| Key uses of kava:
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• Anxiety
• Depression
• Insomnia
General description
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Kava (Piper methysticum) is a
member of the pepper family. It is a hardy, slow-growing perennial that generally
resembles other members of the family Piperaceae. This attractive shrub can attain heights
of more than 3 meters. The plant does not have many leaves, and those are thin, single,
heart-shaped, alternate, petiolate, and 4 to 10 inches long and sometimes wider than they
are long. Although Piper methysticum does flower, it is incapable of
self-reproduction; its propagation is vegetative and solely due to human effort.1,2
The rootstock is used for medicinal purposes. The rootstock is knotty, thick, and
sometimes tuberous, with holes or cracks created by partial destruction of the inner
tissue. In other words, the rootstock is often somewhat pithy. Lateral roots up to 3
meters long extend from the main rootstock.1,2
Chemical composition
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Analysis of the composition of the dried
kava rootstock indicates that it contains approximately 43 percent starch, 12 percent
water, 3.2 percent simple sugars, 3.6 percent proteins, 3.2 percent minerals (primarily
potassium), and 15 percent kavalactones.1,2
On the basis of detailed analyses of kava's active ingredients (a laborious process
spanning the past 110 years), many experts now believe the pharmacological activities of
kava are due mostly, if not entirely, to the presence of the kavalactones (also referred
to as kava alphapyrones). These compounds are found in the fat-soluble resin of the root.
Although the kavalactones are the primary active components, it must be pointed out that
other components appear to contribute to the sedative and anxiolytic activities of kava,
as in one study the sedative activity of a crude preparation was more effective than that
of the isolated kavalactones3. The kavalactone content of the root
can vary between 3 and 20 percent. Therefore, for clinical use, preparations standardized
for kavalactone content are preferred to crude preparations.
History and folk use
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Oceania, that is, the island communities of
the Pacific including Micronesia, Melanesia, and Polynesia, is one of the few areas of the
world that did not have alcoholic beverages before European contact in the eighteenth
century. However, these islanders did possess a "magical" drink used in
ceremonies and celebrations because of its calming effect and ability to promote
sociability. The drink, also called kava, is still used today in this region, where the
people are often referred to as the happiest and friendliest in the world.
The origins of kava usage are not known, as it predates written history in Oceania.1,2
It was first described for the western world by Captain James Cook in the account
of his voyage to the South Seas in 1768. Many myths and legends surround the early use of
kava. The plant itself probably originated in the New Guinea-Indonesia area and was
spread, along with other plants, from island to island by early Polynesian explorers in
canoes. Each culture has its own story on the origins of kava. For example, in Samoa a
story is told about the origins of kava and sugar cane. The story goes that a Samoan girl
went to Fiji, where she married a great chief. After some time, she returned to Samoa, but
before doing so she noticed two plants growing on a hill. A rat was chewing on one of the
plants, and it seemed to fall asleep. She concluded that the plant was a comforting food,
and decided to take this plant (sugar cane) back to Samoa. Then she noticed that the rat
awoke and began to chew the root of another plant-kava. The animal, which had been weak
and shy, became bold, strong, and more energetic. She decided that she would take both
plants back to Samoa. The plants grew very well in Samoa, and soon a chief from a
neighboring island exchanged two laying hens for roots of the two plants. Hence, the
Samoans take credit for the spread of both the sugar cane and kava.
In Tonga, the legend is told of a great chief named Loau, who lived on the island of Eua
Iki and was visited by his servant Fevá anga. Fevá anga wanted to give a feast in honor
of his chief, but it was a time of great famine. In desperation he and his wife killed and
cooked their only daughter to be served to the chief. However, Loau recognized the human
flesh in the food when it was served and would not eat it. He instructed Fevá anga to
bury his daughter, and to bring him the plant that would spring forth. On receiving the
mature plant, Loau instructed that a drink be prepared from it and consumed with due
ceremony.
The Kava Ceremony
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Regardless of exactly how kava originated,
it has been used in ceremonies by the Oceanic people for thousands of years. There are
three basic kava ceremonies: the full ceremonial as enacted on every formal occasion; that
performed at the meeting of village elders, chiefs, and nobles and for visiting chiefs and
dignitaries; and the less formal kava circle common to social occasions1,2.
