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Vitamin B1 (Thiamine)

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Last Update: January 31, 2024.

Continuing Education Activity

Thiamine, also known as thiamin and vitamin B1, is one of the 8 B-complex vitamins and is classified as a water-soluble B vitamin. Thiamine occurs naturally in specific diets, is added to food products, and is available in dietary supplements. Brown rice, whole grains, pork, poultry, soybeans, nuts, peas, dried beans, and fortified or enriched grain products such as bread, cereals, and infant formulas are rich sources of thiamine. Multivitamins supplement an additional 1.5 mg of thiamine to a diet already abundant in this essential vitamin.

In prolonged or untreated vitamin B1 deficiency cases, individuals may experience advanced-stage symptoms, which can lead to the development of the Wernicke-Korsakoff syndrome. Thiamine is approved by the United States Food and Drug Administration (FDA) for the treatment of Wernicke encephalopathy, infantile beriberi, and cardiovascular disease resulting from thiamine deficiency. Vitamin B1 deficiency may present with early or advanced symptoms. Early symptoms mainly arise from neurological, cardiac, and gastrointestinal systems. Due to thiamine's limited storage duration before rapid excretion, maintaining adequate blood serum levels requires a consistent and regular dietary intake. This activity outlines the indications, mechanism of action, administration methods, significant adverse effects, contraindications, and monitoring protocols for vitamin B1. This activity also equips clinicians to guide patient therapy in treatment or supplementation scenarios where thiamine is indicated by collaborating with dieticians, pharmacists, and primary care clinicians as part of the interprofessional team to enhance patient outcomes.


  • Identify early and advanced symptoms of vitamin B1 deficiency, including neurological, cardiac, and gastrointestinal manifestations.
  • Screen patients at risk of vitamin B1 deficiency, considering factors such as alcohol use disorder, poor nutrition, fasting, restricted food access, persistent vomiting, and impaired thiamine absorption.
  • Implement evidence-based interventions for vitamin B1 deficiency, utilizing appropriate treatment modalities such as dietary recommendations, thiamine supplementation, or multivitamin therapy.
  • Collaborate with interprofessional healthcare teams to coordinate comprehensive care plans for individuals with vitamin B1 deficiencies, considering the broader context of patient health and lifestyle.
Access free multiple choice questions on this topic.


Thiamine, also known as thiamin and vitamin B1, is one of the 8 B-complex vitamins and is classified as a water-soluble B vitamin. Thiamine occurs naturally in specific diets, is added to food products, and is available in dietary supplements.[1] Foods rich in thiamine include brown rice, whole grains, pork, poultry, soybean, nuts, peas, dried beans, and fortified or enriched grain products such as bread, cereals, and infant formulas.[2][3][4] Multivitamins provide an additional 1.5 mg of thiamine in addition to a diet rich in thiamine.[5]

Thiamine is approved by the United States Food and Drug Administration (FDA) for the treatment of Wernicke encephalopathy, infantile beriberi, and cardiovascular disease resulting from thiamine deficiency. It is also approved for use when administering intravenous (IV) dextrose to individuals with marginal thiamine status to prevent heart failure. Parenteral thiamine is also FDA-approved for patients with established thiamine deficiency who can't take thiamine orally due to severe anorexia, nausea, vomiting, and malabsorption.

Thiamine or vitamin B1 deficiency occurs if the recommended daily intake (RDI) is not maintained. However, deficiency may also occur due to impaired intestinal absorption or high excretion rates, such as in people with alcohol dependency, acquired immunodeficiency syndrome (AIDS), and malnutrition.[6][7] Due to thiamine's limited storage duration before rapid excretion, maintaining adequate blood serum levels requires a consistent and regular dietary intake. Individuals with certain medical and non-medical conditions are more susceptible to vitamin B1 deficiency, such as alcohol dependency, older age, diabetes, post-bariatric surgery, malignant disease, gastrointestinal disease, pregnancy, lactation, fasting, starvation, use of unbalanced diets, hyperthyroidism, renal failure on hemodialysis, and systemic infections.[8][9]

Vitamin B1 deficiency may present with early or advanced symptoms. Early symptoms mainly arise from neurological, cardiac, and gastrointestinal systems, presenting as weight loss, anorexia, confusion, short-term amnesia, malaise, muscle weakness, and cardiac symptoms.

