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Vitamin B1 (Thiamine)

Nutrient Name: Vitamin B1, thiamine.
Synonyms: Thiamin, thiamine.
Related Substances: Aneurine hydrochloride, thiamine hydrochloride, thiaminium chloride hydrochloride; benfotiamine; tetrahydrofurfuryl disulfide (TTFD).

Summary Table
Drug/Class Interaction TypeMechanism and SignificanceManagement

Antacids interfere with the absorption of thiamine and other nutrients.Separate intake of thiamine sources and antacids by at least 2 hours.

Repeated or protracted administration of broad-spectrum antibiotics can destroy beneficial intestinal flora and disrupt healthy gut ecology, including production of B vitamins. Mechanism is widely recognized, but clinical significance and long-term implications are just beginning to be acknowledged and understood.Administration of diverse probiotic is judicious after significant antibiotic therapy. Multivitamin supplementation may be indicated if deficient.
Fluorouracil (5-FU)
Antimetabolite chemotherapeutic agents
/ /
Fluorouracil interferes with conversion of thiamine to thiamine pyrophosphate as a means of inhibiting DNA and RNA synthesis and tumor cell proliferation. Mechanism and probability of this interaction are axiomatic, and its clinical significance is fundamental to use as chemotherapeutic strategy.Thiamine restriction and depletion essential, but intermittent dietary enhancement or supplementation may be appropriate. Supervision and monitoring critical.
Loop diuretics
/ /
Furosemide and other loop diuretics can increase urinary thiamine excretion and induce thiamine depletion, which can contribute to cardiac insufficiency and aggravate congestive heart failure. With mechanism and prevalence of this adverse effect reaching consensus, so has appreciation of its profound clinical significance and long-term implications. Changes in medical practice are emerging.Coadminister with diuresis longer than 1 month. Monitor for deficiency symptoms.
Tricyclic antidepressants (TCAs)
Response improved with coadministration of antidepressants, including nortriptyline and TCAs, and B vitamins, particularly thiamine. Mechanism undetermined: prevention of nutrient depletion or promotion of active synergistic effect, or both. Evidence preliminary but with strong positive trend. Clinical significance and individual patient factors still undefined.B-complex coadministration judicious and considered safe, especially with probable deficiency.
Oral contraceptives (OCs)
Variable decreases in levels of thiamine and other nutrients associated with OC use. Clinical significance controversial; evidence mixed.B-complex coadministration judicious and considered safe, especially with probable deficiency.
Anticonvulsant medications
Phenytoin interferes with thiamine function, particularly in brain, CNS, and CSF. Antiepileptic drugs may deplete thiamine (and folate), and supplementation may enhance therapeutic effect.Coadminister with anticonvulsant therapy longer than 1 month. Monitor for deficiency symptoms.
Scopolamine may interfere with CNS functions of thiamine, particularly involving acetylcholine. Preliminary evidence of reduced adverse effects with thiamine coadministration. Clinical significance probable.Coadminister; may require high doses under supervision.
Reverse-transcriptase inhibitor (nucleoside) antiretroviral agents
Thiamine used to counter severe lactic acidosis associated with stavudine, alone or with HAART protocols, particularly in patients with genetic susceptibility or preexisting vitamin deficiency. Evidence from anecdotal reports, but pattern consistent.Preventive B-complex coadministration prudent. Intravenous thiamine administration indicated in critical cases. Close supervision, monitoring.
Tetracycline antibiotics

Thiamine and other B-complex vitamins may interfere with tetracycline pharmacokinetics. Concomitant intake may significantly impair bioavailability. Evidence minimal but not controversial.Avoid thiamine and B vitamins. If necessary, separate intake by 4 hours.
CNS , Central nervous system; CSF , cerebrospinal fluid; HAART , highly active antiretroviral therapy.
nutrient description

Chemistry and Forms

In 1926, thiamine was the first B vitamin isolated, as a crystalline, water-soluble, yellowish white powder with a salty, slightly nutty taste. By 1936 it had been synthesized and its chemical structure determined. This substance is heat and oxygen stable in its dry form, heat and alkali reactive in solution, and stabilized by acid.

Physiology and Function

Thiamine uptake by active transport is highest in the jejunum and ileum, with both passive diffusion and active, carrier-mediated transport. Throughout the small intestine, and generally by cells in various organs, absorption is mediated by a saturable, high-affinity transport system, and once absorbed, thiamine is primarily transported in the serum bound to albumin. In humans, thiamine can be synthesized in the large intestine as thiamine pyrophosphate (TPP). Too large a molecule to be absorbed across the intestinal mucosa, TPP requires the use of an enzyme to cleave the smaller thiamine molecule out of the compound. Skeletal muscle, heart, liver, kidneys, and the brain are sites of particularly high concentrations, although only small amounts of thiamine (30-70 mg) are typically stored in the body.

