Kava

• 1. Introduction

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  The scientific name of kava, Piper methysticum, joins the Latin word for pepper to a Latinized Greek word meaning intoxicating. The everyday name tells a different story. It comes from Tongan and Marquesan, where it means bitter. Kava belongs to the pepper family and grows natively in the Pacific Islands. The word can mean the plant itself or the psychoactive drink made from its root. Communities across Polynesia, Micronesia and Melanesia have long treated that drink as both ceremony and recreation. Kava bars now serve it in many countries far from the Pacific. Where did this plant come from, and how did it travel across so much ocean? Why do islands that grow it prize some roots and forbid others? And why have governments argued so fiercely over a drink that people describe as calming?

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• 2. Cloned in Vanuatu

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  Around 3,000 years ago, farmers in northern Vanuatu began selecting a wild plant called Piper wichmannii, and the result was kava. Kava is conspecific with that wild ancestor, which shows it was domesticated from it. Today it exists only as sterile cultivars, each one a clone of the wild stock. Hundreds of cultivars are now grown across the Pacific, and each has its own growing needs, its own appearance and its own psychoactive character.

  A survey of where the plants grow points back to Vanuatu. Cultivated Piper methysticum turned up on numerous islands of Micronesia, Melanesia, Polynesia and Hawaii. Specimens of the wild Piper wichmannii came only from Papua New Guinea, the Solomon Islands and Vanuatu.

  The Lapita culture carried kava east into the rest of Polynesia after contact. The plant is endemic to Oceania and does not occur in other Austronesian groups. It reached Hawaii. It never took hold in New Zealand, where the climate is too cold for it to grow.

  Betel nut tells a parallel story. Chewing it is ubiquitous elsewhere among Austronesian peoples, yet in Oceania the habit was lost, and kava is believed to be the reason. Linguists have also reconstructed an ancient word, *kava, that once pointed at a different plant altogether.

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• 3. Names and False Kava

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  According to Lynch, writing in 2002, the Proto-Polynesian word kava descends from the Proto-Oceanic kawaR. That older word meant a bitter root, or a potent root used as fish poison. It originally named Zingiber zerumbet, a plant used in Austronesian rituals to brew a similar, mildly psychoactive bitter drink.

  The word survives in many tongues. Pohnpeian has sa-kau, while Tongan, Niue, Rapa Nui, Tuamotuan and Rarotongan all say kava. Samoan, Tahitian and Marquesan speakers say ava, and Hawaiians say ʻawa. In Māori, the cognate kawa has drifted to mean bitter, sour or acrid. Fiji uses yaqona or yagona, Kosrae uses seka, and parts of Vanuatu use malok or malogu.

  In the Cook Islands, the doubled forms kawakawa and kavakava name unrelated members of the genus Pittosporum. Futunan compounds such as kavakava atua name other species of Piper. Doubling a word in these languages signals falsehood or likeness, so the sense is false kava.

  New Zealand holds the best-known false kava. The Māori name kawakawa belongs to Piper excelsum, a plant endemic to New Zealand and to nearby Norfolk Island and Lord Howe Island. Māori applied the name drawing on earlier knowledge of kava, which could not survive the colder climate. Kawakawa is a sacred tree, a symbol of death that pairs with the rangiora, Brachyglottis repanda, the symbol of life. It has no psychoactive properties. Its link to kava rests on a similar appearance and a bitter taste.

  The Kava Society of New Zealand suggests that "in all likelihood, the kava plant was known to the first settlers of Aotearoa." The society says the settlers named another pepper-family plant kawa-kawa "in memory of the kava plants they undoubtedly brought with them and unsuccessfully attempted to cultivate." It adds that the Māori word kawa also means ceremonial protocol, recalling the stylized drinking typical of Polynesian societies. Kawakawa itself serves in Māori traditional medicine for skin infections, wounds and cuts, and as a tea for stomach upsets and other minor illnesses.

  Scholars of the real plant draw their own line between two kinds, and that line decides which roots may leave Vanuatu.

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• 4. Noble and Tudei

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  Scholars separate noble kava from non-noble kava, a group that includes tudei, meaning two-day, kavas, medicinal kavas and wild Piper wichmannii. Traditionally, only noble kavas were used for regular drinking. Their mix of kavalactones and other compounds gives pleasanter effects, with less chance of nausea or the so-called kava hangover. Polynesian and Melanesian migrants spread only noble cultivars around the Pacific. That is why non-noble ones remain limited to the islands of Vanuatu, where they began.

  Tudei is cheaper and quicker to grow. Noble kava can take up to 5 years to mature, while non-noble varieties can often be harvested a year after planting. Reports describe farmers in Hawaii trying to grow the non-noble cultivars isa and palisi, and dried tudei imported into Fiji for re-export.

