Kava

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Kava
Young Piper methysticum
Young Piper methysticum
Scientific classification
Kingdom: Plantae
Division: Magnoliophyta
Class: Magnoliopsida
Order: Piperales
Family: Piperaceae
Genus: Piper
Species: P. methysticum
Binomial name
Piper methysticum
G.Forst.

Kava (Piper methysticum) (Piper Latin for "pepper", methysticum Greek for "intoxicating") is an ancient crop of the western Pacific. Other names for kava include ʻawa (Hawaii), 'ava (Samoa), yaqona (Fiji), and sakau (Pohnpei). The word kava is used to refer both to the plant and the beverage produced from it. In some parts of the Western World, kava extract is marketed as herbal medicine against stress and anxiety.

Preparation and consumption

File:Kava fiji.jpg
Kava root drying in Lovoni village, Ovalau, Fiji

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. Chewing is followed by depositing into a bowl, mixing with water and straining through the cloth-like fiber of a coconut tree. 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 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 kavalactone droplets in starch. 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. Various sources incorrectly state that it is because saliva enzymes act on the plant. Fresh, undried kava produces a stronger beverage than old, dry kava. The strength also depends on the species and techniques of cultivation.

Fijians commonly share a drink called "grog", made by pounding sun-dried kava root into a fine powder and mixing it with cold water. Traditionally, grog is drunk from the shorn half-shell of a coconut, called a "bilo." Despite tasting very much like dirty water, grog is very popular in Fiji, especially among young men, and often brings people together for storytelling and socializing.[1]

File:Kava vanuatu.jpg
Kava root being prepared for consumption in Asanvari village on Maewo Island, Vanuatu

Effects

A moderately potent kava drink causes effects within 20-30 minutes that last for about two and a half hours, but can be felt for up to eight hours.

The sensations, in order of appearance, are slight tongue and lip numbing caused by the contraction of the blood vessels in these areas (the lips and skin surrounding may appear unusually pale); mildly talkative and euphoric behavior; anxiolytic (calming) effects, sense of well-being, clear thinking; and relaxed muscles. Sleep is often restful and there are pronounced periods of sleepiness correlating to the amount and potency of kava consumed.

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 that the psychoactives are absorbed into the bloodstream more quickly.

A potent drink results in a faster onset with a lack of stimulation, somnolence, and then deep, dreamless sleep within 30 minutes. Unlike alcohol-induced sleep, after wakening the drinker does not experience any mental or physical after effects.

It is reported that many people experience rather vivid dreams after drinking kava. [1]

Kava culture

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

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. It is used primarily at social gatherings to increase amiability and to relax after work. It has great religious significance, being used to obtain inspiration. In some Westernized Pacific peoples, the drink has been demonized and seen as a vice, and youth there often reject its traditional use. However, it has gained a cult following among the youth culture of caucasian people living on Pacific islands.

Botany and agronomy

There are several cultivars of kava, with varying concentrations of primary and secondary psychoactive substances. 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 2,000mm/yr). Ideal growing conditions are 20-35 degrees Celsius (70-95 Fahrenheit), 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 propagation is entirely due to human efforts by the method of striking.

Traditionally, plants are harvested around 4 years of age, as older plants have higher concentrations of kavalactones. But in the past two decades farmers have been harvesting younger and younger plants, as young as 18 months. After reaching about 2m height, plants grow a wider stalk and additional stalks, but not much taller. The roots can reach 60cm depth.

Composition

Fresh kava root contains on average 80% water. Dried root contains approximately 43% starch, 20% fibers, 15% kavalactones, 12% water, 3.2% sugars, 3.6% proteins, 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.

Basic research on anti-cancer potential

On 15 February 2006, the Fiji Times and Fiji Live reported that researchers at the University of Aberdeen in Scotland and the Laboratoire de Biologie Moleculaire du Cancer in Luxembourg had discovered that kava may treat ovarian cancer and leukemia. Kava compounds inhibited the activation of a nuclear factor that led to the growth of cancer cells. The Aberdeen University researchers published in the journal The South Pacific Journal of Natural Science that kava methanol extracts had been shown to kill leukaemia and ovarian cancer cells in test tubes. The kava compounds were shown to target only cancerous cells but not healthy cells.

Fiji Kava Council Chairman Ratu Josateki Nawalowalo welcomed the findings, saying that they would boost the kava industry. For his part, Agriculture Minister Ilaitia Tuisese called on the researchers to help persuade members of European Union to lift their ban on kava imports.

