Botanical Name: Piper methysticum, Piperaceae

Common names: Kava, Ava, Awa, Yaqona, Grog

Plant description: Kava is described as a robust, mostly succulent, perennial, dioecious shrub, with erect knotted stems and many branches, attaining a height of up to 3 m. The yellowish to pale green leaves are alternate, cordate, with a wavy, entire margin, and an abrupt, acute point, and can be up to 28 cm long.. The petiole is about 2-3 cm long, dilated at the base, and supplied with linear, erect stipules. The leaf veins are prominent, and number between 12 and 13, diverging from the base of the leaf-blade. The flowers are small, without petals, and are arranged on slender spikes. Kava plants bearing male flowers are axillary and solitary, whereas in female specimens the spikes are numerous and larger.  From the rootstalk, which is sometimes incorrectly referred as a rhizome, arise a fringe of lateral roots up to 3 m in length.  The color of the rootstalk varies from white to dark yellow, depending upon the amount of kava lactones, which impart a yellowish color.  According to Singh and Blumenthal, the Polynesian people recognize many different varieties, classified primarily according to morphology, such as the intensity of leaf color, and the color and shape of the stem (1997, 40).

Habitat, ecology and distribution: Kava is thought to have originated in Indonesia and Papua New Guinea, and in other areas of South East Asia, from where it was brought by early explorers by canoe to the various islands of Polynesia, including the Solomon Islands, Fiji, Tonga, Tahiti and Hawaii.  Wild specimens are said to thrive in stony ground at elevations of between 150 and 300 m, but Kava has since been cultivated.  Mills and Bone state that P. methysticum is a cultigen derived from P. wichmannii (2000, 457). The name "Kavakava" is a Maori name that refers to a related species (P. excelsum) that was used in religious ceremonies but was not consumed as a ceremonial or recreational beverage (Singh and Blumenthal 1997, 37).

Part used: rootstock or stump, leaves

History: Kava has long been an important ceremonial and religious plant used by peoples of Polynesia.  Each group has a rich mythology surrounding the usage of this plant, which is consumed both for religious and ceremonial purposes, as well as for recreation.  The task of preparing the drink traditionally fell upon young boys or girls, who masticated the root after it has been scraped from the rootstalk and pounded into smaller particles by a mortar and pestle.  The result was then strained into a special ceremonial bowl and mixed with water.  In more recent times this practice has largely been superceded by simply pounding and mixing the pulverized root with water, which is then strained.  Kava is considered to be an important ceremonial herb among the Polynesian peoples, offered to honored guests to welcome them, but is also used in communal disputes to allay hostile feelings between the participants, and simply as a recreational beverage to alleviate tensions in social gatherings, much like alcohol in used in the West.  Kava ceremonies typically begin in the late afternoon or early evening, and can continue all night long. 

Constituents: Kava is noted for its kava pyrones (or lactones) contained within the resin of the plant, comprising between 5-9% of the total constituents depending on the variety and location in which the plant is grown.  The kava pyrones, or 6-stytyl-4-methoxy-alpha-pyrone derivatives, include kavain (kawain), dihydrokavain (DHK) and methysticin as major components, dihydromethysticin (DHM), yangonin and desmthoxyyangoni as minor constituents, and 11-methoxynoryangonin and 11-methoxyyangonin in trace amounts.  Additionally, Kava contains two flavonoid pigments called flavokawin A and flavokawin B, and an alkaloid derived from the leaves called pipermethystine (Mills and Bone 2000, 457; Singh and Blumenthal 1997, 46-47).