  Flavokavains drive the worry about non-noble kava. These compounds are present in high concentrations in non-noble varieties and in no significant concentration in noble ones. Some researchers suggest that tudei in the manufacture of kava products may explain the rare adverse reactions seen among users in Europe. Government regulators and non-profit groups have since set up bodies to monitor kava quality, publish regular reports, certify vendors who sell proper noble kava, and warn customers about products that may contain tudei.

  Vanuatu allows only noble cultivars to be exported. Its laws also require exported kava to be at least five years old and organically farmed. Only the most desirable everyday cultivars count as noble, which keeps quality under control. Common noble cultivars include Borogu, also called Borongoru, from Pentecost Island, and Melomelo from Aoba Island, which is called Sese in the north of Pentecost. Palarasul comes from Espiritu Santo. Tudei is reserved for special ceremonial occasions and may not be exported, and palisi is a common tudei variety.

  Hawaii keeps its own roster of cultivars, among them Mahakea, Moʻi, Hiwa and Nene. The Aliʻi, the kings of precolonial Hawaii, coveted the Moʻi variety, which had a strong cerebral effect because the kavalactone kavain predominates in it. It was so sacred that only royalty could ever experience it, "lest they suffer an untimely death."

  Nathaniel Bright Emerson recorded a chant that E. S. Craighill and Elizabeth Green Handy later quoted, showing the reverence for Hiwa. It refers to the cup of sacramental ʻawa brewed from the strong, black ʻawa root, which the kumu hula drank sacramentally. One line promises "An insight won by the black sacred 'awa, A vision like that of a god!" Winter describes a hula prayer for inspiration containing the line He ʻike pū ʻawa hiwa. Pukui and Elbert translated it as "a knowledge from kava offerings." Winter explains that ʻawa, especially Hiwa, was offered to hula deities in return for knowledge and inspiration.

  Far from the Pacific, specialized varieties have been introduced to South Florida, acclimated to its soil and climate and resistant to pests and disease. As of 2024, only a small number of commercial farms and backyard growers cultivate them.

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• 5. Bowl and Nakamal

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  In Fiji, a formal yaqona ceremony often accompanies important social, political or religious functions. It usually includes a ritual presentation of bundled roots as a sevusevu, or gift, followed by the drinking of the yaqona itself. Across the Pacific, kava serves medicinal, religious, political, cultural and social purposes, and these cultures hold the plant in great respect.

  The nakamal is traditionally the central meeting place in Vanuatu. Kava drunk there supports communal gathering, dialogue, and the exchange of knowledge across different groups and generations.

  Christian missionaries in the 18th and 19th centuries tried to prohibit kava drinking. They objected to its place in religious rituals and to a preparation method that looked unhygienic from a Western point of view. The pressure changed the drink itself. Kava had historically been made from fresh root, and preparation from dried kava emerged in response to the missionaries' efforts.

  A typical serving starts with 1.0-1.5 g of root, macerated, ground or pounded, then mixed with 100-150 mL of water or coconut milk. The mixture is agitated and strained through cloth or bark filters into a communal bowl. The resulting drink is grey and slightly pungent. Fresh root gives a stronger and more complex drink than dried root, because it retains volatile compounds.

  Fresh roots are peeled, then chewed or mechanically ground into a fine, fibrous pulp. Dried roots are finely ground, placed in a porous cloth and infused in water. In Vanuatu, fresh root is common. Outside the Pacific, dried root powder is usually soaked for 30 minutes at about one tablespoon per cup, then strained. On Pohnpei in Micronesia, cooks mix the root with the fibrous bark of Hibiscus tiliaceus before pressing it.

  Between 2012 and 2017, the number of kava bars in American cities grew to around 180. They operate as social, alcohol-free spaces.

  In 1886, one of the earliest Western publications on kava reported that "A well prepared Kava potion drunk in small quantities produces only pleasant changes in behavior." The same account said the drink "relaxes the body after strenuous efforts, clarifies the mind and sharpens the mental faculties." Modern descriptions agree broadly. Noble kava tends to bring calmness, relaxation and well-being without diminishing cognitive performance. An early talkative stage may give way to muscle relaxation and eventual sleepiness. Effects vary with the cultivar, the age of the plant and the way the drink is taken.

  The mouth feels the drink first. Kavalactones act as a local anesthetic, so the beverage numbs and tightens the mouth. Chewing the root has local anesthetic effects similar to cocaine and longer lasting than benzocaine. Kava is not considered physically addictive, and its use does not lead to dependency.

  Whether the drink is entirely harmless is a harder question, and it begins with what the root actually holds.