Thiamine is required for all tissues as a coenzyme in the metabolism of carbohydrates and branched-chain amino acids, particularly in the tricarboxylic acid (TCA) cycle and pentose phosphate shunt. Thiamine needs to be phosphorylated to become metabolically active, and thiamine diphosphate is its active form. Thiamine diphosphate is a cofactor for several important enzymes involved in the biosynthesis of neurotransmitters and various cell constituents, for the production of reducing equivalents used in oxidative stress responses, and for the biosyntheses of pentoses (e.g., ribose, deoxyribose) used as nucleic acid precursors. When it combines with two molecules of phosphoric acid, thiamine will form TPP. Functioning as a co-carboxylase, TPP is required for the oxidative decarboxylation of pyruvate to form active acetate and acetyl coenzyme A. It is also required for the oxidative decarboxylation of other alpha keto acids such as α-ketoglutaric acid and the 2-keto-carboxylates derived from the amino acids methionine, threonine, leucine, isoleucine, and valine. TPP is also involved as a coenzyme for the transketolase reaction, which functions for the pentose monophosphate shunt pathway. With a specific role in neurophysiology separate from its coenzyme function, TPP works at the nerve cell membrane to allow displacement so that sodium ions can freely cross the membrane. Although thiamine is needed for the metabolism of carbohydrates, fat, and protein, it is especially central to carbohydrate metabolism in the brain. In addition to providing TPP, thiamine becomes part of thiamine triphosphate, which appears to have an important function in brain cell viability. Thiamine is also required in acetylcholine and fatty acid synthesis.

Research is ongoing into the genetic and biochemical factors contributing to interindividual differences in susceptibility to development of disorders related to thiamine deficiency, as well as the differential vulnerabilities of various tissues and cell types.

nutrient in clinical practice

Known or Potential Therapeutic Uses

Thiamine deficiency manifests primarily as disorders of the nervous, cardiovascular, muscular, and gastrointestinal systems. Deficiency symptoms include: fatigue, weight loss, depression, irritability, memory loss, mental confusion, heart palpitations, tachycardia, anorexia, indigestion, edema, neuritis, neuropathies, paresthesia, hyporeflexia (especially of legs), defective muscular coordination, muscular weakness, and sore muscles (especially calves).

Historical/Ethnomedicine Precedent

Beriberi, the classic thiamine deficiency disease.

Possible Uses

Alcoholism, Alzheimer's disease, anxiety, atherosclerosis, canker sores, chronic dieting, congestive heart failure (CHF), Crohn's disease, depression, diabetes mellitus, dysmenorrhea, fibromyalgia, glaucoma, hepatitis, human immunodeficiency virus and acquired immunodeficiency syndrome (HIV/AIDS) support, insomnia, Kearns-Sayre syndrome, Leigh's disease, minor injuries, mosquito repellant, multiple sclerosis, neuropathy (especially benfotiamine), roundworms, sciatica, sensory neuropathy (diabetic), trigeminal neuralgia, Wernicke-Korsakoff syndrome; diets consisting primarily of highly processed, refined foods; treatment of thiamine deficiency–related disorders, including cardiovascular (wet) beriberi, nervous (dry) beriberi, Wernicke's encephalopathy syndrome, and peripheral neuritis associated with pellagra (vitamin B3deficiency); alcoholic patients with altered sensorium; various genetic metabolic disorders, such as thiamine-responsive megaloblastic anemia.

Dietary Sources

Pork, liver, chicken, fish, beef, wheat germ, dried yeast, cereal products, lentils, potatoes, brewer's yeast, rice polishings, most whole-grain cereals (especially wheat, oats, and rice), all seeds and nuts, beans (especially soybeans), milk and milk products, vegetables such as beets, green leafy vegetables.

Most plant and animal foods contain some thiamine, but the richest dietary sources are brewer's yeast and organ meats.

Thiamine deficiency is one of the most common nutritional deficiency patterns in modernized societies. Almost half the U.S. population consumes less than half the recommended daily allowance (RDA) of thiamine, according to the U.S. Department of Agriculture. Although whole grains may be rich in thiamine, processing of grains significantly reduces their thiamine content. Likewise, because thiamine is water soluble and heat sensitive, cooking largely results in the loss or destruction of this vitamin, especially when chlorinated water is used.

Clinical signs of thiamine deficiency primarily involve the nervous, cardiovascular, muscular, and gastrointestinal systems. Adults have the following symptoms:

  • Mental confusion, anorexia, muscle weakness, calf muscle tenderness, ataxia, indigestion, constipation, tachycardia with palpitations.
  • Wet beriberi: edema starting in the feet and progressing upward into the legs, trunk, and face, eventually resulting in death from cardiac enlargement and CHF.
  • Dry beriberi: worsened polyneuritis in early stages (particularly peripheral neuritis), difficulty walking, and muscle wasting, especially atrophy of the legs.

The distinction between wet (cardiovascular) and dry (neuritic) manifestations of beriberi usually relates to the duration and severity of the deficiency, the degree of physical exertion, and the caloric intake. The wet or edematous condition results from severe physical exertion and high carbohydrate intake. The dry or polyneuritic form stems from relative inactivity with caloric restrictions during the chronic deficiency.

Wernicke-Korsakoff syndrome is the classical manifestation of central nervous system (CNS) deficiency of thiamine caused by alcoholism. Patients present with impaired memory and cognitive function, irritability, and nystagmus caused by weakness in the sixth cranial nerve; coma is a common end state. Vitamin B1is necessary for the metabolism of alcohol, but alcohol interferes with its absorption, making malnourished alcoholics often severely thiamine deficient. Alcoholics given intravenous (IV) glucose without thiamine are at high risk of developing Wernicke-Korsakoff syndrome and sustain permanent neurological damage, because the glucose, which also requires thiamine for its metabolism, rapidly depletes remaining tissue levels of brain thiamine. For this reason, an IV “cocktail” of glucose, thiamine, and a narcotic antagonist is typically administered in emergency rooms to unconscious patients who present with unconsciousness of unknown etiology.

