Haren et al. BMC Public Health 2010, 10:454 http://www.biomedcentral.com/1471-2458/10/454 overall prevalence of elevated GGT (defined in this study as ≥61 U/L) was 22.4% (males 34.9%, females 10.7%). Over two thirds of this population were Aborigi- nal and had an elevated GGT prevalence of 28.6% com- pared with 8.8% in non-aboriginals [32]. It has been suggested that the high prevalence of type 2 diabetes in North American indigenous populations may indicate a high prevalence of NAFLD [33], and despite a lack of published data, this may also be true in Indigenous Aus- tralians. Elevated serum GGT and diagnosed NAFLD have also been shown to predict incident cardiovascular events in the general population [34], and more strongly in diabetics [34,35] and alcohol drinkers [34]. Almost 80% of Indigenous males and 59% of Indigen- ous females in this study reported that they currently drink alcohol. These percentages appear higher than Australian population estimates for Indigenous Austra- lians generally [36] and reflects near universal access to alcohol from “wet” canteens in these remote commu- nities in far north Queensland at the time of the study. In these communities, drinking alcohol was associated with a 3.6 to 6.2-fold increase in the chance of having elevated GGT after adjustment for age, gender and eth- nicity and the effect increased from moderate to risky alcohol consumption. The association between alcohol intake and GGT is well described [11] with modifica- tions of this association by sex [37], ethnicity [38-40] and age [41]. In these communities, the observed dou- bling in risk of elevated GGT from drinking in males compared with females, and in Aboriginal compared with TSI peoples was directly related to the prevalence of high risk alcohol consumption by males compared with females and Aboriginal compared with TSI people. Thus, irrespective of sex or ethnicity, people who drink alcohol at risky levels have equivalent odds of elevated GGT. Limitations to this study include a possible downward response bias to 7-day recall of alcohol consumption [42], the sole use of GGT as an outcome and indicator of NAFLD due to the limited ability to perform more advanced investigations in very remote communities, and a small degree of missing data on major exposure variables that differentially occurred in participants who were female, older and had lower blood pressure. Conclusions Taken together, drinking was most strongly associated with elevated GGT in a dose dependent manner. Abori- ginal men were at particularly high risk of elevated GGT from drinking, due largely to the high prevalence of risky drinking in this group. In this Indigenous popu- lation, an adverse metabolic profile conferred 3 times the risk of elevated GGT in risky drinkers than in abstainers, independent of sex and ethnicity. Page 9 of 10 Interventions need to target modifiable community determinants of both the population’s metabolic risk sta- tus and risky alcohol drinking behaviour to achieve greater reduction in population GGT levels. The effects of such strategies on the rates of new diabetes, CHD and stroke cases (major contributors to the Indigenous health gap in Australia) require further investigation. Additional material Additional file 1: Expectation Maximisation Cluster analysis and Partial Least Squares expanded methods. This file contains an expanded discussion of the EM cluster and PLS analysis methods. Additional file 2: Disagreement between IDF metabolic syndrome classification and MR cluster membership. This file contains two tables that show (1) the level of disagreement between the metabolic syndrome classification and MR cluster membership, and (2) the demographic and metabolic characteristics of cases in which disagreement occurred. Acknowledgements Kerry Arabena, Phillip Mills, Dympna Leonard and the Indigenous Health Workers contributed to various aspects of the work including study design and acquisition of data but have not qualified for authorship. Thank you to the participants in the community surveys. This work was support by the National Health and Medical Research Council of Australia (NH&MRC) [grant number 278402] to R.A.M. M.T.H is supported by an NH&MRC Training Fellowship (Public Health) [grant number 511345]. Author details 1Spencer Gulf Rural Health School (SGRHS), University of South Australia and The University of Adelaide, Whyalla Norrie SA, Australia. 2Centre for Rural Health and Community Development (CRHaCD), University of South Australia, Whyalla Norrie SA, Australia. 3Sansom Institute, Division of Health Sciences, University of South Australia, Adelaide SA, Australia. 4Applied Statistics Unit, Centre for Regional Engagement, University of South Australia, Mount Gambier SA, Australia. Authors’ contributions MTH contributed to the analysis and interpretation of data, drafting of the manuscript and critical revision of the manuscript for important intellectual content and data analysis. ML performed the data analysis and contributed to interpretation of data, drafting of the manuscript, critical revision of the manuscript for important intellectual content. JP performed data analysis and contributed to interpretation of data, drafting and critical revision of the manuscript for important intellectual content. RAM was involved in the conception and design of the study, acquisition of data, interpretation of data and critical revision of the manuscript for important intellectual content and for obtaining funding and administrative, technical and material support. ML had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. All authors read and approved the final manuscript. Competing interests The authors declare that they have no competing interests. Received: 15 March 2010 Accepted: 3 August 2010 Published: 3 August 2010 References 1. Moreno-Sanchez D: [Epidemiology and natural history of primary nonalcoholic fatty liver disease]. Gastroenterol Hepatol 2006, 29(4):244-254. 2. Tahan V, Canbakan B, Balci H, Dane F, Akin H, Can G, Hatemi I, Olgac V, Sonsuz A, Ozbay G, et al: Serum gamma-glutamyltranspeptidase