Thiamine Deficiency in Alcoholic Brain Disease
Thiamine deficiency is the established cause of an alcohollinked neurological disorder known as WernickeKorsakoff syndrome (WKS). The role of thiamine in the development of WKS is supported by findings that giving this nutrient to patients with WKS reverses many of the acute symptoms of the disease.
Thiamine, also known as vitamin B1, is an essential nutrient required by all tissues, including the brain. The human body itself cannot produce thiamine but must ingest it with the diet.
Thiamine is required for several enzymes that are important for the metabolism of sugar (carbohydrate catabolism). Proper functioning of these enzymes is required for critical biochemical reactions in the body, including the synthesis of certain brain chemicals (i.e., neurotransmitters); production of the molecules making up the cells genetic material (i.e., nucleic acids); and production of fatty acids, steroids, and certain complex sugar molecules. In addition, inadequate functioning of the thiamineusing enzymes can interfere with the bodys defense against the damage (i.e., oxidative stress) caused by harmful, highly reactive oxygen molecules called free radicals.
Three enzymes that require thiamine as a cofactor. These enzymes are called transketolase, pyruvate dehydrogenase (PDH) and alphaketoglutarate dehydrogenase (KGDH); they all participate in the catabolism of sugar molecules (i.e., carbohydrates) in the body. As a result, thiamine deficiency causes suboptimal levels of functional enzymes in the cell, in addition to interfering with the activity of those enzymes.
Transketolase is an important enzyme in a biochemical pathway called the pentose phosphate pathway. In this set of biochemical reactions, a molecule called glucose6phosphate, which is derived from the sugar glucose, is modified by transketolase, yielding two productsa sugar called ribose5phosphate and a molecule called reduced nicotinamide adenine dinucleotide phosphate (NADPH). Both of these molecules are essential for the production of numerous other important molecules in the cell.
Thiamine deficiency can lead to cell damage in the central nervous system through:
Several mechanisms have been identified through which alcoholism may contribute to thiamine deficiency:
Thiamine, also known as vitamin B1, is an essential nutrient required by all tissues, including the brain. The human body itself cannot produce thiamine but must ingest it with the diet.
Thiamine is required for several enzymes that are important for the metabolism of sugar (carbohydrate catabolism). Proper functioning of these enzymes is required for critical biochemical reactions in the body, including the synthesis of certain brain chemicals (i.e., neurotransmitters); production of the molecules making up the cells genetic material (i.e., nucleic acids); and production of fatty acids, steroids, and certain complex sugar molecules. In addition, inadequate functioning of the thiamineusing enzymes can interfere with the bodys defense against the damage (i.e., oxidative stress) caused by harmful, highly reactive oxygen molecules called free radicals.
Three enzymes that require thiamine as a cofactor. These enzymes are called transketolase, pyruvate dehydrogenase (PDH) and alphaketoglutarate dehydrogenase (KGDH); they all participate in the catabolism of sugar molecules (i.e., carbohydrates) in the body. As a result, thiamine deficiency causes suboptimal levels of functional enzymes in the cell, in addition to interfering with the activity of those enzymes.
Transketolase is an important enzyme in a biochemical pathway called the pentose phosphate pathway. In this set of biochemical reactions, a molecule called glucose6phosphate, which is derived from the sugar glucose, is modified by transketolase, yielding two productsa sugar called ribose5phosphate and a molecule called reduced nicotinamide adenine dinucleotide phosphate (NADPH). Both of these molecules are essential for the production of numerous other important molecules in the cell.
Thiamine deficiency can lead to cell damage in the central nervous system through:
- cell necrosis
- cellular apoptosis
- oxidative stress
Several mechanisms have been identified through which alcoholism may contribute to thiamine deficiency:
- Inadequate nutritional intake
- Decreased absorption of thiamine from the gastrointestinal tract and reduced uptake into cells
- Impaired utilization of thiamine in the cells
