Kava is mainly used for its anxiolytic effects. It has the unique ability of calming the nerves, without causing sedation or any loss of cognition (within therapeutic range).
It's a ceremonial brew used on many of the scattered Pacific Islands. Kava isn't psychadelic, but it does have potent relaxant and slightly euphoric effects when consumed in higher doses.
In the modern era, kava has become a staple used by herbalists around the world. It's one of the most reliable anti-anxiety herbs available, and has additional uses for treating pain and insomnia.
- Acute stress
- Depression (mild)
- Generalised anxiety disorder
- Menopausal symptoms
- Muscle spasms
- Tension headaches
- To improve cognitive performance
- Urinary tract infections
- Pregnancy or lactation.
- Hypnotic (in high doses)
- Relaxing nervine
- Sedative (mild)
- Local anasthetic
- Urinary Antiseptic
How Is Kava Used?
Kava is used traditionally in ceremonies. Modern medicinal uses of the herb involves anxiety-related conditions, muscle tension, insomnia, and acute stress.
+ Western Herbal Medicine
Traditional uses in Western herbal medicine includes neuralgia, dizziness, chronic bronchitis, cystitis, dysuria, rheumatism, anorexia, leukorrhea, gonorrhea, gout, and joint pain .
- (1:2 Liquid Extract)
- View Dosage Chart
Pacific Islands (numerous)
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Constituents of Interest
- Kava lactones
- Awa (Hawaii)
- Ava (Samoa)
- Yaqona (Fiji)
- Sakau (Pohnpei)
- Malok (Vanuatu)
- Avoid use during pregnancy.
Duration of Use
- Long ter use acceptable in smaller doses.
Kava is a modest plant, bearing only a small amount of leaves. The leaves have a characteristic heart shape.
In the Piperaceae family, there are about 2400 species distributed through only 10 genera. The Piper genus accounts for about 2000 of these species.
Harvesting Collection, and Preparation
Kava extracts are usually standardised to 30% kava lactones. The kava lactone content can vary from 3-20% naturally .
Pharmacology & Medical Research
+ Neurological Activity
The pyrones contained within kava have been shown through various studies to provide multiple beneficial actions on the neurological system from analgesic, antispasmodic, anti-convulsant, neuroprotective, and recovery support after cerebral ischemic attacks [9-18]. The suggested mechanisms of action for this wide range of neurological improvements is via:
- Calcium channel agonism [19, 20]
- Blocking of sodium channels [21-23]
- Monoamine oxidase inhibition 
- Noradrenalin uptake inhibition 
- GABA modulation 
Compelling evidence has been found to suggest kava extracts can act selectively on the limbic structures to reduce anxiety without causing sedation .
Kava extracts have also been show to interact with glutamate , dopamine (water soluble fractions only) , noradrenalin , and serotonin (water soluble fractions only [27, 19, 20].
+ Generalised Anxiety Disorder
An 8-week randomised, double blind clinical trial involving 129 individuals found that a 400 mg Kava extract was as effective at treating generalised anxiety disorder as 10 mg Buspirone, and 100 mg Opipramol .
Kava contains kava lactones (3.5-15% of the dried root), flavonoids (flavokawains), methystcin, dihydromethysticin, kavain, dihydrokavain, chalcones (flavokavains A-C). [4, 5].
Clinical Applications Of Kava:
Kava is useful as an anxiolytic, anti-insomniac, and muscle relaxant. It has also shown to be beneficial in treating and recovering from cerebral ischemic attacks (stroke).
Avoid use of kava if pregnant, breastfeeding, or experiencing liver dysfunction.
Due to the dopamine antagonising actions of kava, care should be taken with those on dopaminergics, or with dopamine disorders like Parkinsons disease. .
Allergies to kava or kavapyrones have been reported [3, 6-8].
Do not use with any patient experiencing liver disease or dysfunctions .
The LD50 of kavalactones is 3-400 mg/kg .
Products Containing Kava:
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(Updated November 2018)
Recent Blog Posts:
Uebelhack, R., Franke, L., & Schewe, H. J. (1998). Inhibition of platelet MAO-B by kava pyrone-enriched extract from Piper methysticum Forster (kava-kava). Pharmacopsychiatry, 31(05), 187-192.
Meyer HG. Pharmakologie der wirksamen prinzipien de kawarhizoms (Piper methysticum Forst.). Arch Int Pharmacodyn Ther 1962; 138: 505-536
Ulbricht, C. (2002). Kava Monograph. Journal Of Herbal Pharmacotherapy, 2(4), 65-91. doi:10.1300/J157v02n04_07
Hoffmann, D. (2003). Medical herbalism: The science and practice of herbal medicine. Rochester, VT: Healing Arts Press.
Bone, K. (2003). A clinical guide to blending liquid herbs: Herbal formulations for the individual patient. Edinburgh [u.a., MO: Churchill Livingstone.
Jappe U, Franke I, Reinhold D, et al. Sebotropic drug reaction resulting from kava-kava extract therapy: a new entity? J Am Acad Dermatol 1998; 38 (1): 104 106.
