Kava Kava

Kava kava, an extract of the Piper methysticum plant, is employed for its proposed anxiolytic, antiepileptic, antidepressant, antipsychotic, and sedative properties (Nowakowska et al. 1998, Skidmore-Roth 2001, Uebelhack et al. 1998). Some of the active ingredients of kava kava include the lactones or pyrones, kawain, methysticin, dihydrokawain, and dihydromethys-ticin (Jellin et al. 2002, Volz and Kieser 1997). Kava extracts available commercially are usually found to contain approximately 30-70% kava lactones (Jellin et al. 2002).

The extract WS 1490 has been investigated to determine its effectiveness in the treatment of anxiety (Volz and Kieser 1997). WS 1490 has been shown to be effective in anxiety disorders as a treatment alternative to benzodiazepines and tricyclic antidepressants and reported not to have the problems associated with those two classes of drugs (Volz and Kieser 1997).

However, therapeutic effect may take up to 4 weeks and data have indicated treatment for 1-8 weeks to obtain significant improvement (Jellin et al. 2002, Forget et al. 2000).

Although the exact mechanism of kava kava's effects on the central nervous system is largely unknown, the pyrones have demonstrated competitive inhibition of the monoamine oxidase B enzyme (Jellin et al. 2002). Inhibition of this enzyme may result in the psychotropic effects related to kava kava use as this enzyme is responsible for the breakdown of amines that play a role in psychoses (Seitz et al. 1997).

Regarding adverse effects, patients who experience hepatic adverse reactions are known as "poor metabolizers." Typically, these patients have a deficiency in the cytochrome P-450 2D6 isoenzyme (Jellin et al. 2002). Therefore, it is recommended that patients who use kava kava receive routine liver function tests to monitor the development of hepatotoxicity (Jellin et al. 2002). Furthermore, there have been 24 documented cases of hepatotoxicity following the use of kava kava and, in some cases, death or liver transplant occurred after 1-3 months of use (Jellin et al. 2002). In countries such as Germany and Australia, kava kava use for longer than 3 months is not recommended (Forget et al. 2000). Other side effects of kava kava use include visual changes, a pellagra-like syndrome with characteristic ichthyosiform dermopathy, and hallucinations (Jellin et al. 2002, Winslow and Kroll 1998, Garner and Klinger 1985).

Regarding drug interactions, kava kava may react adversely with the benzodiazepine alprazolam, other central nervous system depressants, statins, alcohol, and levodopa, consequently resulting in excessive sedation among other side effects; therefore the supplement should be avoided in those patients with endogenous depression (Jellin et al. 2002, Jellin et al. 1990, Jamieson and Duffield 1990, Gruenwald et al. 1998). Finally, kava kava may also affect platelets in an antithrombotic fashion by inhibiting cyclooxygenase and, thus, attenuating thromboxane production (Jellin et al. 2002). Pain relief mechanisms utilized by the herbal may be similar to local anesthetic responses and could be dependent on a non-opiate sensitive pathway (Jamieson and Duffield 1990, Singh 1983).

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