Haren et al. BMC Public Health 2010, 10:454 http://www.biomedcentral.com/1471-2458/10/454 R E S E A R C H A R T I C L E Open Access Alcohol, metabolic risk and elevated serum gamma-glutamyl transferase (GGT) in Indigenous Australians Matthew T Haren1,2,3*, Ming Li3, John Petkov2,4, Robyn A McDermott3 Abstract Background: The interaction between overweight/obesity and alcohol intake on liver enzyme concentrations have been demonstrated. No studies have yet examined the interaction between metabolic syndrome or multiple metabolic risk factors and alcohol intake on liver enzymes. The aim of this study was to examine if alcohol consumption modifies the effect of metabolic risk on elevated serum GGT in Indigenous Australians. Methods: Data were from N = 2609 Indigenous Australians who participated in a health screening program in rural far north Queensland in 1999-2000 (44.5% response rate). The individual and interactive effects of metabolic risk and alcohol drinking on elevated serum GGT concentrations (≥50 U/L) were analyzed using logistic regression. Results: Overall, 26% of the population had GGT≥50 U/L. Elevated GGT was associated with alcohol drinking (moderate drinking: OR 2.3 [95%CI 1.6 - 3.2]; risky drinking: OR 6.0 [4.4 - 8.2]), and with abdominal obesity (OR 3.7 [2.5 - 5.6]), adverse metabolic risk cluster profile (OR 3.4 [2.6 - 4.3]) and metabolic syndrome (OR 2.7 [2.1 - 3.5]) after adjustment for age, sex, ethnicity, smoking, physical activity and BMI. The associations of obesity and metabolic syndrome with elevated GGT were similar across alcohol drinking strata, but the association of an adverse metabolic risk cluster profile with elevated GGT was larger in risky drinkers (OR 4.9 [3.7 - 6.7]) than in moderate drinkers (OR 2.8 [1.6 - 4.9]) and abstainers (OR 1.6 [0.9 - 2.8]). Conclusions: In this Indigenous population, an adverse metabolic profile conferred three times the risk of elevated GGT in risky drinkers compared with abstainers, independent of sex and ethnicity. Community interventions need to target both determinants of the population’s metabolic status and alcohol consumption to reduce the risk of elevated GGT. Background Non-alcoholic fatty liver disease (NAFLD) has become the most common cause of chronic liver disease and cryptogenic cirrhosis in developed countries. The increasing prevalence of obesity, type 2 diabetes, and metabolic syndrome may be important drivers of increasing rates of NAFLD diagnoses [1]. An elevated serum gamma-glutamyl transferase (GGT) has been demonstrated as a biomarker of NAFLD [2] and, although it is not the only marker of chronic liver dis- ease, it does predict future diabetes, coronary heart dis- ease and stroke [3,4]. * Correspondence: Matt.Haren@unisa.edu.au 1Spencer Gulf Rural Health School (SGRHS), University of South Australia and The University of Adelaide, Whyalla Norrie SA, Australia The Australian indigenous population has an excess of metabolic syndrome and type 2 diabetes relative to the non-indigenous population [5-7]. BMI-specific incidence rates for type 2 diabetes in Australian Aboriginal adults are among the highest in the world [8]. The overall inci- dence rate in rural Far North Queensland indigenous communities from 2000 to 2006 was 29 per 1000 person years (predicted to equate to 120 new diabetes diagnoses per year) [9]. Diabetes and CVD account for 7% and 14%, respectively of the overall burden of disease in Indigenous Australians, and for 12% and 24% respec- tively, of the health gap between indigenous and non- indigenous Australians [10]. Heavy and moderate drinkers are more likely to have elevated serum GGT when compared to abstainers [11]. The metabolic effects of alcohol include an increase in © 2010 Haren et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.