Published scientific literature shows that alcoholism directly contributes to thiamine deficiency, notes the United States National Institute on Alcohol Abuse and Alcoholism (NIAAA). The effects of excessive alcohol consumption in terms of thiamine deficiency occur via several mechanisms of action, which include insufficient intake of thiamine from dietary sources, reduced absorption of thiamine from the digestive tract and poor thiamine utilization in the cells.
Thiamine deficiency due to alcoholism is present in up to 80 percent of people with a history of chronic alcohol abuse, states the NIAAA. Most individuals need at least 0.33 milligrams of thiamine for every 1,000 calories consumed from foods. However, those who drink heavily tend to derive less than 0.29 milligrams for every 1,000 caloric intake.
Research shows that alcoholics have considerably reduced concentrations of a phosphate-containing form of thiamine compound, although there is an abundance of free thiamine in the body. This may indicate that increased amounts of alcohol in the body inhibit the synthesis of phosphate-containing thiamine from the free form of thiamine.
Animal studies reveal that exposure to acute levels of alcohol hinders the activity of the enzyme thiamine diphosphokinase (TPK), which facilitates the transport of thiamine from the gastrointestinal tract into the blood stream to be delivered throughout the body. As of 2015, there is inadequate clinical data to establish whether alcohol positively impacts TPK in humans.
However, scientists theorize that there is decreased activity of TPK in alcoholics. This presumption stems from the fact that alcoholics contain only a small proportion of phosphorylated thiamine compared to non-alcoholics.