Kava, sometimes referred to twice as kava-kava, is a potent anti-anxiety. It has the useful ability of being a strong anti anxiety agent without causing any loss in alertness within the therapeutic range. In fact, kava can actually improve concentration rather than diminish it.
In higher doses, kava kava is a sedative.
The main constituent in kava kava is reported to be the kava lactones. These can vary greatly in the plant from 3.5% to 15% of the total dried plant weight.
The main uses of kava kava are to calm the nerves before public speaking, treat general anxiety and depression, and to increase focus during anxious tasks.
- Hypnotic (higher doses)
- Relaxing nervine
- Sedative (mild)
- Skeletal muscle relaxant
- Local anaesthetic
- Analgesic (mild)
- Antipruritic (topical)
Dried Herb Equivalent:
Liquid Extract (1:2):
A note about the dose:
The dosage for kava depends mainly n the amount of kava lactones present. The recommended dosage for this is the equivalent of 60-120 mg kavalactones taken 3 times a day .
- Menopausal symptoms
- Depression (mild)
- Muscle tension or spasms
- To improve cognitive performance
Traditional uses in Western herbal medicine includes neuralgia, dizziness, chronic bronchitis, cystitis, dysuria, rheumatism, anorexia, leukorrhea, gonorrhea, gout, and joint pain .
Still compiling research
Habitat Ecology, and Distribution:
Still compiling research
Harvesting Collection, and Preparation:
Kava extracts are usually standardised to 30% kava lactones. The kava lactone content can vary from 3-20% naturally .
Kava contains kava lactones (3.5-15% of the dried root), flavonoids (flavokawains), methystcin, dihydromethysticin, kavain, dihydrokavain, chalcones (flavokavains A-C). [4, 5].
Pharmacology and Medical Research:
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 
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].
Toxicity and Contraindications:
- Contraindicated during pregnancy and lactation. Based off of a lack of safety data. .
- Do not use with any patient experiencing liver disease or dysfunctions .
- The LD50 of kavalactones is 3-400 mg/kg .
- 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].
Traditional Chinese Medicine:
Still compiling research.
Still compiling research.
Recent Blog Posts:
- 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 (5): 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, et al. Effects of kawain and dihydromethysticin on field potential changes in the hippocampus. Prog Neuropsychopharmacol Biol Psychiatry 1997; 21 (4): 697-706.
- Walden J, von Wegerer J, Winter U, et al. Actions of kavain and dihydromethysticin on ipsapirone-induced field potential changes in the hippocampus. Human Psychopharm 1997; 12: 265-270.
- Gleitz J, Friese J, Beile A, et al. Anticonvulsive action of (+/2)-kavain estimated from its properties on stimulated synaptosomes and Na+ channel receptor sites. Eur J Pharmacol 1996; 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, Schule A, Gleitz J. [3H]-monoamine uptake inhibition properties of kava pyrones. Planta Med 1997; 63 (6): 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.