Medical Research: Due to its popularity Kava has undergone a significant degree of scientific investigation, and has been the subject of several clinical trials to determine its efficacy in the treatment of anxiety and sleep disorders.  Most of the pharmacological work has concentrated on the water-soluble pyrones, either in combination or in isolation.
•Sedative: Two  standardized extracts containing 105 mg of kavalactones and another containing 210 mg of kavalactones were assessed in a placebo controlled clinical trial in healthy volunteers.  These extracts shortened the time it took to fall asleep, increasing the length of deep sleep, and decreasing the duration of wakeful phases in sleep EEG recording, without affecting the duration of REM sleep.  These results compare favorably to benzodiazepines and barbituates that have an adverse effect upon REM sleep (Mills and Bone 2000 458).  In another study, mice were given an extract of Kava and Passionflower (Passiflora incarnata), and while both had a sedative effect they worked via different mechanisms.  When combined however, their sedative properties were more pronounced (Mills and Bone 2000, 458).  The sedative and anxiolytic properties of Kava are thought to include a variety of mechanisms, including the blockade of voltage-gated sodium ion channels, enhanced ligand binding to gamma-aminobutyric acid (GABA) type A receptors, diminished excitatory neurotransmitter release due to calcium ion channel blockade, reduced neuronal reuptake of noradrenaline (norepinephrine), reversible inhibition of monoamine oxidase B and suppression of the synthesis of the eicosanoid thromboxane A(2), which antagonises GABA(A) receptor function (Singh and Singh 2002).
•Anxiolytic: Despite the fact that Kava was not used therapeutically as an anxiolytic in Polynesian society, the usage of Kava in such conditions has caught the attention of medical researchers.  In one reported case, s 37-year-old female outpatient with generalized anxiety disorder was treated with Kava, and within 4 weeks the symptoms had improved by 75% and by 6 months there was an almost total remission of symptoms (Boerner 2001). Similarly, clinical trials have demonstrated the efficacy of Kava in anxiety and depression.  In an early double-blind placebo controlled clinical trial using purified kavain at a dose of 400 mg per, kavain was found to improve memory and reaction time in patients with anxiety (Mills and Bone 2000, 460).  When compared to oxazepam, another double-blind placebo controlled study determined that kavain had similar effects in patients with anxiety neurosis (Mills and Bone 2000, 460-61).  In another clinical trial 300 mg of standardized extract of kava (210 mg kava pyrones, equivalent to 4 g crude herb) was shown to exhibit significant effects in reducing anxiety, comparable to barbiturates such as bromazepam and oxazepam, without the same side-effects (Mills and Bone 200 461).  Longer term clinical trials with Kava in the treatment of anxiety and depression have similarly demonstrated a superior outcome compared with placebo, although a few studies have indicated that Kava has little effect in severe anxiety (Pittler and Ernst 2002; Connor and Davidson 2002).  The modes by which Kava exerts its anxiolytic effects are diverse, thought to be similar to antiepileptic drugs such as carbamazepine and valproic acid that have been observed to be successful mood stabilizers, albeit with adverse reactions.  These drugs exhibit a characteristic pattern of action on ion fluxes, affecting the movement of Na+- and Ca2+ inward and K+ outward across membranes, as well as interacting with the metabolism and receptor occupation of a variety of biogenic amines and excitatory and inhibitory amino acids.  Kava pyrones appear to have a weak Na+ antagonistic effect that may contribute to their antiepileptic properties.  Kava pyrones also have pronounced Ca2+ channel antagonistic properties and act as positive modulators of the movement K+ outward across membranes, two actions that are thought to be importance in mood stabilization.  In addition, kava pyrones have demonstrated additive effects with the serotonin agonist ipsapirone, probably contributing to their anxiolytic and sleep-inducing effects.  The kava pyrones also display a distinct pattern of action on glutamatergic and GABAergic transmission, without affecting long-term potentiation (Grunze et al 2001).
•Antispasmodic: Kava pyrones have demonstrated potent antispasmodic properties in experimental models, and in one study, were shown to be 10 times more effective than mephenesin in convulsions induced by strychnine.  Kava pyrones have also demonstrated an antispasmodic property on smooth muscle similar to papavarine (Mills and Bone 2000 459).
•Antiepileptic: Kava extracts and purified kava pyrones (esp. dehydromethysticin) have demonstrated efficacy in the treatment of grand mal seizures, but have not been recommended for use because of the adverse skin effects associated with the high doses necessary to control the symptoms (Mills and Bone 2000, 461).
•Analgesic: An aqueous extract of Kava and a lipid soluble extract of the resin were tested in mice, by the tail immersion and abdominal constriction methods. Both extracts showed analgesic effects in both tests.  Eight of the purified pyrones from the lipid soluble extract were also tested for activity in the tail immersion test, and kavain, dihydrokawain, methysticin and dihydromethysticin were found to be highly effective in producing analgesia.  To demonstrate the pathway by which Kava exerts its analgesic activities, researchers used naloxone to inhibit morphine-induced analgesia, which was completely ineffective in reversing the antinociceptive activities of the kava extracts, indicating that analgesia produced by Kava occurs via non-opiate pathways (Jamieson and Duffield 1990a).
•Antimicrobial: Although Kava has traditionally been used to treat urinary tract infections, kava pyrones have not demonstrated an antibacterial property in vitro, although they have demonstrated a potent antifungal activity, excluding species of Candida (Mills and Bone 2000, 460).
•Antioxidant: Dihydrokawain and yangonin have demonstrated significant cyclooxygenase-I and cyclooxygenase-II inhibitory activities in a cyclooxygenase enzyme inhibitory assay, whereas yangonin and methysticin showed only moderate antioxidant activities in a free radical scavenging assay (Wu et al 2002).
•Anticancer: One study indicates that the more Kava consumed by a population the lower the cancer incidence for that population, suggesting a close inverse relationship between cancer incidence and Kava consumption (Steiner 2000).
•Schizophrenia: Kava is reported to display a dopamine antagonist property, and has been observed to be of benefit in treating symptoms of schizophrenia (Mills and Bone 2000, 463).

