Species of plant
Kava or kava kava (Piper methysticum: Latin 'pepper' and Latinized Greek 'intoxicating') is a plant in the pepper family, native to the Pacific Islands. The name kava is from Tongan and Marquesan, meaning 'bitter'. Kava can refer to either the plant or a psychoactive beverage made from its root. The beverage is a traditional ceremonial and recreational drink from Polynesia, Micronesia, and Melanesia. Nakamals and kava bars exist in many countries. Traditional kava is made by grinding fresh or dried kava root, mixing it with water or coconut milk, and straining it into a communal bowl. Outside the South Pacific, kava is typically prepared by soaking dried root powder in water and straining it. It is consumed socially for its psychoactive effects, comparable to those produced by alcohol but without significant cognitive impairment or addiction risk. Kava also produces a numbing sensation in the mouth.
Kava consists of sterile cultivars clonally propagated from its wild ancestor, Piper wichmanii. It originated in northern Vanuatu, where it was domesticated by farmers around 3,000 years ago through selective cultivation. Historically, the beverage was made from fresh kava; preparation from dry kava emerged in response to the efforts of Christian missionaries in the 18th and 19th centuries to prohibit the drinking of kava.
According to in vitro research, the pharmacological effects of kava stem primarily from six major kavalactones that modulate GABAA, dopamine, norepinephrine, and CB1 receptors, and inhibit MAO-B and ion channel mechanisms. Kava reduces short-term, situational anxiety, but its specific efficacy for generalized anxiety disorder appears to not be supported by the evidence.
Many countries banned or restricted kava in 2002 due to safety concerns. The World Health Organization (WHO) subsequently reviewed kava’s safety and concluded that moderate consumption of kava in its traditional form, as a water-based suspension of roots, presents an "acceptably low level of health risk". However, WHO and other health authorities have also concluded that consumption of kava extracts produced with organic solvents or excessive amounts of low-quality kava products may be linked to an increased risk of adverse health outcomes, including liver injury.
Safety at a Glance
High Risk- Noble vs. Tudei Varieties
- Only consume noble kava varieties. Reputable vendors will specify the cultivar or chemotype
- Toxicity: Studies have shown that kava can and will induce a low level of hepatic apoptosis similar to how paracetamol affects ...
- Dangerous with: Dissociatives
- Overdose risk: overdose has ever been recorded. The consumption of 'noble' kava root has very low toxicity, howe...
If someone is in crisis, call 911 or Poison Control: 1-800-222-1222
Dosage
oral
Duration
oral
Total: 3 hrs – 6 hrsHow It Feels
Kava announces itself first on the tongue. The traditional preparation -- muddy, earthy, faintly bitter water strained from the pounded root -- produces an immediate and distinctive numbing of the mouth and lips, a mild local anesthesia that is the first tangible sign that something pharmacologically interesting has entered the body. The lips tingle, the tongue grows slightly thick, and there is a warmth that begins in the throat and descends into the stomach. This oral numbing is kava's calling card, and it arrives within seconds, well before the systemic effects begin.
Within twenty to forty minutes, the first wave of the kavalactones reaches the brain, and the world begins to shift. Anxiety loosens its grip, not with the dramatic totality of benzodiazepines but with a gentler, more organic softening. The muscles relax, particularly in the face and shoulders, and there is a growing sense of calm sociability -- a willingness to engage with others that feels warm and genuine rather than chemically imposed. The mind remains clear, even sharpened in some respects, while the emotional undercurrent of worry simply fades to background noise. There is a physical pleasure to the relaxation that is distinctly kava's own -- a warm, slightly heavy sensation in the limbs that has been likened to sinking into a warm bath.
