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This article is about the kava plant. For the class of pharmacological derivatives, see Kavalactone. For other uses, see Kava (disambiguation).
Starr 070515-7054 Piper methysticum.jpg
Piper methysticum leaves
Scientific classification
Kingdom: Plantae
(unranked): Angiosperms
(unranked): Magnoliids
Order: Piperales
Family: Piperaceae
Genus: Piper
Species: P. methysticum
Binomial name
Piper methysticum

Kava or kava-kava (Piper methysticum: Latin "pepper" + Latinized Greek "intoxicating") is a crop of the western Pacific.

The name kava(-kava) is from Tongan and Marquesan;[1] other names for kava include ʻawa (Hawaiʻi), ava (Samoa), yaqona (Fiji), sakau (Pohnpei), and malok or malogu (parts of Vanuatu).

The roots of the plant are used to produce a drink with sedative anesthetic, and entheogenic properties. Kava is consumed throughout the Pacific Ocean cultures of Polynesia, including Hawaii, Vanuatu, Melanesia and some parts of Micronesia. (See canoe plants.) Kava is sedating and is primarily consumed to relax without disrupting mental clarity. Its active ingredients are called kavalactones. A Cochrane Collaboration systematic review of its evidence concluded it was likely to be more effective than placebo at treating short-term social anxiety.[2]


The several cultivars of kava vary in concentrations of primary and secondary psychoactive alkaloids. The largest number are grown in the Republic of Vanuatu, and so it is recognised as the "home" of kava. Kava was historically grown only in the Pacific islands of Hawaii, Federated States of Micronesia, Vanuatu, Fiji, the Samoas and Tonga. Some is grown in the Solomon Islands since World War II, but most is imported. Kava is a cash crop in Vanuatu and Fiji.

The kava shrub thrives in loose, well-drained soils where plenty of air reaches the roots. It grows naturally where rainfall is plentiful (over 2,000 mm/yr). Ideal growing conditions are 70–95 °F (21–35 °C) and 70–100% relative humidity. Too much sunlight is harmful, especially in early growth, so kava is an understory crop.

Kava cannot reproduce sexually. Female flowers are especially rare and do not produce fruit even when hand-pollinated. Its cultivation is entirely by propagation from stem cuttings.

Traditionally, plants are harvested around four years of age, as older plants have higher concentrations of kavalactones. After reaching about 2 m height, plants grow a wider stalk and additional stalks, but not much taller. The roots can reach a depth of 60 cm.

Strains and origins[edit]

A painting showing women preparing kava

One of the most potent strains is called "Isa" in Papua New Guinea, and also called "Tuday" in Hawaii. In Vanuatu, it is considered a type of "Tudei" kava, pronounced as "two-day" because it is said to have effects lasting two days due to its chemical profile being high in the kavalactone dihydromethysticin. The plant itself is a strong, very hardy, fast-growing variety with multiple light to dark green stems covered with raised dark spots.

In Vanuatu, exportation of kava is strictly regulated. Only strains they deem as "noble" varieties that are not too weak or too potent are allowed to be exported. Only the most desirable strains for everyday drinking are selected to be noble varieties to maintain quality control. In addition, their laws mandate that exported kava must be at least five years old and farmed organically. Their most popular noble strains are "Boroguu" or "Boronggoru" from Pentecost Island, "Melomelo" from Ambae island (called sese in North Pentecost), and "Palarasul" kava from Espiritu Santo Island. In Vanuatu, Tudei (two-days) kava is reserved for special ceremonial occasions and exporting it is not allowed. "Palisi" is a popular Tudei variety.

In Hawaii, there are many other strains of kava. Some of the most popular strains are the "Mahakea," "Mo'i," "Hiwa" and "Nene" varieties. The Ali'i (kings) of old Hawaii coveted the special kava they called "Mo'i" that had a strong cerebral effect due to a predominant amount of the kavalactone kavain. This sacred variety was so important to them that no one but royalty could ever experience it, "lest they suffer an untimely death". The reverence for Hiwa in old Hawai‘i is evident in this portion of a chant recorded by N.B. Emerson and quoted by Handy and Handy. "This refers to the cup of sacramental‘awa brewed from the strong, black ‘awa root (‘awa hiwa) which was drunk sacramentally by the kumu hula":

The day of revealing shall see what it sees:
A seeing of facts, a sifting of rumors,
An insight won by the black sacred ‘awa,
A vision like that of a sacred god!