Schmidt P, Boehncke WH. Delayed-type hypersensitivity reaction to kava-kava extract. Contact Dermatitis 2000; 42 (6): 363-364.
Suss R, Lehmann P. [Hematogenous contact eczema caused by phytogenic drugs exemplified by kava root extract]. Hautarzt 1996; 47 (6): 459-461.
Brüggemann F, Meyer HJ. Die analgetische wirkung der Kawa-inhaltsstoffe dihydrokawain und dihydromethysticin. Arzneimittelforschung 1963; 13: 407-409.
Hänsel R. Characterization and physiological activity of some Kawa constituents. Pacific Science 1968; 22: 293-313.
Kretzschmar R, Meyer HJ. [Comparative studies on the anticonvulsant activity of the pyrone compounds of Piper methysticum Forst]. Arch Int Pharmacodyn Ther 1969; 177 (2): 261-277.
Kretzschmar R, Meyer HJ, Teschendorf HJ. Strychnine antagonistic potency of pyrone compounds of the kavaroot (Piper methysticum Forst.). Experientia 1970; 26 (3): 283-284.
Kretzschmar R, Teschendorf HJ, Ladous A, et al. On the sedative action of the kava rhizome (Piper methyst.). Acta Pharmacol Toxicol 1971; 29(4):26. Monograph from Natural Standard 85
Meyer HJ. [Spasmolytic effect of dihydromethysticin, a constituent of Piper methysticum Forst]. Arch Int Pharmacodyn Ther 1965; 154 (2): 449-467.
Meyer HJ, Meyer-Burg J. Hemmung des elektrokrampfes durch die kawapyrone dihydromethysticin und dihydrokawain. Arch Int Pharmacodyn 1964; 148 (1-2): 97-110.
Singh Y, Blumenthal M. Kava: an overview. Distribution, mythology, botany, culture, chemistry and pharmacology of the South Pacific’s most revered herb. Herbal Gram 1997; 39 (Suppl 1): 34-56.
Backhauss C, Krieglstein J. Extract of kava (Piper methysticum) and its methysticin constituents protect brain tissue against ischemic damage in rodents. European Journal of Pharmacology 1992; 215 (2-3): 265-269.
Kleiser B, Diepers M, Wagner N, et al. Treatment of intracerebral hematomas with kava in rats. Neurology 1998; 50 (4): a398.
Walden, J., Von Wegerer, J., Winter, U., Berger, M., & Grunze, H. (1997). Effects of kawain and dihydromethysticin on field potential changes in the hippocampus. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 21(4), 697-706.
Walden, J., Von Wegerer, J. Ö. R. G., Winter, U., & Berger, M. (1997). Actions of Kavain and Dihydromethysticin on Ipsapirone‐Induced Field Potential Changes in the Hippocampus. Human Psychopharmacology: Clinical and Experimental, 12(3), 265-270.
Gleitz, J., Friese, J., Beile, A., Ameri, A., & Peters, T. (1996). Anticonvulsive action of (±)-kavain estimated from its properties on stimulated synaptosomes and Na+ channel receptor sites. European journal of pharmacology, 315(1), 89-97.
Gleitz J, Gottner N, Ameri A, et al. Kavain inhibits non-stereospecifically veratridine-activated Na+ channels. Planta Med 1996; 62: 580-581.
Magura EI, Kopanitsa MV, Gleitz J, et al. Kava extract ingredients, (+)-methysticin and (+/2)-kavain inhibit voltage-operated Na(+)-channels in rat CA1 hippocampal neurons. Neuroscience 1997; 81 (2): 345-351.
Seitz, U., Schüle, A., & Gleitz, J. (1997). [3H]-monoamine uptake inhibition properties of kava pyrones. Planta medica, 63(06), 548-549.
Gleitz J, Beile A, Peters T. (+/2)-kavain inhibits the veratridine- and KCl-induced increase in intracellular Ca2+ and glutamate-release of rat cerebrocortical synaptosomes. Neuropharmacology 1996; 35 (2): 179-186
Holm E, Staedt U, Heep J, et al. [The action profile of D,L-kavain. Cerebral sites and sleep-wakefulness-rhythm in animals]. Arzneimittelforschung 1991; 41 (7): 673-683
Baum SS, Hill R, Rommelspacher H. Effect of kava extract and individual kavapyrones on neurotransmitter levels in the nucleus accumbens of rats. Prog Neuropsychopharmacol Biol Psychiatry 1998; 22 (7): 1105-1120.
Jussofie, A., Schmiz, A., & Hiemke, C. (1994). Kavapyrone enriched extract fromPiper methysticum as modulator of the GABA binding site in different regions of rat brain. Psychopharmacology, 116(4), 469-474. [animal studies].
Boerner, R. J., Sommer, H., Berger, W., Kuhn, U., Schmidt, U., & Mannel, M. (2003). Kava-Kava extract LI 150 is as effective as Opipramol and Buspirone in Generalised Anxiety Disorder–an 8-week randomized, double-blind multi-centre clinical trial in 129 out-patients. Phytomedicine, 10, 38-49. [RCT].