The first step in any kava ceremony was the preparation of the beverage. A description of
the classic process was given in 1777 by Georg Forster, a young naturalist on James Cook's
second Pacific voyage:1
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[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 naseous stuff as fast as
possible; and some old topers value themselves on being able to empty a great number of
bowls.
This traditional method of preparation was
frowned on or outlawed by colonial governments and missionaries, and more
"sanitary" methods of preparation, involving grinding or grating, took its place
in many parts of Oceania.
The full kava ceremony reserved for very highly honored guests involves leading all of the
guests to a platform. The ceremony begins with the arrival of a group of young men dressed
in ceremonial attire and carrying a bowl of the kava drink and necessary utensils. The
bowl is placed between the kava preparers and the visitors. The kava is placed in a cup by
a specially selected individual, the cup bearer, who then turns and faces the visitor and
delivers the beverage to the chief guest. The guest is instructed to hold the cup with
both hands and drink from it. If the whole cup is drained without stopping, everyone says a
maca (pronounced "a matha," meaning "it is empty") and claps
three times with cupped hands. The cup bearer then refills the kava bowl and proceeds to
serve the person next in rank or importance.
Important people visiting Fiji and other islands of Oceania still participate in 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.
The Effects of Drinking
Kava
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Kava drinkers relate a pleasant sense of
tranquillity and sociability on consumption. Subjective reports given by scientists who
have sampled kava themselves are relatively abundant. One of the first scientific studies
on kava was performed by the noted pharmacologist Louis Lewin in 1886. A later
description, written in 1927, is as follows:1
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 conscious 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.
A more recent description is provided by
researcher R. J. Gregory, who writes from his own experience:1
Kava seizes one's 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
(approximately 100 to 150 milliliters) 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.
Standardized preparations of kava are now gaining greater popularity in Europe and the
United States as mild sedatives and anxiolytics.
Pharmacology
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Many of the the first comprehensive studies
on the activities of kavalactones were conducted by a team of scientists from the Freiburg
University Institute of Pharmacology in Germany, led by Hans J. Meyer, during the 1950s
and 1960s.3 Altogether, this research has determined that
kavalactones exhibit sedative, analgesic, anticonvulsant, and muscle relaxant effects in
laboratory animals. These studies seemed to confirm earlier empirical and subjective
observations.
More recent studies, including those conducted by Dana D. Jamieson and colleagues at the
University of New South Wales, have confirmed and/or elaborated on these effects. Most
notable are the studies demonstrating that kavalactones exert many of their effects by
nontraditional mechanisms. For example, most sedative drugs, including the benzodiazepines
(e.g., Valium, Halcion, and Tranxene), work by binding to specific receptors
(benzodiazepam or GABA [gamma-aminobutyric acid] receptors) in the brain, which then leads
to the neurochemical changes (potentiation of GABA effects) that promote sedation. Studies
in animals have shown that the kavalactones do not bind to benzodiazepam or GABA receptors4.
Instead, the kavalactones somehow modify receptor domains rather than interact
specifically with receptor-binding sites. In addition, other studies have indicated that
the kavalactones appear to act primarily on the limbic system-an ancient part of the brain
that affects all other brain activities and is the principal seat of the emotions.5
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 used
to identify how a substance promotes a calming effect are simply not sophisticated enough
to evaluate the kavalactones.
In another example of the uncharacteristic pharmacological qualities of kava, a study
designed to evaluate its pain-relieving effects could not demonstrate any binding to
opioid receptors.6 The significance of this finding is that the
study used models in which nonopiate analgesics such as aspirin and other nonsteroidal
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. What all
of these findings mean is that kava reduces pain in a manner unlike morphine, aspirin, or
any other pain reliever.
An interesting effect of kava compared to many anxiolytic drugs is that, unlike the drugs,
kava does not lose effectiveness with time. Loss of effectiveness of a drug is known as
"tolerance." Kavalactones, even when administered in huge amounts, demonstrated
absolutely no loss of effectiveness in animal studies.7 Again, this
is another example of the uncharacteristic qualities of kava.
