Thiamin (vitamin B-1)

Thiamin (vitamin B-1) is a water-soluble substance, consisting of thiazole and pyrimidine rings joined by a methylene bridge, with both moieties needed for full biologic action. Thiamin is found in high concentrations in skeletal muscle, the heart, liver, kidneys and brain. The total amount in an adult is about 30 mg and the biologic half-life in the body is about 15 days. It is not surprising that a state of severe depletion can be seen in patients on a strict thiamin-deficient diet in 18 days.

Thiamin pyrophosphate (TPP) is the coenzyme for pyruvate dehydrogenase, transketolase, and a-ketoglutarate. Decarboxylation in the tricarboxylic cycle is essential for generation of energy and production of the neurotransmitter acetylcholine. The pentose cycle generates NADPH (fatty acid synthesis) and pentoses for nucleic acid formation. TPP has been implicated also in sodium movement and impulse initiation in neuronal membranes.

In animals, thiamin is absorbed from the small intestine by an active (energy-requiring) process at concentrations below 2 µmoles/L and by passive (diffusion) transfer at higher levels. In rodents active transport is inhibited by ethanol, but this has not been documented in man. Malnutrition in man may contribute to decreased thiamin absorption, but this, too, requires more study. In blood, thiamin is present in erythrocytes as well as in plasma where it is bound largely to albumin.

Deficiencies: 1) Neurologic problems. These consist of central nervous manifestations including mystagmus, ophthalmoplegia, ataxia and memory deficit usually termed collectively as Wernicke's syndrome. This may merge into more extensive mental confusion with confabulation, usually called Korsakoff's psychosis. Another manifestation of thiamin deficiency, often in the setting of alcoholism, is peripheral neuropathy. 2) Cardiac problems. Cardiomegaly and congestive heart failure, with a characteristic high cardiac output presumably related to low peripheral resistance, is seen in thiamin deficiency and is termed cardiac (Shoshin) beriberi. The precise pathogenic mechanisms of these clinical syndromes are still uncertain, but are felt to be reflections of deranged carbohydrate metabolism, likely affecting the decarboxylation pathway. Detection of thiamin deficiency depends on a high index of suspicion (i.e. the syndrome may be seen with poor food intake, prolonged vomiting, intake of thiaminases in some types of fish and not just alcoholism) and the use of confirmatory laboratory tests. These include the measurement of erythrocyte transketolase activity and its enhancement on in vitro addition of thiamin pyrophosphate (TPP effect) and blood thiamin levels. The TPP effect may not be seen with chronic thiamin loss.

Clinical uses: Therapy in deficiency consists of parenteral administration of thiamin (intramuscular or intravenous) as 50-100 mg/day for 7-14 days, followed by oral therapy. In clinical disorders related to thiamin deficiency, therapy is urgent and should bypass the intestinal tract.

Diet recommendations: The Recommended Dietary Allowance for children and adults is 0.5 mg (1.9 µmoles) per 1000 Kcalories. A minimal intake of 1.0 mg/day is advised. In pregnancy an additional increment of 0.4 mg is suggested.

Food sources: Thiamin is present in many dietary products, but is found in large amounts in lean pork, legumes and yeast. Thiamin is destroyed by cooking at high temperature and by a pH above 8. As it is water-soluble, significant amounts may be lost in cooking water.

Toxicity: There is no toxicity with oral thiamin. There are only a few reports of toxic reactions to intravenous thiamin.

For further information:

Tanphaichitr, V. (1994) Thiamin. In: Modern Nutrition in Health and Disease (Shils, M.E., Olson, J.A., & Shike, M., eds.), 8th ed., vol. 1, pp. 359-365. Lea & Febiger, Philadelphia, PA

Tan, G.H., Farnell, G.F., Hensrud, D.D. & Litin, S.C. (1994) Acute Wernicke's encephalopathy attributable to pure dietary thiamine deficiency. Mayo. Clin. Proc. 69: 849-850.

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