Introduction

In Pacific island societies, kava (Piper methysticum Forst. f.) has been used for centuries as aqueous extracts of the plant's crushed roots or lower stems (Brunton, 1989; Lebot et al, 1997). Aboriginal Australians in Arnhem land (Northern Territory, NT) have used it in similar ways since 1982 when it was first brought from the Pacific (Cawte, 1985; Clough et al, 2000). A possible association between heavy kava use and sudden death in Aboriginal Australians is an unresolved concern (Young et al, 1999). While clinical observation suggests that sudden deaths have occurred in Arnhem Land among heavy kava users, no clear evidence for increased risk of ischaemic heart disease was found in a recent case–control study (unpublished data) or of atherogenesis in a cross-sectional study (Clough et al, 2003). Poor nutrition, which contributes to high rates of coronary heart disease (CHD) in Aboriginal Australians (Thomson, 1991; Rowley et al, 2001), may add to this concern.

In one Arnhem Land community, 6 y after kava was introduced, 'heavy' and 'very heavy' kava users showed signs of malnutrition with 20% lower body weight and 50% less subcutaneous fat (Mathews et al, 1988). These same kava users had unusual lipid profiles with elevated high-density lipoprotein (HDL) cholesterol (Mathews et al, 1988). In a recent study, continuing kava users were compared with less regular users and a group of nonusers. Lower body mass index (BMI), higher total cholesterol and a tendency for higher HDL-cholesterol were found in kava users, while other CHD risk markers (C-reactive protein and homocysteine) were generally elevated (Clough et al, 2003).

This short report seeks to clarify the inter-relationships between kava use, biomarkers of dietary quality and CHD risk, and nutritional status.

Methods

In March 2000, a sample of 98 people (62 males, 36 females) was opportunistically recruited in an eastern Arnhem Land Aboriginal community (340 people aged >15 y). Of these, 32 males and four females reported using kava; 17 males and nine females had ceased using it 1 y before the study, while 13 males and 23 females never used kava. Self-reported kava consumption was confirmed by knowledgeable Aboriginal health workers and documentary evidence. Details of the study setting, methods for assessing exposure to kava and other substance use (alcohol, tobacco, and cannabis), and ethical approvals are described elsewhere (Clough et al, 2003). Participants gave written informed consent with procedures explained by health workers.

Sitting and standing heights (stadiometer) and skinfold thicknesses (calipers) were measured and BMI was calculated (Wang et al, 2001). Per cent body fat was measured using a Tanita Body Fat (TBF 521) instrument. Plasma samples (nonfasting) were analysed for lipids (Clough et al, 2003), carotenoids and micronutrients (Rowley et al, 2001).

Variations in continuous outcomes across kava using groups were tested using general linear modelling including tests for a linear trend (SPSS V-11.0). Models included kava use (never, former and current) and gender as fixed factors and, for lipid-soluble antioxidants, plasma cholesterol as a covariate. Data for triglycerides, homocysteine, triceps and subscapular skinfold thicknesses, folate, - and -tocopherol and carotenoids were skewed and were reported as geometric mean (95% confidence interval).

Results

In all, 53% of continuing kava users and just 4% (n=1) of past users (P<0.001) showed dermopathy characteristic of prolonged use (Norton & Ruze, 1994). Adjusted for age, cholesterol levels beyond a reference range indicating increased CHD risk (Table 1) were more likely in continuing kava users than in never users for total cholesterol (OR=2.9, 1.2–7.0, P=0.005) and low-density lipoprotein (LDL) (OR=2.5, 1.4–4.5, P=0.001), but less likely for HDL (OR=0.4, 0.2–0.7, P=0.001).

Table 1 - Coronary risk profile of survey participants stratified by kava use.

Full table

Table 1 shows the following. Total-, LDL- and HDL-cholesterol levels were highest in kava users and lowest in never users. Elevated HDL was less evident in kava users who had abstained for at least 1 y. BMI varied significantly by kava use with a nonsignificant tendency for a linear decrease. There were significant linear decreases in percent body fat and subscapular skinfold thickness, but not midupper-arm circumference, across never, former and current kava use categories. Triceps skinfold varied significantly by kava usage, with no evidence of a linear trend. Compared to never users, current kava users had a significantly lower percent body fat (P=0.031) and subscapular skinfold thickness (P=0.027).

