Kava Kava: Adverse Reactions

In RCT, the incidence of adverse effects to kava kava has been found to be similar to placebo. Two post-marketing surveillance studies involving more than 6000 patients found adverse effects in 2.3% and 1.5% of patients taking 120-240 mg standardised extract. The most common side-effects appear to be gastrointestinal upset and headaches.


A systematic review assessing the safety of kava which included a total of 7078 patients taking kava extract equivalent to 10 mg to 240 mg kavalactones per day for 5-7 weeks identified no cases of hepatotoxicity. Considering that case reports of hepatotoxicity exist, they should be considered a very rare event based on the evidence.


Most adverse effects, such as yellow discolouration of the skin, hair and nails, have been associated with excessive long-term use. This temporary condition is known as ‘kava dermopathy’ and reverses once kava use is discontinued. A 2003 report found no evidence of brain dysfunction in heavy and long-term kava users.

Clinical note

Commercial kava products and links to hepatotoxicity

Conflicting reports abound. On 15 August 2002, the TGA initiated a voluntary recall of all products containing kava kava. The response was undertaken due to incoming details from European countries of case reports of hepatotoxicity apparently associated with the use of commercial kava products. The decision to remove kava from the market has been viewed as controversial and questioned by many people. Toxicological and clinical studies have shown that kava extracts are virtually devoid of toxic effects and when assessed primarily by the British regulatory authority (MCA) and a German research group, a critical analysis of the suspected cases in Germany reveals that a very probable causal relationship could be established in only one patient. It is suspected that a rare, immunologically mediated, idiosyncratic mechanism may be responsible and the extraction process used to produce kava products also had an influence. It now appears that the aqueous method results in extraction of glutathione, in addition to kava lactones, an important factor for protecting the liver from potential damage, whereas the acetone extraction method does not. As a result, kava products made with the acetone extraction process are more toxic than those produced via aqueous extraction methods. This is an important distinction to make as most European products were made using acetone extraction, whereas Australian products were chiefly made via aqueous extraction. Interestingly, fulminant hepatic failure has not been documented with traditional use in Pacific countries nor in the Northern Territory where Aboriginal kava drinkers consume kava lactones in doses estimated to be 10-50-fold the recommended levels. Several reports published in 2003 have found no evidence of aqueous kava extracts inducing irreversible liver toxicity in vivo or in humans. One study involving long-term users of aqueous kava extracts found that although changes to liver function could occur at moderate levels of consumption, they are reversible and begin to return to baseline after 1-2 weeks’ abstinence from kava. Genetic polymorphism of many cytochrome enzymes, leading to inter-individual variation in drug metabolism, may be another important factor in the marked discrepancy in hepatotoxic response to kava.

Australia was not alone, and other countries also issued health advisory cautions or banned kava-containing products from sale. Although these actions effectively removed kava products from the market, the traditional kava beverage continued to be consumed in the Pacific Islands and the kava-producing countries of the Pacific found the controversy surprising given the long history of apparent safe use in the Pacific. In January 2003 the Kava Evaluation Group was established in Australia to review the accumulating safety data and by August that same year the Complementary Medicine Evaluation Committee recommended to the TGA that certain forms of kava could be considered safe. The TGA accepted these recommendations and amended the regulations accordingly. Currently, there is a limit of 125 mg kavalactones allowable per tablet or capsule and all products must not provide more than 250 mg kavalactones in the recommended daily dose.