Español | 日本語


  • Thiamin pyrophosphate (TPP), the active form of thiamin, is involved in several enzyme functions associated with the metabolism of carbohydrates, branched-chain amino acids, and fatty acids. (More information)
  • Severe thiamin deficiency leads to beriberi, a disease that affects multiple organ systems, including the central and peripheral nervous systems. (More information)
  • Wernicke's encephalopathy refers to an acute neurologic disorder secondary to thiamin deficiency. The Wernicke-Korsakoff syndrome results in persistent alterations in memory formation, along with the encephalopathy-related symptoms. (More information)
  • Thiamin deficiency can result from poor dietary intake, inadequate provision in parenteral nutrition, reduced gastrointestinal absorption, increased metabolic requirements, or excessive loss of thiamin. Chronic alcohol consumption is the primary cause of thiamin deficiency in industrialized countries. (More information)
  • Alteration in glucose metabolism has been associated with decreased plasma thiamin concentrations in diabetic patients. Correction of thiamin deficiency may reduce the risk of vascular complications in diabetic subjects. (More information)
  • Thiamin deficiency and decreased thiamin-dependent enzyme activity are associated with Alzheimer's disease. Although thiamin supplementation markedly reverses cognitive impairment in animal models of thiamin deficiency, the effect of thiamin supplementation in Alzheimer's disease patients is not yet known. (More information)
  • Diuretic-induced thiamin excretion may increase the risk of thiamin deficiency and disease severity in subjects with congestive heart failure. Further studies are needed to assess the inclusion of thiamin supplementation in the management of this disease. (More information)

Thiamin (also spelled thiamine) is a water-soluble B vitamin, also known as vitamin B1 or aneurine (1). Isolated and characterized in the 1930s, thiamin was one of the first organic compounds to be recognized as a vitamin (2). Thiamin occurs in the human body as free thiamin and as various phosphorylated forms: thiamin monophosphate (TMP), thiamin triphosphate (TTP), and thiamin pyrophosphate (TPP), which is also known as thiamin diphosphate.


Coenzyme function

The synthesis of TPP from free thiamin requires magnesium, adenosine triphosphate (ATP), and the enzyme, thiamin pyrophosphokinase. TPP is required as a coenzyme for four multi-component enzyme complexes associated with the metabolism of carbohydrates and branched-chain amino acids.

Pyruvate dehydrogenase, α-ketoglutarate dehydrogenase, and branched-chain α-ketoacid dehydrogenase (BCKDH) each comprise a different enzyme complex found within cellular organelles called mitochondria. They catalyze the decarboxylation of pyruvate, α-ketoglutarate, and branched-chain amino acids to form acetyl-coenzyme A (CoA), succinyl-CoA, and derivatives of branched-chain amino acids, respectively. All products play critical roles in the production of energy from food through their connection to the citric acid (Krebs) cycle (2). Branched-chain amino acids (BCAA), including leucine, isoleucine, and valine, are eventually degraded into acetyl-CoA and succinyl-CoA to fuel the citric acid cycle. The catabolism of the three BCAAs also contributes to the production of cholesterol and donates nitrogen for the synthesis of the neurotransmitters, glutamate and γ-aminobutyric acid (GABA) (3). In addition to the thiamin coenzyme (TPP), each dehydrogenase complex requires a niacin-containing coenzyme (NAD), a riboflavin-containing coenzyme (FAD), and lipoic acid.

Transketolase catalyzes critical reactions in another metabolic pathway occurring in the cytosol, known as the pentose phosphate pathway. One of the most important intermediates of this pathway is ribose-5-phosphate, a phosphorylated 5-carbon sugar required for the synthesis of the high-energy ribonucleotides, such as ATP and guanosine triphosphate (GTP). Nucleotides are the building blocks of nucleic acids, DNA, and RNA. The pentose phosphate pathway also supplies various anabolic pathways, including fatty acid synthesis, with the niacin-containing coenzyme NADPH, which is essential for a number of biosynthetic reactions (1, 4). Because transketolase decreases early in thiamin deficiency and, unlike most thiamin-dependent enzymes, is present in red blood cells, measurement of its activity in red blood cells has been used to assess thiamin nutritional status (2).


