Alcohol, metabolic risk and elevated serum gamma-glutamyl transferase (GGT) in Indigenous Australians

Abstract

BackgroundThe 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.MethodsData 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.ResultsOverall, 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]).ConclusionsIn 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.

Independent and Supra-Additive Effects of Alcohol Consumption, Cigarette Smoking, and Metabolic Syndrome on the Elevation of Serum Liver Enzyme Levels

“…However, our present study did not link alcohol consumption to fatty liver disease, but to elevated liver enzyme levels. Moreover our findings suggested that even an alcohol consumption lower than that referred to in previous studies (i.e., lower than ≥30 g/day or ≥40 g/day) 21,40 may confer some risk.…”

“…Some previous studies showed the combined risk of alcohol consumption and metabolic syndrome on liver enzyme levels and fatty liver disease [26], [40]. However, their results were not consistent and their magnitudes of risk and the supra-additive effect of these factors were not clear.…”

“…However, their results were not consistent and their magnitudes of risk and the supra-additive effect of these factors were not clear. Haren and colleagues reported that adverse metabolic risk cluster profile increased the risk in risky drinkers (>40 g/day in men, >20 g/day in women) than in nondrinkers by three-fold [40].Adams and colleagues found no synergistic effect between alcohol consumption and BMI or waist circumference on ALT or GGT levels [26]. Moreover, the risk of moderate alcohol consumption (<24 g/day) and its synergistic relationship with metabolic syndrome were not explored in most of the previous studies.…”

Albuminuria and its associated biomedical factors among indigenous adults in Far North Queensland: a 7-year follow up study

“…We have reported that GGT predicts hypertension incidence [ 37 ] and is highly correlated with overweight and obesity. Metabolic syndrome and alcohol drinking magnifies the association between GGT and metabolic components among this population [ 38 , 39 ]. Further exploration of its association with cardiovascular conditions and diabetes is needed to understand the additional independent impact of GGT on albuminuria found in this population for better risk evaluation or stratification in Indigenous population.…”

Synergistic Effect of Alcohol Consumption and Body Mass on Serum Concentrations of Cytokeratin‐18

“…TPS concentrations in obese risky drinkers were higher than expected for the simple addition of these 2 factors, that is, the body mass index modified the effect of alcohol consumption on TPS levels. It is well known that alcohol consumption and body mass have a synergistic effect on the elevation of liver enzyme levels (Alatalo et al., 2008; Haren et al., 2010; Loomba et al., 2009; Shen et al., 2010) and on the risk for liver disease (Naveau et al., 1997; Raynard et al., 2002), hepatocellular carcinoma (Marrero et al., 2005), and liver disease‐related mortality (Hart et al., 2010). The present study extends this to cytokeratin‐18 (TPS) concentration, which can be regarded as a particular marker of liver damage.…”