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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
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
  • Evidence: Furosemide (Lasix).
  • Extrapolated, based on similar properties: Bumetanide (Bumex), ethacrynic acid (Edecrin), torsemide (Demadex).
Drug-Induced Nutrient Depletion, Supplementation Therapeutic, Not Requiring Professional Management
Prevention or Reduction of Drug Adverse Effect
Adverse Drug Effect on Nutritional Therapeutics, Strategic Concern

Probability: 1. Certain
Evidence Base: Consensus

Effect and Mechanism of Action

Several studies have suggested that loop diuretics, especially furosemide (Lasix), can cause thiamine depletion due to increased urinary excretion, contributing to cardiac insufficiency in patients with CHF. 16-21 Further research has indicated that the compromised thiamine status of individuals with CHF may be caused by altered metabolism, rather than simple deficiency, of thiamine. In a study of the diuretic effects of single IV doses of furosemide on six healthy volunteers, Rieck et al. 22 observed a doubling of thiamine excretion rate, along with the expected increased urine volume and sodium excretion. Another study examined cardiac function and status of select nutrients in 30 patients with idiopathic dilated cardiomyopathy using diuretics, compared with a similar number of healthy control individuals. Measuring the activity of erythrocytic transketolase and the effect of TPP, da Cunha et al. 22a determined the presence of thiamine deficiency in 33% of the patients with heart disease (vs. 10% of controls).

Even though all loop diuretics work by inhibiting sodium and chloride reabsorption in the thick ascending limb of Henle's loop, no conclusive research on the effects of other loop diuretics on thiamine has been published. However, CHF is characteristic of wet beriberi, caused by thiamine deficiency. Patients receiving furosemide are likely to have compromised kidney function, decreased metabolic function associated with aging, malnourishment, alcoholism and other lifestyle factors, and other variables aggravating thiamine depletion, deficiency, and dysregulation. 17,19,23


As noted earlier, numerous studies have determined that thiamine depletion is a common phenomenon among patients undergoing loop diuretic therapy. For example, an investigation of 38 sequential patients in a cardiology clinic assessed thiamine status by in vitro erythrocyte transketolase activity assay and dietary intake of thiamine. Thiamine deficiency was found in 21% of the patients and evidence of risk for dietary thiamine inadequacy in 25%. 19

A small pilot study in 1991 examined the effects of long-term furosemide therapy (80-240 mg for 3-14 months) in hospitalized patients with CHF to determine the occurrence of clinically significant thiamine deficiency caused by urinary loss. 17 Elevated levels of thiamine pyrophosphate effect (TPPE), indicating thiamine deficiency, were found in 21 of 23 furosemide-treated patients and in 2 of 16 age-matched controls. Biochemical evidence of thiamine deficiency tended to be more common among patients with poor left ventricular ejection fractions (LVEF). A 7-day course of IV thiamine, 100 mg twice daily, lowered TPPE levels to normal in six of the subjects, indicating normal thiamine utilization capacity, and improved LVEF in four of five patients, as demonstrated by echocardiography. These preliminary findings suggest that long-term furosemide therapy may be associated with clinically significant thiamine deficiency, presumed to result from urinary loss, and contribute to impaired cardiac performance in patients with CHF. Further, this apparent drug-induced depletion pattern responded to appropriate thiamine administration within an inpatient setting.

In 1995 the same research team conducted a double-blind, placebo-controlled trial in which they initially randomized 30 subjects to 1 week of either IV thiamine (200 mg/day) or placebo within inpatient care. 18 In the second phase, all individuals were discharged and given oral thiamine (200 mg/day) for 6 weeks. After the initial IV thiamine, thiamine status normalized, and LVEF increased significantly in those who received IV thiamine, in contrast to no measurable response in thiamine status among those given IV placebo. After the 7-week intervention, the 27 remaining subjects showed 22% improvement in LVEF. The researchers concluded that cardiac function in CHF patients may be exacerbated by thiamine depletion attributable to long-term furosemide therapy; thiamine supplementation or systematic dietary enhancement may avert or correct this adverse effect and its probable sequelae in patients with moderate to severe CHF.

Although there is consensus on an association between loop diuretic therapy and compromised thiamine status, conclusive evidence is lacking to confirm a consistent causal relationship. Using high-pressure liquid chromatography (HPLC) to assess blood thiamine and thiamine ester concentrations in erythrocytes of 41 elderly patients with CHF treated with furosemide (and a control group), a Swedish team found reduced thiamine diphosphate (TPP), the storage form of thiamine, but not thiamine phosphate (TP). The researchers concluded that the observed change in CHF patients taking furosemide was most likely not an expression of a thiamine deficiency, but rather of altered thiamine metabolism not yet explained. 24

Zenuk et al. 25 investigated the thiamine status of 32 patients with CHF who received either 40 to 80 mg or 80 mg or more of furosemide daily. Using erythrocyte transketolase enzyme activity and the degree of TPPE, these researchers found that 96% (24 of 25) of those receiving the higher diuretic dose demonstrated biochemical evidence of severe thiamine deficiency, as did 57% (4 of 7) of patients taking 40 mg furosemide daily. No other clinical variables showed a significant association with thiamine status.

Thus, collectively, the body of evidence suggests that thiamine deficiency occurs in a substantial proportion of CHF patients being treated with furosemide.

Nutritional Therapeutics, Clinical Concerns, and Adaptations

Long-term diuretic administration remains a central pharmacological therapy of heart insufficiency and hypertension in conventional practice. However, loop diuretics can aggravate the high-risk status inherent to many conditions for which these medications are prescribed, especially among hospitalized or chronic care elderly patients. Thiamine supplements should be considered in patients undergoing sustained diuresis, particularly when dietary deficiency may be present. Investigating the risk posed by diuretic use for subclinical thiamine deficiency in elderly patients, Swiss researchers suggested that low-dose thiamine supplementation may help prevent the development of subclinical wet beriberi in such patients. 20 Pending conclusive evidence to the contrary, patients taking furosemide, and possibly other loop diuretics, would most likely benefit from thiamine support of 100 mg per day, orally.

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
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  • .[No authors listed.] Thiamine: monograph. Altern Med Rev 2003;8(1):59-62. (Review)
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