Beriberi, the disease resulting from severe thiamin deficiency, was described in Chinese literature as early as 2600 B.C. Thiamin deficiency affects the cardiovascular, nervous, muscular, gastrointestinal, and central and peripheral nervous systems (2). Beriberi has been subdivided into dry, wet, cerebral, or gastrointestinal, depending on the systems affected by severe thiamin deficiency (1, 5).

Dry beriberi

The main feature of dry (paralytic or nervous) beriberi is neuropathy. Early in the course of the neuropathy, "burning feet syndrome" may occur. Other symptoms include abnormal (exaggerated) reflexes, as well as diminished sensation and weakness in the legs and arms. Muscle pain and tenderness and difficulty rising from a squatting position have also been observed (6).

Wet beriberi

In addition to neurologic symptoms, wet (cardiac) beriberi is characterized by cardiovascular manifestations of thiamin deficiency, which include rapid heart rate, enlargement of the heart, severe swelling (edema), difficulty breathing, and ultimately congestive heart failure. The Japanese literature describes the acute fulminant form of wet beriberi as "shoshin" (7).

Cerebral beriberi

Cerebral beriberi may lead to Wernicke's encephalopathy and Korsakoff's psychosis, especially in people who abuse alcohol. The diagnosis of Wernicke's encephalopathy is based on a "triad" of signs, which include abnormal eye movements, stance and gait ataxia, and cognitive impairments. If left untreated, irreversible neurologic damage can cause additional clinical manifestations known as Korsakoff's psychosis. This syndrome—also called Korsakoff's dementia, Korsakoff's amnesia, or amnestic confabulatory syndrome—involves a confused, apathetic state and a profound memory disorder, with severe amnesia and loss of recent and working memory.

Thiamin deficiency affecting the central nervous system is referred to as Wernicke's disease when the amnesic state is not present and Wernicke-Korsakoff syndrome (WKS) when the amnesic symptoms are present along with the eye-movement and gait disorders. Rarer neurologic manifestations can include seizures (8). Most WKS sufferers are alcoholics, although it has been observed in other disorders of gross malnutrition, including stomach cancer and AIDS. Administration of intravenous thiamin to WKS patients generally results in prompt improvement of the eye symptoms, but improvements in motor coordination and memory may be less, depending on how long the symptoms have been present. Evidence of increased immune cell activation and increased free radical production in the areas of the brain that are selectively damaged suggests that oxidative stress plays an important role in the neurologic pathology of thiamin deficiency (9).

Gastrointestinal beriberi

TPP is critical for metabolic reactions that utilize glucose in glycolysis and the citric acid cycle (Figure 1). A decrease in the activity of thiamin-dependent enzymes limits the conversion of pyruvate to acetyl-CoA and the utilization of the citric acid cycle, leading to accumulation of pyruvate and lactate. Lactic acidosis, a condition resulting from the accumulation of lactate, is often associated with nausea, vomiting, and severe abdominal pain in a syndrome described as gastrointestinal beriberi (5).

Figure 1. Metabolic Pathways Requiring Thiamin Pyrophosphate (TPP). As explained in the article text, TPP is critical for metabolic reactions that utilize glucose in glycolysis and the citric acid cycle. Specifically, TPP is needed for the following enzymes: transketolase in the pentose phosphate cycle, which converts ribose-5-phosphate to glyceraldehyde-3-phosphate; branched chain alpha-ketoacid dehydrogenase complex (BCKDH) in the branched amino acid catabolic pathway, which converts branched-chain alpha-ketoacids to branched chain acyl-CoA; pyruvate dehydrogenase, which converts pyruvate to acetyl-CoA (shown here, acetyl-CoA enters the citric acid cycle where it is metabolized); and alpha-ketoglutarate dehydrogenase, which coverts alpha-ketoglutarate to succinyl-CoA in the citric acid cycle.

