The risk factors presently (2010) known are: * Quantity of alcohol taken: Consumption of 60–80g per day (14g is considered one standard drink in the US, i.e., 1.5 fl oz hard liquor, 5 fl oz wine, 12 fl oz beer; drinking a six-pack of 5% ABV beer daily would be 84g and just over the upper limit) for 20 years or more in men, or 20g/day for women significantly increases the risk of hepatitis and fibrosis by 6% to 41%, * Pattern of drinking: Drinking outside of meal times increases up to 3 times the risk of<unk> . * Sex: Women are twice as susceptible to alcohol-related liver<unk> , and may develop<unk>  with shorter durations and doses of chronic consumption. The lesser amount of alcohol dehydrogenase secreted in the gut, higher proportion of body fat in women, and changes in fat absorption due to the menstrual cycle may explain this phenomenon. * Hepatitis C infection: A concomitant hepatitis C infection significantly accelerates the process of liver injury. * Genetic factors: Genetic factors predispose both to<unk> m and to<unk> . Both monozygotic twins are more likely to be<unk> s and to develop liver cirrhosis than both dizygotic twins. Polymorphisms in the enzymes involved in the metabolism of alcohol, such as ADH,<unk> H, CYP4502E1, mitochondrial dysfunction, and cytokine polymorphism may partly explain this genetic component. However, no specific polymorphisms have currently been firmly linked to<unk> . * Iron overload (hemochromatosis) * Diet: Malnutrition, particularly vitamin A and E deficiencies, can worsen alcohol-induced liver damage by preventing regeneration of hepatocytes. This is particularly a concern as<unk> s are usually malnourished because of a poor diet, anorexia, and encephalopathy.
Alcoholic liver disease
Porphyria
Alcoholic hepatitis
Fatty liver disease
Viral hepatitis
Non-alcoholic fatty liver disease
Autoimmune hepatitis
Ischemic hepatitis