Kava is highly regarded in Europe as an effective treatment for anxiety. Numerous clinical studies have verified its efficacy. A randomized placebo-controlled trial evaluated Kava’s effectiveness in 101 patients with anxiety of non-psychotic origin. Subjects were followed for 6 months. Symptoms were evaluated using the Hamilton Anxiety Scale (HAM-A).Significant improvements were seen at 8 weeks (reduction of HAM-A score from 30-17) and continued for another 16 weeks. At the end of the trial the HAM-A score was reduced to 9.
Similar, but quicker results were seen in a placebo-controlled double blind study of 40 women with menopause-related symptoms of anxiety. However, unlike the previous study there was a significant decrease (measured by HAM-A) in symptoms after just 1 week of treatment. Improvement continued throughout the full study period.
Several studies have been conducted comparing Kava with other agents. A double-blind study of 174 patients with anxiety compared Kava with other agents. Patients were followed for 6 weeks. Similar improvements in HAM-A scores were seen in all treatment groups. Statistically there was no difference in the outcome of the therapies. Kava was well tolerated with none of the side effects associated with the other agents. A recent meta-analysis reviewed several clinical trials to determine the efficacy of Kava for the treatment of anxiety. The reviewers concluded that Kava was superior to placebo as a symptomatic for anxiety. The authors agreed that Kava is an herbal option for the treatment of anxiety.
The exact mechanism of Kava on the central nervous system is unknown. One possible mode of action is that Kava may interact with Gama-Aminobutyric acid (GABA) receptors. Early in vivo and in vitro research found that Kavalactones demonstrated only weak GABA receptor binding actions. However, a more recent study found that Kava pyrones mediate effects in GABA-A receptors, particularly in the hippocampus and amygdala. Other possible mechanisms include inhibition of noradrenaline uptake and activation of mesolimbic dopaminergic neurons. It is likely that there is more than one pathway responsible for Kava's activity on the central nervous system.