At the peak, the experience divides into two broad streams depending on the kava variety. Heady cultivars produce a more cerebral, uplifting effect -- enhanced sociability, a brightening of mood, a sense of mental spaciousness. Heavy cultivars push toward deeper sedation -- a profound muscular relaxation, a drowsiness that pulls the eyelids downward, and a body-centered tranquility that makes sitting motionless feel like the most natural and rewarding activity imaginable. Both paths share a common anxiolytic baseline and a sense of peaceful well-being that is kava's most universal gift. At higher doses, coordination diminishes noticeably, and there is a visual softening that makes the world appear gently out of focus.
The comedown is gentle and generally pleasant. The calm persists as the more pronounced effects recede, leaving behind a mellow afterglow that can last for hours. Sleep, when it follows a kava session, is deep and restful, and the morning after is typically clear and refreshed -- there is no hangover comparable to alcohol's, though the stomach may feel slightly tender from the root's astringent properties. The overall impression of kava is of a profoundly civilized intoxicant -- warm, social, anxiolytic, and remarkably forgiving, a substance that seems designed for the communal evening rather than the solitary escape.
Subjective Effects
The effects listed below are based on the Subjective Effect Index (SEI), an open research literature based on anecdotal reports and personal analyses. They should be viewed with a healthy degree of skepticism. These effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects.
Physical Effects
Physical(17)
- Dehydration— A state of insufficient bodily hydration manifesting as persistent thirst, dry mouth, and physical d...
- Dizziness— A sensation of spinning, swaying, or lightheadedness that impairs balance and spatial orientation, o...
- Headache— A painful sensation of pressure, throbbing, or aching in the head that can range from a dull backgro...
- Increased libido— A marked enhancement of sexual desire, arousal, and sensitivity to erotic stimuli that can range fro...
- Increased salivation— Increased salivation (hypersalivation or sialorrhea) is the excessive production of saliva beyond wh...
- Motor control loss— A distinct decrease in the ability to control one's physical body with precision, balance, and coord...
- Mouth numbing— Mouth numbing is a localized loss of sensation in the tongue, gums, cheeks, and surrounding oral tis...
- Muscle relaxation— The experience of muscles throughout the body losing their rigidity and tension, becoming noticeably...
- Nausea— An uncomfortable sensation of queasiness and stomach discomfort that may or may not lead to vomiting...
- Pain relief— A suppression of negative physical sensations such as aches and pains, ranging from dulled awareness...
- Perception of bodily heaviness— Perception of bodily heaviness is the subjective feeling that one's body has become dramatically hea...
- Physical euphoria— An intensely pleasurable bodily sensation that can manifest as waves of warmth, tingling electricity...
- Respiratory depression— A dangerous slowing and shallowing of breathing that can progress from barely noticeable reductions ...
- Sedation— A state of deep physical and mental calming that manifests as a progressive desire to remain still, ...
- Spatial disorientation— Spatial disorientation is the inability to accurately perceive one's position or orientation within ...
- Temporary erectile dysfunction— Temporary erectile dysfunction is the substance-induced inability to achieve or sustain a penile ere...
- Vibrating vision— Vibrating vision is the subjective experience of the visual field rapidly oscillating or shaking due...
Cognitive & Perceptual Effects
Visual(3)
- After images— A visual phenomenon in which a faint, ghostly imprint of a previously viewed image persists in the v...
- Colour enhancement— An intensification of the brightness, vividness, and saturation of colors in the external environmen...
- Visual haze— A translucent fog or haze overlays the visual field, softening the environment and reducing clarity....
Cognitive(10)
- Addiction suppression— Addiction suppression is the experience of a marked decrease in or complete cessation of the craving...
- Amnesia— A complete or partial inability to form new memories or recall existing ones during and after substa...
- Anxiety— Intense feelings of apprehension, worry, and dread that can range from a subtle background unease to...
- Anxiety suppression— A partial to complete suppression of anxiety and general unease, producing a calm, relaxed mental st...
- Cognitive euphoria— A cognitive and emotional state of intense well-being, elation, happiness, and joy that manifests as...
