1.1 Background of study
In chemistry, an alcohol is an organic compound in which the hydroxyl functional group (-OH) is bound to a carbon atom. In particular, this carbon center should be saturated, having single bonds to three other atoms (Nic et al., 2006).
Alcohols are neutral colourless and a water miscible organic solvent and it distributes itself throughout the body. This means that the concentration within tissues will be similar to that in the blood. Alcohol (ethanol) is consumed widely in the form of beer, wines and spirit. Excessive alcohol consumption with its associated consequences is a leading cause of economic, social and medical problems throughout the world. Besides the short term effects most pathophysiological consequences of ethanol abuse are associated with chronic consumption over a long period.
Alcohol is consumed by about 70 % of U.S. adults (Breslow et al.,2008). Consumption of this dietary component has both risks and benefits. Low to moderate doses of alcohol lower the risk of cardiovascular disease and all-cause mortality(USDA, 2010). The Dietary Guidelines for Americans 2010 and American Heart Association’s dietary guidelines suggest that if alcohol is consumed, males consume no more than two alcoholic drinks per/day (28 g/day) and women no more than one per/day (14 g/day) (Lichtenstein et al., 2006).
However, approximately 38 million adults in the United States report binge drinking an average of four times per month and consuming an average of eight drinks per episode (Kanny et al., 2013). Excessive alcohol intake was responsible for approximately 10 % of deaths among working age adults in the United States during 2006–2010 (Stahre et al., 2014) and cost the United States $223.5 billion in 2006. It is estimated to be the fourth leading preventable cause of death in the United States (Mokdad et al., 2000). Heavy drinking, including binge drinking, increases the risk of liver disease, hypertension, stroke, type II diabetes, gastrointestinal cancers, injuries and violence (USDA, 2010). Alcohol abuse is the leading cause of liver-related morbidity and mortality (USDA, 2010). In alcoholic patients increased levels of several liver-derived biomarkers are associated with excessive ethanol intake and alcoholic liver disease, and a number of studies have reported induction of liver enzyme function due to excessive alcohol consumption (Sharpe, 2001; Niemela, 2006). However, only a few small studies have investigated the effects of moderate alcohol consumption on liver enzymes (Alatalo et al., 2009)
1.2 JUSTIFICATION
Alcohol is consumed by about 70 % of U.S. adults (Breslow et al., 2008).Consumption of this dietary component has both risks and benefits. Low to moderate doses of alcohol lower the risk of cardiovascular disease and all-cause mortality (USDA, 2010). Excessive alcohol consumption can cause liver diseases including fatty liver, hepatitis and cirrhosis (Zakhari and Li, 2007; Schwartz and Reinus, 2012). Since alcohol is mainly metabolized by the liver, it is a primary site of alcohol-induced adverse health effects. Changes in liver enzymes activities are biomarkers of liver damage and are routinely assessed for diagnostic purposes and as part of physical examinations (Woreta and Alqahtani, 2013).
Previous studies have suggested the presence of a graded dose–response relationship between alcohol intake and risk of liver disease (Bellentani and Tiribelli, 2001; Day, 1997) and that GGT induction can be initiated at low doses of alcohol intake (Alatalo et al.,2009). But no such research has been done in this part of the world where the intake of alcohol is on the increase. Hence it becomes imperative to carry out this research.