitis, gastric erosions, ulcers and duodenitis, and the patients presented with haematemesis and hypotension within fifteen minutes to six hours (Indian Journal of Gastroenterology, 2011). An anticoagulated or antiplatelet-treated patient who sustains that mucosal injury has no capacity to stop the bleed. There is no antidote for cucurbitacin toxicity; management is supportive only.
Clinical note: Do not recommend bottle gourd juice to any patient on an anticoagulant or antiplatelet. Tell patients on these drugs plainly that a bitter-tasting gourd, juice or cooked dish must be spat out and discarded, not finished. Any haematemesis after such an ingestion is an emergency.
NSAIDs, aspirin and systemic corticosteroids
The endoscopic picture after bitter bottle gourd ingestion is the same pattern of erosive injury that NSAIDs and corticosteroids cause, so the two insults are additive on the same tissue. The case series and single case reports consistently describe erosive oesophagitis, pangastritis and duodenitis, and hypotension requiring crystalloid and inotropic support.
Clinical note: Avoid the juice entirely in patients on chronic NSAIDs or steroids. If exposure has occurred, treat as a chemical gastritis: withhold the NSAID, start a proton pump inhibitor and arrange endoscopy if there is bleeding.
Antihypertensive drugs and diuretics
Hypotension is one of the defining features of bottle gourd poisoning and was present across the reported case series, requiring fluids and inotropes. Cucurbitacin D increases capillary permeability, so the fall in pressure reflects fluid shift out of the vasculature as well as gastrointestinal loss, and it does not correct quickly. Bottle gourd juice is, ironically, promoted in India precisely as a remedy for hypertension, so the patients most likely to drink it are the ones already on blood-pressure-lowering drugs.
Clinical note: Ask hypertensive patients directly whether they drink lauki or ghia juice as a health tonic. In a patient who presents hypotensive after such a drink, hold the antihypertensive, resuscitate with fluids, and do not attribute the low pressure to the medication alone.
Digoxin and other drugs sensitive to potassium loss
Repeated vomiting and diarrhoea are constant features of the poisoning syndrome, and the resulting potassium and magnesium depletion lowers the threshold for digoxin toxicity and for arrhythmia on QT-prolonging drugs. The mechanism is the well-understood consequence of gastrointestinal fluid loss rather than any direct chemical interaction with the cucurbitacins.
Clinical note: Check potassium and magnesium and obtain an ECG in any digoxin-treated patient presenting after bitter gourd ingestion.
Insulin and oral hypoglycaemic drugs
Bottle gourd juice is widely promoted in Indian folk practice for diabetes, so diabetic patients are a high-exposure group. The realistic hazard is not a pharmacodynamic glucose-lowering effect, for which human evidence is absent, but the vomiting and inability to eat that follow a toxic ingestion in a patient who has already taken insulin or a sulphonylurea that morning.
Clinical note: Ask diabetic patients about bottle gourd juice use. If a patient becomes unwell after drinking it, treat as sick-day rules: check glucose, adjust or hold the hypoglycaemic agent and rehydrate.
All orally administered medication
Vomiting begins within fifteen minutes to six hours of ingestion of the toxic juice and is followed by diarrhoea. Every oral drug taken in that window is at risk of being lost, which matters most for anticonvulsants, antiretrovirals, immunosuppressants and oral contraception.
Clinical note: Review which oral doses were due around the time of ingestion and replace or reschedule them; consider parenteral cover for critical drugs.
Ku Hu Lu and other bitter Cucurbitaceae drugs (Citrullus colocynthis, Momordica charantia, Trichosanthes species)
A caution specific to how this drug sits in a Chinese materia medica. Ku Hu Lu is the deliberately bitter gourd, Lagenaria siceraria var. gourda, used in Chinese medicine as a drastic water-expelling and emetic drug precisely because it is loaded with cucurbitacins; Hu Lu Ke is the ordinary non-bitter gourd used as a bland diuretic. These are the same species in different varieties and with opposite risk profiles, and their names and dried material are easily confused. Stacking a bitter Cucurbitaceae drug on top of a bottle gourd preparation, or receiving the bitter variety when the bland one was intended, multiplies the cucurbitacin dose.
Clinical note: Specify the variety when prescribing or sourcing. Taste is the practical assay: any bottle gourd material intended as the bland drug that tastes bitter is the wrong material and must be rejected. Do not combine with colocynth or other drastic Cucurbitaceae purgatives.
Dosage Calculator
⚖ Dosage Calculator
A weight-based mathematical estimate for Calabash. Not a prescription.
Evidence Tier
7 studies on recordRecorded studies by study design, strongest design at the top. This is a study-design tier only, not a GRADE rating: it does not weigh risk of bias, consistency or precision.