- Delusion— A delusion is a fixed, false belief that is held with unshakeable certainty and is impervious to con...
- Depression— A persistent state of low mood, emotional numbness, hopelessness, and diminished interest or pleasur...
- Disinhibition— A marked reduction in social inhibitions, self-consciousness, and behavioral restraint that manifest...
- Dream potentiation— Enhanced dream vividness, complexity, and recall, often occurring as REM rebound after discontinuing...
- Increased sense of humor— A general amplification of one's sensitivity to finding things humorous and amusing, often causing p...
Transpersonal(1)
- Spirituality enhancement— A profound intensification of spiritual feelings, mystical awareness, and a sense of sacred connecti...
Pharmacology
Pharmacologically, kava's effects stem from 18 different chemicals found within the plant called kavalactones, six of which have been found to be directly psychoactive in the body. The first of these are methysticin, dihydromethysticin, dihydrokavain, all of which act on the GABAA receptor and behave as an agonist, creating the well-known anxiolytic effects. Dihydromethysticin is also a reversible selective Monoamine Oxidase Inhibitor, specifically acting upon the MAO-B enzyme. Next is yangonin, which is unique in its ability to activate the CB1 receptor in the endocannabinoid system. Desmethoxyyangonin is also an MAO-B inhibitor and is able to increase dopamine levels in the Nucleus Accumbens. This, along with the potential increases of serotonin and other catecholamine concentrations, may be responsible for the purported attention-promoting effects of kava. Lastly is kavain. Kavain has shown evidence to be a serotonin-norepinephrine reuptake inhibitor (SNRI). It also shows evidence of being an activator of NMDA receptors. Kavain has also been proven to be an effective GABAA receptor agonist and a positive allosteric modulator of GABA efficacy. Kavain is also weak anti-epileptic due to its sodium ion (Na+) channel antagonism. It is also an effective mood stabilizer, working as an antagonist on Ca2+ (calcium ion) channels and as a positive modulator on K+ channels (potassium ion). Its effects on calcium ion channels also make it an effective anticonvulsant and, in synergy with yangonin, makes an effective analgesic (Pain reliever) working with both calcium ion channels and the endocannabinoid system.
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.
Some research has been done into finding the LD50 of kavalactones with results stating that around 300-400 Mg/Kg daily would be the likely lethal dose based on animal studies.
Kava is known to produce a "reverse tolerance" in many users, in a similar fashion to substances like kanna. This means that continued use is required in order to experience full effects. Some users do not experience this.
Kava is traditionally regarded as non-addictive especially in comparison to other chemically related drugs such as benzodiazepines. In some Pacific Island communities, there is some record of people who have a psychological addiction to kava and drink it like an alcoholic drinks alcohol.
- Hepatic Route drugs - Kava inhibits several liver enzymes in the CYP family. Consequentially, combining kava with drugs metabolized via CYP pathways, such as paracetamol, may cause adverse effects. For a list of medications click here A 2010 review concluded that it's possible that ethanol combined with kava may be the cause of kava hepatotoxicity.
- Anticoagulants - Kava may increase the risk of bleeding if taken with anticoagulants. Specifically the kavalactone kavain. A list of anticoagulants can be found here
- Antiplatelet - Kava may increase the risk of bleeding if taken with antiplatelet agents. Specifically the kavalactone kavain. A list of antiplatelet agents can be found here
In some countries, kava has been banned but in most, it is simply regulated.
Australia** - Kava is regulated by the National Code of Kava Management. Only 18 year olds may have it and can only possess 2 Kg in their baggage.
United Kingdom** - In the UK it is illegal to sell, supply or import any medicinal product containing kava for human consumption. It is legal to possess kava for personal use, or to import it for purposes other than human consumption (e.g. for animals).
United States** - In the U.S., kava was once noted as a potential "Liver Damaging substance" but this remark has since been archived by the FDA and kava is legal for sale, trade, possession, use, and all other uses.
