Alcohol is a major cause of cirrhosis of the liver in the US. Cirrhosis usually occurs only after a decade of drinking, but other types of injury can occur much earlier.
Alcohol can cause liver injury that ranges from fatty infiltration and inflammation (hepatitis) to full-blown cirrhosis. The main factors that contribute to alcoholic liver disease are: quantity of alcohol consumed, duration of alcohol consumption, nutritional status, and genetic or metabolic disposition.
In the United States, annual alcohol consumption is estimated at ten liters of pure ethanol per person. Approximately 15 million people abuse or are dependent on alcohol, and men are nearly three times as likely as women to abuse alcohol.
While only 10 to 20% of alcoholics eventually develop cirrhosis, drinking more than 60 grams of alcohol daily (about five drinks) for two to four weeks induces fatty liver in otherwise healthy men. 80 gm/day can lead to alcoholic hepatitis, and 160 grams daily for a decade can lead to cirrhosis. (The Merck Manual, 18th Edition 2006:211-214)
Factors that Increase Susceptibility to Alcoholic Liver Damage
Female gender: Women are more susceptible than men to alcohol-induced liver damage, even when adjusting for smaller body size. Women possess less alcohol dehydrogenase in their stomach linings, thus increasing the amount of alcohol from any given beverage that is absorbed directly into the bloodstream.
Familial tendency: Alcoholic liver disease often runs in families. This may represent a deficiency of cellular enzymes that metabolize alcohol.
Malnutrition: Alcohol is preferentially metabolized by the liver at the expense of other metabolic processes. A lack of specific nutrients, particularly proteins and B vitamins, slows the oxidation of alcohol, reduces the levels of antioxidant molecules in the liver, and leaves the liver susceptible to damage by other toxins.
Diets high in unsaturated fats: The liver prefers fatty acids as a fuel source. Fatty acids that aren’t used immediately are normally placed into triglyceride “packets” which are then routed to other organs and tissues. When alcohol is present, fatty acid metabolism and transport are delayed.
Iron deposition: Iron increases oxidative stress within liver cells. Certain diseases (e.g., hemochromatosis) increase the amount of iron stored in the liver. Indeed, chronic alcohol use itself leads to increased stores of liver iron.
Age: As people age, liver function (and the ability to metabolize alcohol) declines.
Chronic liver disease: The presence of other liver diseases, particularly hepatitis C, significantly increases one’s susceptibility to alcohol-related liver damage.
Stages of Alcoholic Liver Damage
Fatty liver (steatosis): As noted above, alcohol interferes with the normal metabolism of fatty acids in the liver. Drinking for only a short period of time can induce significant accumulation of lipids. Fatty liver is potentially reversible.
Alcoholic hepatitis: Continued exposure to alcohol leads to progressive damage to liver cells, accompanied by inflammation and various degrees of liver dysfunction. Alcoholic hepatitis may range from a mild, reversible illness (fatigue, fever, jaundice, abdominal pain) to a life-threatening condition (jaundice, liver failure, electrolyte abnormalities, bleeding).
Cirrhosis: As liver damage progresses, extensive scarring replaces the normal architecture of the liver. Cirrhosis is irreversible (and increases the risk of liver cancer), but the liver possesses a remarkable ability to regenerate. With abstinence from alcohol, small islands of remaining cells may recover and continue to offer some level of liver function.
The key to preventing alcoholic liver disease is limiting alcohol consumption. “Sensible” drinking limits have generally been defined as:
For men, no more than two drinks daily
For women, no more than one drink daily
For individuals over 65 years old, no more than one drink daily
One-drink equivalents are:
One 12-ounce beer
4-5 ounces of wine
1 ounce of 100-proof distilled spirits
The copyright of the article Alcohol and Liver Disease in Alcohol Abuse is owned by Stephen Allen Christensen. Permission to republish Alcohol and Liver Disease in print or online must be granted by the author in writing.