Table 2 shows that plasma levels of carotenoids were extremely low compared to other populations (Ito et al, 1990; Ford & Giles, 2000) for example, they were approximately one-quarter of the carotenoid levels in non-Aboriginal subjects from Melbourne (unpublished data). The average retinol and -tocopherol concentrations were within normal ranges, but not particularly low relative to other populations and did not vary by kava usage. After adjustment for plasma cholesterol levels, there were no differences between kava users and nonusers for these biomarkers of dietary quality (with the exception of -tocopherol). High-plasma homocysteine levels across all groups were consistent with low dietary folate intake and increased CHD risk.

Table 2 - Dietary markers stratified by kava use.

Full table

Discussion

The loss of total and upper body fat (indicated by low percent body fat and subscapular skinfold thickness, respectively) was striking among current kava users compared to those who had never used it and this remained evident in former users. Although kava users had a significantly lower body fat, low levels of biomarkers of dietary quality that were similar to those already reported for other Aboriginal Australian populations (Lee et al, 1995; Rowley et al, 2001), were not further compromised in kava users. Loss of body fat in kava users has been described as similar to that in anorexia nervosa (Mathews et al, 1988, p 545). In Pacific island kava drinkers evidence for such weight loss, by contrast, is equivocal (Frater, 1952; Ruze, 1990), which along with kava's association with feasting in Pacific traditions (Holmes, 1967; Singh, 1992), implies the likely influence of social factors. Psychosocial factors are plausible causal agents for loss of body fat and are further indicated in Aboriginal Australian kava drinkers. For example, some Arnhem Land aboriginal people have used kava continuously for up to 18 y (Clough et al, 2003) and unpublished participants' observations suggest that drinkers even constrain their eating in order to maximise kava's mood-altering effects. Therefore, notwithstanding possible economic deprivation and appetite suppression in kava users, an obsession with kava drinking may be a significant contributing factor.

While we could not identify associations of kava use with carotenoids, antioxidant vitamins, folate and homocysteine, concentrations of carotenoids and homocysteine were adversely low in all groups and suggested a severe lack of cardioprotection associated with diets high in vegetables and fruits. We previously reported the tendency for elevated plasma cholesterol, including HDL, associated with kava use, but not triglycerides (Clough et al, 2003). However, the cholesterol levels in kava users were unremarkable relative to cholesterol levels in Caucasian populations. While a low HDL in kava users was less likely, the ratio of LDL–HDL cholesterol (data not shown) did not differ across kava-using groups (P_ANOVA=0.591, P_{linear trend}=0.872).

Tobacco, cannabis, and alcohol users generally had cholesterol levels within a reference range. Alcohol was used by 48% of participants and cannabis by 40% and both were associated with kava use (Fisher's exact P<0.001, data not shown). Tobacco was used by 83% of participants but was not associated with kava use (Clough et al, 2003) (Fisher's exact P=0.110, data not shown) and generally low antioxidant levels did not vary across kava-using groups (Table 2). Nonetheless, greater risk of atherogenesis in kava users is biologically plausible if there is a greater proportion of small, dense LDL particles that may be more susceptible to oxidative modification, especially in the absence of adequate antioxidant levels, with possible additional tobacco-related CHD risk.

Confounding effects of excess alcohol use on lipid metabolism are possible (Stone, 1994). Strong confounding effects seem unlikely, however, since triglycerides were not elevated overall (Table 1). Not all alcohol users in the sample used it excessively. Health workers described 44% of alcohol users as 'heavy' users, that is, using >318 g/month of pure alcohol (data not shown). While these 'heavy' alcohol users also tended to be less likely to have a low HDL (OR=0.3, 0.1–1.1, P=0.064, age-adjusted), when they were excluded from the analysis, continuing kava users remained less likely to have a low HDL (OR=0.5, 0.3–0.9, P=0.015). There were no associations between cannabis use and cholesterol levels. Drug-induced intrahepatic cholestasis is known to disrupt lipid profiles (Stone, 1994). But it is not known whether the obstructive hepatic response already reported in these same kava users (Clough et al, 2003) could lead to atherogenesis with increased CHD risk (Naschitz et al, 2000). Moreover, liver function changes are not necessarily accompanied by weight loss, unlike the dyslipidaemia of anorexia nervosa (Stone, 1994). Further research is warranted to consider the inter-relationships of these factors with other measures of CHD risk.

In conclusion, although causal mechanisms are not known, we have found kava use to be associated with low body fat and dyslipidaemia. Biomarkers of fruit and vegetable consumption were also very low, but no more so than in other community members. These effects were less evident among former kava users. Thus, while kava use among Aboriginal people is associated with malnutrition this effect is at least partly reversible.

