The role of thiamine deficiency in alcoholic brain disease

Alcohol Res Health. 2003;27(2):134-42.


A deficiency in the essential nutrient thiamine resulting from chronic alcohol consumption is one factor underlying alcohol-induced brain damage. Thiamine is a helper molecule (i.e., a cofactor) required by three enzymes involved in two pathways of carbohydrate metabolism. Because intermediate products of these pathways are needed for the generation of other essential molecules in the cells (e.g., building blocks of proteins and DNA as well as brain chemicals), a reduction in thiamine can interfere with numerous cellular functions, leading to serious brain disorders, including Wernicke-Korsakoff syndrome, which is found predominantly in alcoholics. Chronic alcohol consumption can result in thiamine deficiency by causing inadequate nutritional thiamine intake, decreased absorption of thiamine from the gastrointestinal tract, and impaired thiamine utilization in the cells. People differ in their susceptibility to thiamine deficiency, however, and different brain regions also may be more or less sensitive to this condition.

Publication types

  • Review

MeSH terms

  • Alcohol Amnestic Disorder / metabolism
  • Alcohol Amnestic Disorder / pathology
  • Alcohol-Related Disorders / metabolism*
  • Alcohol-Related Disorders / pathology
  • Animals
  • Brain / metabolism*
  • Brain / pathology
  • Humans
  • Thiamine / metabolism
  • Thiamine Deficiency / metabolism*
  • Thiamine Deficiency / pathology
  • Wernicke Encephalopathy / metabolism
  • Wernicke Encephalopathy / pathology


  • Thiamine