Heavy drinking is the daily consumption of five to six standard drinks, each drink equivalent to approximately 12 ounces of beer, 5 ounces of wine, or 1.5 ounces of distilled spirits. A friend of mine is considered a heavy drinker, he drinks constantly. Last week I found out he went to the doctor and was diagnosed with Alcohol-induced liver disease (ALD). I had never heard of ALD before so I decided to do some research on ALD to give myself knowledge of what he has and what he will be going through.
Alcohol-induced liver disease (ALD) is a major cause of illness and death in the United States. Fatty liver, the most common form of ALD, is reversible with abstinence. More serious ALD includes alcoholic hepatitis, characterized by persistent inflammation of the liver, and cirrhosis, characterized by progressive scarring of liver tissue. Either condition can be fatal, and treatment options are limited. During the past 5 years, research has significantly increased our understanding of the mechanisms by which alcohol consumption damages the liver.
Approximately 10 to 35 percent of heavy drinkers develop alcoholic hepatitis, and 10 to 20 percent develop cirrhosis. In the United States, cirrhosis is the seventh leading cause of death among young and middle-age adults. I also found out that Approximately 10,000 to 24,000 deaths from cirrhosis may be attributable to alcohol consumption each year.
Factors that influence vulnerability to ALD include:
Genetic Factors- Structural of functional variability in any of the cell types and biochemical substances discussed above could influence a person’s susceptibility to ALD. Researchers are seeking genetic factors that may underlie this variability. Results of this research may provide the basis for future gene-based therapies.
Dietary Factors- Nutritional factors influence the progression of ALD. For example, a high-fat, low-carbohydrate diet promotes liver damage in alcohol-fed rats, and high amounts of polyunsaturated fats may promote the development of cirrhosis in animals.
Gender- Women develop ALD after consuming lower levels of alcohol over a shorter period of time compared with men. In addition, women have a higher incidence of alcoholic hepatitis and a higher mortality rate from cirrhosis than men. The mechanisms that underlie gender-related differences are unknown.
Hepatitis C- Many patients with ALD are infected with hepatitis C virus (HCV), which causes a chronic, potentially fatal liver disease. The presence of HCV may increase a person’s susceptibility to ALD and influence the severity of alcoholic cirrhosis. For example, alcohol- dependent patients infected with HCV develop liver injury at a younger age and after consuming a lower cumulative dose of alcohol than do those without HCV. Patients with HCV are often treated with an antiviral substance called interferon. However, interferon is less effective in patients with chronic HCV who are heavy drinkers, compared with those who are not. What scares me is my friend does have HCV.
Treatment effectiveness includes abstinence, it’s the cornerstone of ALD therapy. With abstinence, fatty liver and alcoholic hepatitis are frequently reversible, and survival is improved among patients with ALD, including those with cirrhosis. For terminally ill patients, liver transplantation remains the only effective treatment. Research has established the effectiveness of liver transplantation in patients with alcoholic cirrhosis. More recently, Bell and colleagues summarized follow up medical data on all persons who received liver transplants in the United States between 1988 and 1995. Deaths among these subjects were not alcohol related. That is, alcohol-dependent patients are rare. Hepatitis C infection in patients with ALD does not appear to affect survival after liver transplantation, despite the continued presence of the virus in the bloodstream.
Medication interactions include chronic alcohol consumption, it may increase the adverse side effects of medications used to treat conditions other than ALD. In particular, excessive use of the widely used pain killer acetaminophen has been associated with liver damage in people drinking heavily.
Prospects for future treatment, the multiple mechanisms of ALD development provide several potential targets for medical intervention. Some promising lines of inquiry are summarized below. The role of endotoxin in the inflammatory response suggests the possibility of inhibiting ALD development at its earliest stages. For example, suppression of endotoxin- producing intestinal bacteria reduced signs of liver damage in alcohol fed rats. An adequate daily supply of total carbohydrates is important in