Canada** - While Health Canada has similar remarks to the U.S. regarding kava, there is no ban on the substance.
Benzodiazepines
Kava (Wikipedia)
Kava (Erowid Vault)
Detection Methods
Urine Detection
Kava (Piper methysticum) contains kavalactones as the primary psychoactive constituents. Kavalactones are not targeted by any standard immunoassay drug panel. Specialized LC-MS/MS methods can detect kavalactone metabolites in urine for approximately 48 to 96 hours after consumption. The primary metabolites include hydroxylated and demethylated kavalactone derivatives.
Blood and Serum Detection
Kavalactones reach peak plasma concentrations within 1 to 2 hours after oral consumption of kava. The half-lives of individual kavalactones range from 1 to 9 hours. Blood detection by LC-MS/MS is feasible for approximately 12 to 48 hours.
Hair Follicle Detection
Hair testing for kavalactones has not been validated for routine use. Research methods exist but are not available in clinical or forensic laboratories.
Standard Drug Panel Inclusion
Kava is NOT included on any standard drug panel (5-panel, 10-panel, or 12-panel). Kavalactones do not cross-react with any immunoassay target. Kava use does not produce false-positive results on routine drug screening.
Confirmatory Methods
LC-MS/MS can identify specific kavalactones and their metabolites. This testing is available only in specialized research or forensic settings. For practical purposes, kava use is undetectable by routine drug testing.
Interactions
| Substance | Status | Note |
|---|---|---|
| Dissociatives | Dangerous | — |
History
Kava has been consumed in Pacific Island communities for over 3,000 years in both social and religious rituals, often as a drink. Kava's constituents have a sedative effect and act mainly on the GABA and dopamine receptors, as well as the sodium and calcium ion channels, but have also been found to have action upon the endocannabinoid system, specifically the CB1 receptor sites. Kava has been likened to the effects of alcohol without the heavy mental effects. Kava is primarily used to relieve anxiety (anxiolytic), to relieve pain (analgesic), and to boost sociability.
Commonly, kava is drank throughout the day by Pacific Islanders such as those on Vanuatu or the Islands of Hawaii. This drink is popularly consumed before spiritual rituals and before social events due to its mild psychotropic effects and its more potent sociability inducing effects. Kava replaces alcohol in many Pacific communities.
Kava cultures are the religious and cultural traditions of western Oceania which consume kava.
Kava is found to contain eighteen different chemicals called kavalactones. Kava's effects are believed to only relate to six psychoactive and medicinal kavalactones: methysticin, dihydromethysticin, kavain, dihydrokavain, yangonin, and desmethoxyyangonin.
Pharmacologically, kava's effects stem from 18 different chemicals found within the plant called kavalactones, six of which have been found to be directly psychoactive in the body. The first of these are methysticin, dihydromethysticin, dihydrokavain, all of which act on the GABAA receptor and behave as an agonist, creating the well-known anxiolytic effects. Dihydromethysticin is also a reversible selective Monoamine Oxidase Inhibitor, specifically acting upon the MAO-B enzyme. Next is yangonin, which is unique in its ability to activate the CB1 receptor in the endocannabinoid system. Desmethoxyyangonin is also an MAO-B inhibitor and is able to increase dopamine levels in the Nucleus Accumbens. This, along with the potential increases of serotonin and other catecholamine concentrations, may be responsible for the purported attention-promoting effects of kava. Lastly is kavain. Kavain has shown evidence to be a serotonin-norepinephrine reuptake inhibitor (SNRI). It also shows evidence of being an activator of NMDA receptors. Kavain has also been proven to be an effective GABAA receptor agonist and a positive allosteric modulator of GABA efficacy. Kavain is also weak anti-epileptic due to its sodium ion (Na+) channel antagonism. It is also an effective mood stabilizer, working as an antagonist on Ca2+ (calcium ion) channels and as a positive modulator on K+ channels (potassium ion). Its effects on calcium ion channels also make it an effective anticonvulsant and, in synergy with yangonin, makes an effective analgesic (Pain reliever) working with both calcium ion channels and the endocannabinoid system.
