Kava Kava, otherwise known as kava, is a native of the South Pacific, where it has been enjoyed as social drink for centuries. Kava has a rich history as a ceremonial plant as well, being prepared and used in rituals by native Pacific Islanders. 
The first westerners exposed to kava were those that traveled with the famous Captain Cook, who purportedly gave the plant the name “intoxicating pepper.”  Used safely for thousands of years, kava has undergone great medical scrutiny when it was blamed for causing roughly 68 cases of liver problems in recent years. As a result of this allegation, some European countries have gone so far as to ban the sale or use of kava, to the detriment of the overall usefulness of this herb in human health; as well as the economies of Pacific Island nations that export this beneficial herb. 
The decision to ban this herb because of its association with comparatively few cases of liver problems (which in itself is still inconclusive) is shocking; considering the high rates of death associated with pharmaceutical medicines that remain for sale despite their much higher health risks. In fact, one large study estimated that approximately 32,000 to 106,000 people die each year in the U.S. from adverse pharmaceutical drug reactions each year, yet none of these drugs have been banned thus far. 
Kava’s medicinal effects are derived from the root, rhizome (underground root projections), and the stem. The pharmacologic activity of kava is attributed to a group of constituents known as kava-lactones.  As a medicine, the herb is typically available in dried form, standardized to contain a minimum of 3.5% kava-lactones. Water - extracted preparations tend to contain less kava-lactones than those forms prepared by ethanol extraction. Additionally ethanol extracted preparations tend to yield higher amounts of the active constituents. 
Kava is best known for relieving anxiety. There is a sizable amount of research that demonstrates the efficacy of kava for this condition as well. Kava is considered comparable to the leading types of drug (i.e. benzodiazepines) prescribed for the treatment of anxiety.  The majority of research regarding kava’s use in anxiety-related symptoms demonstrated its effectiveness after 1 to 8 weeks of treatment. [7, 8] Because its efficacy in treating anxiety is similar to that of benzodiazapene drugs, it is thought that kava may be a useful treatment for mitigating benzodiazapene withdrawl. 
Kava may also be useful in treating anxiety stemming from menopausal symptoms; one week of treatment with standardized kava led to a reduction in anxiety symptoms that were related to hormonal changes in women. 
Kava’s pharmacologic effects have been identified as:
- anesthetic (localized)
While the exact mechanism of these effects are not completely understood, researchers suspect that kava works through several mechanisms on neurotransmitter levels and receptors. [11-13]
Taking kava for relieving anxiety will not lead to impairment of cognitive function, however.  Kava has been used ceremonially to help with relaxation; it is also thought to affect the part of the brain that controls emotion.  Kava can make a person feel more at ease, happier, and perhaps, more sociable. 
For treatment of anxiety-related conditions, most of the research has utilized a dose of 100 milligrams (standardized to contain 70 milligrams of kava-lactones) three times per day. 
For assisting with discontinuation of benzodiazapenes, kava can be taken at a dose starting at 50 milligrams per day to 300 milligrams per day over the course of one week, while simultaneously tapering benzodiazepine usage.
Note: kava-lactone content will vary between products, therefore dosing should reflect these varied levels.
Kava Kava Side effects
As mentioned earlier, kava has been associated with a handful of cases in which liver damage occurred, even when these people took accepted doses for short periods of time. Some of these cases occurred after taking kava for only one month, and the worst outcomes were the need for liver transplant and death. 
On the other hand, the validity of these reports are often questioned; the majority of those who suffered negative consequences from taking kava were heavy users of alcohol, had existing liver disease or other advanced disease conditions. One astounding fact regarding these episodes (all occurring in Europe within a short time frame) is that the kava in question was extracted using acetone, rather than alcohol. Acetone is a known toxin.
Other than these isolated episodes, kava has been attributed to stomach upset, GI distress, headaches, drowsiness, and dizziness, Other, more rare side effects may include, visual-spatial disturbances, dry mouth, and skin rash.  Taken in normal doses, the use of kava may interfere with ability to operate or drive machinery.
Kava Kava General interactions (supplement, herb, food, lab)
- Supplements: Taking kava with other herbs with sedative properties may lead to enhanced sedation.
- Food: Taking kava with alcohol may lead to increased side effects of drowsiness and slowed reflexes.  There is also the concern that taking kava with alcohol may predispose one to liver toxicity.
- Labs: Kava may elevate liver function tests (LFT) in some people. LFTs should be monitored in those taking high doses over prolonged periods.
