Jewel Vine (Derris elliptica)

🔴 This page exists to correct a mistake. Derris elliptica — jewel vine, tuba root, akar tuba — is the classical botanical source of rotenone. Rotenone is an insecticide and a piscicide: a fish poison. Across Southeast Asia the pounded root has been thrown into dammed streams for centuries to stun fish so they can be scooped out by hand. That is what this plant is for. It is not a remedy, it has never been an internal remedy in any major traditional system, and it should never be swallowed.

Rotenone blocks complex I of the mitochondrial electron transport chain — it switches off the cell's ability to make ATP from NADH. In rodents, systemic rotenone reliably destroys dopamine neurons in the substantia nigra and produces α-synuclein inclusions, which is why it is one of the standard laboratory models of Parkinson's disease. Epidemiological work in farmworkers has associated occupational rotenone use with a higher risk of Parkinson's in humans. Deliberate ingestion of rotenone products has killed adults and at least one small child.

Jewel vine appears on herb lists mostly because of database contamination and name confusion — in particular with Derris scandens, a genuinely medicinal relative used in Thai traditional medicine with real clinical trials behind it. Those are different plants. This page explains what Derris elliptica actually is, how it is genuinely used, and why there is no dosage section below.

Table of Contents

  1. 🔴 Safety Flag: This Is a Pesticide, Not a Remedy
  2. Overview
  3. Names and Identification
  4. Traditional Use: Tuba Fishing and Parasite Control
  5. Active Compounds: Rotenone and the Rotenoids
  6. How Rotenone Works: Shutting Down Complex I
  7. Why Fish Die So Easily and Mammals Less So
  8. Rotenone and Parkinson's Disease
  9. Human Poisoning
  10. Regulatory Status and the "Natural Pesticide" Lesson
  11. Why It Turns Up on Herb Lists
  12. Forms and Preparations
  13. Dosage: There Is No Safe Oral Dose
  14. Cautions and Contraindications
  15. Key Research Papers
  16. Connections

🔴 Safety Flag: This Is a Pesticide, Not a Remedy

Four statements, plainly:

  1. Derris elliptica root is a commercial insecticide raw material. Between roughly the 1920s and the 1950s it was farmed on plantations in Malaya and the Dutch East Indies and shipped worldwide as "derris dust" and "derris root". The trade was priced on rotenone content, the way coffee is priced on grade.
  2. Its traditional use is to poison fish and external parasites, not to treat illness from the inside. Tuba fishing is a harvesting technique. Derris dust on cattle is delousing. Neither is internal medicine.
  3. Swallowing rotenone has killed people. There are published forensic cases of fatal rotenone poisoning after deliberate ingestion of pesticide products, and a documented paediatric death.
  4. Rotenone is the standard laboratory tool for causing Parkinsonian brain damage in animals. Researchers use it precisely because it works: it kills the dopamine neurons that Parkinson's disease kills.

If you have been offered Derris elliptica, "tuba root", "derris root" or "jewel vine" as a supplement, a detox, a parasite cleanse or a traditional tonic, that offer is wrong on the facts. Do not take it. If someone has swallowed a derris or rotenone product, treat it as a poisoning emergency and contact your national poisons centre or emergency services immediately.

Overview

Derris elliptica (Wall.) Benth. is a woody climbing legume in the pea family, Fabaceae — the same family as beans, peanuts, liquorice and clover. It is a vigorous liana that scrambles into forest edges and secondary growth, with pinnate leaves of glossy leaflets and drooping sprays of pink-to-white pea flowers. It is native to Southeast Asia: Malaysia, Indonesia, the Philippines, mainland Indochina and adjacent regions, and it has been planted well outside that range.

The part used is the root, and the active material is concentrated there. Roots are dug, washed, sliced or pounded, and either used fresh — the crushed root releases a milky sap — or dried and ground for storage and trade. Historically the dried powder was sold on assay: commercial derris root was traded on its rotenone percentage, commonly a few percent of dry root weight and reported considerably higher in selected cultivated strains. That variation is one reason the material is unpredictable.

A note on taxonomy: some floras now place this species in the segregate genus Paraderris, as Paraderris elliptica (Wall.) Adema. Both names refer to the same plant, and older literature and the entire pesticide record use Derris elliptica.

Names and Identification

Binomial: Derris elliptica (Wall.) Benth., also treated as Paraderris elliptica.  Family: Fabaceae (Leguminosae).  NCBI Taxonomy entry.

⚠️ The confusion that matters: Derris elliptica is not Derris scandens

This is the single most important identification point on the page, because it is the likeliest reason someone lands here looking for a herb.