Winter describes a hula prayer for inspiration which contains the line, He ‘ike pū ‘awa hiwa. Pukui and Elbert translated this as "a knowledge from kava offerings". Winter explains that ‘awa, especially of the Hiwa variety, was offered to hula deities in return for knowledge and inspiration. [pg. 34, Hawaiian 'Awa, Views of an Ethnobotanical Treasure, 2006].

Other strains are found in Fiji, Tonga, and Samoa.


Fresh kava root contains on average 80% water. Dried root contains approximately 43% starch, 20% dietary fiber, 15% kavalactones,[3] 12% water, 3.2% sugars, 3.6% protein, and 3.2% minerals. Kavalactone content is greatest in the roots and decreases higher up the plant. Relative concentrations of 15%, 10% and 5% have been observed in the root, stump, and basal stems, respectively.

The mature roots of the kava plant are harvested after a minimum of four years (at least five years ideally) for peak kavalactone content. Most kava plants produce around 50 kg (110 lb) of root when they are harvested. Kava root is classified into two categories: crown root (or chips) and lateral root. Crown roots are the large-diameter pieces that look like (1.5 to 5 inches (38 to 127 mm) diameter) wooden poker chips. Most kava plants consist of approximately 80% crown root upon harvesting. Lateral roots are smaller-diameter roots that look more like a typical root. A mature kava plant is about 20% lateral roots. Kava lateral roots have the highest content of kavalactones in the kava plant. "Waka" grade kava is made of lateral roots only.



The general structure of the kavalactones, without the R1-R2 -O-CH2-O- bridge and with all possible C=C double bonds shown.

A total of 18 different kavalactones (or kavapyrones) have been identified to date, at least 15 of which are active.[4] However, six of them, including kavain, dihydrokavain, methysticin, dihydromethysticin, yangonin, and desmethoxyyangonin, have been determined to be responsible for about 96% of the plant's pharmacological activity.[4] Some minor constituents, including three chalcones, flavokavain A, flavokavain B, and flavokavain C, have also been identified,[4] as well as a toxic alkaloid, pipermethystine.[5]


The following pharmacological actions have been reported for kava and/or its major active constituents:[4][6]

Other effects include significant reduction of the inhibitory effects of muscimol (a GABAA receptor agonist) in the solitary nucleus of the brain stem of rats (by "kavalactones or dihydrokavain"), and elevation of dopamine levels in the nucleus accumbens of rats (by high concentrations of kavain and desmethoxyyangonin).[4]

In addition to the above, receptor binding assays have revealed direct interactions of leaf extracts of kava (which appear to be more active than root extracts) with the GABA (i.e., main) binding site of the GABAA receptor, the D2 receptor, the μ- and δ-opioid receptors, and the H1 and H2 receptors.[8][9] Weak interaction with the 5-HT6 and 5-HT7 receptors and the benzodiazepine site of the GABAA receptor was also observed.[8]

Potentiation of GABAA receptor activity may underlie the anxiolytic effects of kava, while elevation of dopamine levels in the nucleus accumbens and agonism of the μ-opioid receptor likely underlie the moderately euphorigenic effects the plant can produce.[10] However, failure of the GABAA receptor inhibitor flumazenil to reverse the anxiolytic effects of kava in mice suggests that an alternative mechanism may be responsible for this effect.[11]

Heavy, long-term use of kava has been found to not reduce ability in saccade and cognitive tests, but has been associated with elevated liver enzymes.[12]


Recent usage of kava has been documented in forensic investigations by quantitation of kavain in blood specimens. The principal urinary metabolite, conjugated 4'-OH-kavain, is generally detectable for up to 48 hours.[13]

Preparation and consumption[edit]

Kava root drying in Lovoni village, Ovalau, Fiji

Traditional preparation[edit]

Kava is consumed in various ways throughout the Pacific Ocean cultures of Polynesia, Vanuatu, Melanesia and some parts of Micronesia and Australia. Traditionally, it is prepared by either chewing, grinding or pounding the roots of the kava plant. Grinding is done by hand against a cone-shaped block of dead coral; the hand forms a mortar and the coral a pestle. The ground root/bark is combined with only a little water, as the fresh root releases moisture during grinding. Pounding is done in a large stone with a small log. The product is then added to cold water and consumed as quickly as possible.

