Nutritional Management of Alcoholic Liver Disease

by National Institute of Health

(Page 6 of 7)

As discussed in the previous sections, alcohol consumption and alcohol metabolism can lead to harmful effects on the liver through numerous pathways related to the drinker's nutrition and metabolism. Alcoholic liver disease typically develops in several sequential and partially overlapping stages. The first stage, fatty liver, is characterized by fat accumulation in the liver; it is sometimes associated with inflammation, and is called steatohepatitis or alcoholic hepatitis, when severe. At this stage, liver cells may begin to die and scar tissue may form, leading to the next stage of liver disease, fibrosis. Excessive scar tissue formation, in turn, eventually destroys the normal liver structure, resulting in cirrhosis, the most severe type of liver disease.

Treatment of alcoholic liver disease must be started as early as possible in the disease process because patients are more likely to die as the disorder advances. For example, one study of patients with alcoholic liver disease found that 70 percent of patients with fatty liver still were alive after 4 years, whereas less than 50 percent of patients with cirrhosis still were alive after the same amount of time. If the cirrhosis was associated with inflammation (alcoholic hepatitis), the outlook was even worse, with only about 33 percent of patients still alive after 4 years. Unfortunately, these high mortality rates, higher than those for many cancers, attract relatively little attention from the public or the medical profession because many people believe that no effective treatment of alcoholic liver disease is available. However, new insights into the mechanisms contributing to the disorder have resulted in prospects for improved treatments, including nutritional management approaches that can lead to better outcomes.

Management of Nutritional Deficiencies

Many drinkers who consume more than 30 percent of their total calories as alcohol ingest less than the recommended daily amounts of carbohydrates; proteins; fats; vitamins A, C, and B (especially thiamine); and minerals, such as calcium and iron. Deficiencies in these essential nutrients may exacerbate the effects of alcohol itself, resulting in serious disorders. To prevent these deficiencies, clinicians can provide alcoholics with a complete diet comparable to that of nonalcoholics. Even a complete, balanced diet, however, cannot prevent some of the organ damage that results from alcohol's direct toxic effects, including alcoholic liver disease.

Nevertheless, dietary supplements may prevent or ameliorate some of alcohol's harmful effects. For example, brain damage resulting from a lack of vitamin B₁ (thiamine), which can lead to conditions such as Wernicke-Korsakoff syndrome, can be reversed to some extent. Vitamin B₁ generally can be administered with a great margin of safety; therefore, all alcoholics undergoing treatment should be presumed to have a vitamin B₁ deficiency and should receive 50 mg of thiamine per day (either by injection if the patients are hospitalized or by mouth). Alcoholics also should receive supplements of vitamins B₂ (riboflavin) and B₆ (pyridoxine) at the dosages usually found in standard multivitamin preparations. Adequate folic acid levels can in most cases be achieved with a normal diet, unless there is evidence of a severe deficiency. As discussed before, vitamin A should be given only to those alcoholics who have a well-documented deficiency and who can stop or at least moderate their alcohol consumption, because of the potential harmful effects of vitamin A when combined with alcohol.

In addition to an improved diet to reverse nutritional deficiencies, alcoholics with moderate malnutrition also might benefit from treatment with anabolic steroids. These compounds, which are derived from the male hormone testosterone, can be used in the short term to promote overall body buildup and therefore may help the alcoholic recover from malnutrition.

Prevention of Fatty Liver

As mentioned, alcohol's interference with the normal metabolism of fatty acids promotes the deposit of dietary fat in the liver. Consequently, decreasing the amount of fat in the diet can reduce the severity of the alcoholic fatty liver. Another means of influencing the extent of alcoholic fatty liver is to change the type of fats consumed. For example, researchers found that consumption of fat molecules known as long-chain triglycerides promotes fatty liver, whereas medium-chain triglycerides (MCTs) significantly reduce alcoholic fatty liver. This difference probably results from the fact that MCTs are more likely to be broken down in the body than long-chain triglycerides and therefore are less likely to be deposited in the liver. Animal studies have confirmed that MCTs can protect against fat deposition in the liver. Thus, providing a diet rich in MCTs may be a promising therapeutic approach, particularly for relatively short-term interventions in patients who are recovering from alcohol-induced liver injury. MCTs generally are available only in health food stores as a dietary supplement.

Antioxidant Therapy to Reduce Oxidative Stress

Alcohol-induced oxidative stress in the liver cells plays a major role in the development of alcoholic liver disease. This condition results from several processes related to alcohol metabolism: Changes in the NAD/NADH ratio resulting from alcohol breakdown by ADH. Production of ROS during alcohol breakdown by the MEOS. This is particularly important after chronic alcohol consumption, which stimulates the activity of the MEOS. Reduced levels of the antioxidant GSH in the liver. GSH is a small molecule consisting of three amino acids, including cysteine. Acetaldehyde, the first product of alcohol breakdown, can bind to GSH and specifically to cysteine, thereby removing active GSH from the liver cells. In addition, alcohol itself inhibits the production of new GSH.

Both increased ROS production and GSH depletion lead, among other harmful effects, to the abnormal breakdown of fat molecules (lipid peroxidation). This process results in the formation of toxic compounds that can stimulate scarring and damage liver cells, thereby contributing to alcoholic liver disease. Accordingly, it is important to prevent or reduce the oxidative stress associated with alcohol metabolism. One approach to achieve this is to ensure that the cells have adequate levels of antioxidants, particularly GSH, that can "capture" ROS and break them down or convert them to less harmful molecules. Because GSH depletion plays a key role in alcoholic liver injury, it is therapeutically important to increase GSH levels in the liver. GSH cannot be administered directly, however, because the molecule cannot penetrate directly into the liver cells. Similarly, the amino acid cysteine, which is most important for ensuring adequate GSH levels, cannot be used as a supplement because it cannot enter the liver cells. Therefore, clinicians have tried to administer precursors of cysteine, such as the compound acetylcysteine or the molecule S-adenosylmethionine (SAMe) (discussed in the following section), which can reach the cells and be converted to cysteine there.

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