Pharmacology

Kavas active principal ingredients are the kavalactones, of which at least 15 have been identified and are all considered psychoactive. Only six of them produce noticeable effects, and their concentrations in kava plants vary. Different ratios can produce different effects.

Kava has been considered very safe. Yet, some kava herbal supplements have been accused of contributing to very rare but severe hepatotoxic reactions (see section on safety) such may have been due to their use of plant parts other than the root, such as stems or peelings that are known to have been exported to Europe manufacturers. Kava is considered to be not addictive.

Pharmacodynamics

Desmethoxyyangonin, one of the six major kavalactones, is a reversible MAO-B inhibitor (Ki 280 nM)[2] and is able to increase dopamine levels in the nucleus accumbens. This finding might correspond to the slightly euphoric action of kava.[3]
Kavain in both enantiomeric forms inhibit the reuptake of noradrenalin at the transporter (NAT), but not of serotonin (SERT).[4] An elevated extracellular NA level in the brain may account for the reported enhancement of attention and focus.

Safety

Incidents and regulation

In the year 2001 concerns were raised about the safety of commercial kava products.[5] There have been allegations of severe liver toxicity, including liver failure in some people who had used dietary supplements containing kava extract. The possbility of liver damage consequently prompted action of many regulatory agencies in European countries where the legal precautionary principle so mandated. In the UK, the Medicines for Human Use (Kava-kava) (Prohibition) Order 2002 prohibits the sale, supply or import of most derivative medicinal products. Kava is banned in Switzerland, France and The Netherlands[citation needed]. The health agency of Canada issued a stop-sale order for kava in 2002. But legislation in 2004 made the legal status of kava uncertain. The United States CDC has released a report[6] expressing reservations about the use of kava and its possibly adverse side effects (specifically severe liver toxicity), as has the Food and Drug Administration (FDA).[7] The Australian Therapeutic Goods Administration has recommended that no more than 250 mg of kavalactones be taken in a 24 hour period.[8] According to the Medicines Control Agency in the U.K., there is no safe dose of kava, as there is no way to predict which individuals would have adverse reactions.[9] However, none of these regulatory actions and took into account the fact that when kava preparations are made with the peeled root of the plant no toxicity is found.[10][citation needed]

Toxicology

File:Kava pyridine alkaloids.svg
Piperidine alkaloids from the kava plant

The legal intervention stimulated research, and hepatotoxic substances were found in the plant. Researchers from the University of Hawaii at Manoa found that an alkaloid called pipermethystine (formula 1), contained in stem peelings and leaves, had toxic effects on liver cells in vitro[11] and in vivo.[12] In rats fed with 10 mg/kg pipermethystine for two weeks, indications of hepatic toxicity were found. Comparable signs of toxicity were not detected with kava rhizome extracts (100 mg/kg, 2 weeks)[12], (73 mg/kg, 3 months).[13]

Flavokavain B, found in the plant's rhizome, may also contribute to toxic effects.[14] And, it is known that some of the kavapyrones block several subtypes of the enzyme cytochrome P450[15], which can result in adverse interactions with other drugs used concomitantly.

The plant also contains glutathione. In extracts its concentration varies depending on the lipophilicity of the applied solvent; the amount is higher in aqueous extracts. Glutathione in kava preparations is able to provide a certain protection of liver cells.[16]

Before 2002, substantial amounts of aerial parts of the kava plant were being exported to North America and Europe and obviously used for the production of commercial prepartions. For traditional use in the South Pacific, stem peelings and leaves are discarded, and only the rhizomes are used and extracted with water. This may explain why native populations that make heavy use of kava experience side effects that are mild, temporary, and confined to the skin, whereas industrialized countries that have newly adopted kava occasionally show severe, acute responses.

Outlook

The issue has long been controversial and the debate fuelled by conflicting economic interests of monopoly-driven pharmaceutical companies, concerned with competition in anti-anxiety drug sales, and kava-exporting nations of the Pacific Islands as well as disagreements between the medical establishment and proponents of herbal and natural medicine. The German Federal Institute for Drugs and Medical Devices (BfArM), which in 2002 temporarily inactivated kava registrations, asked the producers to provide new clinical data by June 2007, in which case a reinstitution of the kava products on the market might again be possible.[17]

A New Zealand committee from the New Zealand Association of Medical Herbalists that considered the issue commented in its summary: "A comparison with paracetamol-associated hepatotoxicity, results in the conclusion that these potential risks for kava are dramatically less than that of a popular non prescription drug widely sold through grocery outlets."[18][19] The NZ government is currently only considering requiring a suitable warning label standard to go on kava products.