Infant symptoms appear suddenly and severely, involving cardiac failure and cyanosis.

The etiology of thiamine deficiency can be traced to an exclusive diet of milled, nonenriched rice or wheat, raw fish consumption (microbial thiaminases), large amounts of tea, alcoholism (impaired absorption and storage, poor nutrition, increased thiamine utilization), use of loop diuretics, and several inborn errors of metabolism.

Special Populations

Individuals with alcoholism, anorexia, CHF, Crohn's disease, folate deficiency, malabsorption syndrome, and multiple sclerosis are at increased risk of developing thiamine deficiency, as are those undergoing long-term diuretic therapy, hemodialysis, or peritoneal dialysis.

Alcoholic individuals frequently develop a deficiency of thiamine because the vitamin is a necessary cofactor in the metabolism of alcohol. Because many alcoholics tend to eat less and drink more, and usually their alcohol-based drinks are low in thiamine, they frequently develop a thiamine deficiency. In hospitals it is routine for alcoholics to receive intramuscular (IM) injections of thiamine on admission.

Elderly persons demonstrate a general decline in thiamine levels that is apparently related more to age than to coexisting illness or health status. This increased susceptibility enhances the risk for adverse effects of drug-induced depletion, especially in regard to cardiovascular health and cognitive stability. 1

Nutrient Preparations Available

Thiamine, water soluble. Thiamine hydrochloride is generally considered the preferred supplemental form of thiamine. Thiamine mononitrate is also available. Thiamine supplementation is usually provided in vitamin B–complex formulations, in most multivitamin preparations, and in vitamin-enriched foods, such as breakfast cereals.

Benfotiamine is a lipid-soluble form of thiamine developed and patented in Japan, now widely used in neuropathy therapies.

Dosage Forms Available

Capsule, liquid, tablet, effervescent tablet; liposomal spray. Parenteral form may be administered by IM or slow IV injection.

Source Materials for Nutrient Preparations


Dosage Range

The RDA for thiamine varies slightly with gender and life stage.

  • Men (>19 years): 1.2 mg/day
  • Women (>19 years): 1.1 mg/day
  • Pregnancy and breastfeeding (any age): 1.4 mg/day


  • Supplemental/Maintenance:   Dependent on dietary intake, usually 1 to 2 mg/day. A paper on the “ideal” daily thiamine intake reported that the healthiest people consumed more than 9 mg/day. 2
  • Pharmacological/Therapeutic:   1.5 to 200 mg/day. In research studies, therapeutic dosage for most conditions ranges from 10 to 100 mg/day, in divided doses. In clinical practice, 200 to 600 mg/day may be given, and some clinicians have used oral dosages as high as 8 g/day, in divided doses, for a variety of metabolic disorders.
  • Thiamine deficiency (beriberi):   5 to 30 mg per dose, intramuscularly (IM) or intravenously (IV), three times daily (if critically ill); then orally 5 to 30 mg/day in single or divided doses, three times daily for 1 month.
  • Wernicke's encephalopathy:   100 mg IV initially, then 50 to 100 mg/day IM or IV until consuming a consistently balanced and nutritious diet.
  • Toxic:   There is no defined upper limit (UL) for thiamine because of its relative safety.

Pediatric (<18 years)


  • Infants: 0.3 to 0.5 mg/day
  • Children: 0.5 to 1 mg/day
Pharmacologic/Therapeutic, for thiamine deficiency (beriberi): 10 to 25 mg per dose, IM or IV, daily (if critically ill), or 10 to 50 mg per dose orally every day for 2 weeks, then 5 to 10 mg per dose orally daily for 1 month.
  • Toxic:   No toxic intake level known to date.

safety profile


Thiamine is generally considered virtually nontoxic, even in very high doses orally. Being water soluble, thiamine excretion is rapid; the vitamin is not stored in the body, and accumulation to toxic levels is highly improbable using oral intake. No adverse effects associated with thiamine intake from food sources or nutritional supplements have been reported. Rare occurrences of adverse effects of thiamine have been documented, although they appear to be largely associated with allergic reactions to thiamine injections.

Nutrient Adverse Effects

General Adverse Effects

Adverse effects are theoretically possible but rare with oral supplemental thiamine intake. Oral doses greater than 200 mg have been reported to cause drowsiness in some individuals. In a study of 989 patients, 100 mg/day IV thiamine hydrochloride resulted in a burning effect at the injection site in 11 subjects and pruritus in one. 3

Large doses of vitamin B1over an extended period may cause imbalance among various B vitamins.

Administration of IV or IM thiamine warrants caution because anaphylactic or allergic reaction infrequently occurs. Allergic reactions to thiamine injections are rare (<1%) but can be severe and include cardiovascular collapse and death, angioedema, paresthesia, warmth, and rash.

Adverse Effects Among Specific Populations

High oral intakes might have some unknown potential for adverse reactions in select, metabolically compromised populations because of pharmacogenomic susceptibility, but such data are only recently under consideration.