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• 6. Chemistry of the Root

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  Most kava plants yield around 50 kg of root at harvest, which traditionally comes at about four years. Older plants hold higher concentrations of kavalactones, so the mature roots are taken after a minimum of four years, and ideally at least five. A plant stops gaining height at about 2 m, then grows a wider stalk and additional stalks. Its roots can reach a depth of 60 cm.

  Growers sort the harvest into two kinds of root. Crown roots, or chips, are large pieces 1.5 to 5 inches across that look like wooden poker chips, and they make up roughly 80% of a plant. Lateral roots are thinner, make up the other 20%, and carry the highest kavalactone concentration in the plant. Waka grade kava is made only from lateral roots.

  Dried root is about 43% starch, 20% dietary fiber and 15% kavalactones. The rest is 12% water, 3.2% sugars, 3.6% protein and 3.2% minerals. Fresh root is on average 80% water. Kavalactones thin out higher up the plant, at observed relative concentrations of 15% in the root, 10% in the stump and 5% in the basal stems. Plant variety, maturity, location and time of harvest also shift the balance.

  Researchers have identified 18 kavalactones, also called kavapyrones, and at least 15 are active. Six of them account for about 96% of the plant's pharmacological activity: kavain, dihydrokavain, methysticin, dihydromethysticin, yangonin and desmethoxyyangonin. Minor constituents include three chalcones, flavokavain A, B and C. A toxic alkaloid called pipermethystine also occurs, but not in the parts of the plant that people drink. It is found in the roots and leaves.

  Laboratory studies point to several actions. Kavain, dihydrokavain, methysticin, dihydromethysticin and yangonin strengthen the activity of GABAA receptors. Kavain and methysticin inhibit the reuptake of norepinephrine, and kavain and desmethoxyyangonin possibly do the same for dopamine. Yangonin binds to the CB1 receptor. Kavain and methysticin inhibit voltage-gated sodium and calcium channels, and all six major kavalactones reversibly inhibit monoamine oxidase B. Methanol extracts of Hawaiian kava leaves bound several receptors more strongly than root extracts, including GABAA, dopamine D2, opioid and histamine receptors. That suggests compounds beyond the main kavalactones may matter.

  The gut absorbs kavalactones quickly. They act mainly on the limbic system, the amygdala and the reticular formation, though their exact molecular mechanisms are not fully understood. In rats, kavain showed a bioavailability of approximately 50%. After a 100 mg/kg dose, over 90% left the body within 72 hours through urine and feces, as the original compound or as metabolites. No bioaccumulation has been seen in rats, mice or humans.

  Forensic investigators have documented recent kava use by measuring kavain in blood. The main urinary metabolite, conjugated 4'-OH-kavain, is generally detectable for up to 48 hours. In people, kavain goes through extensive metabolism in the liver, driven by cytochrome P450 enzymes, and that detail sits at the center of the safety debate.

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• 7. The Liver Dispute

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  Supplement and pharmaceutical companies make pills standardized to between 30% and 90% kavalactones, extracting them with solvents such as supercritical carbon dioxide, acetone and ethanol. Water extraction is the traditional method. Scholars and regulators have raised concerns about the solvent products, and one group argues that organic solvents pull compounds into the pill that may affect the liver. Compared with water, solvents extract vastly larger amounts of flavokavains, which are scarce in noble kava.

  Glutathione is a key part of the argument. Unlike traditional water-based preparations, solvent products do not contain this liver-protecting compound. The same group notes that "the extraction process may exclude important modifying constituents soluble only in water." Other researchers concluded that the difference in toxicity comes from the extraction process, acetone versus water, because pulling out glutathione along with the kava lactones protects against hepatotoxicity, meaning damage to the liver.

  Low-quality raw material makes matters worse. Extracts are often made from plant material that includes the toxic aerial parts holding the hepatotoxic alkaloid pipermethystine, non-noble varieties, or moldy plants. Solvents can draw far larger amounts of potentially toxic compounds from this material than water can.

  In 2002, many countries banned or restricted kava, and the World Health Organization then reviewed its safety. It concluded that moderate drinking of kava in traditional form, as a water-based suspension of roots, carries an "acceptably low level of health risk." The WHO and other health authorities also linked ethanolic and acetonic extracts, and excessive amounts of low-quality products, to a higher risk of adverse outcomes including liver injury. The WHO says products should be developed from water-based suspensions of kava. Warnings from health authorities in the United States, Australia and Canada followed, and kava was omitted from the US Pharmacopeia.

  Heavy use looks different from moderate use. Adverse effects such as skin rashes, higher body mass index, elevated gamma-glutamyl transferase levels and higher lymphocyte counts may begin at roughly 240-440 g of kava powder per week. That equals 3,500-6,440 mg of kavalactones per day. One shell of kava averages 250 mg of kavalactones, so recreational drinking can pass these levels. Clinical anxiety studies used aqueous extracts of 140-250 mg once daily for six weeks and showed no significant toxicity. Long-term liver damage remains an inconclusive question.

