In this paper an attempt has been made to identify important factors governing the supply of thiamine and to examine the relative roles of thiamine and ethanol in the pathogenesis of alcoholic brain damage.Thiamine depletion occurs in alcoholics principally through decreased intake, impaired absorp tion and reduced hepatic storage. The kinetics of thiamine uptake and turnover in brain are such that any fall in circulating levels of the vitamin may significantly impair the supply to the brain.The brain depends on an adequate supply of glucose both as an energy source and as a donor of carbon fragments for protein and lipid biosynthesis. Glucose utilisation is, however, thiamine dependent and it is likely that this is a major factor in the production of thiamine deficient brain damage.Ethanol alone can cause a number of structural alterations in brain tissue and these lesions may be found in alcoholics either in association with or in the absence of thiamine deficient lesions. It is also probable that ethanol and thiamine deficiency act synergistically to produce structural damage.Recurrent deficiences of many different kinds also play a part in the production of cumulative brain damage in the alcoholic.
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