(Source: SaluGenecists, Inc.)


Kava, a member of the pepper family that originates from Melanesia, Micronesia, and Polynesia, is a large perennial shrub with a thick, pithy rootstock, which is the part used for medicinal purposes. Kava usage predates written history in the Pacific Islands, being used ceremoniously by Pacific Islanders for thousands of years.

The rootstock contains many constituents including starch, simple sugars, minerals and flavonoids as well as the phytonutrients known as kavalactones (also referred to as kavapyrones). While the kavalactones are thought to be the primary active components, other components such as kavas flavonoids (flavokavains) also appear to contribute to its activities. The dried herb typically provides 3.5% kavalactones, but kava extracts commercially available are generally formulated to provide from 30-70% kavalactones. Kava is generally available in tablet or liquid form.

Kavalactones exert sedative effects through mechanisms that are different than most other sedatives, including benzodiazepines, in that they do not bind to specific receptors (including GABA receptors) in the brain. Although it is still unclear through which specific mechanisms kava exerts its sedative actions, it is suggested that it works on the higher centers of the brain, the limbic system. In addition to its sedative effects, kava also has a variety of other suggested physiological actions including analgesic, anticonvulsant, anxiolytic, muscle-relaxant, anti-ischemia, and antimicrobial effects.

Healthcare applications for which kava may be useful include anxiety, prevention of benzodiazepine (sedative drugs) withdrawal, and menopausal symptoms.

Although adverse effects are not expected when kava is used at the recommended dosage, rarely kava has been found to cause side effects such as gastrointestinal upset, headache, dizziness, drowsiness, enlarged pupils, disturbances of oculomotor equilibrium and accommodation, dry mouth, and allergic skin reactions. High doses may cause kava dermopathy, a skin condition characterized by a scaly eruption; liver toxicity; and other adverse events.

Kava is contraindicated for those with Parkinsons disease, hepatitis (active case or history of disease), depression, and genetic cytochrome P450 2D6 (CYP2D6) isozyme susceptibility as well as for women who are pregnant or lactating.

Theoretically, using kava along with potentially hepatotoxic drugs, herbs and nutritional supplements might increase the risk of developing liver damage, particularly in individuals with genetic deficiency in the cytochrome P450 2D6 (CYP2D6) isozyme (see Drug/Nutrient/Herb Interactions section for more detail). Using kava along with other sedative agents may increase the risk of excessive drowsiness. Other agents which have shown an interaction with kava include Alprazolam, levadopa, and central nervous system depressants such as alcohol, barbiturates, and benzodiazepines.

Typical dosage varies depending upon the form being used and the health care application for which it is being used.

Key Constituents

The pharmacologically active constituents of kava are found in the root. Analysis of the composition of the dried kava rootstock indicates that it contains approximately 43% starch, 12% water, 3.2% simple sugars, 3.6% proteins, 3.2% minerals (primarily potassium), and 15% kavalactones (also referred to as kavapyrones). Found in the fat-soluble resin of the root, the kavalactones, which include kavain (or kawain), dihydrokavain (or dihydrokawain), methysticin, dihydromethysticin, yangonin and desmethoxyyangoin, are thought to be the primary active components.

Other components such as kavas flavonoids (flavokavains) also appear to contribute to the sedative and anxiolytic activities of kava, as one study found the sedative activity of a crude preparation to be more effective than the isolated kavalactones. The kavalactone content of the root can vary between 3 and 20% depending upon geographical location.

The dried herb typically provides 3.5% kavalactones, but but kava extracts commercially available are generally formulated to provide from 30-70% kava-lactones.

Evidence suggests that crude extracts standardized for kavalactone content may offer the greatest therapeutic benefit since the whole complex of kavalactones and other compounds naturally found in kava have been shown to produce greater pharmacological activity than isolated kavalactones. (This evidence is discussed below under Typical Forms.)

Historical Use

Kava usage predates written history in the Pacific Islands. The plant itself probably originated in the New Guinea/Indonesia area and was spread from island to island by early Polynesian explorers in canoes, along with other plants.