References

1. Brunton R (1989): The Abandoned Narcotic: Kava and Cultural Instability in Melanesia. Cambridge: Cambridge University Press.
2. Cawte J (1985): Psychoactive substances of the south seas: betel, kava and pituri. Aust. NZ J. Psychiatr. 19, 83–87.
3. Clough AR, Burns CB & Mununggurr N (2000): Kava in Arnhem Land: a review of consumption and its social correlates. Drug Alcohol Rev. 19, 319–328.
4. Clough AR, Jacups SP, Wang Z, Burns CB, Bailie RS, McDonald SP, Cairney SJ, Guyula T & Currie BJ (2003): Health effects of kava use in an eastern Arnhem Land Aboriginal community. Int. Med. J. 33, 336–340.
5. Ford ES & Giles WH (2000): Serum vitamins, carotenoids, and angina pectoris: findings from the National Health and Nutrition Examination Survey III. Ann. Epidemiol. 10, 106–116. | Article | PubMed |
6. Frater AS (1952): Medical aspects of yaqona. Trans. Proc. Fijian Soc. 5, 31–39.
7. Holmes L (1967): The function of kava in modern Samoan culture, In Ethnopharmacological Search for Psychoactive Drugs, ed. D Efron, publication no. 1645. Washington: US Public Health Service.
8. Ito Y, Ochiai J, Sasaki R, Suzuki S, Kusuhara Y, Morimitsu Y, Otani M & Aoki K (1990): Serum concentrations of carotenoids, retinol, and alpha-tocopherol in healthy persons determined by high-performance liquid chromatography. Clin. Chim. Acta 194, 131–144. | Article | PubMed |
9. Lebot V, Merlin M & Lindstrom L (1997): Kava, The Pacific Elixir: the Definitive Guide to its Ethnobotany, History and Chemistry, 2nd Edition. Rochester, Vermont: Healing Arts Press.
10. Lee AJ, Bonson APV & Yarmirr D (1995): Sustainability of a successful health and nutrition program in a remote Aboriginal community. Med. J. Aust. 162, 632–635. | PubMed |
11. Mathews J, Riley M, Fejo L, Munoz E, Milns NR, Gardner ID, Powers JR, Ganygulpa E & Gununuwawuy BJ (1988): 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. | PubMed |
12. Naschitz JE, Slobodin G, Lewis RJ, Zuckerman E & Yeshurun D (2000): Heart diseases affecting the liver and liver diseases affecting the heart. Am. Heart. J. 140, 111–120. | Article | PubMed | ISI | ChemPort |
13. Norton SA & Ruze P (1994): Kava dermopathy. J. Am. Acad. Dermatol. 31, 89–97. | Article | PubMed |
14. Rowley KG, Su Q, Concotta M, Skinner M, Skinner K, Pindan B, White GA & O'Dea K (2001): Improvements in circulating cholesterol, antioxidants, and homocysteine after dietary intervention in an Australian Aboriginal community. Am. J. Clin. Nutr. 74, 442–448. | PubMed | ISI | ChemPort |
15. Ruze P (1990): Kava-induced dermopathy: a niacin deficiency? Lancet 335, 1442–1445. | Article | PubMed |
16. Singh Y (1992): Kava: an overview. J. Ethnopharmacol. 37, 13–45. | Article | PubMed |
17. Stone NJ (1994): Secondary causes of hyperlipidemia. Med. Clin. North. Am. 78, 117–141. | PubMed | ISI | ChemPort |
18. Thomson NJ (1991): Recent trends in Aboriginal mortality. Med. J. Aust. 154, 235–239. | PubMed |
19. Wang Z, Hoy W & McDonald S (2001): Body mass index in Aboriginal Australians in remote communities. Aust. NZ J. Public Health 24, 570–575.
20. Young M, Fricker P, Thomson N & Lee K (1999): Sudden death due to ischaemic heart disease in young Aboriginal sportsmen in the Northern Territory, 1982–1986. Med. J. Aust. 170, 425–428. | PubMed |

Acknowledgements

We are grateful to Dr Qing Su and her laboratory staff for carrying out the carotenoid assays. Carotenoid assays were funded by National Health and Medical Research Council, Australia (NHMRC) Grant #981010 and the lipid levels and physical assessments from NHMRC Grant #980434. We thank Dr Chris Burns and Prof Bart Currie for project development and Ms Kath Flyn for data collection and compilation, Mr Terrence Guyula, Roslyn Wunungmurra and Susan Ninikirri for assistance with the research. We declare that the paper's publication creates no conflict of interest. Dr Rowley is a VicHealth Public Health Research Fellow.