Kava Stats - Substance Search

Pharmacology

DrugBank

State Solid

Receptor Profile

Receptor Actions

Agonists

CB1 receptor agonist (yangonin)

Inhibitors

Monoamine oxidase-B inhibitor (reversible)

Norepinephrine reuptake inhibitor (kavain)

Modulators

GABA-A receptor positive allosteric modulator (non-benzodiazepine site)

Other

Voltage-gated sodium channel blocker

L-type calcium channel blocker

Dopamine modulation (nucleus accumbens)

Receptor Binding

norepinephrine reuptake inhibitor

History & Culture

Kava originated in northern Vanuatu, where it was domesticated by farmers approximately 3,000 years ago through selective cultivation. The plant was subsequently spread eastward by the Austronesian Lapita culture into the rest of Polynesia, becoming endemic to Oceania while remaining absent from other Austronesian groups. The beverage reached Hawaii but could not establish itself in New Zealand due to the colder climate. In memory of the kava plants they brought with them and unsuccessfully attempted to cultivate, the Māori gave the name kawa-kawa to another Piperaceae species (M. excelsum). The Māori word "kawa" also came to mean "ceremonial protocol," reflecting the stylized consumption practices typical of Polynesian societies. Kava consumption is believed to be the reason betel nut chewing, otherwise ubiquitous among Austronesian peoples, was abandoned in Oceania.

Kava has been consumed in Pacific Island communities for over three millennia in religious, political, cultural, and social contexts, typically prepared as a beverage. Throughout the Pacific, the plant is treated with great respect and holds an important place in local cultures, though each society has developed its own distinct traditions alongside shared practices. In Fiji, formal yaqona ceremonies accompany significant social, political, and religious functions, usually involving a ritual presentation of bundled roots as a sevusevu (gift) followed by communal drinking. In precolonial Hawaii, the Aliʻi (kings) coveted the Moʻi variety for its strong cerebral effects, attributed to a predominant concentration of the kavalactone kavain. This sacred cultivar was restricted exclusively to royalty, with commoners forbidden from experiencing it on pain of death. In Vanuatu, the nakamal serves as the traditional central meeting place and cultural hub where kava consumption facilitates communal gathering, dialogue, and the exchange of knowledge across generations. In many Pacific communities, kava functions as a replacement for alcohol and is consumed throughout the day, particularly before spiritual rituals and social gatherings. Historically, it has been recognized as an entheogen of Pacific Island and Polynesian communities, playing an important role in various spiritual and ritualistic rites.

1778–present

Western interest in kava began with Captain Cook's voyages to the Pacific islands in 1778, though the beverage was initially regarded as inferior to alcohol. During the 18th and 19th centuries, Christian missionaries made efforts to prohibit kava drinking, which inadvertently led to changes in preparation methods. Historically, the beverage had been made exclusively from fresh kava root; in response to missionary restrictions, preparation from dried kava emerged as an alternative practice. In recent decades, facilitated largely by the internet, kava has become available to users worldwide and has been adopted by increasing numbers of people outside the Pacific region. Nakamals and kava bars now exist in many countries, where the beverage can be consumed in a social setting similar to traditional practices. As a major traditional producer, Vanuatu has introduced legislation focused on regulating the quality of its kava exports rather than restricting domestic availability.

Toxicity

PsychonautWiki

Studies have shown that kava can and will induce a low level of hepatic apoptosis similar to how paracetamol affects the liver and also can affect hepatic enzymes. Because of this, certain medications can make kava unsuitable and even dangerous for some users. Noble kava root alone can not, without consuming very large amounts of the substance, induce toxic levels and no overdose has ever been recorded. The consumption of 'noble' kava root has very low toxicity, however consumption 'tudei' kava and the stems and leaves of kava plants may increase the risk of liver damage.