Kava has been used in ceremonies by the Pacific Islanders for thousands of years, but was brought to the attention of the West by Captain Cook who named the plant intoxicating pepper. Kava was prepared in a defined ritual manner and used for ceremonial purposes in the South Pacific. Three basic kava ceremonies were: a full ceremonial enacted on every formal occasion; the ceremony performed at the meeting of village elders, chiefs, and nobles and for visiting chiefs and dignitaries; and a less formal kava circle common on social occasions.

The first step of all kava ceremonies was the preparation of the beverage. A description of the classic process was written in 1777 by Georg Forster, a young naturalist on Captain James Cooks second Pacific voyage:

[Kava] is made in the most disgustful manner that can be imagined, from the juice contained in the roots of a species of pepper-tree. This root is cut small, and the pieces chewed by several people, who spit the macerated mass into a bowl, where some water (milk) of coconuts is poured upon it. They then strain it through a quantity of fibres of coconuts, squeezing the chips, till all their juices mix with the coconut-milk; and the whole liquor is decanted into another bowl. They swallow this nauseous stuff as fast as possible; and some old topers value themselves on being able to empty a great number of bowls.

In most parts of Oceania, this traditional method of preparation has largely been replaced by more sanitary methods involving grinding or grating the root. Commercially available kava extracts are prepared from the dried root with an ethanol-water mixture to produce extracts containing 30% kavalactones (also called kavapyrones) and with an acetone-water mixture to produce extracts containing 70% kavalactones.

When consumed, kava confers a pleasant sense of tranquility and sociability, as verified not only by traditional lore but a number of subjective reports given by scientists who have sampled kava themselves.

One of the first scientific studies of kava was performed by noted pharmacologist Louis Lewin in 1886. A later description written in 1927 is as follows: When the mixture is not too strong, the subject attains a state of happy unconcern, well-being and contentment, free of physical or psychological excitement. At the beginning, conversation comes in a gentle, easy flow and hearing and sight are honed, becoming able to perceive subtle shades of sound and vision. Kava soothes temperaments. The drinker never becomes angry, unpleasant, quarrelsome or noisy, as happens with alcohol. Both natives and whites consider kava as a means of easing moral discomfort. The drinker remains master of his consciousness and his reason. When consumption is excessive, however, the limbs become tired, the muscles seem no longer to respond to the orders and control of the mind, walking becomes slow and unsteady and the drinker looks partially inebriated. He feels the need to lie down. He is overcome by somnolence and finally drifts off to sleep.

Researcher R.J. Gregory provides the following more recent description:

Kava seizes ones mind. This is not a literal seizure, but something does change in the processes by which information enters, is retrieved, or leads to actions as a result. Thinking is certainly affected by the kava experience, but not in the same ways as are found from caffeine, nicotine, alcohol, or marijuana. I would personally characterize the changes I experienced as going from lineal processing of information to a greater sense of being and contentment with being. Memory seemed to be enhanced, whereas restriction of data inputs was strongly desired, especially with regard to disturbances of light, movements, noise and so on. Peace and quiet were very important to maintain the inner sense of serenity. My senses seemed to be unusually sharpened, so that even whispers seemed to be loud while loud noises were extremely unpleasant.

Drinking about half a coconut shell (100150mL) of certain varieties of kava is enough to put most people into a deep, dreamless sleep within 30 minutes. Unlike alcohol and other sedatives, kava does not produce any morning hangover. The kava drinker awakens having fully recovered normal physical and mental capacities.

Important people who visit Fiji and other islands of Oceania still participate in the kava ceremonies. For example, during a 1992 presidential campaign visit to Hawaii, Hillary Clinton participated in a kava ceremony conducted by the Samoan community on Oahu.

Physiological Effects

In the 1950s and 60s, a team of scientists led by Hans J. Meyer from the Freiburg University Institute of Pharmacology in Germany conducted many of the first comprehensive studies on the activities of kavalactones. Their research, which found that kavalactones exhibit sedative, analgesic, anticonvulsant, and muscle-relaxant effects in laboratory animals, confirmed earlier empirical and subjective observations. More recent studies have provided further evidence to support these early studies and have utilized better-defined kava extracts.

