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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
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