Ava, awa, intoxicating pepper, kava-kava, kava pepper, kawa, kawa-kawa, kew, Piper methysticum, sakau, tonga, yagona
Kava has been an important part of the Pacific island ceremonial cultures for many centuries, where its main use has been to induce relaxation in kava ceremony participants. Obtained from dried rhizome and root of Piper methysticum, a member of the black pepper family (Piperaceae), kava is used to make the beverage of the same name. Kava contains seven major and several minor kava lactones, both aqueous and lipid soluble. Pharmacologic effects result from lipid soluble lactones. Their mechanism of action differs from that of benzodiazepines and opiate-agonists. Kava affects the limbic system, modulating emotional processes to produce anxiolytic effects. Kava lactones inhibit MAO type B, producing psychotropic effects. They also inhibit voltage-gated calcium and sodium channels, producing anticonvulsant and skeletal muscle relaxant effects. The kava lactone, kawain, inhibits cyclooxygenase and thromboxane synthase, producing antithrombotic effects on human platelets.
Kava is available as liquid extract, capsules, soft gel caps, liquid spray, and tea bags, in products such as Kavacin, Kava Tone, and St. John’s Plus Kava Kava.
Kava is used orally to treat nervous anxiety, stress, and restlessness. It’s used as a sedative, and to treat headaches, seizure disorders, the common cold, respiratory tract infection, tuberculosis, and rheumatism. Kava is also used to treat urogenital infections including chronic cystitis, venereal disease, uterine inflammation, menstrual problems, and vaginal prolapse. Some herbal practitioners consider kava an aphrodisiac. Kava is used orally to promote wound healing. Kava juice is used topically to treat skin diseases, including leprosy. It’s also used as a poultice for intestinal problems, otitis, and abscesses.
- Anxiety: Dosage is 50 to 70 mg purified kava lactones three times a day, equivalent to 100 to 250 mg of dried kava root extract per dose. (By comparison, the traditional bowl of raw kava beverage contains about 250 mg of kava lactones.)
- Restlessness: Dosage is 180 to 210 mg of kava lactones taken as a tea 1 hour before bedtime, or 1 cup three times a day. Tea is prepared by simmering 2 to 4 g of the root in 5 oz boiling water for 5 to 10 minutes, and then straining.
Kava causes mild euphoric changes characterized by feelings of happiness, fluent and lively speech, and increased sensitivity to sounds. Adverse effects of kava include morning fatigue, headache, drowsiness, impairment of motor reflexes, visual accommodation disorders, pupil dilation and disorders of oculomotor equilibrium, mild GI disturbances, mouth numbness, hematuria, increased RBC count, decreased platelets and lymphocytes, pulmonary hypertension, scaly rash with chronic use, and reduced levels of albumin, total protein, bilirubin, and urea with chronic use.
Possible additive effects may occur when kava is used with antiplatelet drugs or MAO type B inhibitors. Kava lactones potentiate the effects of central nervous system (CNS) depressants, leading to t?xicity. Kava may cause reduced effectiveness of levodopa therapy in patients With Parkinson’s disease, apparently be cause of dopamine antagonism. Use of kava with calamus, calendula, California poppy, capsicum, catnip, celery, couch grass, elecampane, German chamomile, golden seal, gotu kola, hops, Jamaica dogwood, lemon balm, sage, sassafras, shepherd’s purse, Siberian ginseng, skullcap, stinging nettle, St. John’s wort, valerian, wild lettuce, or yerba mate may lead to additive sedative effects. There’s an increased risk of CNS depression and liver damage when kava is used with alcohol.
Patients hypersensitive to kava or any of its components should avoid use. Depressed patients should avoid kava because of possible sedative activity; those with endogenous depression should avoid it because of possible increased risk of suicide. Pregnant women should avoid kava because of possible loss of uterine tone; those who are breast-feeding should also avoid it. Children younger than age 12 shouldn’t use kava.
- Patients shouldn’t use kava with conventional sedative-hypnotics, anxiolytics, MAO inhibitors, other psychopharmacologic drugs, levodopa, or antiplatelet drugs without first consulting health care provider.
- Adverse effects of kava are minimal at therapeutic dosages, and may occur at start of therapy but are transient.
- Oral use is probably safe for 3 months or less; use for longer than 3 months may be habit forming.
- Kava can cause drowsiness and may impair motor reflexes.
- Patients should avoid taking kava with alcohol because of increased risk of CNS depression and liver damage.
- Periodic monitoring of liver function tests and CBC may be needed.
- Heavy kava users are more likely to complain of poor health. Some 20% of these patients are underweight with reduced levels of albumin, total protein, bilirubin, urea, platelets, and lymphocytes. They demonstrate increased HDL cholesterol and RBCs, hematuria, puffy faces, scaly rashes, and some evidence of pulmonary hypertension. These symptoms resolve several weeks after kava is stopped. Extreme use (more than 300 g per week) may increase gamma-glutamyl transferase levels. Toxic doses can cause progressive ataxia, muscle weakness, and ascending paralysis, all of which resolve when kava is stopped.
- Encourage patients to seek medical diagnosis before taking kava.
- Tell patient to notify pharmacist of any herbal and dietary supplements that he’s taking when obtaining a new prescription.
- Advise patient to consult his health care provider before using an herbal preparation because a conventional treatment with proven efficacy may be available.
Kava lactones are responsible for its mild sedative effects, which are additive with alcohol or benzodiazepines. Kava root is approved for conditions of nervous anxiety, stress, and restlessness by the German Commission E, and has also been presented in British pharmaceutical journals. However, it shouldn’t be used for more than 3 months at a time.