STUDY OF KAVA WATER EXTRACT CONSUMPTION

BY ABORIGINES IN AUSTRALIA  

            reviewed by Francis Brinker, N.D.

J.D. Mathews, M.D. Riley, L. Fejo, E. Munoz, N.R. Milns, I.D. Gardner, J.R. Powers

(The Menzies School of Health Research);

E. Ganygulpa, B.J. Gununuwawuy

(Northern Territory Department of Health and Community Services).

“Effects of the heavy usage of kava on physical health: summary of a pilot survey in an Aboriginal community,” The Medical Journal of Australia, vol. 148, pp. 548-555, June 6, 1988.

        With the controversy over potential adverse effects of kava (Piper methysticum) preparations on the liver, it is useful to consider evidence as it applies to the use of water extracts of kava root and rhizomes, since this is the traditional form used in the South Pacific. This retrospective study is the only one that compares the effects of long-term regular use of kava with a matched control group. However, the practices documented in this report lie outside of the traditional Polynesian context of ceremonial and social use of fresh kava root juice in water. Also, a high level of morbidity apart from kava consumption existed in the community studied.

        In the early 1980s kava was introduced as a beverage to an Australian Aboriginal community in Arnhem Land in an attempt to replace rampant alcohol abuse. Alcohol use was banned in this community, and as a result the consumption of kava water extract became common. About 80% of the men and 20% of the women drank kava. In 1987 a survey of the kava use of 73 members of this community was carried out. All male non-users in the community were included and age-matched randomly with 1 of 4 of the male users; all female users were studied and age-matched randomly with 1 of 4 of the female non-users. All subjects were over age 16.

        Individual users estimated the grams (gm) of dried kava powder extracted with cold water and drunk each week, and health workers familiar with the subjects ranked the users by consensus. There were four distinct patterns of kava consumption in those studied: 34 were non-users, 4 were occasional users (100 gm/week on average), 15 were heavy users (310 gm/week ave., up to 600 gm/week), and 20 were very heavy users (440 gm/week ave., up to 900 gm/week). Consumption levels were corroborated by urinalysis. The per-capita kava consumption of this community appeared to be greater than that in the South Pacific. Within each category of users, men tended to drink more kava than women. Cigarette smoking was prevalent, but petrol-sniffing was no longer practiced. Alcohol use over the previous year was rare (19% of subjects admitted drinking, but less than once monthly) and took place at distant sites, though some kava users had drunk alcohol heavily prior to 1980.

        A variety of physical and biochemical parameters were studied in these individuals for comparison. The only physical signs and symptoms with a steadily increasing frequency with increasing kava usage were weight loss, skin rash, and red eyes. The only laboratory chemical signs indicating a highly significant trend with increasing kava use were non-acidic urine (pH > 6.5), dilute urine (specific gravity < 1.010), increased average red blood cell hemoglobin content and volume, diminished plasma urea and bilirubin, and increased plasma levels of gamma-glutamyl transferase (GGT).

        Only the GGT elevation was clearly outside of normal variation ranges. The high GGT levels in heavy and very heavy kava users were considered strong circumstantial evidence for potential kava hepatotoxicity. This enzyme elevation did not correlate with hepatitis B surface antigen carriers. GGT elevations within each group were greater in men than in women, including the non-user group. The male occasional users had GGT levels slightly above normal but not greatly in excess of the male non-users. GGT was normal in female occasional users and actually lower than female non-users, even though average daily use was equivalent to a half-ounce (over 14 grams) dried kava root extracted daily. Greatly elevated GGT was only seen at the heavy consumption level of over 44 grams of kava powder (about an ounce and a half) extracted daily. In addition, both male and female very heavy users had lower GGT levels than heavy users, though consuming on average 42% more (an additional 18.5 grams daily, or a total of over 62 grams dried root extracted) each day.

Reviewer’s Observations

       The conclusions based on this study are not entirely clear, due to uncertainty about a number of important parameters. These include the complicating influence of malnutrition and duration of kava use, which appeared to be for years in this group. Another concern is the accuracy of the estimated consumption, and the range of consumption within each category. Also, the relative potency of the kava powder used is not defined in terms of content of total kavalactones, nor is the cultivar(s) with its specific kavalactone chemical profile known. The methods of extracting the kava also varied somewhat between individuals, and it is uncertain what percentage of kava lactones in the dried kava were effectively extracted. It does seem, however, that abusive consumption of kava caused some toxic effect on the liver. At what level of intake does this become a realistic concern?

        Making conservative assumptions in an attempt to assess the general kavalactone exposure in the Aborigine community can lead to some pertinent estimations. Given that the total kavalactone content of the kava powder could have been as low as 5% (though kava roots/rhizomes typically have up to 4.5 times this much, ranging from 5% to 22%) and that only half of these lactones are usually extracted by the cold water (2.5% of dried kava weight, or 25 mg kavalactones consumed for each gram of kava powder used), this would lead to a minimum total kavalactone consumption of 350 mg daily for the occasional user (25 mg lactones per gram times 14 grams = 350 mg). Following these same assumptions, the estimated kavalactone intake of the heavy user would be at least 1100 mg, while the very heavy Aborigine user was consuming over 1550 mg of kavalactones daily. These levels of consumption may have occurred for up to five years or more with no physical signs or symptoms directly indicative of liver toxicity, which was suggested only by an elevated GGT enzyme level.

        Even the relatively safe level of intake of the occasional Aborigine water extract user (minimum 350 mg kavalactones on average daily) is well in excess of the maximum recommended dosage as found in concentrated standardized extracts of kava root made with chemical solvents. These standardized extracts typically contain 60% to 70% kavalactones. A dosage of 60-70 mg of kavalactones two or three times daily, or 120-210 mg kavalactones per day is usually recommended on product labels. Total kavalactone intake slightly above this range, over 240 mg per day, for even a few weeks or months has been implicated by some in the phytopharmaceutical industry as a possible cause of reported hepatotoxicity using these concentrated extracts.

        It seems apparent from comparison of these different extracts that the cause of hepatotoxicity is not merely one of total kavalactone intake, but must be associated with specific components. The responsible compound(s) could be derived from either large amounts of water extracts or relatively small amounts of concentrated chemical solvent extracts. Otherwise, if total kavalactone consumption itself were the only cause for adverse liver effects, a great many inhabitants of Polynesia, where water extracts are consumed in relatively large quantities regularly over a lifetime for generations, would necessarily be suffering from overt endemic liver failure.

        The differences between these two completely different types of kava preparations are great enough to not assume toxicological equivalence on the basis of total kavalactone content. If perhaps unusual metabolism of kavalactones is a major contributing factor in hepatotoxic outcomes, then the influence of other components in the water extract that are not in the chemical solvent extract, or vice versa, could significantly modify the metabolic process. The metabolic breakdown products of the specific kavalactones could also account for their different beneficial or toxic effects.

        Aside from the type of preparation, the type of cultivar is very important when considering the effects and appropriate duration of kava use. Specific kavalactones are known to have different effects, and their proportions vary between cultivars as shown by the particular chemical profiles. For example, the tudei (2-day) cultivars are not used daily in Vanuatu, the ancestral home of kava, because they are considered too potent. Their chemical profile is high in the kavalactone dihydromethysticin. The cultivar borogu is preferred for daily use; it is high in the kavalactone kavain and low in dihydromethysticin. (The cultivar kelai, which is even higher in kavain and lower in dihydromethysticin, is reputed to have even more pleasant effects.) So, to achieve the same level of exposure to the potent dihydromethysticin, much greater consumption of a preparation from borugu would be required than if tudei were used.