Systematic review / meta-analysis
0
Randomized controlled trial
0
Other clinical trial
0
Observational / case report
6
4 verified · 2 unverified
Show 6 studies
- Gastrointestinal toxicity due to bitter bottle gourd (Lagenaria siceraria)─a report of 15 cases
- Bottle gourd (Lagenaria siceraria) juice poisoning
- Bottle Gourd Juice: Poison or Panacea
- Health Drink Poisoning - An Unusual Case of Bottle Gourd Toxicity
- Bottle gourd (Lagenaria siceraria) toxicity: A rare case report
- Bottle gourd juice poisoning misdiagnosed as portal hypertension
In vitro / animal
1
0 verified · 1 unverified
Other / unclassified
0
Verified: design read from PubMed for a DOI that resolves to the cited paper Unverified: taken from the study's recorded description
Clinical Studies
Gastrointestinal toxicity due to bitter bottle gourd (Lagenaria siceraria)─a report of 15 cases
Consecutive case series of fifteen patients who developed toxicity after drinking bitter bottle gourd juice. Presentation was abdominal pain, vomiting, haematemesis, diarrhoea and hypotension within fifteen minutes to six hours of ingestion. Endoscopy showed oesophagitis, gastric erosions, ulcers and duodenitis. Hypotension needed crystalloid and inotropic support. All fifteen recovered within one to four days and the mucosal lesions healed within two weeks. This is the single most useful human dataset on the drug and it is observational, not a trial.
Bottle gourd (Lagenaria siceraria) juice poisoning
Single case report of a 52-year-old woman presenting with repeated haematemesis and shock after drinking bottle gourd juice, resuscitated with fluids, proton pump inhibitors and antiemetics and admitted for urgent endoscopy; she was discharged stable after four days. The authors state explicitly that there is no known antidote for cucurbitacin toxicity and that treatment is symptomatic only.
Bottle Gourd Juice: Poison or Panacea
Two further cases of poisoning with severe abdominal pain and haematemesis; both patients were hypotensive with oesophagitis, pangastritis and duodenitis on evaluation and were discharged after five days of conservative management. The authors note that the risk is higher in water-stressed arid regions, since drought stress is what drives cucurbitacin accumulation in the fruit.
Health Drink Poisoning - An Unusual Case of Bottle Gourd Toxicity
Case report of a 35-year-old man who drank concentrated bottle gourd juice as a health tonic and developed repeated vomiting, bloody diarrhoea and giddiness, requiring crystalloid resuscitation, proton pump inhibitors and antiemetics and four days of critical care. The authors again record that there is no specific antidote and that management is symptomatic.
Bottle gourd (Lagenaria siceraria) toxicity: A rare case report
Case report published in a United Kingdom general medical journal, which matters because it shows the poisoning presenting outside South Asia in diaspora populations who use the juice as a tonic. Clinicians unfamiliar with the exposure are the ones most likely to miss it.
Bottle gourd juice poisoning misdiagnosed as portal hypertension
Case report in which bottle gourd juice poisoning was initially mistaken for variceal bleeding from portal hypertension. Directly relevant to practice: a patient bleeding after drinking the juice can be worked up for the wrong diagnosis, and the exposure history is what prevents that.
Novel detection method to rapidly quantify toxic cucurbitacin in Lagenaria siceraria (bottle gourd)
Develops a molecularly imprinted polymer assay for cucurbitacin B and applies it to commercial bottle gourd juice and to fresh peel and pulp, finding 2.81, 3.37 and 2.39 mg per 100 g respectively. The safety-relevant finding is that neither gamma irradiation nor beta-glucosidase treatment significantly reduced cucurbitacin concentration, which undercuts any assumption that processing renders a bitter fruit safe.
Historical Texts
Shen Nong Ben Cao Jing (Divine Husbandman's Classic of Materia Medica), entry for Ku Hu, the bitter gourd
Han dynasty compilation, traditionally dated to around the 1st to 2nd century CE (Chinese tradition)Ben Cao Gang Mu, Li Shizhen, entries for Hu Lu (the bland gourd) and Ku Hu (the bitter gourd)
Ming dynasty, completed 1578, first printed 1596 (Chinese tradition)Sushruta Samhita, Alabu Avacharana among the raktamokshana (bloodletting) procedures
Ayurvedic classical surgical tradition, compiled in its received form by roughly the 3rd to 4th century CE (Ayurvedic tradition)Ayurvedic dietetic and nighantu tradition distinguishing sweet alabu from bitter (tikta) alabu
Classical and mediaeval Ayurvedic tradition (Ayurvedic tradition)References
- Saeed M, Khan MS, Amir K, Bi JB, Asif M, Madni A, Kamboh AA, Manzoor Z, Younas U, Chao S. Lagenaria siceraria fruit: A review of its phytochemistry, pharmacology, and promising traditional uses . Frontiers in Nutrition (2022) [DOI]
- Wang HX, Ng TB. Lagenin, a novel ribosome-inactivating protein with ribonucleolytic activity from bottle gourd (Lagenaria siceraria) seeds . Life Sciences (2000) [DOI]
- Rojas-Sandoval J. Lagenaria siceraria (bottle gourd) . CABI Compendium (2018) [DOI]
This information is for educational purposes only and is not intended to replace professional medical advice. Always consult a qualified healthcare provider before using any herbal remedy, especially if you are pregnant, nursing, or taking medications.
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