Alcoholic Liver Disease (Fatty Liver, Hepatitis and Cirrhosis)

The liver is the central processing point of nutrients and wastes in the body. It filters and stores blood, regulates the way nutrients are metabolized and stores excess micro- and macroutrients, forms bile to discard wastes from the body and contributes to blood clotting. The liver is capable of contending with a range of chemical irritants but certain more toxic compounds can have a detrimental effect if consumed in excess or over a long period. Alcohol is one of the compounds and its widespread use globally is one of the leading causes of liver disease.

In most cases alcohol and its byproducts are broken down by the liver enzymes. 80% of alcohol is metabolized by the enzyme alcohol dehydrogenase (ADH) and the remaining 20% by the enzyme cytochrome CYP2E1. This yields harmless substances that can easily be excreted from the system. With alcoholic liver disease, the inability to metabolize alcohol and its byproducts allow these compounds to damage liver tissue.

What is alcoholic liver disease?

Alcoholic liver disease (ALD) is damage to liver tissue induced by alcohol that leads to acute or chronic reversible or irreversible changes that compromise liver function. Despite the term “alcoholic”, this type of liver disease is not only seen in those with an alcohol addiction. Many alcohol users exceed the maximum allowance that can be tolerated by the liver without causing significant toxicity or damage to the liver tissue. This will lead to three patterns of liver injury which may be similar and overlap to a certain degree – fatty liver disease (hepatic steatosis), alcoholic hepatitis and cirrhosis.

Different Types of Alcoholic Liver Disease

It is important to note that these different forms of alcoholic liver disease are not isolated to alcohol abuse or misuse. It is simply patterns of injury that may also be seen with other pathological causes like infection, drugs and toxins, blood disorders and autoimmune diseases.

Fatty liver disease is usually the first changes to be seen with long term alcohol misuse. With severe abuse, fatty liver may progress to alcoholic hepatitis which is the acute inflammation of the liver induced by alcohol. However, alcoholic hepatitis can also arise in the previously normal liver if there is severe alcohol abuse.

Both fatty liver disease and alcoholic hepatitis are reversible. Abstinence from alcohol may see the liver return to normal. A person who has fatty liver disease with continued exposure to alcohol will eventually suffer with cirrhosis. Similarly, repeated attacks of alcoholic hepatitis may also lead to cirrhosis. This stage of alcoholic disease is irreversible.

Alcoholic Fatty Liver Disease

Also known as hepatic steatosis, this pattern of liver injury can occur even with moderate alcohol intake. Droplets of lipid (fat) builds up in the liver cells (hepatocytes). This initially starts as small microscopic vesicles which enlarge with continued alcohol use. It eventually becomes large enough to be seen macroscopically as a larger than normal liver which is yellow and greasy. Usually there is little or no fibrosis at this stage of alcoholic liver disease but with continued alcohol use, fibrotic scarring may be seen especially around the hepatic veins.

Alcoholic Hepatitis

In alcoholic liver disease, there is acute inflammation marked by swollen hepatocytes (liver cells) and death of some liver cells. The build up of proteinaceous filaments in clumps within the cell (Mallory bodies)  is then seen but this change is seen in many types of liver injury. Eventually a large number of neutrophils, a type of white blood cell, congregate in the liver lobules around the damaged and dying liver cells. Fibrotic scarring of the liver may then ensue especially if there is repeated bouts of alcoholic hepatitis. Bile flow may be inhibited to varying degrees.

Alcoholic Cirrhosis

This the final stage of alcoholic liver disease. The irreversible changes seen with alcoholic cirrhosis is seen after long term alcoholic fatty liver disease and/or repeated bouts of alcoholic hepatitis. It develops slowly and the shrinks from a large fatty liver to a small brown nodular liver. Fibrous bands (septa) extend into the liver tissue especially at areas of liver cell death (necrosis) and nodules. This eventually creates a pattern of hard pale areas of scar tissue. The production and release of bile from the liver is also compromised significantly.

Causes of Alcoholic Liver Disease

As previously mentioned, the patterns of liver injury seen with alcoholic liver disease is not only seen with alcohol consumption. However with regards to alcoholic liver disease, the injury is seen as soon as 5 years with excessive drinking with cirrhosis setting in by the 8th year on average. Moderate to heavy drinking can also lead to alcoholic liver disease with 10 to 20 years. A mild form of alcoholic fatty liver disease can even be seen within days if there is extremely excessive drinking on a daily basis.

How much of alcohol before liver disease?

Alcoholic liver disease is unlikely to occur in a person who drinks under the weekly threshold of :

  • 28 units for men
  • 21 units for women

Men are advised not exceed 21 units of alcohol per week or no more than 4 units per day while women are advised not to exceed 14 units per week with no more than 3 units per day.

The number of units depends on the volume percentage of alcohol and quantity of alcohol. A simple breakdown of popular alcoholic beverages is as follows :

  • Light beer (1 pint) = 2 units
  • Regular beer (1 pint) = 3 to 4 units
  • Wine (1 bottle) = 9 units
  • Sherry (1 bottle) = 12 to 13 units
  • Vodka / rum / gin (1 bottle) = 28 to 30 units
  • Whiskey / brandy = 28 units


Individual tolerance and underlying risk factors have to also be taken into account and may explain why alcoholic liver disease sets in so early in some patients and much later or not at all in others. These risk factors may include :

  • Gender. Women are more susceptible and this could be associated with the lower female body mass. Despite this, most alcoholic liver disease patients are men. It may also be associated with social and cultural factors associated with alcohol misuse among men and women.
  • Genetics. Despite a strong familial link and alcoholic liver disease being more frequently seen among monozygotic twins (identical) than dizygotic twins (fraternal), there is no conclusive evidence to indicate a genetic link as yet. It is believed that a genetic variant of aldehyde dehydrogenase (ALDH) may impair the liver’s ability to breakdown byproducts of alcohol. These byproducts are extremely toxic to liver tissue.
  • Nutrition. Those with a choline deficient diet are more likely to develop alcoholic liver disease. Foods rich in choline include meat, fish, eggs, nuts, wheat germ, brocolli and brussel sprouts.
  • Pre-existing conditions like viral hepatitis (HBV and HCV particularly) and/or hemochromatosis (iron overload).

The type of alcohol consumed does not change the risk but alcoholic liver disease is more likely to occur in those who drink continuously compared to binge drinkers.

Signs and Symptoms

The clinical features of alcoholic liver disease may vary significantly. Early diagnosis is therefore mainly dependent on liver function testing in individuals with known alcohol misuse.

  • Alcoholic Fatty Liver Disease (Hepatic Steatosis)
    • This stage is usually asymptomatic and patients are almost never aware of any changes in the liver tissue.
    • Hepatomegaly (enlarged liver) may not be present.
    • It is usually only discovered by routine liver function test (LFT) indicating elevated liver enzymes.
  • Alcoholic Hepatitis (Rapidly developing symptoms)
    • Jaundice
    • Hepatomegaly
    • Mild cases are often asymptomatic.
    • Severe cases may also present with sudden gastrointestinal bleeding, blood clotting disorders (prolonged prothrombin time), mental confusion and coma (hepatic encephalopathy).
  • Alcoholic Cirrhosis (Slowly developing signs and symptoms)
    • Jaundice
    • Hepatomegaly
    • Blood clotting disorders
    • Mental confusion
    • Coma


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