Causes of thiamin deficiency

Thiamin deficiency may result from inadequate thiamin intake, increased requirement for thiamin, excessive loss of thiamin from the body, consumption of anti-thiamin factors in food, or a combination of these factors.

Inadequate intake

Inadequate consumption of thiamin is the main cause of thiamin deficiency in developing countries (2). Thiamin deficiency is common in low-income populations whose diets are high in carbohydrate and low in thiamin (e.g., milled or polished rice). Breast-fed infants whose mothers are thiamin deficient are vulnerable to developing infantile beriberi. Alcoholism, which is associated with low intake of thiamin among other nutrients, is the primary cause of thiamin deficiency in industrialized countries. Some of the non-alcoholic conditions associated with WKS include anorexia, bariatric surgery (weight-loss surgery), gastrointestinal malignancies, and malabsorption syndromes (10-13). Cases of Wernicke's encephalopathy have also been linked to parenteral nutrition lacking vitamin supplementation (14, 15).

Increased requirement

Conditions resulting in an increased requirement for thiamin include strenuous physical exertion, fever, pregnancy, breast-feeding, and adolescent growth. Such conditions place individuals with marginal thiamin intake at risk for developing symptomatic thiamin deficiency. Malaria patients in Southeast Asia were found to be thiamin deficient more frequently than non-infected individuals (16, 17). Malarial infection leads to a large increase in the metabolic demand for glucose. Because thiamin is required for enzymes involved in glucose metabolism, the stresses induced by malarial infection could exacerbate thiamin deficiency in predisposed individuals. HIV-infected individuals, whether or not they had developed AIDS, were also found to be at increased risk for thiamin deficiency (18). Further, chronic alcohol abuse impairs intestinal absorption and utilization of thiamin (1); thus, alcoholics have increased requirements for thiamin. Thiamin deficiency is also observed as a complication of the refeeding syndrome: the introduction of carbohydrates in severely starved individuals leads to an increased demand for thiamin in glycolysis and the citric acid cycle that precipitates thiamin deficiency (19).

Excessive loss

Excessive loss of thiamin may precipitate thiamin deficiency. By increasing urinary flow, diuretics may prevent reabsorption of thiamin by the kidneys and increase its excretion in the urine (20, 21). The risk of thiamin deficiency is increased in diuretic-treated patients with marginal thiamin intake (22) and in individuals receiving long-term, diuretic therapy (23). Individuals with kidney failure requiring hemodialysis lose thiamin at an increased rate and are at risk for thiamin deficiency (24). Alcoholics who maintain a high fluid intake and high urine flow rate may also experience increased loss of thiamin, exacerbating the effects of low thiamin intake (25).

Anti-thiamin factors (ATF)

The presence of anti-thiamin factors (ATF) in foods also contributes to the risk of thiamin deficiency. Certain plants contain ATF, which react with thiamin to form an oxidized, inactive product. Consuming large amounts of tea and coffee (including decaffeinated), as well as chewing tea leaves and betel nuts, have been associated with thiamin depletion in humans due to the presence of ATF (26, 27). ATF include mycotoxins (molds) and thiaminases that break down thiamin in food. Individuals who habitually eat certain raw, fresh-water fish; raw shellfish; and ferns are at higher risk of thiamin deficiency because these foods contain thiaminase that normally is inactivated by heat in cooking (1). In Nigeria, an acute neurologic syndrome (seasonal ataxia) has been associated with thiamin deficiency precipitated by a thiaminase in African silkworms, a traditional, high-protein food for some Nigerians (28).

The Recommended Dietary Allowance (RDA)

The RDA for thiamin, revised in 1998 by the Food and Nutrition Board of the Institute of Medicine, was based on the prevention of deficiency in generally healthy individuals (29; Table 1).

