The classic signs of vitamin deficiency only occur in states of extreme 
depletion and are unreliable indicators for early treatment or prophylaxis of 
alcoholic patients at risk. Post-mortem findings demonstrate that thiamine 
(vitamin B1) deficiency sufficient to cause irreversible brain damage is not 
diagnosed ante mortem in 80-90% of these patients. The causes of vitamin 
deficiency are reviewed with special attention to the inhibition of oral 
thiamine hydrochloride absorption in man caused by malnutrition present in 
alcoholic patients or by the direct effects of ethanol on intestinal transport. 
As the condition of the patient misusing alcohol progresses, damage to brain, 
liver, gastrointestinal tract, and pancreas continue (with other factors 
discussed) to further compromise the patient. Decreased intake, malabsorption, 
reduced storage, and impaired utilization further reduce the chances of unaided 
recovery. Failure of large oral doses of thiamine hydrochloride to provide an 
effective treatment for Wernicke's encephalopathy emphasizes the need for 
adequate and rapid replacement of depleted brain thiamine levels by repeated 
parenteral therapy in adequate doses.