Pregnancy and Nursing

A review of the medical literature reveals no substantial reports of adverse effects related to fetal development during pregnancy or to breast-fed infants.

Infants and Children

A review of the medical literature reveals no substantial reports of adverse effects specifically related to the use of thiamine in infants and children.


No contraindications are known to date, except hypersensitivity to thiamine or to any component of any compound formulation. Some clinicians and researchers are proposing that cancer patients undergoing chemotherapy may benefit from restricted thiamine intake during treatment.

Precautions and Warnings

Use with caution with parenteral administration, especially with IV administration.

Laboratory Values

Whole-blood thiamine: Level less than 70 nmol/L indicates deficiency.

Erythrocyte transketolase (EKTA): Low activity of EKTA (<5 U/mmol hemoglobin) indicates deficiency, as does increase in EKTA (>16 U/mmol) after stimulation by the addition of TPP.

Therapeutic reference range: 1.6-4.0 mg/dL.

interactions review

Strategic Considerations

Thiamine plays a critical role in a range of metabolic processes, especially the Krebs cycle and adenosine triphosphate (ATP) synthesis. Vitamin B1depletion by diet, lifestyle, or medications increases several risk factors, especially for the cardiovascular and nervous systems. Although thiamine is central to metabolic vitality and cardiovascular health, the use of loop diuretics increases the risk of clinically significant thiamine depletion. However, adverse effects caused by drug depletion can be safely and effectively treated with thiamine supplementation, while further supporting healthy cardiac function. Thiamine intake during chemotherapy is challenging, and personalized integrative care may clarify paradoxical data. In other, simpler situations, the potential for adverse effects from unintentional depletion of thiamine by pharmacological agents can be corrected through supplementation at typical therapeutic levels.

