Kava, also known as kava kava, is a plant that originated in the warm South Pacific islands of Hawaiʻi, Tonga, Micronesia, Fiji, Vanuatu, and the Samoas. Kava use in Polynesia and Micronesia takes place within a traditional or cultural context, leading to different patterns of use than are seen elsewhere.^[67][68] In Polynesian and Micronesian cultures, kava is often consumed as a drink as part of group sessions. These kava sessions, which take place in a community setting and involve conversation, may last for several hours.^[69][49] Although kava may be consumed differently in cultures where it is not a native plant, the reasons for consumption (e.g., anxiety, relaxation, socialization) are generally similar.^[29]

Kava root has been traditionally used by the Indigenous people of Hawaiʻi. Hawaiian cultural uses for kava include a range of conditions, from easing stomach upset in children to gynecological aids, in addition to its better-known use as a relaxant.^[28]

Traditionally, kava root is macerated, then steeped in a liquid (e.g., water, coconut milk, alcohol) and strained before being drunk.^[70] Some reported traditional medicinal uses also incorporate plant parts other than the root.^[28]

Less-traditional kava preparations include (but aren’t limited to) tinctures, teas, capsules, and dried powders. When researchers tested different preparations, they found a wide variety of kavalactone content, sometimes inconsistent with the labeling.^[71] Kava extracts have been used in cosmetics, but there is still insufficient evidence regarding both kava’s toxicity and efficacy when applied topically.^[70]

Standardized preparations of kava also exist and can be found throughout the scientific literature. The standardized preparations cited most frequently in clinical trials include kava root extractions (ethanol-in-water or acetone) standardized to 30–70% kavalactones.^[13][36]

Anxiety reduction is the best-known use case for kava. Clinical studies indicate that standardized kava preparations (210–300 mg, containing either 30 or 70% kavalactones depending on standardization used) could be a safe and effective alternative to benzodiazepines for the treatment of short-term anxiety.^{[36][14][19][37][31][38][32][18][10]} Clinical evidence still appears to be mixed, however, regarding the effectiveness of kava for generalized anxiety disorder (GAD). Trials of standardized preparations (300–400 mg/day) have had the strongest results, possibly through effects on vasovagal response.^[72][15][13] Similar studies using different doses and/or preparations do not support kava use for GAD.^[73][17][74]

Kava has also been studied for other anxiety disorders. People experiencing postmenopausal anxiety saw reductions in symptoms when hormone replacement therapy was combined with lower doses (100 mg/day) of kava extract for periods of three to six months.^[34][35] Clinical studies including both menopausal and perimenopausal women similarly saw improvements in menopause-related anxiety with kava extract (100–300 mg/day over 8 to 12 weeks) compared to a control.^[33][9]

Finally, there is some indication that kava can boost mood in individuals without apparent health conditions. One trial noted that a single 300 mg dose of kava extract (containing 90 mg kavalactones) resulted in mood boosts that occurred within about an hour.^[12]

The effects of kava on cognition have also been a point of interest since the current standard therapy medications for anxiety can reduce cognitive functioning, while kava may not.^{[30][12][16][39][40]}

Two randomized clinical trials which compared an “acute dose” of kava (containing 180 mg of kavalactones) to benzodiazepines found that, while the lower kava dose couldn’t reduce anxiety as well as benzodiazepines, anxiety did not increase for kava users either. Kava users were also able to maintain alertness in cognitive tasks such as driving, which was not the case for participants taking benzodiazepines.^[16][30]

Similar clinical studies using kava doses at 300 mg or more suggest that it doesn’t impair the cognitive skills required for operating a motor vehicle and could even improve cognitive tasks requiring accuracy or quicker response time.^[12][69]

When kava is combined with alcohol, reports vary on whether this amplifies the short-term negative effects of alcohol consumption.^[26][27] Mixing kava and alcohol may increase both the sedative effects and the liver damage caused by either alone.^[22]

One clinical study, in which kava was combined with St. John's Wort (990 μg of hypericin and 50 mg of kavalactones per capsule, taken 3 times a day for 4 weeks), found a reduction of depression-related symptoms of anxiety. There were also some reports of heightened emotional sensitivity and disturbed sleep in individuals taking the combination, but no conclusions could be made regarding the combination’s synergistic effects.^[25]

Commonly reported side effects of kava use include headaches, sleepiness, sedation, diarrhea, and distinctive skin rashes called “kava dermopathy”.^{[49][50][51][52][20]} Kava use may increase the risk of low birth weight when consumed during pregnancy; however, this was reported in an observational study, so other risk factors leading to kava use (stress, for example) may have played a role.^[53] Upset stomach is a rarely-mentioned side effect but is sometimes reported to occur more with kava than in placebo groups.^[19][75]

The use of kava powder in very high doses (205 grams) has resulted in clinical effects similar to alcohol intoxication.^[29][24] Occasionally, this may be called “kava intoxication”, since it’s been described as a somewhat-less-aggressive and happier state of “drunkenness”.^[76] Consuming the herb in much larger quantities (3.6 to 13L of traditionally prepared kava beverage, estimated to be the equivalent of over 8,000 mg of kavalactones per day) as part of traditional kava sessions may put users at risk for short-term impairments in motor vehicle operation and cognitive response as well.^{[69][23][24][77]}

There are clinical reports of herb-induced liver injury with kava use, especially when taken consistently for longer than a month.^[1] Prolonged kava use has been associated with lower body weight and depressed markers of immune function similar to those seen in alcoholics.^[23][24] Reports of multiple adverse events, liver dysfunction (e.g., hepatotoxicity, hepatitis, hepatic failure), and, in some instances, death have also been reported, but the dose and duration of kava aren’t always consistent or clearly stated in these reports.^{[29][3][44][45][46]}

These accounts, however, may be mistaken in the assumption that kava alone is to blame. While some adverse event reports identify the use of individual kavalactones (rather than a whole root extract), other reports note that kava was taken in addition to another substance with the potential for hepatotoxicity.^[29][47][44]

Additionally, no controlled trials using a standardized kava intervention (i.e, 200–300 mg of standardized extracts, taken for less than 2 months) have reported liver toxicity with the use of moderate dosing. However, not all studies measure liver enzymes or function either.^[14][48] Regardless of whether kava alone or in combination with other factors is to blame for adverse events, caution is advised until clearer evidence is established.

Higher doses of kava (greater than 1,000 mg/day of root extract over 4 weeks) are associated with an increased risk of impaired cytochrome P450 (CYP450) function.^[5] Inhibition of CYP450 is possibly due to kava containing methysticin, as demonstrated by in vitro studies.^[78] In vitro studies have also identified that some kavalactones (desmethoxyyangonin, methysticin, and dihydromethysticin) could inhibit liver enzymes CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4, and CYP4A9/11.^[79][80][81] However, the kavalactone kavain is not yet known to inhibit liver enzymes.^[79]