Int. J. Environ. Res. Public Health 2010, 7 1882 Ammonia remains the key gut-derived neurotoxin implicated in the pathogenesis of hepatic encephalopathy [39]. 7. Current Treatment There is a wide range of therapeutic options for treating ALD and alcohol use disorders. The aim of all therapeutic strategies for ALD is to improve liver function. In alcoholic patients the goal attempts to reduce ethanol intake significantly, looking forward abstinence, thus avoiding further hepatic damage. 7.1. Alcoholic Liver Disease Prognosis of individual patients with ALD depends on the degree of histological injury, patient’s nutritional status, presence of complications of advanced disease, other comorbid conditions such as HCV infection, and the patient's ability to eradicate destructive drinking patterns. The cornerstone in ALD therapy is a daily life style modification, including drinking cessation and treatment of decompensation, if appropriate. Abstinence from alcohol is vital in order to prevent further ongoing liver injury, fibrosis, and possibly hepatocellular carcinoma [33]. 7.1.1. Nutrition Several studies support the notion that nutritional status is a determinant factor in the outcome after any therapy. Nutritional intervention has shown to play a positive role on both, in-patient and out-patient basis. Data has described patients with alcoholic liver injury who voluntarily consumed >3,000 kcal/ day had virtually no mortality, whereas those consuming <1,000 kcal/day had a mortality greater than 80% at 6-month. Moreover, the undernourishment degree in cirrhosis was correlated with the development of severe complications such as encephalopathy, ascites and hepatorenal syndrome. Jonas et al. found that alcoholic fatty liver decreased significantly in rats with fatty acids supplemented diet, this was observed when oxidative/nitrosative levels were normalized in rats fed with alcohol-fatty acids-supplementes diet [40]. The molecular mechanism of DHA/AA, (decosahexaenoic acid/arachidonic acid) essential fatty acids, against liver steatosis is poorly understood. However, it has been observed that steatosis increases in diets with greater amounts of polyunsaturated fatty acids. This fact indicates a sharpened threshold between therapeutic and harmful effects [5]. In cirrhotic patients it has been demonstrated that a nutritious diet improved the 5-year outcome compared with patients consuming an inadequate diet. 7.1.2. Pharmacotherapy The progression of ALD continues according to the amount of alcohol consumed. Complications appear when there is a considerable liver fibrosis tissue, few functional hepatocytes, and when chronic inflammation affects the structure and function of the liver. When progression renders alcoholic hepatitis, corticosteroids are widely used in selected patients and treatment with pentoxifylline appears to be a promising anti-inflammatory therapy. Recent studies have indicated anti-TNFα therapy, at least for alcoholic hepatitis, although further clinical trials must be designed due to the disparity in the results of some research data. However antioxidant therapy, alone or in combination with