Experience Report Analysis

Erowid BlueLight

188 Reports

123 Single-substance

1998–2022 Date Range

71 With Age Data

19 Effects Detected

Demographics

Gender Distribution

Age Distribution

Reports Over Time

Effect Analysis

Erowid + Bluelight

Effects aggregated from 129 experience reports (123 single-substance Erowid + 6 Bluelight)

129 Reports

36 Effects Detected

22 Positive

7 Adverse

7 Neutral

Effect Sentiment Distribution

Confidence Distribution

Each bar is the share of reports mentioning the effect; its whisker, and the band on the rows below, is the 95% interval: where the share could plausibly be with other reports of the same kind.

Rows resting on fewer than 20 reports show a count (“3 of 7”) instead of a bar. Why 20?

Positive Effects 22

Euphoria 27.1% 75%

Sedation 22.5% 88%

Music Enhancement 20.1% 80%

Stimulation 17.9% 70%

Color Enhancement 14.6% 70%

Pain Relief 13.2% 85%

Empathy 12.2% 70%

Tactile Enhancement 10.6% 70%

Body High 10.0% 85%

Focus Enhancement 7.0% 85%

Contentment 4 of 6 84%

Sociability Enhancement 2 of 6 88%

Peace 2 of 6 88%

Happiness 2 of 6 88%

Thought Deceleration 1 of 6 90%

Muscle Relaxation 1 of 6 95%

Clarity 1 of 6 90%

Memory Enhancement 1 of 6 80%

Drowsiness 1 of 6 85%

Motor Enhancement 1 of 6 75%

Adverse Effects 7

Nausea 15.4% 70%

Headache 7.3% 70%

Motor Impairment 4.9% 70%

Confusion 4.7% 75%

Memory Suppression 2.4% 70%

Depression 1 of 6 80%

Ataxia 1 of 6 80%

Show 7 neutral or unclassified mentions

Visual Distortions 6.5%

Auditory Effects 5.7%

Dissociation 4.1%

Hospital 3.3%

Heaviness 2 of 6

Body Load 2 of 6

Numbness 1 of 6

Also reported in combinations. In the 65 Kava reports where another drug was taken too, 2 (3.1%) mention hospital, emergency services or an overdose, 0 (0.0%) a seizure and 0 (0.0%) psychosis. In the 123 single-substance reports: 3.3%, 0.0% and 0.8%. These are not in the figures above: they cannot be put down to Kava alone, and a mention is not always something that happened to the writer.

Dose-Response Correlation

How effect frequency changes across dose levels. Whiskers, and the numbers' hover text, give each figure's 95% interval.

Not drawn, too few reports (a dose tier needs 20): Oral Heavy (n=18). Why 20?

Dosage Distribution

Dose distribution from experience reports, one dose per report (the first listed). Doses above Q3 + 3×IQR, far above what people typically take, are left out of the median and range and listed under each route: most are real heavy doses or overdoses, not mistakes.

Median: 1000.0 mg IQR: 412.5–1735.0 mg n=30

3 reports gave a dose above the typical range (15,500–25,000 mg), so they are not in the figures above. Listing a dose here does not mean it is safe.

Show the reports

25,000 mg
24,000 mg · another drug taken too
15,500 mg

Real-World Dose Distribution

Erowid

From 86 of 290 recorded dose entries: those that state a weight (mg, g or µg), in routes with at least five of them. Values above Q3 + 3×IQR, far above what people typically take, are left out; they can include real heavy doses and overdoses, not only mistakes.

Oral (n=84)

Median: 1288.0mg 25th: 500.0mg 75th: 3675.0mg 90th: 6250.0mg

Common Combinations

Most co-occurring substances, as a share of all 188 reports filed under Kava; whiskers are 95% intervals

Form / Preparation

Most common forms and preparations, as a share of the 162 reports that give one; whiskers are 95% intervals

Body-Weight Dosing

Dose per kg of body weight, one dose per report (the first listed), from reports giving a weight of 30–250 kg. Doses above Q3 + 3×IQR, far above what people typically take, are left out of the median and range and listed under each route.

Median: 13.89 mg/kg IQR: 5.514–22.395 mg/kg n=28

4 reports gave a dose above the typical range (121.429–408.497 mg/kg), so they are not in the figures above. Listing a dose here does not mean it is safe.