Beriberi is a disorder caused by vitamin B1 deficiency, which can present as wet or dry types. Wet beriberi presents as a high-output cardiac failure with signs of edema, an enlarged heart, warm extremities, tachycardia, and respiratory distress. Dry beriberi is predominantly a neurological complication involving the peripheral nervous system and presents with peripheral neuropathy, malaise, muscle weakness, seizures, or brisk tendon reflexes.[8] Infants and children are also susceptible to vitamin B1 deficiency, presenting as infantile or childhood beriberi. Usually, infants present with edema, ill appearance, pallor, anorexia, coffee-ground vomiting, and diarrhea. Neurological signs include a hoarse cry due to vocal cord paralysis, head lag, seizures, coma, and sudden infant death syndrome. Juvenile beriberi is uncommon and often misdiagnosed due to overlapping symptoms of meningitis.[10]

In cases of prolonged or untreated vitamin B1 deficiency, individuals may experience advanced-stage symptoms, which can lead to the development of Wernicke-Korsakoff syndrome. This syndrome manifests in 2 phases—Wernicke encephalopathy and Korsakoff psychosis. The syndrome is more common in the United States and 8 to 10 times more common among people with chronic alcohol consumption/misuse, severe gastrointestinal disorders, malignancies, drug use, and AIDS. Wernicke encephalopathy occurs early and presents with polyneuropathy, ataxia, ophthalmoplegia, and gait abnormalities. If left untreated, it can eventually evolve into Korsakoff psychosis with signs of severe short-term amnesia, disorientation, confabulation, and hallucinations.[11][12][13]

5-fluorouracil-induced depletion of thiamine has been described in the literature. 5-FU rapidly increases thiamine pyrophosphate (TPP) levels, which could quickly deplete the cellular thiamine stores. The condition is reversible with thiamine supplementation as an off-label indication.[14]

Mechanism of Action

In blood, the thiamine diphosphokinase enzyme converts thiamine into its active form, TPP. TPP plays different roles during distinct steps of metabolism, glycolysis, the Krebs cycle, and the pentose phosphate pathway.

  1. TPP works with enzyme functions while metabolizing carbohydrates, lipids, and branched-chain amino acids.
  2. TPP acts as a cofactor at several steps during glycolysis and oxidative decarboxylation of carbohydrates.[15]
  3. TPP acts as a coenzyme for the mitochondrial enzyme complexes such as α-ketoglutarate dehydrogenase and pyruvate dehydrogenase. These enzymes are critical in the Krebs and tricarboxylic acid cycles. Thiamine deficiency decreases these enzymes' activity, impairing lactate conversion into pyruvate, leading to the accumulation of lactic acid. Lactic acidosis may cause focal damage to specific brain structures, such as mamillary bodies and the posteromedial thalamus, as seen on MRI.[1] 
  4. The presence of TPP is required by the erythrocyte transketolase enzyme during the pentose phosphate pathway of nucleotide synthesis and provides reduced nicotinamide adenine dinucleotide phosphate for several synthetic pathways.[16]


Absorption: The intestinal enzyme phosphatase hydrolyzes thiamine into a free form, which is then absorbed by the small intestine. Thiamine is actively absorbed and passively diffused by the small intestine at nutritional and pharmacological doses, respectively. It has a short half-life of 14 to 18 days; therefore, regular dietary intake of thiamine is necessary.

Distribution: The phosphorylated form of thiamine gets distributed to various organs. Limited quantities of thiamine are stored in the liver, heart, kidney, and brain for a short duration.

Metabolism: Thiamine gets metabolized through phosphorylation. In the human body, thiamine exists mainly as thiamine diphosphate (TDP), also known as TPP. TPP is the metabolic form of thiamine and serves as a cofactor for various enzymes during the metabolism of glucose, lipids, and proteins.[10]

Elimination: Thiamine is a water-soluble vitamin; excess thiamine is exerted in the urine.[17]


Available Dosage Forms and Strengths

Thiamine is available as a tablet and capsule formulation as an over-the-counter supplement. Parenteral thiamine (100 mg/mL) requires a prescription.

