Thiamine deficiency as predisposition to, and consequence of, increased alcohol consumption

Alcohol Alcohol. 1996 Jul;31(4):421-7. doi: 10.1093/oxfordjournals.alcalc.a008172.


It was found that the activity of the marker thiamine-dependent enzyme, transketolase (TK), was decreased (down to 61-79% of control) in blood, liver and brain of inbred rats following a 6-month consumption of 15% ethanol as their only source of drinking fluid. After ethanol withdrawal, the enzyme activity was gradually restored, but did not reach the control values until 1 month following cessation of alcohol consumption. Moreover, in rats preferring ethanol, the decrease of TK activity was more pronounced than in water-preferring rats. Another experiment showed that thiamine deficiency induced by the thiamine antagonist, oxythiamine (200 mg/kg), led to a prolonged increase of the preferential intake of ethanol solutions in inbred rats. Significantly lower liver TK activities and thiamine pyrophosphate content were found in Finnish AA line rats as opposed to ANA line rats which had been obtained by selective outbreeding for high and low voluntary alcohol intake, respectively. Significantly lower TK activity was also found in the whole brain (89%), cerebellum (79%) and pons-medulla oblongata (87%) of AA rats as compared to ANA animals. Our own findings and the literature data confirm the hypothesis that thiamine deficiency can be both predisposing to and a consequence of, increased alcohol consumption.

MeSH terms

  • Alcoholism / genetics*
  • Alcoholism / physiopathology
  • Animals
  • Brain / physiopathology
  • Genotype
  • Liver / physiopathology
  • Male
  • Oxythiamine / pharmacology
  • Rats
  • Rats, Inbred Strains
  • Risk Factors
  • Thiamine Deficiency / genetics*
  • Thiamine Deficiency / physiopathology
  • Thiamine Pyrophosphate / blood
  • Transketolase / blood


  • Oxythiamine
  • Transketolase
  • Thiamine Pyrophosphate