Sedative and Hypnotic Effects

Most notable are studies demonstrating that kavalactones exert many of their effects through non-traditional mechanisms. For example, most sedative drugs including the benzodiazepines (e.g., Valium, Halcion, Tranxene, etc.) work by binding to specific receptors (benzodiazepine or GABA receptors) in the brain, which then leads to the neurochemical changes (potentiation of GABA effects) that promote sedation. Although more recent studies suggest that kavalactones do have an effect on GABA-A receptor binding via increasing the number of GABA-binding sites, the majority of animal studies have found that kava resin and kavalactones do not bind to benzodiazepine or GABA receptors. Other preliminary evidence suggests kavas sedative effects might be partially due to dopamine antagonism.

Both kava extracts and kavalactones have demonstrated sedative effects in a variety of animal models. Studies using isolated hippocampal tissue of guinea pigs suggest that kavain and dihydromethysticin may have additive effects and may enhance the effects of the anxiolytic serotonin-1A agonist ipsapirone. The activation of NMDA receptors (a class of glutamate receptors characterized by an affinity for N-methyl-D-aspartate) and/or voltage-dependent calcium channels may also be involved in the elementary mechanism of action.

Kavalactones given to rabbits produced EEG changes similar to sedative drugs. These modifications to EEG patterns suggest that kava and kavain induce sleep by acting on the limbic system, specifically the amygdala complex&mdash an effect different from that of benzodiazepines or tricyclic antidepressants.

Kava extracts and kavalactones have demonstrated sedative effects and induced sleep in a variety of in vivo experimental models.

Dihydrokavain and dihydromethysticin produced sedation and hypothermia in mice. Kava resin inhibited experimentally induced hypermotility and conditioned avoidance responses in mice comparable to antipsychotic drugs, and higher doses caused marked sedation. The major pharmacological effects of reduced motor control and sleep induction have been shown in studies of lactone-free (aqueous) kava extract to be due to components in the resin. In one study, total extract was more active than any isolated kavalactones. Sedative effects have also been observed from injection of aqueous extract of kava.

Efficacy of standardized kava extract was evaluated in a placebo-controlled trial of 12 healthy volunteers over 4 days. Placebo was taken for 3 days, followed by three divided doses totaling either 150 mg kava extract (containing 105 mg kavalactones) or 300 mg extract containing 210 mg kavalactones). When kava was given, lability to fall asleep and the light sleep phase were shortened, while the deep sleep phase was lengthened, the duration of REM sleep was not influenced, and the duration of wakeful phases in sleep EEG recordings was decreased. These effects are favorable, particularly in comparison with orthodox sedatives such as benzodiazepines and barbiturates, both of which depress both REM and deep sleep. Kava, like orthodox sedatives, also increased the density of sleep spindles.

In addition, unlike orthodox sedatives, kava does not negatively affect cognitive performance, but may actually improve it. In a double-blind, crossover study to evaluate the effect on event-related potentials in a word recognition task, 12 healthy volunteers received the benzodiazepine drug oxazepam (3 days of placebo, 15 mg on the day before testing, 75 mg on the morning of testing) and standardized kava extract (600 mg per day for 5 days). With oxazepam, a significant decrease was observed in the quality and speed of responses in several psychometric tests, no changes were observed with kava treatment. In a memory test using word recognition, kava showed a not statistically significant tendency to improve reaction time and correct answers, while oxazepam significantly slowed reaction time and reduced the number of correct answers. Changes in event-related potentials induced by kava during the word recognition task were very different from changes caused by oxazepam.

In another trial of similar design, 12 healthy men were tested in a visual search paradigm assessed by event-related potentials. Kava was shown to have a positive effect on the allocation of attention and processing capacity, whereas oxazepam reduced the capacity to allocate focal attention and reduced processing capacity.

