Folates are polyglutamylated in their dietary forms and circulate in the methylated and reduced mono-glutatate form. Folates function in DNA synthesis and cell turnover, and play a central role in methio-nine metabolism as substrate for the enzyme methio-nine synthase in the conversion of homocysteine to methionine. While originally recognized as a cause of megaloblastic anemia, the expanding consequences of folate deficiency are related to elevated circulating homocysteine and include increased risk for neural tube defects and other congenital abnormalities in newborns and altered cognition in the elderly. Prior to folate fortification in the US, the incidence of low serum folate levels in chronic alcoholics was at about 80%. Megaloblastic anemia, due to the negative effects of folate deficiency on DNA synthesis, has been described in about one-third of patients with alcoholic liver disease. Excessive alcohol use is associated with reversible hyperhomocysteine-mia in chronic alcoholics because of the inhibitory effect of alcohol or its metabolite acetaldehyde on methionine synthase. Furthermore, folate deficiency may play a role in the pathogenesis of alcoholic liver disease by exacerbating abnormalities in the metabolism of S-adenosylmethionine.

The causes of folate deficiency in chronic alcoholism are multiple. With the exception of beer, all alcoholic beverages are devoid of folate, and the typical diet of the chronic alcoholic does not include its fresh vegetable sources. Chronic alcoholism is associated with intestinal folate malabsorption, decreased liver folate uptake, and accelerated folate excretion in the urine. In addition, alcoholic liver disease results in decreased liver stores of folate, so the duration of time for development of folate deficiency with marginal diet is shortened.

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