Table 1. Recommended Dietary Allowance (RDA) for Thiamin
Life Stage Age Males (mg/day) Females (mg/day)
Infants 0-6 months  0.2 (AI) 0.2 (AI)
Infants 7-12 months 0.3 (AI) 0.3 (AI)
Children 1-3 years 0.5 0.5
Children 4-8 years 0.6 0.6
Children 9-13 years 0.9 0.9
Adolescents 14-18 years 1.2 1.0
Adults 19 years and older 1.2 1.1
Pregnancy all ages - 1.4
Breast-feeding all ages  - 1.4

Disease Prevention


A cross-sectional study of 2,900 Australian men and women, 49 years of age and older, found that those in the highest quintile of thiamin intake were 40% less likely to have nuclear cataracts than those in the lowest quintile (30). In addition, a recent study in 408 US women found that higher dietary intakes of thiamin were inversely associated with five-year change in lens opacification (31). However, these cross-sectional associations have yet to be elucidated by studies of causation.

Diabetes mellitus and vascular complications

Low plasma concentrations and high renal clearance of thiamin have been observed in diabetic patients compared to healthy subjects (32), suggesting that individuals with type 1 or type 2 diabetes mellitus are at increased risk for thiamin deficiency. Two thiamin transporters, thiamin transporter-1 (THTR-1) and THTR-2, are involved in thiamin uptake by enterocytes in the small intestine and re-uptake in the proximal tubules of the kidneys. A recent study suggested that hyperglycemia in diabetic patients could affect thiamin re-uptake by decreasing the expression of thiamin transporters in the kidneys (33). Conversely, thiamin deficiency appears to impair the normal endocrine function of the pancreas and exacerbate hyperglycemia. Early studies showed that insulin synthesis and secretion were altered in the endocrine pancreatic cells of thiamin-deficient rats (34, 35). In humans, thiamin deficiency caused by recessive mutations in the gene coding for THTR-1 leads to diabetes mellitus in the thiamin-responsive megaloblastic anemia syndrome (see Metabolic diseases).

In a randomized, double-blind pilot study, high-dose thiamin supplements (300 mg/day) were given for six weeks to hyperglycemic individuals (either glucose intolerant or newly diagnosed with type 2 diabetes). Thiamin supplementation prevented any further increase in fasting glucose and insulin levels compared with placebo treatment but did not reduce the hyperglycemia (36). However, one study suggested that thiamin supplementation might improve fasting glucose levels in type 2 diabetics in early stages of the disease (i.e., pre-diabetes or early diabetes) (37).

Chronic hyperglycemia in individuals with diabetes mellitus contributes to the pathogenesis of micro-vascular diseases. Diabetes-related vascular damage can affect the heart (cardiomyopathy), kidneys (nephropathy), retina (retinopathy), and peripheral nervous system (neuropathy). In diabetic subjects, hyperglycemia alters the function of bone marrow-derived endothelial progenitor cells (EPC) that are critical for the growth of blood vessels (38). Interestingly, a higher daily intake of thiamin from the diet was correlated with more circulating EPC and with better vascular endothelial health in 88 individuals with type 2 diabetes (39). An inverse association has also been found between plasma concentrations of thiamin in diabetic patients and the presence of soluble vascular adhesion molecule-1 (sVCAM-1), a marker of vascular dysfunction (32, 40). Early markers of diabetic nephropathy include the presence of serum albumin in the urine, known as microalbuminuria. Administration of thiamin or benfotiamine (a thiamin derivative) prevented the development of renal complications in chemically-induced diabetic rats (41). A randomized, double-blind study conducted in 40 type 2 diabetic patients with microalbuminuria found that high-dose thiamin supplementation (300 mg/day) decreased excretion of urinary albumin compared to placebo over a three-month period (40). Since thiamin treatment has shown promising results in cultured cells and animal models (42-44), the effects of thiamin and its derivatives on vascular complications should be examined in diabetic patients.

