Int. J. Environ. Res. Public Health 2010, 7 1873 amount and time of exposure to alcoholic beverages. According to the World Health Organization, the average alcohol consumption per capita in adults is 5.1 liters per year, though mean consumption varies worldwide. While in some countries, like Saudi Arabia, alcohol consumption (liters per capita per year) is 0.0, in other countries such as Luxembourg the consumption reaches 17.54 [1]. Table 1. Causes of death related to alcohol abuse. 1 2 3 4 5 6 7 8 Mouth and oropharynx cancer Alcohol use disorders Ischemic heart disease Liver cirrhosis Road traffic accidents Poisonings Falls Intentional injuries The impact and consequences of AD and alcohol abuse have elevated economical costs, as well as negative health and social implications. The most direct health influence of ethanol consumption is reflected in a systemic level; thereby moderate ethanol consumption has been related to a reduced cardiovascular disease, favorable lipid profile and less thrombogenic platelet function [2]. On the other hand, elevated amounts of alcohol intake lead to hepatic damage. Although the mechanisms by which ethanol causes liver damage have been well described, some facts remain to be elucidated. The risk, severity and prognosis of ethanol-mediated liver diseases generally depend on the amount, frequency, and duration of alcohol consumption, as well as the continued presence of liver inflammation, diet, nutritional status and genetic make-up of the host. In this matter, alcoholic steatosis (AS) is the initial pathology found in early stages of the natural history of alcoholic liver disease (ALD). AS is characterized by the accumulation of lipids in the liver. Steatosis caused by alcohol is clinically considered as benign since it is reversible if the stimulus is removed. The progression to alcoholic steatohepatitis (ASH) represents the key step in the development of ALD. Only a small portion of heavy drinkers develop a severe form of the disease, suggesting the involvement of other factors modifying ALD onset and presentation [3]. Alcohol is identified as a harmful agent to the liver, and hepatic stellate cells (HSC) are activated in response to this injury. Activated HSC are recognized as fibrogenic cells and lead to deposition of collagen (particularly collagen type I). HSC are also regulated in a paracrine manner by acetaldehyde and reactive oxygen species (ROS), produced by the metabolism of ethanol in surrounding hepatocytes. Activated Kupffer cells secrete pro-inflammatory cytokines, linking apoptosis in the liver to inflammation [4]. ―Programmed cell death‖, also called apoptosis, plays an important role in the pathogenesis of chronic liver disease. Whenever there is an acute presentation of the disease, it is possible to observe massive hepatocyte apoptosis. This phenomenon induces progressive fibrosis, which is the hallmark of chronic liver damage and, therefore could result in liver failure, cirrhosis, and hepatocellular carcinoma.