In a placebo-controlled, double-blind study of 40 healthy volunteers, standardized kava extract combined with ethanol (0.05% blood alcohol concentration) not only caused no negative effects, but tended to counter the adverse effect of alcohol on mental concentration. However, in an experimental model, high doses of ethanol potentiated the sedative and hypnotic effect of kava resin and markedly increased the toxicity.

In another randomized, double-blind, crossover clinical study, the effect of kava extract (120 mg kavalactones) was compared to that of diazepam (10 mg) or placebo. To compare mental alertness, neurophysiological and psychophysiological tests were conducted immediately before, 2 and 6 hours after administration of the preparations. Results for both kava and diazepam differed significantly from placebo. Kavas effects also differed significantly from diazepam, specifically, the increase in beta-activity typical of benzodiazepines did not occur, and the action of kava was undiminished 6 hours after application. Despite kavas relaxing effects, in one of the psychophysiological tests, performance of complex challenges was better with kava than placebo or diazepam, and these apparently contradictory properties (increased relaxation and increased performance) were confirmed for kava.

In yet another study, the effect of simultaneous administration of kava (120 mg kavalactones twice daily) and bromazepam (4.5 mg twice daily) on safety-related performance was evaluated. A double-blind, randomized, three-way crossover design was used with 18 healthy volunteers who received kava, bromazepam or a combination of the two. Performance was measured at 0, 1, 2, and 14 days after each treatment, with a 7-day washout between treatment periods. Seven computer-assisted computer performance tests were used to assess cognitive performance including visual orientation, extended concentration, acoustic reaction time, discriminative reaction time, stress tolerance, vigilance and motor coordination. Three of the 7 tests showed significant differences between treatments. With bromazepam and the combination, vigilance, stress tolerance and motor coordination worsened, while with kava, it remained unchanged. Bromazepam and the combination produced the most pronounced impairment, mainly fatigue. The studys authors concluded that adding kava to bromazedpam is unlikely to produce greater effects on well-being and mental performance aspects required for safety, but that patients are not exposed to additional side effects or risks while taking both concurrently.

While the specific mechanisms behind kavas sedative effects are still unclear, the kavalactones are thought to somehow modify receptor domains rather than interacting specifically with receptor binding sites. In addition, other studies have indicated that rather than work on the higher centers of the brain, the kavalactones appear to act primarily on the limbic system, the more primitive part of the CNS that affects all other brain activities and is the principle seat of the emotions. It is thought that kava may also promote sleep by altering the way in which the limbic system modulates emotional processes. It appears that many of the laboratory models of identifying how a substance works to promote a calming effect are simply not sophisticated enough to evaluate the physiological effects of kava.

Local Analgesic and Anaesthetic Effects

Kava resin, kavalactones, and a lactone-free (aqueous) extract of kava have all demonstrated analgesic properties in experimental models when given by injection. The analgesia produced by kava is not believed to occur by the opiate pathway because it is not reversible by naloxone.

Kava is thought to work for a variety of inflammatory conditions by inhibiting both COX-1 and COX-2 enzymes, which are the enzymes responsible for converting arachidonic acid to Series 2 (pro-inflammatory) prostaglandins.

Kavalactones have been shown to have anaesthetic potency similar to cocaine and prococaine and have also demonstrated analgesic activity in several experimental models. As an analgesic, the kavalactone dihydrokavain was superior to aspirin but much less potent than morphine. Combined administration of dihydrokavain with aspirin indicated additive synergism between the two, while caffeine diminished the duration but not the intensity of the analgesic effects of dihydrokavain and dihydromethysticin.

Anxiolytic Effects

Standardized extract of kava improved cognitive performance and stabilized emotional disposition without causing sedation in a single-blind study with placebo of six healthy volunteers. EEG measurements indicated that anti-anxiety activity was produced without sedation or hypnotic effects.

ERICis the following a reasonable connection to make? If not, under what physiological effect should this study be placed? Or should we add Anti-depressant Activity to our list of physiological effects? A possible mechanism of action is the ability ot the kavalactones desmethoxyyangonin and methysticin to competitively inhibit monoamine oxidase B (MAO-B).