nutrient-drug interactions
Antacids, Including Aluminum Hydroxide and Magnesium Trisilicate
Antibiotics and Antimicrobial Agents (Systemic)
Fluorouracil and Related Antimetabolite Chemotherapeutic Agents
Furosemide and Related Loop Diuretics
Nortriptyline and Related Tricyclic Antidepressants
Oral Contraceptives: Monophasic, Biphasic, and Triphasic Estrogen Preparations (Synthetic Estrogen and Progesterone Analogs)
Phenytoin and Related Anticonvulsant Medications
Stavudine and Related Reverse-Transcriptase Inhibitor (Nucleoside) Antiretroviral Agents
Tetracycline and Related Tetracycline Antibiotics
nutrient-nutrient interactions
Chlorinated Water and Chlorogenic Acid
B Vitamins and Other Synergistic Nutrients
herb-nutrient interaction
Citations and Reference Literature
  • 1.Wilkinson TJ, Hanger HC, George PM, Sainsbury R. Is thiamine deficiency in elderly people related to age or co-morbidity? Age Ageing 2000;29:111-116.
  • 2.Cheraskin E, Ringsdorf WM Jr, Medford FH, Hicks BS. The “ideal” daily vitamin B1 intake. J Oral Med 1978;33:77-79.View Abstract
  • 3.Wrenn KD, Murphy F, Slovis CM. A toxicity study of parenteral thiamine hydrochloride. Ann Emerg Med 1989;18:867-870.View Abstract
  • 4.Dudeja PK, Tyagi S, Kavilaveettil RJ et al. Mechanism of thiamine uptake by human jejunal brush-border membrane vesicles. Am J Physiol Cell Physiol 2001;281:C786-C792.View Abstract
  • 5.Majoor CL, de Vries LA. [The development of cardiac beriberi with polyneuritis after protracted use of large amounts of magnesium trisilicate. An unpublished observation by Dr. JGG Borst]. Ned Tijdschr Geneeskd 1980;124:1411-1416.View Abstract
  • 6.Deguchi Y MT, Mutai M. Comparative studies on synthesis of water-soluble vitamins among species of bifidobacteria. Agric Biol Chem 1985:13-19.
  • 7.Cummings JH, Macfarlane GT. Role of intestinal bacteria in nutrient metabolism. JPEN J Parenter Enteral Nutr 1997;21:357-365.View Abstract
  • 8.Basu TK, Dickerson JW, Raven RW, Williams DC. The thiamine status of patients with cancer as determined by the red cell transketolase activity. Int J Vitam Nutr Res 1974;44:53-58.View Abstract
  • 9.Aksoy M, Basu TK, Brient J, Dickerson JW. Thiamin status of patients treated with drug combinations containing 5-fluorouracil. Eur J Cancer 1980;16:1041-1045.View Abstract
  • 10.Basu TK. Vitamins–cytotoxic drug interaction. Int J Vitam Nutr Res Suppl 1983;24:225-233.View Abstract
  • 11.Basu TK. The significance of ascorbic acid, thiamin and retinol in cancer. Int J Vitam Nutr Res Suppl 1983;24:105-118.View Abstract
  • 12.Heier MS, Dornish JM. Effect of the fluoropyrimidines 5-fluorouracil and doxifluridine on cellular uptake of thiamin. Anticancer Res 1989;9:1073-1077.View Abstract
  • 13.Boros LG, Brandes JL, Lee WN et al. Thiamine supplementation to cancer patients: a double edged sword. Anticancer Res 1998;18:595-602.View Abstract
  • 14.Cascante M, Centelles JJ, Veech RL et al. Role of thiamin (vitamin B-1) and transketolase in tumor cell proliferation. Nutr Cancer 2000;36:150-154.View Abstract
  • 15.Comin-Anduix B, Boren J, Martinez S et al. The effect of thiamine supplementation on tumour proliferation: a metabolic control analysis study. Eur J Biochem 2001;268:4177-4182.View Abstract
  • 16.Kasper H. [Effect of diuretics on thiamine elimination]. Bibl Nutr Dieta 1969;11:23-29.View Abstract
  • 17.Seligmann H, Halkin H, Rauchfleisch S et al. Thiamine deficiency in patients with congestive heart failure receiving long-term furosemide therapy: a pilot study. Am J Med 1991;91:151-155.View Abstract
  • 18.Shimon I, Almog S, Vered Z et al. Improved left ventricular function after thiamine supplementation in patients with congestive heart failure receiving long-term furosemide therapy. Am J Med 1995;98:485-490.View Abstract
  • 19.Brady JA, Rock CL, Horneffer MR. Thiamin status, diuretic medications, and the management of congestive heart failure. J Am Diet Assoc 1995;95:541-544.View Abstract
  • 20.Suter PM, Haller J, Hany A, Vetter W. Diuretic use: a risk for subclinical thiamine deficiency in elderly patients. J Nutr Health Aging 2000;4:69-71.View Abstract
  • 21.Suter PM, Vetter W. Diuretics and vitamin B1: are diuretics a risk factor for thiamin malnutrition? Nutr Rev 2000;58:319-323.
  • 22.Rieck J, Halkin H, Almog S et al. Urinary loss of thiamine is increased by low doses of furosemide in healthy volunteers. J Lab Clin Med 1999;134:238-243.View Abstract
  • 22a.da Cunha S, Albanesi Filho FM, da Cunha Bastos VL, et al. Thiamin, selenium, and copper levels in patients with idiopathic dilated cardiomyopathy taking diuretics. Arq Bras Cardiol 2002;79(5):454-465. (English, Portuguese)
  • 23.Bohmer T. How prevalent is thiamin deficiency in heart failure patients? Nutr Rev 2001;59:342-344.
  • 24.Hardig L, Daae C, Dellborg M et al. Reduced thiamine phosphate, but not thiamine diphosphate, in erythrocytes in elderly patients with congestive heart failure treated with furosemide. J Intern Med 2000;247:597-600.View Abstract