Kava Kava Drug interactions
Taking kava with any drug(s) that depress the central nervous system, or those that are damaging to the liver (e.g. non-steroidal anti-inflammatories - NSAIDs) may increase the possibility of enhanced effects of those drugs. There are numerous prescription and over-the-counter pharmaceuticals in this category as well; it is advisable to obtain consultation.
- Hepatitis: kava may negatively affect the liver; patients with any liver disease should avoid taking kava. 
- Depression: because of the down-regulatory effects of kava on the brain, it is thought that kava may worsen depression. Therefore, people who are experiencing depression should avoid kava.
- Parkinson’s Disease: kava may antagonize the action of the neurotransmitter dopamine, which is the key neurotransmitter considered problematic in Parkinson's disease. 
1. Singh YN, Blumenthal M. Kava an overview. HerbalGram 1997;39:33-44, 46-55.
2. Norton SA, Ruze P. Kava dermopathy. J Am Acad Dermatol 1994;31:89-97.
3. Moulds RF, Malani J. Kava: herbal panacea or liver poison? Med J Aust 2003;178:451-3.
4. Lazarou, J, Pomeranz, BH, Corey, PN, “Incidence of adverse drug reactions in hospitalized patients: a meta-analysis of prospective studies,” Journal of the American Medical Association (Chicago, IL: American Medical Association, 1998), 1998;279:1200-1205
5. 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;22:1105-1120.
6. Garner LF, Klinger JD. Some visual effects caused by the beverage kava. J Ethnopharmacol 1985;13:307-311.
7. Woelk H, Kapoula O, Lehrl S, et al. [Comparison of kava special extract WS 1490 and benzodiazepines in patients with anxiety]. [Article in German]. Z Allg Med 1993;69:271â€”7.
8. Lehmann E, Kinzler E, Friedemann J. Efficacy of a special Kava extract (Piper methysticum) in patients with states of anxiety, tension and excitedness of non-mental origin- a double-blind placebo-controlled study of four weeks treatment. Phytomedicine 1996;3:113-9.
9. Malsch U, Kieser M. Efficacy of kava-kava in the treatment of non-psychotic anxiety, following pretreatment with benzodiazepines. Psychopharmacology (Berl) 2001;157:277-83.
10. 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.
11. Jussofie A, Schmiz A, Hiemke C. Kavapyrone enriched extract from Piper methysticum as modulator of the GABA binding site in different regions of rat brain. Psychopharmacology 1994;116:469-74.
12. Schelosky L, Raffaup C, Jendroska K, Poewe W. Kava and dopamine antagonism. J Neurol Neurosurg Psychiatry 1995;58:639-40.
13 Seitz U, Schule A, Gleitz J. [3H]-monoamine uptake inhibititon properties of kava pyrones. Planta Med 1997;63:548-549.
14. Cairney S, Maruff P, Clough AR, et al. Saccade and cognitive impairment associated with kava intoxication. Hum Psychopharmacol 2003;18:525-33.
15. Pierce A. The American Pharmaceutical Association Practical Guide to Natural Medicines. New York: The Stonesong Press, 1999:19.
16. Pittler MH, Ernst E. Efficacy of kava extract for treating anxiety: systematic review and meta-analysis. J Clin Psychopharmacol 2000;20:84-9.
17. Escher M, Desmeules J, Giostra E, Mentha G. Drug Points: hepatitis associated with kava, a herbal remedy for anxiety. BMJ 2001;322:139.
18. Schmidt P, Boehncke WH. Delayed-type hypersensitivity reaction to kava-kava extract. Contact Dermatitis 2000;42:363-4.
19. Brinker F. Herb Contraindications and Drug Interactions. 2nd ed. Sandy, OR: Eclectic Medical Publications, 1998.
20. Strahl S, Ehret V, Dahm HH, Maier KP. [Necrotizing hepatitis after taking herbal medication]. [Article in German] (abstract). Dtsch Med Wochenschr 1998;123:1410-4.
21. Bilia AR, Gallori S, Vincieri FF. Kava-kava and anxiety: growing knowledge about the efficacy and safety. Life Sci 2002;70:2581-97.
22. Volz HP, Kieser M. Kava-kava extract WS 1490 versus placebo in anxiety disorders–a randomized placebo-controlled 25-week outpatient trial. Pharmacopsychiatry 1997;30:1-5.
23. Fetrow CW, Avila JR. Professional’s Handbook of Complementary & Alternative Medicines. 1st ed. Springhouse, PA: Springhouse Corp., 1999.