Kava Kava

I first started using Kava as herb in the mid 1970’s, when a Chiropractor group asked me to develop a herbal formula that could help relax the muscle so they could do adjustment easier and more specifically help them hold them in better. I build a formula around kava that became quite useful and we sold a fair amount to local Chiropractor in Calgary Alberta where I live.  We used it successful in our clinical practice for well over 30 years.

Of course it works as a great muscle relaxant, but we have employed it in many other areas. I found that it is quite good for Urinary Tract Infection (UTI), not only reducing the bladder’s negative organism, but also relaxing the Urinary tract, having a slight numbing effect on the urinary tract, thus taking out the stinging feeling. It appears not only are some people anal retentive, they can be urinary retentive also. The first question I ask a woman when she comes in with a UTI is, ‘who they are pissed off at’. It doesn’t always hit pay dirt, but in well over 70% when the patient reflex on it, their UTI reduce a whole lot. Many people hold their pelvic area tightly, for these people Kava is great.

I also have had success with using it for some types of PMS, especially when anxiety is involve. Kava is very useful in many cases of anxiety. We also have found it quite useful for athletes that need to keep their muscle relaxed.

The biggest problem with Kava is that now in Canada it is banned at the health food store level. Herbal practitioners can still use it as it is not a banned substance and therefore Clinical Herbalist can still compound with it in a practitioner setting. Kava just can’t be sold in stores without a NPN and so far as I know, no one has gotten one as yet. There is a presumed toxicity issue with Kava due to a literal smear campaign for it since the early 2000’s

There were some anecdotal and medical reports of a small number of hepatotoxicity in humans associated with Kava ingestion in both Europe and North America at the turn of the millennia, but these finding could not be substantiated by third party investigations. These reported cases of Kava toxicity did stimulate 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.

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.

The use of substandard cultivars has been implicated in kava-associated hepatotoxicity. For example, the “Tu Dei” cultivar is a cheaper and fast-growing cultivar that is not recommended for daily consumption. The Vanuatu government’s 2002 Kava Act No. 7 categorizes the various kava chemotypes and cultivars into noble cultivars, medicinal varieties, Tu Dei kavas, and wild kavas. Noble cultivars have a long history of use as social beverages, and the medicinal varieties have a long history of traditional use by Pacific herbalists. Both of these types are available for export. The export of Tu Dei and wild kavas is no longer permitted. The noble cultivars that are more commonly used in traditional beverages are different from the medicinal varieties that are found in Western kava products. It is possible that the noble cultivars have lower hepatotoxicity compared to the medicinal varieties.[1]

I have included a bit of background information taken from our Western Medica I course to fill is some background:

Botanical Name: Piper methysticum, Piperaceae

Common names: Kava, Ava, Awa, Yaqona, Grog, Gea, Gi, Kao, Kavain, Kavapipar, Kawa Kawa, Kawa Pepper, Kawapfeffer, Kew, Malohu, Maluk, Meruk, Milik, Rauschpfeffer, Sakau, Tonga, Wurzelstock, Yagona, Yangona, Yaqona, Yongona

Part used: root, leaves (not normally used)

 History: The ancient Tahitians used this plant to create a “stupefying” drink and distinguished roughly 40 varieties of the plant. ‘Ava or kava was grown carefully in plantations which were selected for particular humidity and local conditions. In a small dose, kava kava was used as a tonic and stimulant.[2]

The herb is indigenous to Polynesia and Melanesia and was a popular drink used in religious rites. The rhizome is chewed or ground to produce a cloudy milky mash. The mash is intoxicating when it interacts with saliva. It was used to calm and relax a person, as well as increasing their mental activity. It has also been used for gout, bronchial and rheumatic ailments.[3],[4],[5]

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 had 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 superseded by simply pounding and mixing the pulverized root with water; which is then strained. Kava is still considered an important ceremonial herb among the Polynesian peoples. It is offered to honored guests to welcome them, but is also used in communal disputes to allay hostile feelings between the participants. It is also used 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.

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, Polynesian healers used kava as a treatment for syphilis, gonorrhea and chronic cystitis. Kava was also used as a diaphoretic and stomachic to treat colds and flus.[6]

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” (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.