Another pharmacological activity of kava worth mentioning is its ability to protect
against brain damage due to ischemia.8 This effect has been
demonstrated in two animal models of focal cerebral ischemia. The effectiveness of the
kavalactones was due to their ability to limit the infarct area as well to a mild
anticonvulsant effect. Kava extract may prove useful in recovery from a stroke.
Clinical applications
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Several European countries have
approved kava preparations in the treatment of nervous anxiety insomnia, and restlessness
on the basis of detailed pharmacological data and favorable clinical studies.
Earlier clinical trials used DL-kavain, a purified kavalactone, at a dose of 400
milligrams per day. For example, in one double-blind placebo-controlled study of
eighty-four patients with anxiety symptoms, kavain was shown to improve vigilance, memory,
and reaction time.9 In another double-blind study, kavain was
compared to the drug oxazepam (a drug similar to diazepain or Valium) in thirty-eight
patients.10 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 produce side
effects, kavain appeared to be free of these complications.
More recent studies have featured well-defined kava extracts. As mentioned earlier,
evidence suggests that the whole complex of kavalactones together with other compounds
naturally found in kava produce greater pharmacological activity. In addition, studies
have shown that kavalactones are more rapidly absorbed when given orally as an extract of
the root rather than as isolated kavalactones. The bioavailability of lactones, as
measured by peak plasma concentrations, is up to three to five times higher from the
extract than when given as isolated substances.3 Further
evidence that kava root extracts are superior to isolated kavalactones is offered by an
animal study11; in this study isolated kavalactones were taken up
well by brain tissue, but when a crude kava preparation was given the concentration of
lactones was two to twenty times higher.11 From this evidence it
appears that crude extracts standardized for kavalactone content may offer the greatest
therapeutic benefit.
Several clinical trials have featured a special kava extract standardized to contain 70
percent 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
dose of kavalactones and the assurance that the full range of kavalactones is present.
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In perhaps the most significant study, a 70
percent kavalactone extract was shown to exhibit significant therapeutic benefit in
patients suffering from anxiety.12 In this double-blind study,
twenty-nine patients were assigned to receive 100 milligrams of the kava extract three
times daily while another twenty-nine 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 twenty women with menopause-related symptoms
were treated for a period of 8 weeks with a 70 percent kavalactone extract (100 milligrams
three times daily) or placebo.13 The target variable was once again
the Hamilton Anxiety Scale. The group receiving the kava extract demonstrated significant
improvement at the end of the very first week of treatment. Scores continued to improve
over the course of the 8-week study. In addition to improvement in symptoms of stress and
anxiety, a number of other symptoms also improved. Most notably, there was an overall
improvement in subjective well-being, mood, and general symptoms of menopause including
hot flashes. Again, no side effects were noted.
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Two 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.14,15
In one of these studies twelve healthy volunteers were tested in a
double-blind, cross-over manner to assess the effects of oxazepam (placebo on days 1-3, 15
milligrams on the day before testing, 75 milligrams on the morning of the experiment), an
extract of kava standardized at 70 percent kavalactones (200 milligrams three times daily
for 5 days), and a placebo on behavior and event-related potentials in
electroencephalograph readings in 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 event-related potential.
In contrast, kava showed a slightly increased recognition rate and a larger event-related
potential difference between old and new words. The results of this study once again
demonstrate the uncharacteristic effects of kava; in this case it reduced anxiety, but
unlike standard anxiolytics, kava actually improves mental function and at the recommended
levels does not promote sedation.
Dosage
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The appropriate dose of a kava
preparation depends on the level of kavalactones. On the basis of clinical studies using
pure kavalactones or kava extracts standardized for kavalactones, the dosage
recommendation for anxiolytic effects is 45 to 70 milligrams of kavalactones three times
daily. For sedative effects, a dose providing 180 to 210 milligrams of kavalactones can be
taken I hour before retiring.
To put the therapeutic dosage in perspective, remember that a standard bowl of
traditionally prepared kava drink contains approximately 250 milligrams of kavalactones
and several bowls may be consumed at one sitting.
Toxicity
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Although no side effects have been reported
when using standardized kava extracts at recommended levels, it is possible that side
effects may present themselves at high doses. High doses of kava beverage consumed daily
over a prolonged period (a few months to a year or more) is associated with "kava
dermopathy"-a condition of the skin characterized by a peculiar, generalized scaly
eruption known as kani. 16 The skin becomes dry and covered with
scales, especially the palms of the hand, soles of the feet, forearms, the back and shins.