  • 25.Zenuk C, Healey J, Donnelly J et al. Thiamine deficiency in congestive heart failure patients receiving long term furosemide therapy. Can J Clin Pharmacol 2003;10:184-188.View Abstract
  • 26.Hintikka J, Tolmunen T, Tanskanen A, Viinamaki H. High vitamin B12 level and good treatment outcome may be associated in major depressive disorder. BMC Psychiatry 2003;3:17.View Abstract
  • 27.Bell IR, Edman JS, Morrow FD 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.View Abstract
  • 28.Thorp VJ. Effect of oral contraceptive agents on vitamin and mineral requirements. J Am Diet Assoc 1980;76:581-584.View Abstract
  • 29.Wynn V. Vitamins and oral contraceptive use. Lancet 1975;1:561-564.View Abstract
  • 30.Briggs MH, Briggs M. Thiamine status and oral contraceptives. Contraception 1975;11:151-154.View Abstract
  • 31.Ahmed F, Bamji MS. Vitamin supplements to women using oral contraceptives (studies of vitamins B1, B2, B6 and A). Contraception 1976;14:309-318.View Abstract
  • 32.Egoramaiphol S, Migasena P, Supawan V. Effect of oral contraceptive agents on thiamine status. J Med Assoc Thai 1985;68:19-23.View Abstract
  • 33.Vir SC, Love AH. Effect of oral contraceptive agents on thiamin status. Int J Vitam Nutr Res 1979;49:291-295.View Abstract
  • 34.Lewis CM, King JC. Effect of oral contraceptives agents on thiamin, riboflavin, and pantothenic acid status in young women. Am J Clin Nutr 1980;33:832-838.View Abstract
  • 35.Prasad AS, Oberleas D, Moghissi KS et al. Effect of oral contraceptive agents on nutrients. II. Vitamins. Am J Clin Nutr 1975;28:385-391.View Abstract
  • 36.Patrini C, Perucca E, Reggiani C, Rindi G. Effects of phenytoin on the in vivo kinetics of thiamine and its phosphoesters in rat nervous tissues. Brain Res 1993;628:179-186.View Abstract
  • 37.Botez MI, Joyal C, Maag U, Bachevalier J. Cerebrospinal fluid and blood thiamine concentrations in phenytoin-treated epileptics. Can J Neurol Sci 1982;9:37-39.View Abstract
  • 38.Botez MI, Young SN. Effects of anticonvulsant treatment and low levels of folate and thiamine on amine metabolites in cerebrospinal fluid. Brain 1991;114(Pt 1A):333-348.View Abstract
  • 39.Botez MI, Botez T, Ross-Chouinard A, Lalonde R. Thiamine and folate treatment of chronic epileptic patients: a controlled study with the Wechsler IQ scale. Epilepsy Res 1993;16:157-163.View Abstract
  • 40.Meador KJ, Nichols ME, Franke P et al. Evidence for a central cholinergic effect of high-dose thiamine. Ann Neurol 1993;34:724-726.View Abstract
  • 41.Marra A, Lewi D, Lanzoni V et al. Lactic acidosis and antiretroviral therapy: a case report and literature review. Braz J Infect Dis 2000;4:151-155.View Abstract
  • 42.Megarbane B, Goldgran-Toledano D, Guerin JM, Baud F. [Fatal lactic acidosis in a patient infected by HIV and treated with stavudine and didanosine]. Pathol Biol (Paris) 2000;48:505-507.View Abstract
  • 43.Ter Hofstede HJ, de Marie S, Foudraine NA et al. Clinical features and risk factors of lactic acidosis following long-term antiretroviral therapy: 4 fatal cases. Int J STD AIDS 2000;11:611-616.View Abstract
  • 44.Mokrzycki MH, Harris C, May H et al. Lactic acidosis associated with stavudine administration: a report of five cases. Clin Infect Dis 2000;30:198-200.View Abstract
  • 45.Rey C, Prieto S, Medina A et al. Fatal lactic acidosis during antiretroviral therapy. Pediatr Crit Care Med 2003;4:485-487.
  • 46.Robinson BH. Lactic acidemia (disorders of pyruvate carboxylase, pyruvate dehydrogenase). In: Scriver C, ed. The Metabolic and Molecular Bases of Inherited Disease. 7th ed. New York: McGraw-Hill; 1995:1479-1499.
  • 47.Schramm C, Wanitschke R, Galle PR. Thiamine for the treatment of nucleoside analogue–induced severe lactic acidosis. Eur J Anaesthesiol 1999;16:733-735.View Abstract
  • 48.Arici C, Tebaldi A, Quinzan GP et al. Severe lactic acidosis and thiamine administration in an HIV-infected patient on HAART. Int J STD AIDS 2001;12:407-409.View Abstract
  • 49.Omray A, Varma KC. Evaluation of pharmacokinetic parameters of tetracycline hydrochloride upon oral administration with vitamin C and vitamin B complex. Hindustan Antibiot Bull 1981;23:33-37.
  • 50.Ames BN, Elson-Schwab I, Silver EA. High-dose vitamin therapy stimulates variant enzymes with decreased coenzyme binding affinity (increased K(m)): relevance to genetic disease and polymorphisms. Am J Clin Nutr 2002;75:616-658.View Abstract
  • .[No authors listed.] Thiamine: monograph. Altern Med Rev 2003;8(1):59-62. (Review)
  • .Akpan T, Peschard S, Brinkane AH, et al. [Right heart failure caused by thiamine deficiency (cardiac beriberi).] Presse Med 2000;29(5):240-241. [French]
  • .Alston TA. Does metformin interfere with thiamine? Arch Intern Med 2003;163(8):983.
  • .Ames BN, Elson-Schwab I, Silver EA. High-dose vitamin therapy stimulates variant enzymes with decreased coenzyme binding affinity (increased K(m)): relevance to genetic disease and polymorphisms. Am J Clin Nutr 2002;75(4):616-658. (Review)