Adult Dosage

The RDI of thiamine for adults 18 and older is 1.2 mg/d for men and 1.1 mg/d for women. For children, adequate intake levels are lower. For children, the RDI of thiamine is 0.2 mg/d during early infancy and then steadily increases with age. Pregnant women should increase their RDI of thiamine intake to 1.4 mg/d. In the United States, the average daily thiamine intake among children from food is 1.27 mg, 1.54 mg, and 1.68 mg among individuals aged 2 to 5, 6 to 11, and 12 to 19, respectively. Among men and women aged 20 years and above, the average daily intake of thiamine is 1.95 mg and 1.39 mg, respectively. Parenteral multivitamins contain 3 to 3.5 mg of thiamine; the adult enteral formula contains 2.2 to 2.9 mg per 1500 kcal/d. The American Society for Parenteral and Enteral Nutrition recommends a thiamine intake of 1.2 to 10 mg/d.[1][18]

Thiamine can be administered by enteral, intravenous (IV), or intramuscular (IM) routes. The oral route is indicated in patients who do not have IV access. The thiamine hydrochloride form is used to prevent and treat Wernicke encephalopathy. However, a lack of consensus exists regarding the route, dose, and duration of treatment for Wernicke encephalopathy. As per the guidelines from the American Society of Addiction Medicine, it is recommended to administer parenteral thiamine to prevent the development of Wernicke encephalopathy, especially in patients with malabsorption, poor nutritional status, or severe complications related to alcohol withdrawal. The recommended dose is 100 mg IV/IM per day for 3 to 5 days.[19] Thiamine is recommended before food, and a nutritionally appropriate diet should be initiated after recommended thiamine supplementation. When clinical symptoms improve, supplementation can be switched to the oral route with a dose range of 50 to 100 mg daily.[1] Individuals with thiamine deficiency also require other nutrient supplementation, such as magnesium, vitamin B2 (riboflavin), B3 (nicotinamide), B6 (pyridoxine), B12, vitamin C, potassium, and phosphate.

Specific Patient Populations

Hepatic impairment: No information is provided in the product labeling regarding the use of thiamine in hepatic impairment.

Renal impairment: No information is provided in the product labeling regarding the use of thiamine in renal impairment. Thiamine levels may be decreased in patients undergoing dialysis.[20] 

Pregnancy considerations: According to The American College of Obstetricians and Gynecologists (ACOG), persistent vomiting may require treatment with dextrose and vitamins along with IV fluids. Clinicians should prescribe 100 mg of thiamine with IV fluids. Subsequent continuation of multivitamins is advised.[21]

Breastfeeding considerations: Thiamine deficiency can occur mainly in infants breastfed by mothers with an inadequate intake of thiamine; supplementation with thiamine should be considered.[22]

Pediatric patients: Patients on soy-based formula may be prone to thiamine deficiency.[23] The World Health Organization (WHO) recommends an initial IV loading dose of 25 to 50 mg and a daily intramuscular injection of 10 mg weekly. Subsequently, a maintenance dose of 3 mg to 5 mg orally once daily for a minimum of 6 weeks is advised. In a study, infants with acute pulmonary hypertension in early infancy received a 100 mg IV thiamine dose over 30 minutes, followed by enteral supplementation.[24]

Older patients: Approximately 20% to 30% of older adults have a thiamine deficiency, which can be due to inadequate consumption of thiamine-rich foods, chronic health conditions, and polypharmacy. Studies emphasize a significant prevalence of this deficiency among senior residents in institutional care settings.[25][26][27]

Adverse Effects

Thiamine supplementation is reported to be well-tolerated and safe to use. A retrospective study on the adverse effects of thiamine supplementation among more than 300,000 patients found no serious side effects. [28] However, some commonly reported adverse effects include nausea, urticaria, lethargy, ataxia, and impaired gut motility.[1]