Because databases and supplement catalogues often index at genus level — "Derris, used in traditional medicine" — the clinical reputation of D. scandens gets silently attached to D. elliptica. If a product says only "Derris", that is not enough information. Ask for the species.

The same trap exists across the fish-poison plants generally. In the Amazon, barbasco and timbó — species of Lonchocarpus, Deguelia and Tephrosia — are used the same way and contain the same rotenoids. They are botanically distinct plants, but the chemistry and the hazard are the same, and they are indexed under "traditional plant use" for the same reason.

Traditional Use: Tuba Fishing and Parasite Control

Tuba fishing

The method is old, widespread and well documented across Malaysia, Indonesia, the Philippines, Vietnam, Papua New Guinea and the Pacific. A section of slow-moving stream or a tidal pool is dammed or chosen at low water. Roots are pounded on rock until the milky sap runs, then swirled through the water. Within minutes the fish lose coordination, rise to the surface and can be picked up by hand or basket.

It is a communal harvesting practice with real cultural weight, and in many places it was governed by custom — who could do it, where, and how often — because everyone understood it emptied a stretch of water. Many countries now prohibit or restrict it, because it is indiscriminate: it kills every gill-breathing thing in the pool, including juveniles, amphibian larvae and aquatic insects, not just the fish somebody wanted.

The fish were eaten. That is the practice, and it is worth explaining rather than glossing over, because it is the fact people cite when they assume the plant must be safe. Rotenone is poorly absorbed from the mammalian gut and rapidly metabolised, and it does not accumulate much in edible flesh; the concentrations involved in a stunned pool are also low. That is why the practice persisted for centuries without visible mass poisoning. It is not a reason to conclude the root itself is safe to consume — the whole point is that the dose reaching a person eating a fish is a tiny fraction of the dose in a mouthful of root.

External parasiticide

The second genuine traditional and commercial use is external. Derris powder has been dusted or washed onto livestock, dogs and poultry against lice, ticks, mites and fleas, and used on humans in some regions against scabies and head lice. It was also a garden and crop insecticide — the "derris dust" of mid-century gardening manuals.

Even here it is not benign. Rotenone dust is a respiratory irritant, absorption through broken skin is a real route, and some species are unusually sensitive — pigs in particular are noted in the veterinary literature as poorly tolerant of rotenone preparations that other livestock handle.

What it was never used for

There is no established internal medicinal use of Derris elliptica in Ayurveda, in traditional Chinese medicine, in Thai traditional medicine, in Jamu or in Vietnamese thuốc nam. Scattered ethnobotanical surveys record topical applications for skin parasites and, occasionally, use as an abortifacient or a poison — which is a use, but not a therapy.

Active Compounds: Rotenone and the Rotenoids

Rotenone is the headline compound — a rotenoid, a modified isoflavonoid built on a complex five-ring skeleton. It is strongly lipophilic (fat-soluble), which governs almost everything about how it behaves: it crosses cell membranes easily, crosses the blood–brain barrier without needing a transporter, and does not need to be actively pumped into cells. PubChem entry for rotenone.

The root also contains a family of related rotenoids that share the mechanism at varying potency:

Rotenone degrades quickly. Sunlight and warm water break it down within days — a property fisheries managers rely on when treating a lake, and the reason old derris dust loses potency on a shed shelf. Rapid environmental breakdown is genuinely good news for the ecosystem. It says nothing about what a concentrated dose does to a person before it degrades.

How Rotenone Works: Shutting Down Complex I

Every cell in your body runs the same power plant. Food-derived electrons are carried by NADH into the mitochondrial electron transport chain, handed down a series of protein complexes, and used to pump protons across the inner mitochondrial membrane. The proton gradient then drives ATP synthase, and ATP is the currency the cell spends on everything.

Rotenone jams the first station on that line. It binds at the ubiquinone-reduction site of complex I (NADH:ubiquinone oxidoreductase), blocking the transfer of electrons from the complex's terminal iron–sulfur cluster to ubiquinone. Structure–activity work by Ueno and colleagues mapped which parts of the rotenone molecule are required for that inhibition, and Schuler and Casida identified the PSST subunit of complex I as the insecticidal target site.

Two consequences follow, and the second is the reason rotenone is neurotoxic rather than merely energy-depleting:

  1. ATP production falls. Cells with high, unrelenting energy demand feel it first.
  2. Electrons back up and leak. A blocked chain spills electrons onto oxygen, generating superoxide and downstream reactive oxygen species. The cell is now simultaneously short of energy and under oxidative attack — a combination dopamine neurons are unusually bad at surviving, because dopamine metabolism is itself a source of oxidative stress and these neurons have enormous axonal arbors to power.

