Haren et al. BMC Public Health 2010, 10:454 http://www.biomedcentral.com/1471-2458/10/454 conversion of acetyl CoA to triglycerides (TG) which are secreted into the blood as very low density lipoproteins (VLDLs); ectopic fat accumulation in the liver from excess TG production and a rise in GGT and other liver enzymes; and weight gain from energy derived from alcohol (about 29 kj/gram) [12]. Alcohol accounted for 5% of the total Indigenous burden of disease, similar to high cholesterol and blood pressure, and for 4% in the health gap with non-indigenous Australians [10]. Li et al. reported elevated GGT with obesity, meta- bolic syndrome and physical inactivity in Indigenous non-drinkers in this cohort [13]. Little work has been published on NAFLD or alcohol-related liver disease in Indigenous populations worldwide. It is not known whether the additive effects of body fatness and alcohol intake on serum liver enzymes described in Nordic populations [14,15] apply to Indigenous Australians or whether drinking combined with multiple metabolic risk factors (or metabolic syndrome) further increases risk of elevated liver enzymes. Evidence suggests that Aboriginal people have a greater risk of coronary heart disease events than would be expected based on Framingham risk functions [16]. Similar underestimation of risk using these algorithms has been reported in ethnic minorities in the UK [17] with overestimated risk in other ethnic groups [18,19]. Moreover, normative values for waist circumference have not been established for Aboriginal and Torres Strait Islanders (TSI) and these populations differ in a number of metabolic characteristics, relative to fatness [7,20,21]. Due to this uncertainty, we defined population metabolic profiles using cluster analysis and then com- pared the alcohol stratified effects of metabolic risk clus- ter versus International Diabetes Federation (IDF) classified metabolic syndrome on elevated GGT. Methods Population Subjects were participants in The Well Person’s Health Check [22]. Briefly, in 1999 - 2000, all indigenous resi- dents aged 13 years and older, in 23 far north Queens- land rural communities, were invited to participate through printed media, local radio, and word of mouth via the local health service, community council and community groups. A total of 3811 (participation rate 44.5%) participated in the study. The cohort was demo- graphically representative of the indigenous population of the local area when compared to local population census data. Aboriginal and TSI are recognized as dis- tinct ethnic groups and ascertainment of ethnicity was by self-identification in a manner consistent with Aus- tralian national minimum dataset specifications [23]. After exclusion of children under age 15 (N = 496), non-indigenous (N = 482) and individuals reporting Page 2 of 10 joint Aboriginal-TSI descent (N = 224), a total of 2609 participants were included in this analysis. All partici- pants provided informed consent to take part in the study. The study procedures were in accordance with the ethical standards on human research and thereby approved by the Cairns Base Hospital Human Research Ethics Committee with support from the peak Indigen- ous Health Organizations, Apunipima Cape York Health Council and the Torres Strait and Northern Peninsula Area Health Council. Data Collection Height to the nearest 0.1 centimeter (cm) and weight to the nearest 0.1 kilogram (Kg) were measured in partici- pants without shoes and wearing only light clothing. Body mass index (BMI) was calculated (weight (kg)/ height (m2)). Waist circumference was measured mid- way between the lower border of the rib cage and the top of the iliac crest and recorded to the nearest 0.1 centimeter. Data were collected on self-reported medical conditions and none reported known liver disease. Phy- sical activity was measured using a 7-day recall method in which the participants were asked to report daily phy- sical activities of at least moderate intensity, lasting at least 30-minutes, performed during the week before their health check. Physical activity level was defined by American Heart Association criteria in which “active” reflects moderate to vigorous physical activity for at least 30-minutes per day on 5 days in the week before the survey [24]. Smoking behaviour was collected by standard questionnaire. The amount of alcohol con- sumed over a week was collected by 7-day recall diary and converted to number of standard drinks per week (1 standard drink = 10 grams of alcohol). Risky alcohol drinking was defined as greater than 6 standard drinks on any occasion or greater than 4 standard drinks per day in the recall week for males and greater than 4 drinks on any occasion or greater than 2 drinks per day in females [22,25]. Three seated blood pressure measurements were taken at 2 minute intervals after 10 minutes rest using a Dinamap automated oscillometric device (Critikon Corporation, USA) and the average was used in all analyses. Venous blood was sampled in the morning after an 8-hour fast as previously described [22]. GGT was measured using the kinetic photometric procedure with Cobas Integra 800 (Roche Diagnostics, USA). Blood glucose and lipids were measured using photo- metric enzyme endpoint assay with Cobas Integra 700/ 400 (Roche Diagnostics, USA). The outcome variable, GGT, was classified as normal (<50 U/L) or elevated (≥50 U/L) based on laboratory specific reference ranges (Queensland Pathology Service, http://www.health.qld.gov.au/qhcss/qhps/default.asp).