Int. J. Environ. Res. Public Health 2010, 7 1874 To objectively assess damage degree in the hepatic parenchyma, completion of a histological study is required. In steatohepatitis, findings in the lamellae include hepatocyte steatosis, ballooning, apoptosis, and lobular inflammatory infiltrate [4]. When ALD is established, an accumulation of reducing equivalents in the cytosol and the rates of fatty acids biosynthesis and subsequent esterification into triglycerols are markedly increased [5]. 2. Assessing the Problem The World Health Organization reports about two billion alcohol consummers worldwide and 76.3 million people with diagnosable alcohol use disorders [1]. Globally, alcohol causes 3.2% deaths for all causes (1.8 million deaths annually) and accounts for 4.0% of disease burden [2]. Excessive ethanol consumption is an important preventable cause of morbidity. The association between ethanol intake and alcoholic liver disease has been well documented, though liver cirrhosis develops only in a small proportion of heavy drinkers. Twenty percent of alcoholics and heavy drinkers develop fatty liver and only 10 to 15 percent of these will develop cirrhosis. The point prevalence of cirrhosis is 1% in people who drink 30 to 60 g of alcohol a day, and up to 5.7% in those consuming 120 g daily. In this matter, mortality studies have demonstrated that heavy drinkers and alcoholics die from cirrhosis at a much higher rate than the general population [6]. A clear aggregated environmental risk factor for the development of cirrhosis attributable to alcohol consumption is infection with hepatitis C virus (HCV). The risk of cirrhosis in humans infected with HCV increases proportionally with consumption of more than 30 g of alcohol per day; as mentioned above, the highest risk is associated with consumption of more than 120 g per day. Other factors, such as sex, genetic characteristics, and environmental influences (including chronic viral infection), play a role in the genesis of ALD [7]. In addition, alcoholism is a multifactorial brain disorder, according to the DSMIV (Diagnostic and Statistical Manual of Mental Disorders Fourth Revision), therefore the approach should be addressed on neurobiological and genetic strategies for the prevention, diagnosis, and treatment of alcoholism. The identified factors that contribute to the development of alcoholism are included in a social environment (i.e., parents, family, friends, peers, community, society). Possible social co-determinants such as poverty, social inequality, and easy availability of alcoholic beverages might establish alcoholism development. Several studies indicate that AD has a genetic component. The heritability of alcohol dependence is rather high, ranging between 50% and 60%, though it has been shown to be a complex polygenic disorder. There have been associated specific genes and polymorphisms that affect the risk of alcohol use disorders. These genes involve expression of enzymes responsible for alcohol metabolism, such as alcohol dehydrogenase and aldehyde dehydrogenase; those associated with disinhibition, and those that confer a low sensitivity to alcohol [8].