Toxicity: The LD50 for oral administration of dihydrokavain is reported to be 920mg/kg and 1050 mh/kg for dihydromethysticin (Mills and Bone 2000, 462).  Continuous administration of 50mg/kg of dihydrokavain three times a week for 3 months in rats showed no indication of toxicity (Mills and Bone 2000, 462).  The oral LD50 for a kava extract standardized to 70% kava pyrones have been recorded as 16g/kg in rats, and 1.8 mg/kg in mice (Mills and Bone 2000, 462). There are recent anecdotal and medical reports of hepatotoxicity in humans associated with Kava ingestion in both Europe and North America, although whether or not Kava can actually be implicated in all cases is still a subject of debate.  At this point only a small number of the cases are actually a cause for concern, as most of the other cases present additional factors, such as the concurrent use of alcohol, NSAIDs and other drugs, or a history of hepatitis and liver disease.  Nonetheless, these reported cases of Kava toxicity have stimulated a ban on the usage of Kava in Canada and in several European countries, despite previous clinical trials and experimental evidence that have demonstrated the relative safety of Kava.  There has been much speculation about why there have been these recent reports of Kava toxicity, especially since these effects have not been observed in Polynesian society where Kava is consumed frequently and in very high doses.  Some herbalists have speculated that the problem may lie with the processing and standardization of Kava, in which the kava pyrones are highly-purified and presented in a product that bears little similarity to the whole herb that is traditionally consumed.  Another cause for concern is the chronic usage of Kava in disorders such as anxiety and insomnia, which is not a traditional indication in Polynesian society, and nor does it reflect the way herbalists have used this herb over the last few hundred years.  Regardless of the reported cases of toxicity however, considering the amount of Kava that is sold and consumed in both Europe and North America, the statistical evidence still suggests that Kava is fairly safe, much more so than common OTC drugs such as NSAIDs that are well known hepatotoxic agents.

Herbal action: diuretic, urinary antiseptic, antispasmodic, analgesic, nervine relaxant, anaesthetic, anxiolytic

Indications: infection and inflammation of the genitourinary tract, urinary tenesmus, muscular pain, neuralgia, trigeminal neuralgia, neuropathies (e.g. toothache, earache, eye pain etc.)

Contraindications and cautions: Long-term chronic use of high doses of Kava has been associated with a reversible ichthyosiform eruption called kava dermopathy.  While the cause is not clear, it is speculated that Kava may interfere with cholesterol metabolism (Norton and Ruze 1994).  Other researchers have suggested the cause could be a Kava-induced niacin deficiency, although a placebo controlled clinical trial in 14 heavy Kava users failed to validate this hypothesis (Singh and Blumenthal 1997, 53). Ethanol and the lipid soluble extract (Kava resin) have been shown greatly to increase the respective hypnotic activity of each in mice.  Ethanol has also been shown to increase the toxicity of kava markedly (Jamieson and Duffield 1990b).  The German Commission E monographs suggest that Kava may potentiate the activity of alcohol, as well as other drugs, including barbiturates and other psychotropic medications (Blumenthal et al 1998, 156). Kava is reported to increase 'off' periods in Parkinson patients taking levodopa and can cause a semicomatose state when given concomitantly with alprazolam (Izzo and Ernst 2001).