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. Different ratios of the various kava lactones seem to determin the action in a subject’s body. Because of this, great care was given by indigenous cultivators to which variety was used in which situation. Additionally, Kava contains two flavonoid pigments called flavokawin A and flavokawin B, and an alkaloid derived from the leaves called pipermethystine; cepharadione A; ketones; yangonic acid, and cinnamic acids.[7],[8],[9],[10],[11],[12],[13],[14]

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 barbiturates that have an adverse effect upon REM sleep.[15]

In another study, mice were given a combination of Kava and Passion flower (Passiflora incarnata) extract.While both herbs are sedatives, they worked via different mechanisms. When combined however, their sedative properties were found to be  more pronounced. 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 antagonizes GABA(A) receptor function.[16],[17]

Anxiolytic: Despite the fact that Kava was not used therapeutically as an anxiolytic (substance to reduce anxiety) in Polynesian society, the usage of Kava in such conditions has caught the attention of medical researchers. The anti-stress and anti-anxiety effect of Kava has been shown out in many studies as a single herb and in formula.[18],[19] In one reported case, a 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.[20] Similarly, clinical trials have demonstrated the efficacy of Kava in anxiety and depression. In an earliar 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. When compared to oxazepam, another double-blind placebo controlled study determined that kavain had similar effects in patients with anxiety neurosis.[21]  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 side-effects.[22]  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.[23],[24]

People consuming kava have reported feeling more sociable, tranquil, and generally happy .[25]

The modes by which Kava exerts its anxiolytic effects are diverse. They are 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 .[26]

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 .[27]

•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.[28]

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.[29]

The kavapyrones desmethoxyyangonin and methysticin competitively inhibit monoamine oxidase B (MAO-B).[30] Kava is thought to work for a variety of inflammatory conditions by inhibiting both COX-1 and COX-2 enzymes, the enzymes responsible for converting arachidonic acid to prostaglandins.[31]

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.[32]

•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.[33]

•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.[34]

•Schizophrenia: Kava is reported to display a dopamine antagonist property, and has been observed to be of benefit in treating symptoms of schizophrenia.[35]

Menopausal anxiety: Two small trials have shown that kava standardized to 15% or 70% kava-lactones is superior to placebo taken orally for short-term treatment of neurovegetative and anxiety symptoms related to menopause. Significant improvement occurred after one week of treatment.[36]

Toxicity:  Any proven toxicity is at doses several order of magnitude above the typical therapeutic dosage.  The LD50 for oral administration of dihydrokavain is reported to be 920mg/kg and 1050 mh/kg for dihydromethysticin. Continuous administration of 50mg/kg of dihydrokavain three times a week for 3 months in rats showed no indication of toxicity. 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.[37]

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 (redness and/or scaling of the skin) eruption called kava dermopathy. While the cause is not clear, it is speculated that Kava may interfere with cholesterol metabolism.[38]  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.[39] 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.[40]  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.[41] Kava is reported to increase ‘off’ periods in Parkinson patients taking levodopa and can cause a semicomatose state when given concomitantly with alprazolam.[42]

Energetics: Tierra lists Kava Kava as pungent, bitter and warm; entering the Liver and Kidney meridians.[43] The odor is faint, characteristic, taste aromatic, pungent, bitter — more or less anesthetic.[44]

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

[1] Teschke R. Kava hepatotoxicity: pathogenetic aspects and prospective considerations. Liver Int. Jul. 11, 2010. [Epub ahead of print].doi: 10.1111/j.1478-3231.2010.02308.x.

[2]. Flore et Faune Terrestres, Encyclopedie de la Polynesie, (ed. B. Salvat), 1986, p.52

[3]. Weiss RF; Herbal Medicine; translate from sixth German edition; Beaconsfield Pub, Eng. p298, 1988.

[4]. Duke JA; CRC Handbook of Medicinal Herbs; CRC Press; Boca Raton Fl;p381, 1985.

[5]. Culbreth, D.M., A Manual of Materia Medica and Pharmacology, reprint Eclectic Med Pub., Portland, Oregon, 1983, p.149.