See also

References

  1. Kevin Cassell (2005). Fiji: A Visitor's Guide. Retrieved on 2007-04-25.
  2. Uebelhack R, Franke L, Schewe HJ (1998): “Inhibition of platelet MAO-B by kava pyrone-enriched extract from kava-kava.” Pharmacopsychiatry 31(5):187-92. PMID 9832350
  3. Baum SS, Hill R, Rommelspacher H (1998): “Effect of kava extract and individual kavapyrones on neurotransmitter levels in the nucleus accumbens of rats.” Prog Neuropsychopharmacol Biol Psychiatry 22(7):1105-20. PMID 9829291
  4. Seitz U, Schule A, Gleitz J (1997): "[3H]-monoamine uptake inhibition properties of kava pyrones." Planta Med. 63(6):548-9. PMID 9434608
  5. Mark Blumenthal (2002). Kava safety questioned due to case reports of liver toxicity. American Botanical Council. HerbalGram. Retrieved on 2005-12-07.
  6. United States Centers for Disease Control and Prevention (2002). "Hepatic Toxicity Possibly Associated with Kava-Containing Products --- United States, Germany, and Switzerland, 1999—2002". Morbidity & Mortality Weekly Report 51(47): 1065–1067. Retrieved on 2005-09-16.
  7. Center for Food Safety and Applied Nutrition (2002). "Kava-Containing Dietary Supplements May Be Associated with Severe Liver Injury". United States Food and Drug Administration. Retrieved on 2005-06-16.
  8. Kava fact sheet. Therapeutic Goods Administration, Government of Australia (April 2005). Retrieved on 2006-07-10. (Download PDF 44KB)
  9. Kava: A supplement to avoid. Consumer Reports (March 2003). Retrieved on 2006-07-17. )
  10. Kava Safety Facts. KavaZen (March 2004). Retrieved on 2007-09-05.)
  11. Pratibha V. Nerurkar et al. (2004): "In Vitro Toxicity of Kava Alkaloid, Pipermethystine, in HepG2 Cells Compared to Kavalactones", Toxicological Sciences 79, 106-111. Fulltext.
  12. 12.0 12.1 Lim ST et al. (2007): "Effects of Kava Alkaloid, Pipermethystine, and Kavalactones on Oxidative Stress and Cytochrome P450 in F-344 Rats." Toxicol Sci. PMID 17329236
  13. Sorrentino L et al. (2006): "Safety of ethanolic kava extract: Results of a study of chronic toxicity in rats", Phytomedicine, 13(8):542-549. PMID 16904878
  14. Jhoo JW et al. (2006): "In vitro cytotoxicity of nonpolar constituents from different parts of kava plant (Piper methysticum)", J. Agric. Food Chem. 54(8):3157-62. PMID 16608246
  15. a) J.M. Mathews et al. (2005): "Pharmacokinetics and disposition of the kavalactone kawain: interaction with kava extract and kavalactones in vivo and in vitro", Drug. Metab. Dispos. 33(10):1555-63. PMID 16033948; Fulltext
    b) J.M. Mathews et al. (2002): "Inhibition of Human Cytochrome P450 Activities by Kava Extract and Kavalactones", Drug Metab. Dispos. 30(11):1153-1157. Fulltext
  16. Whitton PA et al. (2003): “Kava lactones and the kava-kava controversy”, Phytochemistry 64(3):673-9. PMID 13679089
  17. a) American Botanical Council. German Government Reconsiders Kava. Retrieved on 2006-05-12.
    b) University of the South Pacific. USP plays a major role in the partial lifting of the Kava ban in Germany. Retrieved on 2006-05-12.
  18. New Zealand association of medical herbalists (2005). Submission on proposed reclassification of kava as a prescription medicine (PDF). Retrieved on 2006-05-12.
  19. New Zealand National Nutritional Foods Association (2002). Announcement on the prohibition of Kava-Kava in the UK (HTML). Retrieved on 2007-09-05.

Literature

  • Lebot, Vincent et al. "Kava: The Pacific Drug", New Haven: Yale University Press, 1992. ISBN 0-300-05213-8

External links

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