Because rotenone is lipophilic and uniformly distributed, it inhibits complex I everywhere in the body — and yet the damage in animal models is remarkably selective for the nigrostriatal dopamine system. That selectivity is itself a major finding: it suggests those neurons are the ones living closest to the edge of their energy budget.

Why Fish Die So Easily and Mammals Less So

Fish are killed by rotenone concentrations that would do nothing to a person standing in the same water. Fisheries agencies treat lakes at well under one part per million of active rotenone. The reason is route of exposure, not some special fish biochemistry:

This is a genuinely elegant piece of comparative toxicology, and it is also the origin of a dangerous misreading. "Safe for humans" in the pesticide literature has always meant "at agricultural residue levels, by the oral route, in a healthy adult". It has never meant that concentrated rotenone is harmless to people, and it says nothing about injected, inhaled, or chronic low-level exposure — which is exactly where the Parkinson's signal appears.

Rotenone and Parkinson's Disease

Animal evidence — strong, reproducible, and the reason this compound is famous.

Human evidence — epidemiological, consistent, and not proof of causation.

Tanner and colleagues studied Parkinson's disease and specific pesticide use in a case-control study nested in the US Agricultural Health Study — roughly 110 people with Parkinson's and 358 controls, all farmers or farm spouses with detailed lifetime pesticide-use histories. Use of rotenone was associated with about 2.5 times the odds of Parkinson's disease (95% confidence interval roughly 1.3 to 4.7). Paraquat, which damages the same neurons through a different mechanism, showed a similar association.

Read that carefully, in both directions. It is a real, biologically coherent finding: a compound that produces Parkinsonian pathology in animals is associated with Parkinson's disease in the humans most exposed to it. But it is a case-control study with self-reported exposure history in a farming population exposed to many chemicals, the confidence interval is wide, and the number of Parkinson's cases is small. It establishes a credible hazard, not a dose-response curve. Nobody knows what level of rotenone exposure, over what period, is required — and nobody is going to run the experiment that would find out.

What it means for you. The occupational finding concerns repeated handling of pesticide formulations over years. It is not a statement about eating one tuba-caught fish. But it is the clearest available answer to the question "what could chronic rotenone exposure do to a person?", and the answer is bad enough that no amount of traditional-use framing should persuade anyone to take this root by mouth.

Human Poisoning

Acute rotenone poisoning in humans is uncommon, because people rarely swallow pesticide concentrate. When it happens it is severe, and the case literature is unambiguous:

The clinical picture reflects systemic mitochondrial failure: vomiting, abdominal pain, then metabolic acidosis with a raised lactate as cells switch to anaerobic metabolism, followed by cardiovascular collapse, seizures and multi-organ failure in severe cases. There is no antidote. Treatment is supportive — airway, circulation, correction of acidosis, intensive care.

Published oral LD50 values in rats span a very wide range, from roughly 100 to over 1,000 mg/kg depending on the formulation and the carrier used. That spread reflects how variably rotenone is absorbed, not a comfortable safety margin: rotenone dissolved in oil is far more dangerous than the same amount of dry powder, and pesticide formulations contain solvents and surfactants designed to improve absorption.

Regulatory Status and the "Natural Pesticide" Lesson

The lesson worth carrying away. For decades rotenone was the flagship "botanical" insecticide — plant-derived, biodegradable, permitted in certified organic production, and marketed as the gentle alternative to synthetics. Then the toxicology matured, the Parkinson's model was published, the epidemiology followed, and it was withdrawn from crop use in most of the developed world.

Rotenone is one of the cleanest available demonstrations that "natural" and "plant-derived" are statements about origin, not about safety. A molecule a legume evolved to kill insects is, chemically, a molecule optimised to kill things with mitochondria. We have mitochondria.

Why It Turns Up on Herb Lists

Four mechanisms, all of them mundane, all of them fixable by reading the species name:

  1. Genus-level indexing. Derris scandens has clinical trials and a place on Thailand's essential medicines list. Aggregated databases that index "Derris" inherit that medicinal status for every species in the genus, including this one.
  2. Ethnobotanical survey data taken out of context. Field surveys that record "plant used" do not always distinguish "used to treat a person" from "used to poison fish" or "used to delouse a buffalo". Downstream, a spreadsheet row says Derris elliptica — traditional use: yes.
  3. Anticancer cell-culture literature. Deguelin and rotenone both show cytotoxicity in cancer cell lines, because killing mitochondria kills cells. Papers describing this are real, and they are periodically misrepresented as evidence that the plant is a cancer remedy. Cytotoxicity in a dish is not selectivity in a person; rotenone kills your neurons by the same mechanism.
  4. Content scraping. Herb-list websites copy each other. One misclassification propagates indefinitely.

