Kava (Piper methysticum) is a member of the pepper family (Piperaceae). As a traditional herbal therapy, kava goes by many names. Traditionally, kava has been (and still is) consumed as an infusion of the macerated root/rhizome, which is soaked in a liquid such as water, coconut milk, or alcohol. Traditional Hawaiian uses of kava have also included plant parts beyond the root, extending to the bark, plant ash, buds, young leaves, and even the whole plant.^[28]

Kava is also used recreationally, and although the plant is native to Oceania, it can now be found nearly worldwide. However, due to the potential for liver injury, kava may be restricted in some countries.^[20] Whether used recreationally or traditionally, kava is known to alleviate anxiety, sleep disturbances, and provide a mildly euphoric sensation.^[20][21][29] Individual responses to kava may vary, and at least one clinical trial has suggested that there may be a genetic component to this variability.^[30]

One reported benefit of kava, especially in comparison to many other anxiolytics, is its ability to relieve symptoms without compromising mental clarity. For this reason, claims that kava is a hypnotic or psychedelic may be exaggerations.^[20]

Kava is best known for anxiety reduction but may not affect all types of anxiety. The clinical evidence of its effectiveness for generalized anxiety disorder or anxiety that is comorbid with depression is mixed.^{[25][9][31][32][18][10]} However, clinical evidence for kava’s effectiveness for short-term anxiety and for anxiety resulting from specific circumstances or situations is more consistently positive.^{[33][34][35][36][14][19][37][38]}

Several clinical studies have shown that kava may be able to reduce anxiety without the deleterious effects on cognition seen with other anxiolytics. It has also been suggested that kava could improve cognitive processing, although such cognitive improvements may simply be byproducts of anxiety reduction; more research is needed to clarify this point.^{[30][12][16][39][40]}

Kava use has also been connected with a near-immediate mood boost^[12] and may treat sleep disturbances associated with anxiety.^[11] However, kava is still not widely recommended or accepted as a treatment for insomnia, especially in place of therapies with stronger evidence of safety and efficacy.^[41][42][43]

When taken consistently for longer than a month or in higher doses (1,000 mg/day or more), kava use is more likely to result in liver damage or dysfunction, liver enzyme impairment, and, in rare cases, death.^{[1][29][3][44][45][46]} Some experts suggest that reports of liver damage with kava use may be unfairly blaming kava, when other factors were actually at play.^[29][47][44] While no controlled trials using standardized formulations have reported liver injury, not all trials assess the participants for this adverse event.^[14][48] Until kava’s potential for liver damage has been fully and accurately assessed, caution is advised. See our additional FAQ below,What long-term side effects are associated with kava?, to learn more details.

Kava’s reported side effects include headaches, sleepiness, sedation, diarrhea, and skin rashes.^{[49][50][51][52][20]} Observational research suggests an association between kava use in pregnancy and low infant birth weight, but kava has not been established as a direct cause of the outcome.^[53] Kava powder taken in very high doses (more than 100 times the dose at which liver damage has been observed) may result in a state similar to alcohol intoxication.^[29][24] Long-term kava use has also been associated with negative outcomes similar to those seen in alcoholism, such as increased liver enzymes, which could suggest liver injury, and reductions in the number of lymphocytes, which could negatively impact immune response.^[23][24] The latter finding is particularly interesting, because reducing anxiety and/or stress has generally been associated with improvements in immune response. Combining kava with alcohol may also magnify the effects of both substances.^[26][27]

The kavalactones contained in kava root are a group of bioactive compounds responsible for its effects. The most notable kavalactones include kavain, dihydrokavain, methysticin, dihydromethysticin, yangonin, and desmethoxyyangonin.^[20][54][55] In animal studies, kavalactones have demonstrated the ability to cross the blood-brain barrier, which helps explain why kava has a psycho-emotional effect.^[56] When taken orally at a dosage of 120 mg of kava per kg of body weight, effects have been seen within an hour as kavalactones begin to accumulate in the brain.^[57][12]

Kavalactones may impart their psycho-emotional effects via glutaminergic, GABAergic, dopaminergic, and/or serotonergic signaling. It has so far proved difficult to establish the effects of individual kavalactones for two reasons: first, the effects of any individual kavalactone may be dose-dependent in ways we don’t understand; and second, when kavalactones are combined, they may not only have interactions, but those interactions could potentially vary depending on the ratio of the kavalactones in combination. In addition, both of these factors may affect humans and animal models differently, making it even harder to tease out these complex relationships. For example, case studies have reported seeing clinical signs of dopamine receptor blockage as a result of kava consumption,^[58] but animal studies have not always supported the existence of an antidopaminergic effect.^[59][60][61] Similarly, while a rodent trial found that mixed kavalactones did not affect serotonin levels, isolated dihydromethysticin increased serotonin in rats, while isolated desmethoxyyagonin produced reductions in it.^[59]

While kavain damaged cultured rat neurons in vitro at concentrations of 300 µM or greater (i.e., greater than or equal to 300 micromoles of kavain per liter),^[62] the kavalactones dihydromethysticin and methysticin may hold neuroprotective effects.^[63] Animal and nonclinical studies suggest that dihydromethysticin and methysticin may also impart sedative effects through indirect GABAergic signaling.^{[59][56][64][65][66]}

As with any plant or herbal preparation, factors such as plant part, growth conditions, and extraction methods may affect kavalactone content. Kava preparations with a standardized kavalactone concentration are more likely to produce consistent effects.