Medicinal uses: Upon tasting Kava, the root presents a mildly pungent, bitter and astringent taste with mild sialagogue properties, but impresses more a marked local anaesthetic property upon the tongue, which suggests its usefulness as an analgesic, especially to mucus membranes.  Traditionally, Polynesian peoples used Kava to induce relaxation and counteract fatigue, as well as for urinary tract problems, asthma, rheumatism, headaches and to promote weight loss.  According to early ethnobotanists Kava was used by Polynesian healers as a treatment for syphilis, gonorrhea and chronic cystitis.  Kava was also used as a diaphoretic and stomachic to treat colds and flus (Singh and Blumenthal 1997, 49-50).  In the West, herbalists and the eclectic physicians found Kava to be an indispensable remedy in the treatment of urinary tract disorders, considering it a powerful diuretic with anticatarrhal properties.  Felter and Lloyd considered it of especial importance in "…acute vaginitis or urethritis, allaying the inflammation, causing the pain during micturition to disappear, when dysuria is present, and suppressing the mucopurulent catarrh from the vesico-urethral mucous membrane" (1893).  It was considered to be of primary importance in the treatment of gonorrhea and other sexually transmitted genito-urinary disorders.  It is also recommended in nocturnal incontinence in both the young and old, "…when due most largely to muscular weakness" (Felter and Lloyd 1893).  For this purpose Kava may be best combined with botanicals such Mullein root (Verbascum thapsus) that help to tone the musculature of the bladder.  These anticatarrhal properties also extend themselves to the intestines, when mucus congestion predominates. Kava also finds usefulness as an antispasmodic, relieving not only the tenesmus associated with urinary tract infections, but in dysmenorrhea, arthritis and rheumatism, as well as a symptomatic treatment in neuralgia and neuropathies. Due to its sialagogue and antispasmodic properties Kava has also shown its usefulness in nervous dyspepsia when used in small doses, correcting deficient secretions of the stomach and relieving undue tension in the smooth muscle of the gastrointestinal tract.  In more recent times Kava has been recommended in larger doses or as a standardized extract as an anxiolytic and antidepressant, to treat anxiety and depressive disorders.  Despite comprising the bulk of its usage in these modern times, Kava is at best a symptomatic treatment of these disorders, and should not be relied upon in chronic situations.  Instead, consider trophorestoratives such as Avena and Hypericum, and allied measures such as lifestyle and dietary changes.  Another more modern indication for Kava is as a sedative, but while it has definite muscle-relaxing properties, it tends to excite the mind and promote a feeling of euphoria, which does not necessarily equate with a good night's sleep.  Nonetheless, some patients will find Kava to be a powerful sedative, usually in uncomplicated cases of social stress and concomitant muscle tension.

Pharmacy and dosage:
•Dry Plant Tincture:  1:3, 1:5, 50% alcohol, 3-20 gtt, 3-10 mL
•Powder: 1.5-4 g daily
•Decoction: dried scraped root, 1:20, 30-90 mL
•Standardized extract: 100-200 mg kava pyrones daily

REFERENCES

Blumenthal, Mark ed. et al. 1998. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Austin, TX: American Botanical Council.
Boerner RJ. 2001. Kava kava in the treatment of generalized anxiety disorder, simple phobia and specific social phobia. Phytother Res. Nov;15(7):646-7
Connor KM, Davidson JR. 2002. A placebo-controlled study of Kava kava in generalized anxiety disorder. Int Clin Psychopharmacol Jul;17(4):185-8
Felter, HW and JU Lloyd. 1893. King's American Dispensatory. Digitized version available from http://www.ibiblio.org/herbmed/eclectic/kings/main.html.
Grunze H, Langosch J, Schirrmacher K, Bingmann D, Von Wegerer J, Walden J. 2001. Kava pyrones exert effects on neuronal transmission and transmembraneous cation currents similar to established mood stabilizers--a review. Prog Neuropsychopharmacol Biol Psychiatry. Nov;25(8):1555-70
Izzo AA, Ernst E. 2001. Interactions between herbal medicines and prescribed drugs: a systematic review. Drugs 61(15):2163-75
Jamieson DD, Duffield PH. 1990a. The antinociceptive actions of kava components in mice. Clin Exp Pharmacol Physiol Jul;17(7):495-507
Jamieson DD, Duffield PH. 1990b. Positive interaction of ethanol and kava resin in mice. Clin Exp Pharmacol Physiol Jul;17(7):509-14
Mills, Simon and Kerry Bone. 2000. Principals and Practice of Phytotherapy. London: Churchill Livingstone
Norton SA, Ruze P. 1994. Kava dermopathy.  J Am Acad Dermatol Jul;31(1):89-97
Pittler MH, Ernst E. 2002. Kava extract for treating anxiety. Cochrane Database Syst Rev 2:CD003383
Singh YN, Singh NN. 2002. Therapeutic potential of kava in the treatment of anxiety disorders. CNS Drugs 16(11):731-43
Singh, Y.N and M. Blumenthal. 1997. Kava: an overview.  Distribution, mythology, botany, culture, chemistry and pharmacology of the South Pacific's most revered herb. Herbalgram. No. 39.
Steiner GG. 2000. The correlation between cancer incidence and kava consumption. Hawaii Med J Nov;59(11):420-2
Wu D, Yu L, Nair MG, DeWitt DL, Ramsewak RS. 2002. Cyclooxygenase enzyme inhibitory compounds with antioxidant activities from Piper methysticum (kava kava) roots. Phytomedicine. Jan;9(1):41-7