Forms and Preparations

For completeness and for accurate identification — not as instructions:

There is no legitimate oral herbal preparation of this plant. No tincture, no decoction, no capsule, no standardised extract intended for human consumption. If you encounter one, it is being sold by someone who has confused it with another species or has not checked.

Dosage: There Is No Safe Oral Dose

This page deliberately has no dosing table.

No safe oral dose of Derris elliptica or of rotenone has been established for humans, and none should be sought. There is no therapeutic indication to dose for. There is no clinical trial that would define a threshold. The only human dose-response information in existence comes from poisonings, and the endpoint in those reports is death or intensive care.

Requests for "a small amount" or "a safe traditional dose" are asking the wrong question. The traditional dose of tuba root is the amount that empties a stream of fish, measured in armfuls of pounded root per pool, and it was never intended to enter a human body.

Cautions and Contraindications

🔴 Do not ingest Derris elliptica, derris root, tuba root or any rotenone product, in any amount, for any reason.

Key Research Papers

  1. Betarbet R, Sherer TB, MacKenzie G, et al. Chronic systemic pesticide exposure reproduces features of Parkinson's disease. Nature Neuroscience. 2000;3(12):1301–1306.
  2. Sherer TB, Kim JH, Betarbet R, et al. Subcutaneous rotenone exposure causes highly selective dopaminergic degeneration and alpha-synuclein aggregation. Experimental Neurology. 2003;179(1):9–16.
  3. Cannon JR, Tapias V, Na HM, et al. A highly reproducible rotenone model of Parkinson's disease. Neurobiology of Disease. 2009;34(2):279–290.
  4. Tanner CM, Kamel F, Ross GW, et al. Rotenone, paraquat, and Parkinson's disease. Environmental Health Perspectives. 2011;119(6):866–872.
  5. Schuler F, Casida JE. The insecticide target in the PSST subunit of complex I. Pest Management Science. 2001;57(10):932–940.
  6. Ueno H, Miyoshi H, Inoue M, et al. Structural factors of rotenone required for inhibition of various NADH–ubiquinone oxidoreductases. Biochimica et Biophysica Acta. 1996;1276(3):195–202.
  7. De Wilde AR, Heyndrickx A, Carton D. A case of fatal rotenone poisoning in a child. Journal of Forensic Sciences. 1986;31(4):1492–1498.
  8. Wood DM, Alsahaf H, Streete P, et al. Fatality after deliberate ingestion of the pesticide rotenone: a case report. Critical Care. 2005;9(3):R280–R284.
  9. Rhee J, Yum H, Moon S, et al. Rotenone analysis by liquid chromatography–tandem mass spectrometry with information-dependent acquisition in a fatal case of rotenone poisoning with a commercial organic insecticide being sold in Korea. Journal of Analytical Toxicology. 2016;40(6):460–465.
  10. Patel F. Pesticidal suicide: adult fatal rotenone poisoning. Journal of Forensic and Legal Medicine. 2011;18(7):340–342.
  11. Sayono S, Anwar R, Sumanto D. Evaluation of toxicity in four extract types of tuba root against dengue vector, Aedes aegypti (Diptera: Culicidae) larvae. Pakistan Journal of Biological Sciences. 2020;23(12):1530–1538.
  12. Kuptniratsaikul V, Pinthong T, Bunjob M, Thanakhumtorn S. Efficacy and safety of Derris scandens Benth. extracts in patients with knee osteoarthritis. Journal of Alternative and Complementary Medicine. 2011;17(2):147–153. — note: this is the different, medicinal species.
  13. Puttarak P, Sawangjit R, Chaiyakunapruk N. Efficacy and safety of Derris scandens (Roxb.) Benth. for musculoskeletal pain treatment: a systematic review and meta-analysis of randomized controlled trials. Journal of Ethnopharmacology. 2016;194:316–323. — again, D. scandens, not D. elliptica.

Live PubMed Searches

  1. Derris elliptica + rotenone
  2. Rotenone Parkinson's disease model
  3. Rotenone and mitochondrial complex I inhibition
  4. Human rotenone poisoning — fatal cases
  5. Rotenone as a piscicide in fisheries management
  6. Pesticide exposure and Parkinson's disease — epidemiology
  7. Deguelin and rotenoid pharmacology
  8. Derris scandens clinical trials (the other species)
  9. Fish-poison plants, ethnobotany and rotenoids
  10. α-synuclein aggregation and complex I inhibition

Connections

Back to Table of Contents