Australian Bureau of Statistics
4364.0.55.005 - Australian Health Survey: Biomedical Results for Chronic Diseases, 2011-12
Latest ISSUE Released at 11:30 AM (CANBERRA TIME) 05/08/2013 First Issue
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The liver works as the body's filter, removing toxins from the blood, processing nutrients and regulating its metabolism. A range of factors, including fatty liver disease, infections and excessive alcohol consumption can prevent the liver from performing these functions and if left untreated, can lead to liver damage.1 When the liver is inflamed or damaged, enzymes including alanine aminotransferase (ALT) and gamma glutamyl transferase (GGT) leak from the liver cells into the bloodstream. As a result, elevated levels of ALT and GGT in the bloodstream can indicate the presence of liver disease.
ALANINE AMINOTRANSFERASE (ALT)
ALT is an enzyme found mainly in the liver that helps the liver metabolise food into energy. Elevated levels of ALT in the blood can occur when the liver is damaged or diseased.2
In 2011–12, around 1.9 million (11.0%) people aged 18 years and over had abnormal or elevated levels of ALT in their blood. Men were more likely than women to have elevated ALT (13.8% compared with 8.3%).
The proportion of people with abnormal ALT remained relatively steady through early and middle adulthood, peaking at 13.5% among people aged 45–54 years. Rates then significantly declined to a low of 1.9% among people aged 75 years or over.
Excess body fat is recognised as a risk factor for liver disease.3 This was reflected in the NHMS results, with 19.5% of those who were obese and 11.6% of people who were overweight having elevated ALT, compared with 4.6% of those who were of normal weight or underweight.
In 2011–12, many people with abnormal ALT also had risk factors for cardiovascular disease. They were more likely than those with normal ALT to have high total cholesterol (40.9% compared with 32.3%) and low HDL cholesterol (35.7% compared with 21.9%), as well as high triglycerides (26.6% compared with 12.3%). They were also more likely to have diabetes (9.2% compared with 4.6%). About two in five people (40.4%) who had elevated ALT also had high GGT.
The enzyme GGT is found in many tissues in the body. It exists in a relatively high concentration in the liver but is also found in the tissues of the kidneys, bile duct, pancreas, gallbladder, spleen, heart, and brain. When any of these tissues are damaged or diseased, GGT leaks from the tissue into the bloodstream. High GGT levels may therefore be indicative of a broader range of conditions and not just liver disease.4,5
In 2011–12, around 2.1 million people aged 18 years and over (12.4%) had abnormal or elevated levels of GGT in their blood. Unlike ALT, the proportion of people with abnormal GGT results generally increased with age, peaking at 20.5% among those aged 55–64 years. Overall, rates were similar for males and females (13.3% compared with 11.6%).
Similar to ALT, excess body fat increased the likelihood of having abnormal GGT. Around one in five (21.6%) people who were obese had abnormal GGT compared with 12.2% of people who were overweight and 6.0% who were of normal weight or underweight.
However, unlike ALT, GGT was also associated with blood pressure and smoking. In 2011–12, people with high blood pressure were more likely to have abnormal GGT than people with normal blood pressure (20.2% compared to 10.3%). Similarly, 18.1% of current smokers had abnormal GGT compared with only 9.6% of people who had never smoked.
People with abnormal GGT were more likely than those with normal GGT to have other chronic disease risk factors, including high total cholesterol (43.7% compared with 31.7%), high triglycerides (32.4% compared with 11.2%), and high LDL 'bad' cholesterol (39.0% compared with 32.4%). They were also more likely to have diabetes (11.5% compared with 4.2%) and to have abnormal results for the chronic kidney disease biomarkers, including albuminuria (12.2% compared with 7.0%) and eGFR (5.9% compared with 3.4%).
For more information on ALT and GGT, see Tables 1, 2, 3, 7, 8 and 9 on the Downloads page of this publication.
1 Angulo, P and Lindor, KD, 2002, 'Non-alcoholic fatty liver disease', Journal of Gastroenterology and Hepatology, <http://www.gastrohep.com/conreports/bangkok/jghs2.pdf>, Last accessed 01/08/2013. Back to top
2 Schindhelm, RK, et al. 2006, 'Alanine aminotransferase as a marker of non-alcoholic fatty liver disease in relation to type 2 diabetes mellitus and cardiovascular disease', Diabetes/Metabolism Research and Reviews, <http://dare.ubvu.vu.nl/bitstream/handle/1871/13286/21810_Schindhelm_proefschrift_V3.pdf?sequence=1#page=95>, Last accessed 08/01/2013. Back to top
3 Farrell, GC et al. 2006, 'Nonalcoholic fatty liver disease: From steatosis to cirrhosis', Hepatology, <http://onlinelibrary.wiley.com/doi/10.1002/hep.20973/full>, Last accessed 08/01/2013. Back to top
4 Lee, DS, et al. 2007, 'Gamma Glutamyl Transferase and Metabolic Syndrome, Cardiovascular Disease, and Mortality Risk: The Framingham Heart Study', Arteriosclerosis, Thrombosis, and Vascular Biology, <http://atvb.ahajournals.org/content/27/1/127.full>, Last accessed 08/01/2013. Back to top
5 Ruttman, E, et al. 2005, 'Gamma-Glutamyltransferase as a Risk Factor for Cardiovascular Disease Mortality: An Epidemiological Investigation in a Cohort of 163 944 Austrian Adults', Circulation: Journal of the American Heart Association, <http://circ.ahajournals.org/content/112/14/2130.full>, Last accessed 08/01/2013. Back to top
This page last updated 5 August 2013
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