Description

Kava

Kava or kava kava (Piper methysticum: Latin ‘pepper’ and Latinized Greek ‘intoxicating’) is a crop of the Pacific Islands. The name kava is from Tongan and Marquesan, meaning ‘bitter’; other names for kava include ʻawa (Hawaiʻi), ʻava (Samoa), yaqona (Fiji), sakau (Pohnpei), Seka (Kosrae), and malok or malogu (parts of Vanuatu). Kava is consumed for its sedating effects throughout the Pacific Ocean cultures of Polynesia, including Hawaii, Vanuatu, Melanesia, and some parts of Micronesia. To a lesser extent, it is consumed in nations where it is exported as herbal medicine.

The root of the plant is used to produce a drink with sedative, anesthetic, and euphoriant properties. Its active ingredients are called kavalactones. A systematic review done by the British nonprofit Cochrane concluded it was likely to be more effective than a placebo at treating short-term anxiety.

Moderate consumption of kava in its traditional form, i.e. as a water-based suspension of kava roots, has been deemed as presenting an “acceptably low level of health risk” by the World Health Organization. However, consumption of kava extracts produced with organic solvents, or excessive amounts of poor-quality kava products, may be linked to an increased risk of adverse health outcomes, including potential liver injury. Nevertheless, in Australia, the import and possession of kava is regulated due to particular social health concerns

Characteristics

Kava was historically grown only in the Pacific islands of Hawaii, Federated States of Micronesia, Vanuatu, Fiji, the Samoas, and Tonga. An inventory of P. methysticum distribution showed it was cultivated on numerous islands of Micronesia, Melanesia, Polynesia, and Hawaii, whereas specimens of P. wichmannii were all from Papua New Guinea, the Solomon Islands, and Vanuatu.

The kava shrub thrives in loose, well-drained soils where plenty of air reaches the roots. It grows naturally where rainfall is plentiful, attaining over 78 inches (2,000 mm) per year. Ideal growing conditions are 70–95 °F (21–35 °C) and 70–100% relative humidity. Too much sunlight is harmful, especially in early growth, because 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 meters (6.6 ft) height, plants grow a wider stalk and additional stalks, but not much taller. The roots can reach a depth of 60 centimeters

Pharmacology

Constituents

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.[32] 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. Some minor constituents, including three chalcones, flavokavain A, flavokavain B, and flavokavain C, have also been identified, as well as a toxic alkaloid (not present in the consumable parts of the plant), pipermethystine. Alkaloids are present in the roots and leaves.

Pharmacodynamics

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

  • Potentiation of GABAA receptor activity (by kavain, dihydrokavain, methysticin, dihydromethysticin, and yangonin).
  • Inhibition of the reuptake of norepinephrine (by kavain and methysticin) and possibly also of dopamine (by kavain and desmethoxyyangonin).
  • Binding to the CB1 receptor (by yangonin).
  • Inhibition of voltage-gated sodium channels and voltage-gated calcium channels (by kavain and methysticin).
  • Monoamine oxidase B reversible inhibition (by all six of the major kavalactones).

Receptor binding assays with botanical extracts 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. Weak interaction with the 5-HT6 and 5-HT7 receptors and the benzodiazepine site of the GABAA receptor were also observed.

Potentiation of GABAA receptor activity may underlie the anxiolytic effects of kava, while the elevation of dopamine levels in the nucleus accumbens likely underlie the moderately psychotropic effects the plant can produce. Changes in the activity of 5-HT neurons could explain the sleep-inducing action, However, failure of the GABAA receptor inhibitor flumazenil to reverse the anxiolytic effects of kava in mice suggests that benzodiazepine-like effects are not contributing to the pharmacological profile of kava extracts.

Heavy, long-term use of kava has been found to be free of association with reduced ability in saccade and cognitive tests but has been associated with elevated liver enzymes.