The extract is an emulsion of kavalactone droplets in starch and buttermilk. The taste is slightly pungent, while the distinctive aroma depends on whether it was prepared from dry or fresh plant, and on the variety. The colour is grey to tan to opaque greenish.

Kava prepared as described above is much more potent than processed kava. Chewing produces the strongest effect because it produces the finest particles. Fresh, undried kava produces a stronger beverage than dry kava. The strength also depends on the species and techniques of cultivation. Many find mixing powdered kava with hot water makes the drink stronger.

In Vanuatu, a strong kava drink is normally followed by a hot meal or tea. The meal traditionally follows some time after the drink so the psychoactives are absorbed into the bloodstream quicker. Traditionally, no flavoring is added.

In Papua New Guinea, the locals in Madang province refer to their kava as waild koniak ("wild cognac" in English).

Fijians commonly share a drink called grog made by pounding sun-dried kava root into a fine powder, straining and mixing it with cold water. Traditionally, grog is drunk from the shorn half-shell of a coconut, called a bilo. Grog is very popular in Fiji, especially among young men, and often brings people together for storytelling and socializing. Drinking grog for a few hours brings a numbing and relaxing effect to the drinker; grog also numbs the tongue and grog drinking typically is followed by a "chaser" or sweet or spicy snack to follow a bilo.[14]

Kava root being prepared for consumption in Asanvari village on Maewo Island, Vanuatu


Pharmaceutical and herbal supplement companies extract kavalactones from the kava plant using solvents such as supercritical carbon dioxide,[15] acetone and ethanol to produce pills standardized with between 30% and 90% kavalactones.

Kava culture[edit]

A sign showing a "Kava licence area" at Yirrkala, in the Northern Territory of Australia
Main article: Kava culture

Kava is used for medicinal, religious, political, cultural and social purposes throughout the Pacific. These cultures have a great respect for the plant and place a high importance on it. In Fiji, for example, a formal yaqona (kava) ceremony will often accompany important social, political, religious, etc. functions, usually involving a ritual presentation of the bundled roots as a sevusevu (gift), and drinking of the yaqona itself.[16]

A traditional Fijian yaqona bundle of roots

Effects of consumption[edit]

The effects of a kava drink vary widely with the particular selection of kava plant(s) and amount. A potent drink results in a faster onset with a lack of stimulation; the user's eyes become more sensitive, the person soon becomes somnolent and then has deep, dreamless sleep within 30 minutes. Sleep is often restful and pronounced periods of sleepiness correlate to the amount and potency of kava consumed. Kava drinkers are often perceived as having lazy days after consumption of kava the night before, which can be expected as many active kavalactones have half lives of approximately 9 hours.[17]


Kava is renowned for its many health benefits, but the chiefly among them is its anxiolytic properties. A journal article titled ""Kava: A Comprehensive Review of Efficacy, Safety, And Psychopharmacology." from the Australian & New Zealand Journal of Psychiatry, reviewed all scholarly journal articles related to kava found in scholarly electronic databases, they found that "The current weight of evidence supports the use of kava in treatment of anxiety with a significant result occurring in four out of six studies reviewed" [18]

Other than its anxiolytic uses, kava also has a few therapeutic qualities. Kava is known for having a sleep inducing affect and is good for common restlessness and more serious insomnia.[19][20] Another study found that kava consumption may reduce colon cancer risk based on their results with carcinogen (a substance capable of causing cancer in living tissue) treated rats.[21]