In addition, unlike other anxiolytic drugs, kava does not lose effectiveness with time. In animal studies, kavalactones, even when administered in large dosages, demonstrated no loss of effectiveness over time.

Muscle Relaxant, Spasmolytic and Anticonvulsant Effects

Kava extract and kavalactones have produced relaxation of skeletal muscle in vitro and in vivo. Kavains anticonvulsant activity was investigated on stimulated synaptosomes and sodium channel receptor sites. Results suggest an interaction of kavain with voltage-dependent sodium and calcium channels, thus suppressing induced increases in cytosolic concentrations of sodium and calcium and the release of endogenous glutamate. In vitro tests with kavain indicate that it inhibits veratridine-activated sodium channels non-stereospecifically.

Kavain was also shown to potently inhibit the uptake of labeled noradrenaline from synaptosomes, which may be the mechanism behind the psychotropic properties of kavalactones. Furthermore, kava is thought to produce motor sedation without affecting respiratory processes.

Kavalactones have demonstrated anticonvulsant activity in several experimental models. Kavalactones were ten times more effective than mephenesin against the convulsant effect of strychnine. A lactone mixture similar to that found in the root had a synergistic effect against strychnine-induced convulsions, an anticonvulsant effect more marked when the lactone mixture was given orally, due to enhanced absorption. Despite these promising results, clinical trials have not shown kava to be suitable in the treatment of epilepsy.

Kavalactones have demonstrated spasmolytic activity on smooth muscle in vitro similar to papaverine. Studies of isolated guinea pig ileum suggest kavain may have a general inhibitory effect on contractile activity and may act in a non-specific musculotropic way on the lipid bilayer of the membrane.

Analgesic Effects

In another example of the unusual pharmacological qualities of kava, a study designed to evaluate its pain-relieving effects could not demonstrate any binding to opiate receptors, although when chewed, kava numbs the mouth similarly to cocaine. The significance of this finding is that the study used experimental models where non-opiate analgesics like aspirin and other non-steroidal anti-inflammatory drugs are ineffective. In addition, it was determined that the sedative or muscle-relaxing effects were not responsible for the pain-relieving effects. These findings indicate that kava reduces pain in a manner unlike morphine, aspirin, or any other pain reliever.

Anti-ischemia Effects

Another potentially important pharmacological activity of kava is its ability to protect against brain damage due to ischemia. This effect has been demonstrated in two animal models of focal cerebral ischemia. The effectiveness of kava extract and the kavalactones methysticin and dihydrokavain was due to their ability to limit the infarct area as well as provide an anticonvulsant effect comparable to the anticonvulsant memantine. Kava extract may thus prove useful in recovery from a stroke.

Antithrombotic Activity

Antithrombotic activity observed for kavain in vitro is likely due to inhibition of cyclooxygenase, which results in suppression of the generation of thromboxane A2.

Antibacterial, Antifungal Effects

Although kava has traditionally been used as an antibacterial agent, especially for urinary tract infections, in vitro studies do not confirm significant antibacterial activity. Some kavalactones do, however, exhibit potent fungistatic activity against a wide range of pathogenic fungi, excluding species of Candida.

Typical Use


Positive results in a number of studies suggest that kava is effective when used orally for short-term treatment of anxiety disorders.

Early clinical trials used d,l-kavain, a purified kavalactone, at a dose of 400 mg/day. In one double-blind placebo-controlled study of 84 patients with anxiety symptoms, kavain was shown to improve vigilance, memory, and reaction time. In another double-blind study, placebo-controlled trial of 38 patients with anxiety associated with neurotic disturbances, kavain was compared to oxazepam (a drug similar to diazepam or Valium) and demonstrated equivalent activity. Both substances caused progressive improvements in two different anxiety scores (Anxiety Status Inventory and the Self-rating Anxiety Scale) over a 4 week period. However, while oxazepam and similar drugs are addictive and attended with negative side-effects, kavain appeared to be free of these complications.