Disease Treatment

Alzheimer's disease

Some elderly people are at increased risk for developing subclinical thiamin deficiency secondary to poor dietary intake, reduced gastrointestinal absorption, and multiple medical conditions (45, 46). Since thiamin deficiency can result in a form of dementia (Wernicke-Korsakoff syndrome), its relationship to Alzheimer's disease (AD) and other forms of dementia have been investigated. AD is characterized by a decline in cognitive function in elderly people, accompanied by pathologic features that include β-amyloid plaque deposition and tangles formed by phosphorylated Tau protein (47). Using positron emission tomography (PET) scanning, reduced glucose metabolism was observed in brains of AD patients (48). A large, multicenter PET study using a radio-labeled glucose analog, 18F-Fluoro-deoxyglucose (FDG), correlated a reduction in FDG uptake (a surrogate marker for glucose metabolism) with the extent of cognitive impairment in AD patients. This study, which included 822 subjects over 55 years of age that were cognitively normal (n=229), displayed mild cognitive impairment (n=405), or had mild AD (n=188), demonstrated that brain glucose utilization could predict the progression from mild cognitive impairment to AD (49). Interestingly, a nine-year longitudinal study associated the presence of diabetes mellitus in older people (above 55 years old) with an increased risk for developing AD (50).

A reduction in thiamin-dependent processes in the brain might be related to the altered glucose metabolism in patients with AD (51). A case-control study in 38 elderly women found that blood levels of thiamin, TPP, and TMP were lower in those with dementia of Alzheimer's type (DAT) compared to those in the control group (52). Moreover, several investigators have found evidence of decreased activity of TPP-dependent enzymes, α-ketoglutarate dehydrogenase and transketolase, in the brains of patients who died of AD (53). The finding of decreased brain levels of TPP in the presence of normal levels of free thiamin and TMP suggested alterations in TPP synthesis rather than poor thiamin bioavailability. However it is not clear whether the activities of TPP-metabolizing enzymes (including thiamin pyrophosphokinase) are altered in AD patients (54, 55). Chronic administration of the thiamin derivative benfotiamine alleviated cognitive alterations and decreased the number of β-amyloid plaques in a mouse model of AD without increasing TMP and TPP levels in the brain. This suggested that the beneficial effects of benfotiamine in the brain were likely mediated by the stimulation of TPP-independent pathways (56).

Thiamin deficiency has been linked to increased β-amyloid production in cultured neuronal cells and to plaque formation in animal models (57, 58). These pathological hallmarks of AD could be reversed by thiamin supplementation, suggesting that thiamin could be protective in AD. Moreover, other disorders including mitochondrial dysfunction and chronic oxidative stress have been linked to both thiamin deficiency and AD pathogenesis and progression (9, 59). Presently, there is only slight and inconsistent evidence that thiamin supplements are of benefit in AD. A double-blind, placebo-controlled study of 15 patients (10 completed the study) reported no beneficial effect of 3 grams/day of thiamin on cognitive decline over a 12-month period (60). A preliminary report from another study claimed a mild benefit of 3 to 8 grams of thiamin per day in DAT, but no additional data from that study are available (61). A mild beneficial effect in patients with AD was reported after 12 weeks of treatment with 100 mg/day of a thiamin derivative (thiamin tetrahydrofurfuryl disulfide), but this study was not placebo-controlled (62). A systematic review of randomized, double-blind, placebo-controlled trials of thiamin in patients with DAT found no evidence that thiamin was a useful treatment for the symptoms of Alzheimer's disease (63).

