Vitamin B1 (thiamine) is a water-soluble vitamin. Intake of vitamin B1 is required on a regular basis due to the body's inability to store it in large amounts. Vitamin B1 is absorbed from the lumen of the intestine by an active transport process. In the mucosal cells of the duodenum, vitamin B1 is phosphorylated resulting in thiamine monophosphate (TMP), thiamine pyrophosphate (TPP), and thiamine triphosphate (TTP). The most physiologically active and abundant form of the vitamin in the body is TPP. In carbohydrate metabolism, TPP functions as a coenzyme in the decarboxylation of alpha-ketoacids such as pyruvate and in transketolation. Decarboxylation of alpha-ketoacids produces energy, which can be used by cells, and transketolation reactions yield pentoses, which can be used for nucleic acid synthesis, and NADPH, which is used in fatty acid synthesis. In neuronal cells, a noncoenzymatic role for vitamin B1, in which it modulates brain chloride channels, has also been described.

The disease of vitamin B1 deficiency is called beri beri. Beri beri is characterized by neurological symptoms ('dry' beri beri) and cardiovascular symptoms ('wet' beri beri). Beri beri became widespread in East Asia in the nineteenth century when polished rice, which lacked the vitamin B1-rich husks, became a diet staple. Major causes of vitamin B1 deficiency in today's society are alcoholism and inadequate intake of vitamin B1; the latter occurs mostly in less industrialized countries. Treating beri beri patients with vitamin B1 reduces the symptoms of the disease.

Recent studies suggest a role for vitamin B1 in the management of congestive heart failure. Patients given the loop diuretic furosemide may be at greater risk for vitamin B1 deficiency through urinary loss, which can lead to wet beri beri and can contribute to cardiac insufficiency. In these patients, supplementation with thiamine results in improved cardiac conditions.

Vitamin B1 may also play a negative role in cancer chemotherapy. Researchers have found that the overadministration of vitamin B1 to chemotherapy patients may aid the tumor cells by providing ribose via transketolation as a substrate for nucleic acid synthesis and ultimately tumor growth.

• Pork
• Wheat germ
• Grain cereals
• Brewer's yeast
• White enriched rice
• Soy milk
• Sunflower seeds
• Beans
• Pasta
• Peanuts (unroasted)

Brewer's yeast is the richest source of vitamin B1. Although milk, fruits, and vegetables are not rich in vitamin B1, they contribute significantly to the recommended dietary allowance of vitamin B1 when consumed in sufficient amounts.

The vitamin B1 molecule consists of pyrimidine and thiazole rings connected by a methylene bridge. In its pure form, thiamine hydrochloride is a crystalline yellowish-white powder with a salty, nut-like taste. It is fairly stable in dry form and is only heat-stable in acid form. Its stability in prepared food is dependent on cooking time and temperature, pH, amount of water used and discarded, and whether the water used was chlorinated. Sulfites, which are used in the production and processing of food, destroy the biological activity of vitamin B1 by splitting the molecule into its pyrimidine and thiazole moieties.

Vitamin B1 is available commercially in salt form as thiamine hydrochloride and thiamine mononitrate. Standard preparations are available as 50-mg, 100-mg, and 300-mg doses in vitamin B1 tablets or capsules; 50-mg, 125-mg, and 150-mg doses in B-complex capsules or tablets, and in 1.5-mg doses in multivitamins (both adult and children's chewable).

Therapeutic uses are limited to conditions that are caused by vitamin B1 deficiency and prophylactic treatment of vitamin B1 deficiency.

• Dry beri beri. Symptoms of dry beri beri include peripheral neuritis with sensory disturbances in the extremities, convulsions, exaggeration of tendon reflexes, and the "burning feet syndrome." This is usually observed in chronic alcoholics. Chronic alcoholics with these symptoms should receive up to 40 mg of oral vitamin B1 daily.
• Wernicke's encephalopathy. This is a vitamin B1 deficiency that affects the central nervous system. Classic symptoms are confusion, ophthalmoplegia, nystagmus, and ataxia. A typical treatment consists of 100 mg of intravenous vitamin B1 daily for three days. If left untreated, Wernicke's encephalopathy can lead to Korsakoff's psychosis, which is characterized by confabulation and in most cases is not treatable once established.
• Cardiovascular disease. This is also called wet beri beri and is characterized by heart hypertrophy, dilatation, tachycardia, respiratory distress, and edema of the legs. Treatment with vitamin B1 will lead to striking recovery if vitamin B1 deficiency is the true cause of the disease. A typical therapeutic regimen is 10 to 30 mg of parenteral vitamin B1 tid until symptoms reverse.
• Infantile beri beri. Infantile beri beri is seen mostly in breast-fed infants of vitamin B1-deficient mothers, which mainly occurs in less industrialized countries. Symptoms include loss of appetite, vomiting, constipation, greenish stools, and progressive edema. Loss of laryngeal nerve function, which leads to aphonia, is a diagnostic feature. In acute disease decreased urine output and cardiac failure occurs. Infants with a mild form of the disease can be treated with 10 mg of oral vitamin B1 daily; 25 mg of intravenous vitamin B1 should be administered to infants with acute cardiac failure, although the prognosis is poor. This treatment should be conducted only under physician supervision.
• Gastrointestinal disorders. In some patients vitamin B1 deficiency affects the gastrointestinal tract. When this occurs, vitamin B1 replacement can relieve symptoms such as ulcerative colitis, diarrhea, and gastrointestinal hypotonia.
• Neuritis of pregnancy. This is caused by hyperemesis gravidarum or low vitamin B1 intake. If vitamin B1 deficiency is the cause of the neuritis, clinical improvement will be seen following vitamin B1 therapy. A typical therapeutic regimen is 5 to 10 mg of vitamin B1 daily, given parenterally if vomiting is severe.
• Congenital defects. Maple syrup disease, congenital lactate acidosis, subacute necrotizing encephalopathy, and vitamin B1-responsive megaloblastic anemia are inherited diseases with congenital defects in vitamin B1 metabolism. Vitamin B1 therapy has been reported to improve these conditions.
• Prophylaxis. Patients receiving parenteral nutrition and those whose vitamin B1 status is suspect (comatose patients, alcoholics) should be given vitamin B1 supplementation before receiving dextrose-containing solutions.