Most later clinical trials have used a standardized extract containing 70% kavalactones. In a randomized, placebo-controlled, double-blind study of 58 patients with anxiety not caused by psyhchotic disorders, a standardized kava extract significantly improved measures of anxiety and depression. Patients were given standardized kava extract (300mg per day, containing 210mg kavalactones) or placebo over a 4-week period. Those receiving the kava extract experienced a significant reduction of anxiety as measured by the Hamilton Anxiety Scale (total score, p<0.02). The difference in anxiety between kava and placebo began in the first week and increased during the course of treatment. No adverse effects were reported for kava extract.

In another well-done study, a 70% kavalactone extract was shown to exhibit significant therapeutic benefit in patients suffering from anxiety. The study was double-blind; 29 patients were assigned to receive 100mg of the kava extract three times daily, while another 29 patients received a placebo. Therapeutic effectiveness was assessed using several standard psychological assessments including the Hamilton Anxiety Scale. The result of this 4 week study indicated that individuals taking the kava extract had a statistically significant reduction in symptoms of anxiety including feelings of nervousness and somatic complaints such as heart palpitations, chest pains, headache, dizziness, and feelings of gastric irritation. No side-effects were reported with the kava extract.

In another double-blind study, two groups of 20 women with menopause-related anxiety symptoms were treated for a period of 8 weeks with the 70% kavalactone extract (100 mg three times daily) or placebo. The measured variable was once again the Hamilton Anxiety Scale. The group receiving kava extract demonstrated significant improvement by the end of the first week of treatment, and scores continued to improve over the course of the 8 week study. In addition to improvement in symptoms of stress and anxiety, several other symptoms also improved. Most notable was an overall improvement in subjective well-being, mood, and general symptoms of menopause, including hot flashes. Again, no side-effects were noted.

Additional studies have shown that unlike benzodiazepines, alcohol, and other drugs, kava extract is not associated with depressed mental function or impairment in driving or the operation of heavy equipment. In one of these studies, 12 healthy volunteers were tested in a double-blind cross-over manner to assess the effects of oxazepam (placebo on days 13, 15mg on the day before testing, 75mg on the morning of the experiment), the extract of kava standardized at 70% kavalactones (200mg three times daily for 5 days), and a placebo on behavior and event-related potentials (ERPs) in electroencephalograph (EEG) readings on a recognition memory task. The subjects task was to identify within a list of visually presented words those that were shown for the first time and those that were being repeated. Consistent with other benzodiazepines, oxazepam inhibited the recognition of both new and old words as noted by ERP. In contrast, kava showed a slightly increased recognition rate and a larger ERP difference between old and new words. The results of this study once again demonstrate the unusual effects of kava, which improves anxiety, but unlike standard anxiolytics, actually improves mental function and, at the recommended levels, does not promote sedation.

In another larger randomized, controlled, double-blind study, a standardized extract of kava was compared to the benzodiazepine drugs bromazepam and oxazeepam. One hundred and seventy six outpatients were divided into three groups, one of which received kava extract (210mg kavalactones per day), a second group which received 15 mg of oxazepam per day, and a third group which was given 9mg of bromazepam daily. After 6 weeks of treatment, the total Hamilton Anxiety Score was reduced from 27.3 to 15.6 in those given kava compared to 27.3 down to 13.4 for bromazepam and 27.7 to 16.6 for oxazepam. Statistical analysis showed kava treatment was equivalent to the benzodiazepine drugs. Side effects, however, were higher in the conventional drug groups.

