Tang Center for Herbal Medicine Research


Common names: intoxicating pepper, kawa, kava kava, ava pepper


Kava is an herbal medication derived from the dried root of the pepper plant Piper methysticum. Kava has a long history of use as a ceremonial intoxicant in the South Pacific islands. It was relatively unknown to the rest of the world until missionaries introduced it into Australian aboriginal society in the 1980s. The missionaries intended kava to substitute for alcohol which was abused by the aboriginal population. Unfortunately, kava misuse became an additional public health problem, and it was eventually outlawed in many aboriginal communities. Australian physicians provided many of the earliest descriptions of the medical effects of kava.


Kava has gained popularity as an over-the-counter anxiolytic and sedative. It is purported to be a safe alternative to benzodiazepines. Kava and alcohol do not appear to have synergistic effects on cognitive and psychomotor impairment. Several randomized controlled trials have compared kava to placebo for the treatment of anxiety (diagnosed by DSM-III-R criteria), situational anxiety, and anxiety associated with menopause. A meta-analysis of clinical trials suggested that kava has therapeutic potential in the treatment of the symptoms of anxiety. Kava has been advocated for the treatment of insomnia, but its effect on sleep in humans has not been well characterized.

Phytochemistry and pharmacology

Kava contains many pharmacologically active constituents that act synergistically to produce effects greater than those achieved with any single compound. The kavalactones, also known as kavapyrones or -pyrones, are responsible for most of the pharmacological effects. The six major kavalactones that have been identified are kawain, dihydrokawain, methysticin, dihydromethysticin, yangomin, and desmethoxyyangonin.

Kava produces dose-dependent effects on the CNS. The antiepileptic and neuroprotective properties of kavalactones have been demonstrated in animal models. Kavalactones produced centrally mediated skeletal muscle relaxation in vivo and smooth muscle relaxation in vitro. Unlike other CNS depressants, kava does not depress cognitive function or electroencephalographic event-related potentials. However, the ability of kavalactones to significantly increase barbiturate sleep time has been demonstrated in animals. Kavalactones also have significant local anesthetic properties. Kawain is equipotent to cocaine in producing topical anesthesia.

The mechanism of action of kava has not been fully elucidated, but multiple effector sites are involved. The anxiolytic and sedative effects of kava suggest that it potentiates γ-aminobutyric acid (GABA) inhibitory neurotransmission. The first investigation addressing this effect found no evidence of binding in the mouse brain frontal cortex or cerebellum. A later investigation showed that kavalactones mediate their effect through GABAA in the limbic structures of the brain. In this study, the kavalactones and pentobarbital also produced a synergistic effect on [³H] muscimol binding to GABA. Kavalactones inhibit voltage-dependent sodium and calcium channels in vitro, possibly explaining the antiepileptic and local anesthetic effects. Kava may exert its effects through neurotransmitters such as dopamine and serotonin, but evidence of this is less compelling.

Peak plasma levels occur 1.8 hr after an oral dose, and the elimination half-life of kavalactones is 9 hr. In rats, unchanged kavalactones and their metabolites undergo renal and fecal elimination.


In Germany, kava has been linked to twenty-four cases of liver toxicity culminating in 1 death and 3 liver transplants. At this writing, the regulatory status of kava in Germany remains uncertain. Kava may potentiate the sedative effects of prescription medications. With frequent use, kava produces “kava dermopathy,” characterized by reversible scaly cutaneous eruptions. Kava may have abuse potential but whether long-term use results in addiction, tolerance, and acute withdrawal after abstinence has not been satisfactorily investigated.

Use during pregnancy or by nursing mothers is not recommended.

Preparations and dosage

The recommended dosage is 150-300 mg of kava extract divided into two doses or 50 – 240 mg of kavalactones per day.