Piper methysticum Forst.  (Piperaceae).  The common name is kava or kava kava.

Kava was not known to the Western world until the eighteenth century when explorers discovered the islands of Oceania that include Polynesia, Melanesia and Micronesia.  The native people of these islands did not have alcoholic beverages, but instead had kava that was used for religious, ceremonial and social purposes.  It was part of the cultural practices, myths and legends of all the Pacific Islands except New Zealand, New Caledonia and most of the Solomons.  The earliest origin of the kava plant seems to be in the New Guinea-Indonesia areas.  It is still extensively used in the South Pacific, generally with a ceremonial attitude and purpose.  It was also used medicinally, particularly in Hawaii.  It was used to soothe nerves, to promote relaxation and sleep, to counteract fatigue, for congestion of the urinary tract, asthma, rheumatism, weight loss, gonorrhea, and other purposes.

Captain James Cook is credited with introducing kava to Europe in 1768.  By the middle of the nineteenth century scientists began taking an interest in kava and began the process of identifying the chemical group of kava pyrones.1

Kava is a member of the black pepper family, Piperaceae.  It is a large perennial shrub growing up to six feet tall, forming dense thickets.  The leaves are heart-shaped with woody jointed stems.  It requires a warm, moist climate and rich soils.

The root and rhizome are the parts used.  It is available as bulk herb, capsule, and hydroalcoholic extract.  Frequently found in formulas with other herbal relaxants and antidepressants.

There are a group of constituents, collectively called kava lactones or kava pyrones that are thought to be the active ingredients of kava.  The whole plant has been shown to be more effective than the isolated ingredients, however.  Studies have indicated that kava lactones have anxiolytic, analgesic, muscle-relaxing and anticonvulsive effects.   It is used for the treatment of anxiety and nervous tension.   It actually appears to enhance cognitive abilities.2

Studies have shown different results as to whether kava binds to GABA receptors, this could be because of variance in chemical constituents depending on where the plant was grown and other variables.  If there is any binding of GABA sites, it appears insignificant.  Kava does effect the amygdalar complex of the limbic system, which would explain its promotion of sleep without apparent sedation. 3   There is a CNS effect of muscle relaxation and it also has anticonvulsant properties.  It also has antiviral effects.4

The German Commission E recommends kava for conditions of nervous anxiety, stress and restlessnes.5  It is used for menopause, insomnia, depression and as a muscle relaxant.  It is used for its analgesic effects especially as an oral anesthetic because it numbs the mucous membranes.

The kava pyrones are the primary pharmacologically active constituents and good quality rhizomes contain between 5.5 and 8.3%.  These consist of  both water soluble and resinous (lipid soluble) components of dihydrokavin, methysticin, dihydromethysticin, kavain, yangonin, demethoxyyangonin, yangonic acid, cinnamic acids and yangono.6

The German Commission E recommends a daily dosage of 60-120 mg kava pyrones.

Occasional gastric disturbances have been reported.  Intake of large quantities of  kava can lead to a dry, scaly skin rash known as kava dermopathy.  This was first observed in natives of Oceania who used kava on a regular basis, their entire body would be scaly.  It was considered by the natives as a sign of privilege or nobility, as only certain classes were allowed to partake of kava.7  This was thought to be a niacin deficiency, but studies have shown this not to be the cause.8  Kava was introduced into Australia to the Aboriginal population, hoping it would cut down on alcohol consumption.  It quickly became a substance of abuse and sever dermopathy symptoms became evident.  The dermopathy clears with the discontinuation of kava consumption.

Kava is contraindicated in pregnancy and nursing, and endogenous depression.  There is the possibility of kava potenizing the effects of substances that act on the CNS such alcohol, barbiturates and psycopharmalogical agents.  Patients taking benzodiazepine or alprazolam should not take kava.

 


1 Singh,Yadhu N. “Kava: an overview”. Journal of Ethnopharnacology; 37(1). 1992. 13-45.

2 Brown, Donald J, ND. “Kava Kava Clinical Monograph”.  Townsend Letter for Doctors & Patients. July 1997. 166.

3 “Kava-A Safe Herbal Treatment for Anxiety”. MediHerb Professional Newsletter; 38. April, 1994.

4 Bone, Kerry.  “Kava A Safe Treatment for Anxiety”. Townsend Letter for Doctors. June, 1995. 84-7.

5 Blumenthal, Mark, et al. The Complete German Commission E Monographs. The American Botanical Council. 1998. 156.

6 Willard, Terry PhD. The Wild Rose Scientific Herbal. Wild Rose School of Natural Healing.Ltd. 1991. 190-1.

7 Norton, SA, et al. “Kava Dermopathy”. Journal of the American Academy of Dermatology; 31(1). 1994. 89-97.

8 Ruze P. “Kava-Induced Dermopathy: A Niacin Deficiency?”. Lancet; 335(8703). June 1990. 1442-5