In the above controlled trials, none lasted for more than 6 weeks, inclusion criteria were insufficiently defined and patient numbers were relatively small. To address these issues, a randomized, placebo-controlled, double-blind multicenter study of 100 patients presenting with nervous anxiety, tension and restlessness of non-psychotic origin (DSM-III-R) was conducted over a period of 6 months. Patients were randomized to receive either 300mg per day of a concentrated kava extract containing 210mg kavalactones (equal to about 4g dried root) or placebo. Assessment was based on changes in the cumulative Hamilton Anxiety Score (HAMA) in addition to other assessments. Comparison of the pre- and post-therapy HAMA scores revealed a significant (p=0.0015) superiority of the kava treatment as against placebo. The difference between the two groups was apparent at 8 weeks, with kava treatment leading to marked reduction in anxiety symptoms along with its physical and psychic manifestations. Kava also positively affected the accompanying depressive symptoms. During the study, 6 adverse events were reported in 5 patients in the kava group, four of which were rated by the investigator as not related to treatment while two (both cases of stomach upset) were considered possibly related. In contrast, 15 adverse effects from 9 patients were reported in the placebo group. Seven patients dropped out under placebo and 3 under kava (2 of the 3 were due to improvement of symptoms. No significant change was noted in biochemical parameters during the study and overall tolerability of kava was rated as excellent. The authors concluded the results support kavas use as an alternative to tricyclic antidepressants and benzodiazepines in anxiety, with proven long-term efficacy and none of the tolerance problems associated with these drugs.

In an observational study of 3029 patients, treatment with standardized kava extract (800mg per day containing 240mg kava pyrones) over a minimum of 4 weeks resulted in improvement of primary symptoms such as nervousness, restless and anger. Other symptoms including sleep disturbances, menopausal complaints, muscle tension and sexual disturbances were also improved. After 5 weeks of treatment, symptoms of nervousness, restlessness, and fear were reduced in 1673 patients. Mild adverse effects were reported in 69 patients (1.7% of patients) and included allergic reaction, gastrointestinal complaints, headache or dizziness.

Similar improvement in symptoms and a similar percentage of mild adverse reactions were observed in another observational study of 4049 patients treated with standardized kava extract (150mg per day, containing 105mg kavalactones) for 7 weeks.

Prevention of Benzodiazepine Withdrawal

Evidence from one study suggests that upwardly titrating kava over one week while tapering the benzodiazepine over 2 weeks can prevent withdrawal symptoms in some people with non-psychotic anxiety.

Menopausal Neurovegetative Symptoms

Standardized kava extract (210mg kavalactones per day for 8 weeks) produced a significant reduction in anxiety, depression, severity of symptoms, and menopausal symptoms in a randomized, placebo-controlled, double-blind trial of 40 patients. Subjective well-being of patients given kava improved and treatment was well tolerated.

Typical Use

Evidence suggests that crude extracts of the root standardized for kavalactone content may offer the greatest therapeutic benefit since the whole complex of kavalactones and other compounds naturally found in kava produce greater pharmacological activity than isolated kavalactones.

In addition, studies have shown that kavalactones are more rapidly absorbed when given orally as an extract of the root rather than as the isolated kavalactones. Lactone bioavailability, as measured by peak plasma concentrations, is up to three to five times higher from the extract than when given as isolated substances.

Further evidence that kava root extracts are superior to isolated kavalactones is offered by an animal study showing that while isolated kavalactones are well absorbed by brain, crude kava preparations produce brain concentrations of lactones two to 20 times higher.

Several clinical trials have featured a kava extract standardized to contain 70% kavalactones. However, this high percentage of kavalactones may be sacrificing some of the other constituents that may contribute to the pharmacology of kava. More important than the actual percentage of kavalactones is the total dosage of the kavalactones and the assurance that the full range of kavalactones and other important constituents are present.

Kava is also taken as 1 cup of the tea up to 3 times per day. The tea is prepared by simmering 2-4 grams of the root in 150 mL boiling water for 5-10 minutes and then straining.


Hepatotoxic Drugs: Theoretically, concomitant use with other potentially hepatotoxic drugs might increase the risk of developing liver damage, particularly in patients with genetic deficiency in the cytochrome P450 2D6 (CYP2D6) isozyme. Hepatotoxic drugs include acarbose (Precose), amiodarone (Cordarone), atorvastatin (Lipitor), azathioprine (Imuran), carbamazepine (Tegretol), cerivastatin (Baycol), diclofenac (Voltaren), felbamate (Felbatol), fenofibrate (Tricor), fluvastatin (Lescol), gemfibrozil (Lopid), isoniazid, itraconazole, (Sporanox), ketoconazole (Nizoral), leflunomide (Arava), lovastatin (Mevacor), methotrexate (Rheumatrex), nevirapine (Viramune), niacin, nitrofurantoin (Macrodantin), pioglitazone (Actos), pravastatin (Pravachol), pyrazinamide, rifampin (Rifadin), ritonavir (Norvir), rosiglitazone (Avandia), simvastatin (Zocor), tacrine (Cognex), tamoxifen, terbinafine (Lamisil), valproic acid, and zileuton (Zyflo).