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.
Some research has been done into finding the LD50 of kavalactones with results stating that around 300-400 Mg/Kg daily would be the likely lethal dose based on animal studies.
Kava is known to produce a "reverse tolerance" in many users, in a similar fashion to substances like kanna. This means that continued use is required in order to experience full effects. Some users do not experience this.
Kava is traditionally regarded as non-addictive especially in comparison to other chemically related drugs such as benzodiazepines. In some Pacific Island communities, there is some record of people who have a psychological addiction to kava and drink it like an alcoholic drinks alcohol.
- Hepatic Route drugs - Kava inhibits several liver enzymes in the CYP family. Consequentially, combining kava with drugs metabolized via CYP pathways, such as paracetamol, may cause adverse effects. For a list of medications click here A 2010 review concluded that it's possible that ethanol combined with kava may be the cause of kava hepatotoxicity.
- Anticoagulants - Kava may increase the risk of bleeding if taken with anticoagulants. Specifically the kavalactone kavain. A list of anticoagulants can be found here
- Antiplatelet - Kava may increase the risk of bleeding if taken with antiplatelet agents. Specifically the kavalactone kavain. A list of antiplatelet agents can be found here
In some countries, kava has been banned but in most, it is simply regulated.
Australia** - Kava is regulated by the National Code of Kava Management. Only 18 year olds may have it and can only possess 2 Kg in their baggage.
United Kingdom** - In the UK it is illegal to sell, supply or import any medicinal product containing kava for human consumption. It is legal to possess kava for personal use, or to import it for purposes other than human consumption (e.g. for animals).
United States** - In the U.S., kava was once noted as a potential "Liver Damaging substance" but this remark has since been archived by the FDA and kava is legal for sale, trade, possession, use, and all other uses.
Canada** - While Health Canada has similar remarks to the U.S. regarding kava, there is no ban on the substance.
Benzodiazepines
Kava (Wikipedia)
Kava (Erowid Vault)
Harm Reduction
Noble vs. Tudei Varieties
The most important safety distinction in kava is between noble andtudei (or "two-day") varieties. Noble kava cultivars have been selected over centuries by Pacific Island cultures for their pleasant effects and safety profile. Tudei varieties contain higher concentrations of flavokavains (particularly flavokavain B) and dihydrokavain-type kavalactones associated with nausea, lethargy, and potentially hepatotoxicity.
- Only consume noble kava varieties. Reputable vendors will specify the cultivar or chemotype
- Tudei kava can cause a heavy, unpleasant "hangover" lasting up to two days (hence the name)
- The chemotype number (the ordering of the six major kavalactones) is the most reliable indicator: noble varieties typically begin with 2 or 4 (e.g., 246531, 423651)
Liver Safety
Kava's hepatotoxicity risk has been debated extensively. The weight of evidence suggests that traditionally prepared noble kava root consumed in moderation poses minimal liver risk. However:
- Avoid kava extracts made with acetone or ethanol — these extract compounds (flavokavains, pipermethystine from leaves/stems) not present in traditional water-based preparation
- Do not combine kava with alcohol — both are metabolized hepatically, and the combination significantly increases liver enzyme elevation
- Do not take kava with hepatotoxic medications (acetaminophen/paracetamol, statins, certain antibiotics)
- If you have pre-existing liver disease, do not use kava
- Monitor for signs of hepatic stress: jaundice (yellowing of skin/eyes), dark urine, unusual fatigue, right upper abdominal pain
Preparation Matters
Traditional preparation (aqueous extraction by kneading ground root in water or coconut milk) selectively extracts kavalactones while leaving behind potentially harmful compounds found in leaves, stems, and bark. This is why traditional Pacific Island kava use has no documented history of liver toxicity despite centuries of heavy use.