A few studies have shown that kava extracts possessed efficacious anxiolytic activity compared to placebo for the symptomatic treatment for anxiety.[22] As well, kava extracts may be an effective alternative to tricyclic antidepressants and benzodiazepines for the treatment of anxiety disorders.[23]

One study showed that 150 mg/day of the standardized WS 1490 Kava extract in divided doses for four weeks was effective at decreasing anxiety symptoms but was not superior to the alternative dose of 300 mg/day in divided doses used in other studies.[24]

Most of these studies used a standardized WS 1490 Kava extract formulation, which is composed of 70% kavalactones.[25]

Toxicity and safety[edit]

In 2001, concerns were raised about the safety of kava, which led to restrictions and regulations in several countries,[26] as well as reports by the United States CDC [27] and FDA.[28] Most of the concerns were related to a small number of reports indicating potential cases of hepatotoxicity caused by consumption of various commercial products derived from kava. A number of scientists and medical practitioners criticized the poor quality of the reports by pointing out that most of the reported rare cases of hepatotoxicity involved patients with a history of alcohol or prescription drugs abuse or concomitant use of medicines known as potentially hepatotoxic.[29] On June 10, 2014, the German Administrative Court overturned the 2002 ban reinstating the regulatory requirements of 2001. The court stated that risk from kava exposure had not been clearly demonstrated, nor does it appear unusually high, an opinion presumably driven by the very small number of cases of reported toxicity (n ~ 3) with even a certain degree of causality linked to kava in a global kava-consuming community that may number in the millions of doses consumed daily.[30]

According to a recent comprehensive review of the relevant literature by Showman et al. (2014): "Despite the link to kava and liver toxicity demonstrated in vivo and in vitro, in the history of Western kava use, toxicity is still considered relatively rare. Only a fraction of the handful of cases reviewed for liver toxicity could be, with any certainty, linked to kava consumption and most of those involved the coingestion of other medications/supplements. That means that the incident rate of liver toxicity due to kava is one in 60-125 million patients."[30]

Various components of the plant have been labelled as potentially capable of causing toxicity, particularly pipermethystine and flavokavain B. Yet, based on a retrospective study in Germany, the alkaloid pipermethystine is an unlikely cause for the observed hepatotoxicity, as, although it occurs in qualities up to 0.2% of the leaves, it is found in quantities a hundred-fold less in Western extracts.[31] Another suggested culprit, Flavokavain B, is also found in various preparations in the plant, although not in ethanol extracts of noble cultivars, and never in large enough amounts to cause any liver damage.[32] The very rare cases of kava hepatotoxicity may have been due to contamination with aflatoxins or other mold hepatotoxins, but this requires further study.[33]

Other data suggests that the rare cases of toxicity may be due to an intrinsic metabolic cause. Three possible mechanisms for kavalactone hepatotoxicity have been theorized: inhibition of cytochrome P450, possible reduction in liver glutathione content and, more remotely, inhibition of cyclooxygenase enzyme activity. The direct toxicity of kava extracts is relatively small under any analysis, yet the potential for drug interactions and/or the potentiation of the toxicity of other compounds is large.[34]

In line with this reasoning, several adverse interactions with drugs have been documented, both prescription and nonprescription – including, but not limited to, anticonvulsants, alcohol, anxiolytics (CNS depressants such as benzodiazepines), antipsychotics, levodopa, diuretics, and drugs metabolized by CYP450 in the liver.[35]

A few notable potential drug interactions are, but are not limited to:

It has been reported that combined use of alcohol and kava extract can have additive sedative effects in mice.[36] However, this additive effect has not been studied in humans. But separately kava has been shown to induce sedation.[37] Regarding cognitive function, kava has been shown to have additive cognitive impairments while taken with alcohol when compared to taking placebo and alcohol alone.[38]
Anxiolytics (CNS depressants such as benzodiazepines and barbiturates)
Kava may have potential additive CNS depressant effects (such as sedation and anxiolytic effects) with benzodiazepines and barbiturates.[38]
Dopamine Agonist - Levodopa
One of levodopa’s chronic side effects that Parkinson’s patients experience is the "on-off phenomenon" of motor fluctuations where there will be periods of oscillations between "on" where the patient experiences symptomatic relief and "off" where the therapeutic effect wears off early.[39] When taking levodopa and kava together it has been shown that there is an increased frequency of this "on-off phenomenon".[40]