  • .Baker H, Thomson AD, Frank O, et al. Absorption and passage of fat- and water-soluble thiamin derivatives into erythrocytes and cerebrospinal fluid of man. Am J Clin Nutr 1974;27(7):676-680.
  • .Basu TK, Dickerson JW, Raven RW, et al. The thiamine status of patients with cancer as determined by the red cell transketolase activity. Int J Vitam Nutr Res 1974;44(1):53-58.
  • .Basu TK. Vitamins: cytotoxic drug interaction. Int J Vitam Nutr Res Suppl 1983;24:225-233.
  • .Bettendorff L, Mastrogiacomo F, Wins P, et al. Low thiamine diphosphate levels in brains of patients with frontal lobe degeneration of the non-Alzheimer’s type. J Neurochem 1997;69:2005-2010.
  • .Blanc P, Boussuges A. [Cardiac beriberi.] Arch Mal Coeur Vaiss 2000;93(4):371-379. [French]
  • .Blanc P, Boussuges A. [In process citation.] Ann Cardiol Angeiol (Paris) 2001;50(3):160-168. [French]
  • .Bohmer T. How prevalent is thiamin deficiency in heart failure patients? Nutr Rev 2001;59(10):342-344.
  • .Bønaa KH, Njølstad I, Ueland PM, et al. Homocysteine lowering and cardiovascular events after acute myocardial infarction. N Engl J Med 2006;354(15):1578-1588.
  • .Boros LG, Brandes JL, Lee WN, et al. Thiamine supplementation to cancer patients: a double edged sword. Anticancer Res 1998;18(1B):595-602. (Review)
  • .Brady JA, Rock CL, Horneffer MR. Thiamin status, diuretic medications, and the management of congestive heart failure. J Am Diet Assoc 1995;95(5):541-544.
  • .Briggs MH, Briggs M. Thiamine status and oral contraceptives. Contraception 1975;11(2):151-154.
  • .Brozek. Psychologic effects of B1 restriction and deprivation in normal young men. Am J Clin Nutr 1957;5(2):109-120.
  • .Chen MF, Chen LT, Gold M, et al. Plasma and erythrocyte thiamin concentrations in geriatric outpatients. J Am Coll Nutr 1996;15(3):231-236.
  • .Cheraskin E, Ringsdorf WM Jr. Predictive medicine: IX: diet. J Am Geriatr Soc 1971;19(11):962-968.
  • .Cheraskin E, Ringsdorf WM Jr, Setyaadmadja AT, et al. Thiamin consumption and cardiovascular complaints. J Am Geriatr Soc 1967;15(11):1074-1079.
  • .Cummings JH, Macfarlane G. Role of intestinal bacteria in nutrient metabolism. J Parenter Enteral Nutr 1997;21(6):357-365.
  • .Davis RE, Icke GC. Clinical chemistry of thiamin. Adv Clin Chem 1983;23:93-140. (Review)
  • .Doyon S, Roberts JR. Reappraisal of the “coma cocktail”: dextrose, flumazenil, naloxone, and thiamine. Emerg Med Clin North Am 1994;12(2):301-316.
  • .Drewe J, Delco F, Kissel T, et al. Effect of intravenous infusions of thiamine on the disposition kinetics of thiamine and its pyrophosphate. J Clin Pharm Ther 2003;28(1):47-51.
  • .Getz L, Sigurdsson JA, Hetlevik I, et al. Estimating the high risk group for cardiovascular disease in the Norwegian HUNT 2 population according to the 2003 European guidelines: modelling study. BMJ 2005;331(7516):551.
  • .Goldfarb-Rumyantzev AS, Jeyakumar A, Gumpeni R, et al. Lactic acidosis associated with nucleoside analog therapy in an HIV-positive patient. AIDS Patient Care STDS 2000;14(7):339-342.
  • .Goldman RE, Parker DR, Eaton CB, et al. Patients’' perceptions of cholesterol, cardiovascular disease risk, and risk communication strategies. Ann Fam Med 2006;4(3):205-212.
  • .Grant JE, Veldee MS, Buchwald D. Analysis of dietary intake and selected nutrient concentrations in patients with chronic fatigue syndrome. J Am Diet Assoc 1996;96:383-386.
  • .Hathcock JN. Metabolic mechanisms of drug-nutrient interactions. Fed Proc 1985;44(1 Pt 1):124-129. (Review)
  • .Heap LC, Peters TJ, Wessely S. Vitamin B status in patients with chronic fatigue syndrome. J R Soc Med 1999;92:183-185.
  • .Hoffman RS, Goldfrank LR. The poisoned patient with altered consciousness. Controversies in the use of a “coma cocktail.” JAMA 1995;274(7):562-569.
  • .Hoyumpa AM Jr. Mechanisms of thiamin deficiency in chronic alcoholism. Am J Clin Nutr 1980;33(12):2750-2761. (Review)
  • .Hung SC, Hung SH, Tarng DC, et al. Thiamine deficiency and unexplained encephalopathy in hemodialysis and peritoneal dialysis patients. Am J Kidney Dis 2001;38:941-947.
  • .Knopp RH, d’Emden M, Smilde JG, et al. Efficacy and safety of atorvastatin in the prevention of cardiovascular end points in subjects with type 2 diabetes: the Atorvastatin Study for Prevention of Coronary Heart Disease Endpoints in Non-Insulin-Dependent Diabetes Mellitus (ASPEN). Diabetes Care 2006;29(7):1478-1485.
  • .Kositawattanakul T, Tosukhowong P, Vimokesant SL, et al. Chemical interactions between thiamin and tannic acid: II: separation of products. Am J Clin Nutr 1977;30(10):1686-1691.
  • .Kuba H, Inamura T, Ikezaki K, et al. Thiamine-deficient lactic acidosis with brain tumor treatment: report of three cases. J Neurosurg 1998;89(6):1025-1028.
  • .Liu S, Huang H, Lu X, et al. Down-regulation of thiamine transporter THTR2 gene expression in breast cancer and its association with resistance to apoptosis. Mol Cancer Res 2003;1(9):665-673.
  • .Lonsdale D. A review of the biochemistry, metabolism and clinical benefits of thiamin(e) and its derivatives. eCAM 2006;3:49-59. (Review)