[6] Singh, Y.N and M. Blumenthal. 1997; ibid

[7]. Winzheimer E et al; Investigation of Kava Root; Arch Pharm 246 p 338 (CA 3:4296)

[8]. Young RL, Hylin JW, et al; Analysis of Kawa pyrones in extract of Piper methysticum; Phytochemistry 5(4) 795-8 1966.

[9]. Veen AG; Isolation and constitution of narcotic substance from Kawa-kawa (Piper methysticum); Rec. trav chim 58, 521-7 (CA33:62719) 1939.

[10]. Weiss RF; Herbal Medicine; translate from sixth German edition; Beaconsfield Pub, Eng. p298, 1988.

[11]. Duke JA; CRC Handbook of Medicinal Herbs; CRC Press; Boca Raton Fl;p381, 1985.

[12]. Leung, A.Y. and S. Foster, Encyclopedia of Common Natural Ingredients: Used in Food, Drugs, and Cosmetics, John Wiley & Sons, Inc., New York, 1996, p 330-331

[13] Mills, Simon and Kerry Bone. 2000

[14] 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

[15] Mills, Simon and Kerry Bone. 2000. P 458

[16] Singh YN, Singh NN. 2002. Therapeutic potential of kava in the treatment of anxiety disorders. CNS Drugs 16(11):731-43

[17] Mills, Simon and Kerry Bone. 2000. P 458

[18]. Singh N, Ellis CR et al; Kavatrol Reduces Daily Stress and Anxiety in Adults; Medical College of Virgina; 1998; p1-13

[19]. Seitz U, Schule A, et al; Monoamine Uptake Inhibition Properties of Kava Pyrones; Planta Medica; Vol 63, 1997, pp548-549

[20] 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

[21] Mills, Simon and Kerry Bone. 2000. P 460-61

[22] Mills, Simon and Kerry Bone. 2000. P 460

[23] Pittler MH, Ernst E. 2002. Kava extract for treating anxiety. Cochrane Database Syst Rev 2:CD003383

[24] Connor KM, Davidson JR. 2002. A placebo-controlled study of Kava kava in generalized anxiety disorder. Int Clin Psychopharmacol Jul;17(4):185-8

[25] Pierce A. The American Pharmaceutical Association Practical Guide to Natural Medicines. New York: The Stonesong Press, 1999:19

[26] 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

[27] Mills, Simon and Kerry Bone. 2000. P 459

[28] Mills, Simon and Kerry Bone. 2000. P 461

[29] Jamieson DD, Duffield PH. 1990a. The antinociceptive actions of kava components in mice. Clin Exp Pharmacol Physiol Jul;17(7):495-507

[30] Uebelhack R, Franke L, Schewe HJ. Inhibition of platelet MAO-B by kava pyrone-enriched extract from Piper methysticum Forster (kava-kava). Pharmacopsychiatry 1998;31:187-92

[31] Wu D, Yu L, Nair MG, et al. Cyclooxygenase enzyme inhibitory compounds with antioxidant activities from Piper methysticum (kava kava) roots. Phytomedicine 2002;9:41-7

[32] Mills, Simon and Kerry Bone. 2000. P 460

[33] 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

[34] Steiner GG. 2000. The correlation between cancer incidence and kava consumption. Hawaii Med J Nov;59(11):420-2

[35] Mills, Simon and Kerry Bone. 2000. P 463

[36] Warnecke G. [Psychosomatic dysfunctions in the female climacteric. Clinical effectiveness and tolerance of Kava extract WS 1490]. [Article in German]. Fortschr Med 1991;109:119-22

[37] Mills, Simon and Kerry Bone. 2000. P 462

[38] 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

[39] 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

[40] Jamieson DD, Duffield PH. 1990b. Positive interaction of ethanol and kava resin in mice. Clin Exp Pharmacol Physiol Jul;17(7):509-14

[41] Blumenthal, Mark ed. et al. 1998. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Austin, TX: American Botanical Council

[42] Izzo AA, Ernst E. 2001. Interactions between herbal medicines and prescribed drugs: a systematic review. Drugs 61(15):2163-75

[43]. Tierra, M., Planetary Herbology, Lotus Press, Santa Fe, NM, 1988, p.235.

[44]. Culbreth, D.M., Ibid.

Leave a Reply