Congestive Heart Failure (CHF)

Severe thiamin deficiency (wet beriberi) can lead to impaired cardiac function and ultimately congestive heart failure (CHF). Although cardiac manifestations of beriberi are rarely encountered in industrialized countries, CHF due to other causes is common, especially in the elderly. Diuretics used in the treatment of CHF, notably furosemide, have been found to increase thiamin excretion, potentially leading to marginal thiamin deficiency (64). A number of studies have examined thiamin nutritional status in CHF patients and most found a fairly high incidence of thiamin deficiency, as measured by assays of transketolase activity. As in the general population, older CHF patients were found to be at higher risk of thiamin deficiency than younger ones (65). An important measure of cardiac function in CHF is the left ventricular ejection fraction (LVEF), which can be assessed by echocardiography. One study in 25 patients found that furosemide use, at doses of 80 mg/day or greater, was associated with a 98% prevalence of thiamin deficiency (23). In a randomized, double-blind study of 30 CHF patients, all of whom had been taking furosemide (80 mg/day) for at least three months, intravenous (IV) thiamin therapy (200 mg/day) for seven days resulted in an improved LVEF compared to IV placebo (66). When all 30 of the CHF patients in that study subsequently received six weeks of oral thiamin therapy (200 mg/day), the average LVEF improved by 22%. This finding may be relevant because improvements in LVEF have been associated with improved survival in CHF patients (67). However, conclusions from studies published to date are limited due to the small sample sizes of the studies, lack of randomization in some studies, and a need for more precise assays of thiamin nutritional status. Presently, the need for thiamin supplementation in maintaining cardiac function in CHF patients remains controversial.


Thiamin deficiency has been observed in some cancer patients with rapidly growing tumors. Research in cell culture and animal models indicates that rapidly dividing cancer cells have a high requirement for thiamin (68). All rapidly dividing cells require nucleic acids at an increased rate, and some cancer cells appear to rely heavily on the TPP-dependent enzyme, transketolase, to provide the ribose-5-phosphate necessary for nucleic acid synthesis. A recent study found that the levels of THTR-1, transketolase, and TPP mitochondrial transporters were increased in samples of human breast cancer tissue compared to normal tissue, suggesting an adaptation in thiamin homeostasis in support of cancer metabolism (69). Thiamin supplementation in cancer patients is common to prevent thiamin deficiency, but Boros et al. caution that too much thiamin may actually fuel the growth of some malignant tumors (70), suggesting that thiamin supplementation be reserved for those cancer patients who are actually deficient in thiamin. Presently, there is no evidence available from studies in humans to support or refute this theory. However, it would be prudent for individuals with cancer who are considering thiamin supplementation to discuss it with the clinician managing their cancer therapy.

Metabolic diseases

Thiamin supplementation is included in the clinical management of genetic diseases that affect the metabolism of carbohydrates and branched-chain amino acids (BCAAs).

Thiamin-responsive pyruvate dehydrogenase complex (PDHC) deficiency

Mutations in PDHC prevent the efficient oxidation of carbohydrates in affected individuals. PDHC deficiency is commonly characterized by lactic acidosis, neurologic and neuromuscular degeneration, and death during childhood. The patients who respond to thiamin treatment (from few mg/day to doses above 1,000 mg/day) exhibit PDHC deficiency due to the decreased affinity of PDHC for TPP (71, 72). Although the vitamin supplementation can reduce lactate accumulation and improve the clinical features in thiamin-responsive patients, it does not constitute a cure (73).

Maple syrup urine disease

Inborn errors of BCAA metabolism lead to thiamin-responsive branched-chain ketoaciduria, also known as maple syrup urine disease. Alterations in the BCAA catabolic pathway result in neurologic dysfunction caused by the accumulation of BCAAs and their derivatives, branched-chain ketoacids (BCKA). The therapeutic approach includes a synthetic diet with reduced BCAA content, and thiamin (10-1,000 mg/day) is supplemented to patients with mutations in the E2 subunit of the BCKDH complex (74). In thiamin-responsive individuals, the supplementation has been proven effective to correct the phenotype without recourse to the BCAA restriction diet.