  • .Lorber A, Gazit AZ, Khoury A, et al. Cardiac manifestations in thiamine-responsive megaloblastic anemia syndrome. Pediatr Cardiol 2003;24(5):476-481. (Review)
  • .Majumdar SK, Shaw GK, O’Gorman P, et al. Blood vitamin status (B1, B2, B6, folic acid and B12) in patients with alcoholic liver disease. Int J Vitam Nutr Res 1982;52(3):266-271.
  • .Mandel H, Berant M, Hazani A, et al. Thiamine-dependent beriberi in the “thiamine-responsive anemia syndrome.” N Engl J Med 1984;311(13):836-838.
  • .Mendoza CE, Rodriguez F, Rosenberg DG. Reversal of refractory congestive heart failure after thiamine supplementation: report of a case and review of literature. J Cardiovasc Pharmacol Ther 2003;8(4):313-316.
  • .Meyer P. Thiaminase activities and thiamine content of Pteridium aquilinum, Equisetum ramosissimum, Malva parviflora, Pennisetum clandestinum and Medicago sativa. Onderstepoort J Vet Res 1989;56(2):145-146.
  • .Mimori Y, Katsuoka H, Nakamura S. Thiamine therapy in Alzheimer’s disease. Metab Brain Dis 1996;11:89-94.
  • .Morinville V, Jeannet-Peter N, Hauser C. Anaphylaxis to parenteral thiamine (vitamin B1). Schweiz Med Wochenschr 1998;128(44):1743-1744.
  • .Murata K. Actions of two types of thiaminase on thiamin and its analogues. Ann N Y Acad Sci 1982;378:146-156. (Review)
  • .Nolan KA, Black RS, Sheu KF, et al. A trial of thiamine in Alzheimer’s disease. Arch Neurol 1991;48:81-83.
  • .Ordovas JM. Nutrigenetics, plasma lipids, and cardiovascular risk. J Am Diet Assoc 2006;106(7):1074-1081. (Review)
  • .Petrie WM, Ban TA. Vitamins in psychiatry: do they have a role? Drugs 1985;30(1):58-65.
  • .Pinedo HM, Peters GFJ. Fluorouracil: biochemistry and pharmacology. J Clin Oncol 1988;6:1653-1664.
  • .Porter FS, Rogers LE, Sidbury JB Jr. Thiamine-responsive megaloblastic anemia. J Pediatr 1969;74(4):494-504.
  • .Proebstle TM, Gall H, Jugert FK. Specific IgE and IgG serum antibodies to thiamine associated with anaphylactic reaction. J Allergy Clin Immunol 1995;95(5 Pt 1):1059-1060.
  • .Reaves L, Steffen LM, Dwyer JT, et al. Vitamin supplement intake is related to dietary intake and physical activity: the Child and Adolescent Trial for Cardiovascular Health (CATCH). J Am Diet Assoc 2006;106(12):2018-2023.
  • .Reuler JB, Girard DE, Cooney TG. Current concepts: Wernicke’s encephalopathy. N Engl J Med 1985;312(16):1035-1039.
  • .Ridker PM, Torres J. Reported outcomes in major cardiovascular clinical trials funded by for-profit and not-for-profit organizations: 2000-2005. JAMA 2006;295:2270-2274.
  • .Rungruangsak K, Tosukhowong P, Panijpan B, et al. Chemical interactions between thiamin and tannic acid: I: kinetics, oxygen dependence and inhibition by ascorbic acid. Am J Clin Nutr 1977;30(10):1680-1685.
  • .Saif MW. Is there a role for thiamine in the management of congestive heart failure? South Med J 2003;96(1):114-115.
  • .Sandoval E, Borja H, Gatica A. [Wernicke’s encephalopathy as a complication of chronic hemodialysis: report of one case.] Rev Med Chile 1997;125(5):582-585. [Spanish]
  • .Shamir R, Dagan O, Abramovitch D, et al. Thiamine deficiency in children with congenital heart disease before and after corrective surgery. JPEN J Parenter Enteral Nutr 2000;24:154-158.
  • .Shangari N, Bruce WR, Poon R, et al. Toxicity of glyoxals--role of oxidative stress, metabolic detoxification and thiamine deficiency. Biochem Soc Trans 2003;31(Pt 6):1390-1393.
  • .Shivalkar B, Engelmann I, Carp L, et al. Shoshin syndrome: two case reports representing opposite ends of the same disease spectrum. Acta Cardiol 1998;53(4):195-199.
  • .Singleton CK, Martin PR. Molecular mechanisms of thiamine utilization. Curr Mol Med 2001;1(2):197-207. (Review)
  • .Stephen JM, Grant R, Veh CS. Anaphylaxis from administration of intravenous thiamine. Am J Emerg Med 1992;10(1):61-63.
  • .Subramanian VS, Marchant JS, Parker I, et al. Cell biology of the human thiamine transporter-1 (hTHTR1): intracellular trafficking and membrane targeting mechanisms. J Biol Chem 2003;278(6):3976-3984.
  • .Van Haecke P, Ramaekers D, Vanderwegen L, et al. Thiamine-induced anaphylactic shock. Am J Emerg Med 1995;13(3):371-372.
  • .Vir SC, Love AH. Thiamin, riboflavin and vitamin B6 status of aged living at home and in institutions. Ir J Med Sci 1980;149(3):107-116.
  • .Wei L, Murphy MJ, MacDonald TM. Impact on cardiovascular events of increasing high density lipoprotein cholesterol with and without lipid lowering drugs. Heart 2006;92(6):746-751.
  • .Wilkinson TJ, Hanger HC, Elmslie J, et al. The response to treatment of subclinical thiamine deficiency in the elderly. Am J Clin Nutr 1997;66(4):925-928.
  • .Wilkinson TJ, Hanger HC, George PM, et al. Is thiamine deficiency in elderly people related to age or co-morbidity? Age Ageing 2000;29:111-116.
  • .Wrenn KD, Murphy F, Slovis CM. A toxicity study of parenteral thiamine hydrochloride. Ann Emerg Med 1989;18(8):867-870.
  • .Yagi N, Itokawa Y. Cleavage of thiamine by chlorine in tap water. J Nutr Sci Vitaminol (Tokyo) 1979;25(4):281-287.