It was thought at one time that kava dermopathy may be due to interference with niacin.
However, in one double-blind, placebo-controlled study no therapeutic effect with
niacinamide (100 milligrams daily) could be demonstrated.17 It
appears that the only effective treatment for kava dermopathy is reduction or cessation of
kava consumption. Again, no reported cases of kava dermopathy have been noted in
individuals taking standardized kava extracts at recommended levels.
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Other adverse effects following the
consumption of extremely high doses of kava (e.g., more than 310 grams per week) for
prolonged periods include biochemical abnormalities (low levels of serum albumin, protein,
urea, and bilirubin), the presence of blood in the urine, increased red blood cell volume,
decreased platelet and lymphocyte counts, and shortness of breath.18 The
attribution of these adverse effects to kava is questionable, because the subjects also
reported heavy alcohol and cigarette usage. Nonetheless, high doses of kava are
unnecessary and should not be encouraged.
References
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1. Lebot V, Merlin M, and Lindstrom
L: Kava: The Pacific Drug. Yale University Press, New Haven, CT, 1992.
2. Singh Y. Kava: An overview. J Ethnopharmacol 37, 13-45, 1992.
3. Meyer HJ: Pharmacology of kava. In: Ethnopharmacological Search for Psychoactive
Drugs (Holmstedt B and Kline NS, eds.). Raven Press, New York, 1979, pp. 133-140.
4. Davies LP, et al.: Kava pyrones and resin: Studies on GABAa, GABAb
and benzodiazepine binding sites in rodent brain. Pharm Toxicol 71, 120-126,
1992.
5. Holm E, et al.: Studies on the profile of the neurophysiological effects of D,L-kavain:
Cerebral sites of action and sleep-wakefulness-rhythm in animals. Arzneimittel-Forsch
41, 673-683, 1991.
6. Jamieson DD and Duffield PH: The antinociceptive action of kava components in mice. Clin
Exp Pharmacol Physiol 17, 495-508, 1990.
7. Duffield PH and Jamieson D: Development of tolerance to kava in mice. Clin Exp
Pharmacol Physiol 18, 571-578,1991.
8. Backhauss and Krieglstein J: Extract of kava (Piper methysticum) and its
methysticum constituents protect brain tissue against ischemic damage in rodents. Eur
J Pharmacol 215, 265-269, 1992.
9. Scholing WE and Clausen HD: On the effect of dl-kavain: Experience with neuronika. Med
Klin 72, 1301-1306,1977.
10. Lindenberg D and Pitule-Schodel H: D,L-Kavain in comparison with oxazepam in anxiety
disorders. A double-blind study of clinical effectiveness. Forschr Med 108,
49-50, 53-54, 1990.
11. Keledjian J, et al.: Uptake into mouse brain of four compounds present in the
psychoactive beverage kava. J Pharm Sci 77, 1003-1006, 1988.
12. Kinzler E, Kromer J, and Lehmann E: Clinical efficacy of a kava extract in patients
with anxiety yn drome: Double-blind placebo controlled study over 4 weeks. Arzneimittel-Forsch
41, 584 -588, 1991.
13. Warnecke G: Neurovegetative dystonia in the female climacteric. Studies on the
clinical efficacy and tolerance of kava extract WS 1490. Forschr Med 109,
120-122, 1991.
14. Herberg, K.W. The Influence of kava-special extract WS 1490 on safety-relevant
performance alone and in combination with ethyl alchol. Blutalkohol 30, 96-105,
1993.
15. Munte TF, et al.: Effects of oxazepam and an extract of kava roots (Piper
methysticum) on event-related potentials in a word recognition task. Neuropyschobiology
27, 46-53, 1993.
16. Norton SA and Ruze P: Kava dermopathy. J Am Acad Dermatol 31, 89-97,1994.
17. Ruze P: Kava-induced dermopathy: A niacin deficiency. Lancet 335, 1442-1445,
1990.
18. Mathews JD, et al.: Effects of the heavy usage of kava on physical health: Summary of
a pilot survey in an aboriginal community. Med J Aust 148, 548-555,1988.
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