The Australian studies that drove this debate focused on populations with heavy concomitant consumption of alcohol and overall poor health. In these studies, heavy kava use in an Aboriginal community in Arnhem Land was associated with overall poor health, a puffy face, scaly rash, and a slight increase in patellar reflexes.[41][42][43] A 2012 analysis of cases worldwide proposed that mold was the primary cause of hepatotoxicity in kava products.[44]


In 2002 the EU imposed a ban on imports of kava-based pharmaceutical products.[45] The sale of kava plant is regulated in Switzerland, France, and the Netherlands.[46] Some Pacific Island States who had been benefiting from the export of kava to the pharmaceutical companies have attempted to overturn the EU ban on kava-based pharmaceutical products by invoking international trade agreements at the WTO: Fiji, Samoa, Tonga and Vanuatu argued that the ban was imposed with insufficient evidence.[47] The pressure prompted Germany to reconsider the evidence base for banning kava-based pharmaceutical products.[48] On June 10, 2014, the German Administrative Court overturned the 2002 ban reinstating the regulatory requirements of 2001.[30]

Poland is the only EU country with an "outright ban on kava" and where the mere possession of kava is prohibited and may result in a prison sentence.[45]

In the United Kingdom it is a criminal offence to sell, supply or import any medicinal product containing kava.[49] At the same time it is still legal to possess kava (for personal use) or import it for purposes other than human consumption.

In 2002 Health Canada issued an order prohibiting the sale of any product containing kava.[50] While the restrictions on kava were lifted in 2012,[51] Health Canada has not licensed any kava products for sale in Canada.[52]

In Australia, the supply of kava is regulated through the National Code of Kava Management. The importation and licensing of kava is prohibited in Western Australia.[53][54] In the Northern Territory, the police say that "the sale and, in majority of circumstances, possession of kava [...] is illegal".[55] The Australian Therapeutic Goods Administration has recommended no more than 250 mg of kavalactones be taken in a 24‑hour period.[56]

Legislation has been proposed to require that kava products be derived only from noble cultivars, which may be less toxic.[57][58] Other acts have been passed based on the assumption that aqueous solutions are less harmful.[32][58] Exclusion of certain aerial parts of the plant are also often required by law or convention, which contain less pipermethystine and other toxic compounds.[58]

See also[edit]


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  3. ^ Naumov, P., Dragull, K., Yoshioka, M., Tang, C.-S., Ng, S. W. Structural Characterization of Genuine (—)-Pipermethystine, (—)-Epoxypipermethystine, (+)-Dihydromethysticin and Yangonin from the Kava Plant (Piper methysticum), Natural Product Communications(2008), 3(8) 1333—1336.
  4. ^ a b c d e Sarris J, LaPorte E, Schweitzer I (2011). "Kava: a comprehensive review of efficacy, safety, and psychopharmacology". Aust N Z J Psychiatry 45 (1): 27–35. doi:10.3109/00048674.2010.522554. PMID 21073405. 
  5. ^ Olsen LR, Grillo MP, Skonberg C (2011). "Constituents in kava extracts potentially involved in hepatotoxicity: a review". Chem. Res. Toxicol. 24 (7): 992–1002. doi:10.1021/tx100412m. PMID 21506562. 
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  16. ^ There are many variations to this ceremony; one of which is described in: Biturogoiwasa, Solomoni; Walker, Anthony R. (2001). My Village, My World: Everyday Life in Nadoria, Fiji. Suva, Fiji: Institute of Pacific Studies, University of the South Pacific. pp. 17–20. ISBN 978-982-02-0160-6.  There are numerous anthropological studies, one example being: Tomlinson, Matt (2007). "Everything and Its Opposite: Kava Drinking in Fiji". Anthropological Quarterly 80 (4): 1065–81. doi:10.1353/anq.2007.0054. [improper synthesis?]
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