- Use root-only products, never those containing aerial parts (leaves, stems)
- Traditional preparation or products made with water/CO2 extraction are preferred over alcohol-based tinctures
- Micronized kava (finely ground root consumed whole) delivers higher doses of all compounds — start with lower amounts
Dermopathy (Kava Skin)
Chronic heavy kava use can cause kava dermopathy — a reversible ichthyotic (scaly, dry) skin condition that typically appears on the palms, soles, forearms, and shins. This is cosmetic, not dangerous, and resolves completely upon reducing or stopping kava use. Adequate hydration and moisturizing can mitigate symptoms.
Driving and Operating Machinery
Kava impairs reaction time and motor coordination at moderate to high doses. Do not drive or operate heavy machinery after consuming kava, particularly during the first few hours after drinking.
Toxicity & Safety
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.
Lethal dosage
Some research has been done into finding the LD50 of kavalactones with results stating that around 300-400 Mg/Kg daily would be the likely lethal dose based on animal studies.
Tolerance and addiction potential
Kava is known to produce a "reverse tolerance" in many users, in a similar fashion to substances like kanna. This means that continued use is required in order to experience full effects. Some users do not experience this.
Kava is traditionally regarded as non-addictive especially in comparison to other chemically related drugs such as benzodiazepines. In some Pacific Island communities, there is some record of people who have a psychological addiction to kava and drink it like an alcoholic drinks alcohol.
Dangerous interactions
Depressants (1,4-Butanediol, 2M2B, alcohol, benzodiazepines, barbiturates, GHB/GBL, methaqualone, opioids) - This combination potentiates the muscle relaxation, amnesia, sedation, and respiratory depression caused by one another. At higher doses, it can lead to a sudden, unexpected loss of consciousness along with a dangerous amount of depressed respiration. There is also an increased risk of suffocating on one's vomit while unconscious. If nausea or vomiting occurs before a loss of consciousness, users should attempt to fall asleep in the recovery position or have a friend move them into it.
Dissociatives - This combination can unpredictably potentiate the amnesia, sedation, motor control loss and delusions that can be caused by each other. It may also result in a sudden loss of consciousness accompanied by a dangerous degree of respiratory depression. If nausea or vomiting occurs before consciousness is lost, users should attempt to fall asleep in the recovery position or have a friend move them into it.
Stimulants - Stimulants mask the sedative effect of depressants, which is the main factor most people use to gauge their level of intoxication. Once the stimulant effects wear off, the effects of the depressant will significantly increase, leading to intensified disinhibition, motor control loss, and dangerous black-out states. This combination can also potentially result in severe dehydration if one's fluid intake is not closely monitored. If choosing to combine these substances, one should strictly limit themselves to a pre-set schedule of dosing only a certain amount per hour until a maximum threshold has been reached.
Hepatic Route drugs - Kava inhibits several liver enzymes in the CYP family. Consequentially, combining kava with drugs metabolized via CYP pathways, such as paracetamol, may cause adverse effects. For a list of medications click here A 2010 review concluded that it's possible that ethanol combined with kava may be the cause of kava hepatotoxicity.
Anticoagulants - Kava may increase the risk of bleeding if taken with anticoagulants. Specifically the kavalactone kavain. A list of anticoagulants can be found here
Antiplatelet - Kava may increase the risk of bleeding if taken with antiplatelet agents. Specifically the kavalactone kavain. A list of antiplatelet agents can be found here
Addiction Potential
Kava has low but non-zero dependence potential. Unlike most psychoactive substances, kava exhibits a well-documented reverse tolerance phenomenon — effects often become stronger with repeated use rather than diminishing, meaning users tend to decrease rather than escalate their doses over time. Heavy daily use over extended periods has been associated with a dermopathy (kava skin) and potential hepatotoxicity, but clinically significant withdrawal syndromes are not well-documented. Traditional Pacific Islander use patterns spanning centuries suggest that moderate, regular consumption carries low addiction risk.
