Kava Is an Effective and Safe Treatment of Anxiety

Kava Kava (Piper methysticum) is an effective treatment of generalized anxiety

In traditional Polynesian cultures kava is used for ceremonial purposes and as an inebriant. In contrast to benzodiazepines, when a standardized kava extract is used at recommended doses (typically between 60 and 300mg/day), the majority of people do not experience mental slowing or impaired cognitive functioning.

The use of kava as a treatment of anxiety has been extensively reviewed in the biomedical and alternative medical literature. Animal studies suggest that the anxiety-reducing mechanism of action involves serotonin blockade in the amygdala by alpha-pyrones, a principle bioactive constituent of kava. Kava interferes with norepinephrine reuptake and is known to have binding affinity with both GABA and NMDA receptors, both of which modulate anxiety. Kava may also reduce anxiety by influencing vagal heart tone in patients with generalized anxiety (Watkins 2001).

A Cochrane systematic review of 11 controlled double-blind studies that met inclusion criteria and over 600 patients concluded that kava was superior to placebo for the short-term management of generalized anxiety (Pittler 2004). Double-blind studies and a meta-analysis (Singh and Blumenthal, 1996; Hansel 1996) support the use of kava preparations standardized to 70% kava lactones at doses between 70mg to 240mg/day for the treatment of “stress” and moderate anxiety, but not severe anxiety or agitation.

An early systematic review of 7 quality studies involving a total of 377 patients concluded that kKava 300mg/day is more effective than placebo in reducing nonpsychotic anxiety states (Pittler 1998). Daily use of kava 100-200mg/day effectively reduces anxiety symptoms associated with menopause (De Leo 2000).

Kava compares favorably to benzodiazepines (e.g. lorazepam, clonazepam, alprazolam) and other prescription anti-anxiety medications. The findings of a small double-blind controlled trial suggest that generally anxious patients who gradually increase their daily dose of kava (up to 300mg/day of a standardized extract) while tapering off a benzodiazepine do not experience worsening anxiety or benzodiazepine withdrawal (Malsch 2001).

A randomized placebo-controlled multicenter study enrolling 129 outpatients concluded that a standardized kava preparation (LI 150) was as effective as two commonly prescribed anti-anxiety agents (Buspirone™ and Opipramol™) in the treatment of generalized anxiety (Boerner 2003). Three fourths of patients in both the kava group and the conventional drug group were classified as “treatment responders,” and experienced 50% or greater reductions in anxiety as measuredon a commonly used clinical instrument known as the Hamilton Anxiety Rating Scale (HAM-A).

Safety issues associated with kava

Kava is generally well-tolerated even at doses significantly above usual therapeutic doses. Uncommon adverse effects include gastrointestinal upset, rash, headaches and dizziness (Schulz 2001). In recent decades there have been reports of kava inebriation (Matthews 1988), although this phenomenon has not been observed in Europe, where kava preparations are used medicinally to treat anxiety.

Rare case reports suggest that kava may potentiate the action of benzodiazepine tranquilizers, resulting in increased sedation (Almeida 1996). But kava does not potentiate the effects of alcohol consumption in humans.

Rare case reports of hepatitis (Escher 2001) and fulminent liver failure (Kraft 2002) have led to restrictions in the sale of kava products in many European countries and a warning by the FDA. However, independent experts have concluded that most reported cases of liver failure were associated with a processing mistake resulting in potentially toxic levels of alkaloids in a single batch of Kava (Waller 2002; Dragull 2003). Nevertheless, it is judicious to advise patients against taking kava (Bone 1993) when there is a question of alcohol abuse or heavy use of conventional sedative-hypnotics. One case report suggests that kava may interfere with anti-Parkinsonian drugs (Izzo 2001).