• Neonates to 6 months: 0.3 mg/day
• Infants 6 months to 1 year: 0.4 mg/day
• Children 1 to 3 years: 0.7 mg/day
• Children 4 to 6 years: 0.9 mg/day
• Children 7 to 10 years: 1.0 mg/day
• Boys over 11 years, men 18 to 50 years: 1.5 mg/day
• Men over 50 years: 1.2 mg/day
• Girls over 11 years, women 18 to 50 years: 1.1 mg/day
• Women over 50 years: 1.0 mg/day
• Pregnant women: 1.5 mg/day; lactating women: 1.6 mg/day.

Vitamin B1 is relatively nontoxic. Some gastric disturbance may be seen at very high oral doses. Exceeding the RDA for vitamin B1 by more than 100-fold has in rare instances led to an allergic reaction.

Vitamin B1 may play a role in failed chemotherapy in cancer patients who receive doses that are 200-fold over the RDA.

Supplementation with vitamins B1, B2, and B6 (10 mg each) at the start of tricyclic antidepressant therapy improved cognitive functioning and depression ratings in 14 geriatric patients undergoing treatment with nortriptyline titrated to doses yielding blood levels between 50 to 150 ng/mL (Bell et al. 1992). B vitamins may augment the treatment of depression in elderly patients.

In a randomized, double-blind, placebo-controlled, double-crossover clinical trial with 13 healthy subjects, coadministration of thiamine (5 g po) countered the cognitive side effects associated with scopolamine treatment (0.007 mg/kg IM) as compared to placebo (Meador et al. 1993).

In one study, the bioavailability of tetracycline hydrochloride was reduced significantly by concomitant administration of vitamin B complex to healthy subjects (Omray 1981). Patients should be cautioned to take vitamin B complex supplements at different times from tetracycline.

Bell I, Edman J, Morrow F, et al. Brief communication. Vitamin B1, B2, and B6 augmentation of tricyclic antidepressant treatment in geriatric depression with cognitive dysfunction. J Am Coll Nutr. 1992;11:159-163.

Boros LG, Brandes JL, Lee W-N P, et al. Thiamine supplementation to cancer patients: a double-edged sword. Anticancer Res. 1998;18:595-602.

Ekhard ZE, Filer LJ, eds. Present Knowledge in Nutrition. 7th ed. Washington, DC: ILIS Press; 1996:160-166.

Hardman JG, Limbird LE, eds. Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill; 1996:1555-1558.

Leslie D, Gheorghiade M. Is there a role for thiamine supplementation in the management of heart failure? Am Heart J. 1996;131:1248-1250.

Lindberg MC, Oyler RA. Wernick's encephalopathy. Am Fam Physician. 1990;41:1205-1209.

Mahan LK, Arlin MT, eds. Krause's Food, Nutrition and Diet Therapy. 8th ed. Philadelphia, Pa: WB Saunders Co;1992:85-87.

Mason P. Nutrition and Dietary Advice in the Pharmacy. Oxford, UK: Blackwell Scientific; 1994:269-271.

Meador KJ, Nichols ME, Franke P, et al. Evidence for a central cholinergic effect of high-dose thiamine. Ann Neurol. 1993;34:724-726.

National Academy of Science. Recommended Dietary Allowances. Accessed at www.nal.usda.gov/fnic/dietary/rda.html on January 4, 1999.

Omray A. Evaluation of pharmacokinetic parameters of tetracycline hydrochloride upon oral administration with vitamin C and vitamin B complex. Hindustan Antibiot Bull. 1981;23(VI):33-37.