Overdose Information
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.
Some research has been done into finding the LD50 of kavalactones with results stating that around 300-400 Mg/Kg daily would be the likely lethal dose based on animal studies.
Kava is known to produce a "reverse tolerance" in many users, in a similar fashion to substances like kanna. This means that continued use is required in order to experience full effects. Some users do not experience this.
Kava is traditionally regarded as non-addictive especially in comparison to other chemically related drugs such as benzodiazepines. In some Pacific Island communities, there is some record of people who have a psychological addiction to kava and drink it like an alcoholic drinks alcohol.
- Hepatic Route drugs - Kava inhibits several liver enzymes in the CYP family. Consequentially, combining kava with drugs metabolized via CYP pathways, such as paracetamol, may cause adverse effects. For a list of medications click here A 2010 review concluded that it's possible that ethanol combined with kava may be the cause of kava hepatotoxicity.
- Anticoagulants - Kava may increase the risk of bleeding if taken with anticoagulants. Specifically the kavalactone kavain. A list of anticoagulants can be found here
- Antiplatelet - Kava may increase the risk of bleeding if taken with antiplatelet agents. Specifically the kavalactone kavain. A list of antiplatelet agents can be found here
In some countries, kava has been banned but in most, it is simply regulated.
- Australia** - Kava is regulated by the National Code of Kava Management. Only 18 year olds may have it and can only possess 2 Kg in their baggage.
- United Kingdom** - In the UK it is illegal to sell, supply or import any
Dangerous Interactions
The combinations listed below may be life-threatening. Independent research should always be conducted to ensure safety when combining substances.
Tolerance
| Full | Reverse tolerance is commonly reported — effects may increase with repeated use |
| Half | Not applicable (reverse tolerance) |
| Zero | Not applicable (reverse tolerance) |
Cross-tolerances
Legal Status
In some countries, kava has been banned but in most, it is simply regulated.
Australia** - Kava is regulated by the National Code of Kava Management. Only 18 year olds may have it and can only possess 2 Kg in their baggage.
United Kingdom** - In the UK it is illegal to sell, supply or import any medicinal product containing kava for human consumption. It is legal to possess kava for personal use, or to import it for purposes other than human consumption (e.g. for animals).
United States** - In the U.S., kava was once noted as a potential "Liver Damaging substance" but this remark has since been archived by the FDA and kava is legal for sale, trade, possession, use, and all other uses.
Canada** - While Health Canada has similar remarks to the U.S. regarding kava, there is no ban on the substance.
Kava (Wikipedia)
Kava (Erowid Vault)
Experience Reports (6)
Tips (5)
Only use noble kava varieties. 'Tudei' kava can cause nausea, lethargy, and has been linked to liver issues. Reputable vendors will specify their kava is noble cultivar and will have lab testing to back it up.
Do not use kava if you are withdrawing from GABAergic drugs like benzos or gabapentin without medical supervision. Kava hits GABA receptors and while it might seem like it would help, mixing it into an active withdrawal from those substances can complicate things unpredictably.
Kava capsules from random stores are almost always weak and underwhelming. If you want to actually feel kava, get medium grind noble root powder and prepare it traditionally — knead it in a strainer bag with warm water for about 10 minutes. The difference between capsules and properly prepared root is night and day.
Keep a usage log for Kava including dose, time, effects, and side effects. This helps you identify patterns and prevent problematic escalation.
Always start with a low dose of Kava and work your way up. Individual sensitivity varies, and you cannot undo a dose once taken.
Community Discussions (2)
See Also
References (3)
- PubChem: Kava
PubChem compound page for Kava (CID: 5281565)
pubchem - Kava - TripSit Factsheet
TripSit factsheet for Kava
tripsit - Kava - Wikipedia
Wikipedia article on Kava
wikipedia