Potentially Hepatotoxic Botanicals and Nutritional Supplements: Kava can adversely affect the liver in susceptible poor metabolizers, , patients whose cytochrome P450 2D6 (CYP2D6) isozyme is underactive. Theoretically, concomitant use with other potentially hepatotoxic products might increase the risk of developing liver damage. Potentially hepatotoxic botanicals include chaparral, comfrey, germander, pennyroyal oil, skullcap and valerian. Potentially hepatotoxic nutritional supplements include androstenedione, coenzyme Q10 (only in high doses), DHEA, niacin, and red yeast.

Sedative Botanicals and Supplements: Theoretically, concomitant use might increase risk of excessive drowsiness. Potentially sedative botanicals include calamus, calendula, California poppy, catnip, capsicum, celery, couch grass, elecampane, German chamomile, goldenseal, gotu kola, hops, Jamaican dogwood, lemon balm, melatonin, sage, St. John

‘s wort, sassafras, scullcap, shepherd
‘s purse, Siberian ginseng, stinging nettle, valerian, wild carrot, wild lettuce, ashwaganda root, and yerba mansa. Potentially sedative nutritional supplements include 5-HTP.

Alprazolam: One report has been made of an individual who was hospitalized due to lethargy and disorientation that occurred when alprazolam and kava were used concomitantly.

CNS Depressants: Concomitant use of kava and alcohol, barbiturates, benzodiazepines, and other CNS depressants can increase the risk of drowsiness and motor reflex depression.

Levadopa (Larodopa, Dopar): Kava may have dopamine antagonist activity and might therefore decrease the effectiveness of levodopa. In one reported case, kava seemed to reduce efficacy of levodopa.

Alcohol: Concomitant use with alcohol can increase the risk of kava side effects such as drowsiness and motor reflex depression. In addition, concommitant use of kava with alcohol can increase risk of hepatotoxicity, particularly in patients with genetic deficiency in the cytochrome P450 2D6 (CYP2D6) isozyme.


In mice, the LD50 for oral administration of dihydrokavain was 920 mg/kg and for dihydromethysticin was 1050 mg/kg.

Doses of 50 mg/kg of dihydrokavain three times a week for three months to rats produced no evidence of chronic toxicity.

For standardized kava extract containing 70% kavalactones the following LD50 values have been recorded: 16 g/kg (oral, rats), 1.8 g/kg (oral, mice), 370 mg/kg (intraperitoneal, rats) and 380 mg/kg (IP, mice).


Parkinsons Disease: No side-effects have been reported using standardized kava extracts at recommended levels in the clinical studies; however, several case reports have been presented indicating that kava, even at typical doses, may have dopamine antagonist activity, thus worsening Parkinsons disease. Until this issue is resolved, kava extract should not be used in Parkinsons patients.

Pregnancy: Kavalactones might cause loss of uterine tone, so kava should be avoided during pregnancy.

Lactation: Kavalactones might pass into breast milk and could, theoretically, have toxic effects on neonates or infants.

Depression: Kava should be used with caution in depressed patients since it appears to have CNS sedative effects and might theoretically exacerbate depression in some patients.

Hepatitis: Kava might adversely affect liver function, especially if taken for prolonged periods or at high doses. Patients with a recurrent history of hepatitis should not use kava even short-term in normal doses as it might exacerbate hepatitis. Patients with active hepatitis or a history of hepatitis should avoid kava.

Genetic (CYP2D6) Isozyme Susceptibility: Patients with genetic deficiency in the cytochrome P450 2D6 (CYP2D6) isozyme may be at increased risk for hepatotoxicity from kava and should avoid its use.