Drug-Drug Interactions

  • Loop diuretics: Patients treated with a high dose of furosemide for a prolonged period are predisposed to thiamine deficiency. Furosemide increases the excretion of thiamine and can disrupt the reabsorption of thiamine in the kidneys.[29][30]
  • Macrolides: Clinical data obtained from electronic health records indicates a decrease in thiamine levels among patients prescribed erythromycin. The probable mechanism is due to the inhibition of thiamine transport mediated by the SLC19A2 protein.[31]
  • Patiromer: Patiromer can reduce the absorption of orally administered thiamine.[32]


No absolute contraindications against vitamin B1 are reported in the literature. However, individuals with a history of allergic reactions to vitamin supplements should avoid thiamine supplements. Anaphylaxis has been reported after parental administration of thiamine.[33]

Warnings and Precautions

  • Administering IV glucose to a thiamine-deficient patient can trigger or exacerbate Wernicke encephalopathy. Therefore, it is imperative to provide thiamine before glucose in patients with thiamine deficiency.[34]
  • Some parenteral thiamine products may contain aluminum as an excipient. Aluminum accumulation can cause neurotoxicity, especially in patients with renal insufficiency and premature infants.[35]


The serum level of thiamine is not a reliable indicator of thiamine status. However, thiamine function can be measured by erythrocyte transketolase activity (ETKA). An EKTA of 0% to 15% is considered adequate, 15% to 25% is considered a moderate risk, and 25% or higher is considered a high risk for thiamine deficiency.[36][37] Direct measurement of erythrocyte TPP is performed using whole-blood testing and has more sensitivity, specificity, precision, and robustness.[36] The concentration of TPP in the whole blood ranges from 70 to 180 nmol/L.[8] Urinary thiamine excretion can measure adequate dietary intake. However, it does not reflect the thiamine stores in the body. In adults, thiamine excretion of <100 mcg/d suggests inadequate intake and less than 40 mcg/d suggests thiamine deficiency.[38] In Wernicke encephalopathy, clinicians should monitor for clinical improvement. Generally, oculomotor abnormalities usually show rapid improvement. Encephalopathy and ataxia require more time for clinical improvement.[39]


The human body excretes excess thiamine in the urine. No toxicity from high thiamine intake from food or supplements is evident. Food and Nutrition Board (FNB) concluded that excessive thiamine consumption might cause adverse effects despite a lack of solid evidence of toxicity. According to the Institute of Medicine, no established upper limit for thiamine intake that causes toxicity is reported in the literature.

Enhancing Healthcare Team Outcomes

All interprofessional healthcare members should encourage healthy nutrition for their patients. Thiamine deficiency is uncommon in North America but can occur in specific high-risk populations. Deficiency can lead to a severe, life-threatening clinical condition, including irreversible brain damage.

The outcome of patients with thiamine deficiency can be improved by early recognition of the disease and early initiation of the treatment before severe neurological and cardiac manifestations develop. In a retrospective study, IV thiamine was given to adult patients admitted to the internal medicine department. Among 141 patients, 115 (81.6%) received 100 mg IV thiamine daily (low-dose), and 26 (18.4%) received >100 mg IV thiamine daily (high-dose). No significant difference in resolving Wernicke encephalopathy symptoms was noted between high-dose and low-dose thiamine recipients. Diverse thiamine prescription patterns were seen. More extensive studies are required to determine the optimal dose of thiamine for Wernicke encephalopathy.[40] 

Pediatricians play a crucial role in managing beriberi in resource-limited settings. Internists and psychiatrists are essential to improve outcomes related to Wernicke encephalopathy. Dieticians should provide recommendations regarding dietary allowances in at-risk populations and patients receiving parenteral nutrition.[41] Public health officials should ensure the fortification of the diet with thiamine.[42] An interprofessional team approach and open communication between clinicians, pharmacists, dieticians, nurses, and specialists are necessary to optimize patient outcomes with thiamine therapy.

Review Questions


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Disclosure: Connor Kerndt declares no relevant financial relationships with ineligible companies.

Disclosure: Harshit Doshi declares no relevant financial relationships with ineligible companies.

Disclosure: Reddog Sina declares no relevant financial relationships with ineligible companies.

Disclosure: David Franklin declares no relevant financial relationships with ineligible companies.

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