The Nutritional Status of Alcoholics : Vitamins

by National Institute of Health

(Page 3 of 7)

Vitamins are molecules that are present in small amounts in various foods and are essential for normal metabolism; insufficient vitamin levels in the body can lead to serious diseases. Alcoholics, even without liver disease, tend to have clinical and/or laboratory signs of deficiencies in certain vitamins, particularly vitamins B₁ (thiamine), B₂ (riboflavin), B₆ (pyridoxine), and C (ascorbic acid), as well as folic acid. The severity of these deficiencies correlates with the amount of alcohol consumed and with the corresponding decrease in vitamin intake.

Vitamin deficiencies are especially common in patients with cirrhosis and result both from reduced intake with the diet and, at least for some vitamins, from reduced absorption of those vitamins that are ingested. One important example is the vitamin A deficiency frequently found in patients with cirrhosis. Vitamin A (retinol), which is essential for bone growth and normal eye function, can be obtained directly from the diet or can be produced in the body from a precursor compound called beta-carotene.

Alcohol's Effects on Vitamin A Levels. Numerous studies have assessed the effects of alcohol consumption on vitamin A and beta-carotene levels in the liver and blood. In the liver, both heavy alcohol consumption and use of other drugs can lead to reduced vitamin A levels. These drugs enhance the activity of the liver enzymes that break down vitamin A and similar molecules.

In the blood, short-term administration of alcohol results either in unchanged or increased vitamin A levels. Studies using baboons found that long-term feeding of alcohol raised the animals' blood levels of beta-carotene, and increased beta-carotene levels in the blood also were found in human alcoholics. Other investigations compared the levels of beta-carotene, vitamin A, and other molecules related to these two compounds in the blood and livers of patients with alcoholic and nonalcoholic liver disease, normal livers of transplant donors, and blood from normal control subjects. The latter study found that the levels of vitamin A-related compounds, particularly vitamin A itself, were reduced in the livers of patients with liver disease (whether alcohol related or not) compared with the other groups. The decreases were greatest in patients with the most severe form of alcoholic liver disease. Despite their reduced levels of vitamin A in the liver, however, many of these patients exhibited normal levels of beta-carotene in the blood, which suggests that liver disease alters the liver's ability to take up beta-carotene and/or convert it into vitamin A. Impaired conversion of ingested beta-carotene to vitamin A in the liver during alcohol consumption may partially explain why the concentration of vitamin A in the liver is reduced, especially at advanced stages of alcoholic liver disease. In addition, alcohol promotes the secretion of vitamin A from the liver, thereby enhancing its decline in the liver.

As reviewed by Leo and Lieber, studies of rats that were fed alcohol every day for several weeks confirmed that alcohol can reduce vitamin A levels in the liver. After receiving alcohol for 4 to 6 weeks, the animals' vitamin A levels in the liver had declined by 60 percent. This reduction became even more severe after 7 to 9 weeks of alcohol administration. At the same time, the levels of vitamin A in the blood did not change. Even supplementing the animals' diet with five times the usual amount of vitamin A could not prevent the alcohol-induced vitamin A depletion in the liver. Similar results were obtained in baboons that received 50 percent of their calories as alcohol. In these animals, vitamin A levels in the liver declined by 60 percent after 4 months and by 95 percent after 24 to 84 months.

Consequences of Altered Vitamin A Levels. Vitamin A deficiency can impair the ability of the eye to adjust to dark conditions (causing night blindness) and can result in other eye disorders. In the liver, reduced vitamin A levels can change the structures of components of some cells, and these changes may be exacerbated by the consumption of alcohol. However, excess vitamin A also has harmful effects. For example, in the liver, increased vitamin A levels can promote the formation of scar tissue, which also is worsened by concurrent alcohol use.

Alcohol has varying effects on vitamin A and beta-carotene content and metabolism throughout the body. For example, alcohol increases the vitamin A content of some tissues and decreases vitamin A in other tissues. In addition, alcohol can speed up or alter the conversion of vitamin A to other compounds. Some or all of these changes may contribute to alcohol's toxic effects on the liver and to the development of liver fibrosis. Alcohol-mediated alterations of vitamin A status also may play a role in the association of low vitamin A or beta-carotene levels with certain types of cancer.

Vitamin A Therapy. Because alcohol consumption leads to reduced vitamin A levels in the liver, with potentially detrimental effects, it would appear plausible to treat alcoholics with extra vitamin A to compensate for alcohol's effects. However, several factors complicate vitamin A therapy in the setting of alcoholism: it is difficult to assess how much vitamin A actually is stored in the tissues, because vitamin A in the blood does not necessarily reflect levels in the liver. High doses of vitamin A are toxic. Even usual doses of vitamin A are potentially harmful in alcoholics who continue to drink, because alcohol potentiates the toxicity of vitamin A.

Therefore, only modest doses of vitamin A should be given to patients who may continue to drink or use other drugs. Patients with night blindness who have low levels of vitamin A in the blood may be given 2 mg of vitamin A per day for several weeks as a possible therapy. Treatment with zinc also may be necessary, especially in patients with night blindness, because this mineral is needed for vitamin A metabolism.

To avoid or reduce the problems associated with vitamin A therapy, clinicians also have considered treating alcoholics with the vitamin A precursor beta-carotene. However, although beta-carotene is thought to be less hazardous, it also can cause toxic effects in the livers of patients who continue to use alcohol. In addition, beta-carotene increases the risk of lung cancer in smokers. This is important because most smokers also drink alcohol, and researchers have found that the increased lung cancer risk after beta-carotene therapy was related to the smokers' concurrent alcohol use. For this reason, beta-carotene therapy of these patients must be used cautiously.

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