Haren et al. BMC Public Health 2010, 10:454 http://www.biomedcentral.com/1471-2458/10/454 Page 6 of 10 elevated GGT. The overall prevalence of elevated GGT was 25.9%. In this group, people were older, more likely to be male, Aboriginal, obese, smokers, drinkers, dia- betic, be classified as metabolic syndrome, have an adverse MR cluster profile, and be physically inactive, when compared to those with normal GGT. The MR cluster profile of the population is shown in table 3 and represented in standardized units in figure 1. There were two clusters identified in this population, denoted as ‘favorable’, which represented 60% of the population, and ‘adverse’ (40%). All metabolic variables were significantly worse and there were a significantly higher proportion of TSI people in the adverse cluster, when compared with the favorable cluster. The major contributors to cluster membership in descending order were: SBP, DBP, waist circumference, fasting glucose and triglycerides. HDL contributed little to explaining cluster membership. Together these variables explained 64% of individual allocation to each particular cluster. Disagreement between metabolic syndrome and MR cluster membership occurred in 524 cases; 286 cases in the favorable cluster were classified as having metabolic syndrome, whereas 238 in the adverse cluster were not. Aboriginal people when compared to TSI were more likely to be in the adverse cluster but not be classified as having metabolic syndrome (Additional file 2, Tables 1 and 2). The multiple adjusted odds of elevated GGT were sig- nificantly greater in moderate and risky drinkers compared with non-drinkers (moderate: OR 2.3 [95%CI 1.6 - 3.2]; risky: OR 6.0 [4.4 - 8.2]), metabolic syndrome compared with no metabolic syndrome (OR 2.7 [2.1 - 3.5]), adverse compared with favorable MR cluster (OR Table 3 Metabolic risk cluster profiles of Indigenous adults across the studied rural far north Queensland communities Favorable cluster (n = 1430, 60%) Mean or No. SD Adverse cluster (n = 955, 40%) Mean or No. Male * Aboriginal * Age ( years)* WC (cm)* Trigs (mmol/L)‡* SBP (mmHg)* DBP (mmHg)* HDL (mmol/L)* FPG (mmol/L)* 634 (44.3%) 912 (63.8%) 31.8 89.10 1.25 120.24 64.80 1.19 4.73 13.5 14.76 0.65 12.63 9.61 0.32 0.76 516 (54.0%) 543 (56.9%) 45.6 104.63 2.65 145.53 81.56 1.09 7.23 SD 14.2 14.48 1.96 18.25 12.26 0.27 2.61 *significant difference of <0.001 between favorable and adverse MR cluster, using t-test (for continuous variables with normal distribution, and Mann- Whitney rank-sum test for continuous variables with non-normal distribution‡. WC is waist circumference, Trigs is serum triglycerides, SBP is systolic blood pressure, DBP is diastolic blood pressure, HDL is high density lipoprotein cholesterol, FPG is fasting plasma glucose. 3.4 [2.6 - 4.3]), diabetics compared with non-diabetics (OR 2.1 [1.6 - 2.9]), and central and general overweight (central: OR 2.3 [1.6 - 3.2]; general: OR 1.7 [1.4 - 2.2]) and obesity (central: OR 3.7 [2.5 - 5.6]; general: OR 1.7 [1.3 - 2.2]), when compared to normal weight. Ethnicity and sex stratified analyses demonstrated strong interactions between drinking and ethnicity and drinking and sex, on the odds of elevated GGT. Aboriginal drinkers were significantly more likely to have elevated GGT than TSI drinkers (OR 2.2 [1.8 - 2.8], Table 4), and male drin- kers were twice as likely to have elevated GGT as female drinkers (OR 2.0 [1.2 - 3.5], Table 5). Moderate and risky alcohol drinking did not interact with ethnicity or sex on the odds of elevated GGT. There were no observed inter- actions between metabolic risk and either ethnicity or sex on elevated GGT. When stratified by drinking status (Table 6), there was no evidence of a multiplicative effect of moderate or risky drinking with obesity or metabolic syndrome on elevated GGT (interaction terms not shown). However, in people with an adverse MR cluster profile, drinking alcohol at risky levels was associated with a near 3-fold increase in the log of the odds of elevated GGT when compared with non-drinkers (OR 2.8 [1.6 - 4.9]). A post-hoc analysis was performed in order to inves- tigate any possible interfering effects of HDL on the outcomes of the planned analysis, given that increases in both HDL (improvement) and GGT (worsening) result from increased alcohol consumption. Thus, we re-performed all steps of the above analysis, beginning with cluster analysis, excluding HDL. This process yielded two clusters of similar proportions to our pre- vious analysis, the variable means and the proportions of Aboriginal and Torres Strait Islanders between clus- ters were similar to the original analysis (data not shown). Re-analysis of the individual effect of cluster membership on elevated GGT gave similar results (OR 3.5 [95% CI 2. 9 - 4.2] compared with OR 3.4 [2.6 - 4.3] in the original analysis) and re-analysis of table 6 showed very similar results to those of the original analysis, even after adjustment for HDL. The overall effect of the cluster × alcohol interaction term was also similar to the original analysis (OR 1.7 [95% CI 1.0 - 3.0]). When adjusted for HDL, the effect of the interaction term was essentially unchanged (OR 1.8 [95% CI 1.1 - 3.2]). Discussion This study reported high population mean serum GGT in both men (61.0 ± 74.2 U/L) and women (35.0 ± 40.4 U/L) that exceeded the highest population mean con- centrations published previously by a study in north- west Russia (Men: 43.8 ±60.5 U/L; Women: 28.3 ± 38.9 U/L) [29].