  Kanikani, the Fijian name for kava dermopathy, is a reversible skin condition from long, heavy use. It covers the palms, soles and back in dry, scaly skin. Some Pacific Islanders deliberately drink large quantities for several weeks to get the peeling, which leaves a layer of new skin. The effects appeared at weekly intakes from 31 g to 440 g of kava powder. The mechanism is poorly understood but "may relate to interference with cholesterol metabolism." The skin returns to normal within a couple of weeks of reduced or no kava use.

  Drug interactions are documented. Combined with alcohol, kava can add to sedation and cognitive impairment. Taken with the anxiety drug alprazolam, it can cause a semicomatose state in humans. Taken with the Parkinson's drug levodopa, it has been shown to increase the frequency of the on-off phenomenon, a swing between symptom relief and its early loss.

  A 2003 systematic review found that kava extract reduced anxiety symptoms compared with placebo, with a small effect size and mostly mild, transient side effects. Meta-analyses suggest relief sometimes comparable to the medications oxazepam and buspirone, though results were mixed. Current evidence does not support kava for generalized anxiety disorder or other conditions, and it has no proven effects on cancer, cognitive function or microbial infections. A study of heavy, long-term kava users in northern Australia found no cognitive or brain dysfunction, but did find liver enzyme elevation and skin changes.

  Those uncertainties shaped the laws that follow.

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• 8. Laws and Bans

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  Australia regulates kava supply through the National Code of Kava Management. Travellers aged at least 18 may bring up to 4 kg of kava in root or dried form. Restrictions arrived in 2007 after concern about kava abuse in indigenous communities, with an initial limit of 2 kg per person. The limit rose to 4 kg in December 2019, and a pilot program for commercial import began on the 1st of December 2021. The Therapeutic Goods Administration recommends no more than 250 mg of kavalactones in 24 hours. The Northern Territory limits possession to 2 kg per adult. Western Australia lifted its ban in February 2017.

  In 2002, after discussion of kava-derived pharmaceutical products sold in Germany, the European Union imposed a temporary ban on imports of such products. Switzerland and France regulated the sale of the plant, and the Netherlands regulated it in prepared form. Fiji, Samoa, Tonga and Vanuatu argued at the World Trade Organization that the ban rested on insufficient evidence. The pressure led Germany to reconsider. On the 10th of June 2014, the German Administrative Court overturned the 2002 ban, so kava medicine could be sold legally under strict rules. Personal possession was never illegal. German kava pharmaceuticals are now prescription drugs, and brochures warn about side effects. Some leading kava scientists oppose the strictness, and a court case filed in early 2016 against the German Federal Institute for Drugs and Medical Devices argues the new regime is unjustified.

  The United Kingdom makes it a criminal offence to sell, supply or import any medicinal product containing kava for human use, although personal possession is legal. Poland had an outright ban until August 2018, with prison possible for mere possession. Under its new legislation, possession, import and personal use are legal, but selling kava there for human use remains illegal. The Netherlands never lifted its ban and still prohibits preparing, making or trading kava. In 2017, the Committee on Herbal Medicinal Products judged the benefit-risk balance of oral kava for anxiety disorders unfavorable, so no European Union herbal monograph could be made.

  New Zealand treats traditional kava as food under the Food Standards Code, and herbal use falls under the Dietary Supplements Regulations. Only traditional forms, meaning pure roots and water extractions of them, can legally be sold as food or supplements. The aerial parts contain relatively little kavalactone but a mildly toxic alkaloid, pipermethysticine. They and non-water extracts may not be sold for human use, but they may go into cosmetics.

  Health Canada issued an order in 2002 prohibiting sale of any product containing kava. The restrictions were lifted in 2012. As of 2017, Health Canada lists five kava ingredients, and manufactured products need federal approval before marketing. In July 2002, the Health Sciences Authority of Singapore banned kava and its extracts because of liver toxicity risk. Commercial sale, supply and import remain banned there under the Poisons Act.

  In the United States, kava is sold mainly as a dietary supplement, and the FDA has not approved it as a drug. In 2002, the FDA warned that kava supplements may cause rare but severe liver injury, including hepatitis, cirrhosis and liver failure. In 2020, it concluded that kava is not generally recognized as safe for conventional foods, citing toxicity, possible liver damage, possible carcinogenicity, drug interactions and thin safety data.

  Vanuatu, where the plant was first domesticated, has passed legislation to regulate the quality of its exports. The law also bars export or use of leaves and stems, the parts of the plant that the worldwide safety debate keeps returning to.

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