Heavy drinkers are at maximum risk to develop serious alcoholic liver disease. Susceptibility to alcoholic hepatitis and cirrhosis can be further associated with heredity, gender, diet, and co-occurring liver illness. But the majority of alcoholic liver damage is attributed to alcohol metabolism. 

Alcohol may cause liver injury by direct toxicity of metabolic by-products of alcohol or by inflammation induced by these byproducts. Liver cells when exposed to these bacterial toxins develop liver disease. Further increase in this liver injury either toxic, inflammatory, or both, can lead to fibrosis and, ultimately, to cirrhosis. 

Alcohol-related liver diseases may be categorised as Fatty liver disease (which is reversible and does not cause much damage), Alcoholic hepatitis (which causes widespread necrosis of liver tissue and may lead to fibrosis), Alcoholic cirrhosis (which is the most advanced form of liver disease, characterized by extensive fibrosis causing severe functional impairment, secondarily leading to malfunction of other organs).

Researchers have postulated possible mechanisms that influence Alcohol-Induced Liver Damage. These may be due to-

Oxygen- by the formation of free radicals, diminishing antioxidants, increasing hypoxia

Inflammatory agents- by wide spectrum actions of Eicosanoids, stimulation of inflammatory cytokine production, increase in intestinal permeability to endotoxins, Adduct formation, and increased fibrosis.

Risk factors for liver disease have been described as-

Genetic Variations in Enzymes That Metabolize Alcohol-

A study demonstrated more than twice c2 allele in patients with alcoholic liver disease contrasting healthy control subjects or patients with non-alcoholic liver disease. Furthermore, the c2 allele has not been demonstrated in alcoholics without liver disease, indicating the potential importance of this allele as a risk factor.

Gender-

Women are prone to cirrhosis at a much lower cumulative dose of alcohol than men. There are 2 theories that explain female predisposition; one being lower gastric ADH that metabolises alcohol in the stomach; second is the difference in the metabolism of fatty acids, leading to accelerated alcoholic liver injury in women. 

Diet and Nutrition

Deficiencies of glutathione or vitamins A or E decrease the liver’s protection against free radicals. Chronic alcohol consumption promotes absorption and storage of iron which acts as a catalyst of free radical production.

Infection with Hepatitis C Virus (HCV)

 Infection with HCV is known to increase the risk of liver injury in alcoholics. Chronic drinking may increase HCV proliferation, which in turn may accelerate HCV-induced damage.

Tobacco and Coffee

Consuming Alcohol and smoking more than one pack of cigarettes/day increases the risk of cirrhosis 3 folds than those who do not smoke. However, alcoholics who consume four or more cups of coffee daily have a fivefold lower incidence of cirrhosis than those who do not drink coffee. 

Increased understanding of the mechanisms of liver injury has introduced innovative treatments for alcoholic liver disease, like the use of corticosteroids, antioxidants, antibiotics, and certain polyunsaturated fats.

Researches providing additional insight into the biological mechanisms underlying liver damage and new approaches to treat the problem in both alcoholic and nonalcoholic patients are needed.

Source: Maher JJ. Exploring alcohols effects on liver function. Alcohol Health Res World. 1997;21(1):5-12.