Thiamin-responsive megaloblastic anemia

Mutations in THTR-1 that impair intestinal thiamin uptake and cause thiamin deficiency have been found in patients affected by thiamin-responsive megaloblastic anemia. This syndrome is characterized by megaloblastic anemia, diabetes mellitus, and deafness. A review of 30 cases reported additional neurologic, visual, and cardiac impairments (75). Oral doses of thiamin (up to 300 mg/day) maintain health and correct hyperglycemia in prepubescent children. However, after puberty, a decline in pancreatic function results in the requirement of insulin together with thiamin to control the hyperglycemia. One study also reported that the treatment of a four-month-old girl with 100 mg/day of thiamin did not prevent hearing loss at 20 months of age (76).

Biotin-responsive basal ganglia disease

Biotin-responsive basal ganglia disease, also called thiamin metabolism dysfunction syndrome-2, is caused by mutations in the gene coding for THTR-2. The clinical features appear around three to four years of age and include sub-acute encephalopathy (confusion, drowsiness, altered level of consciousness), ataxia, and seizures. A retrospective study of 18 affected individuals from the same family or the same tribe in Saudi Arabia was recently conducted. The data showed that biotin monotherapy (5-10 mg/kg/day) efficiently abolished the clinical manifestations of the disease, although one-third of the patients suffered from recurrent acute crises. Often associated with poor outcomes, acute crises were not observed after thiamin supplementation started (300-400 mg/day) and for a five-year follow-up period. Early diagnostic and immediate treatment with biotin and thiamin led to positive outcomes (77).


Humans obtain thiamin from dietary sources and from the normal microflora of the colon, although the contribution of the latter towards the body's requirement for thiamin is not clear (78).

Food sources

A varied diet should provide most individuals with adequate thiamin to prevent deficiency. In the US the average dietary thiamin intake for young adult men is about 2 mg/day and 1.2 mg/day for young adult women. A survey of people over the age of 60 found an average dietary thiamin intake of 1.4 mg/day for men and 1.1 mg/day for women (29). However, institutionalization and poverty both increase the likelihood of inadequate thiamin intake in the elderly (79). Whole-grain cereals, legumes (e.g., beans and lentils), nuts, lean pork, and yeast are rich sources of thiamin (1). Because most of the thiamin is lost during the production of white flour and polished (milled) rice, white rice and foods made from white flour (e.g., bread and pasta) are fortified with thiamin in many Western countries. A number of thiamin-rich foods are listed in Table 2, along with their thiamin content in milligrams (mg). For more information on the nutrient content of foods, search USDA's FoodData Central (80).

Table 2. Some Food Sources of Thiamin
Food Serving Thiamin (mg)
Lentils (cooked, boiled) ½ cup 0.17
Green peas (cooked, boiled) ½ cup 0.21
Long-grain, brown rice (cooked) 1 cup 0.19
Long-grain, white rice, enriched (cooked) 1 cup 0.26
Long-grain, white rice, unenriched (cooked) 1 cup 0.04
Whole-wheat bread 1 slice 0.10
White bread, enriched 1 slice 0.23
Fortified breakfast cereal (wheat, puffed) 1 cup 0.31
Wheat germ breakfast cereal (toasted, plain) 1 cup 1.88
Pork, lean (loin, tenderloin, cooked, roasted) 3 ounces* 0.81
Pecans 1 ounce 0.19
Spinach (cooked, boiled) ½ cup 0.09
Orange 1 fruit 0.11
Cantaloupe ½ fruit 0.11
Milk 1 cup 0.10
Egg (cooked, hard-boiled) 1 large 0.03
*Three ounces of meat is a serving about the size of a deck of cards


Thiamin is available in nutritional supplements and for fortification as thiamin hydrochloride and thiamin nitrate (81).



The Food and Nutrition Board did not set a tolerable upper intake level (UL) for thiamin because there are no well-established toxic effects from consumption of excess thiamin in food or through long-term, oral supplementation (up to 200 mg/day). A small number of life-threatening anaphylactic reactions have been observed with large intravenous doses of thiamin (29).

Drug interactions

Reduced blood levels of thiamin have been reported in individuals with seizure disorders (epilepsy) taking the anticonvulsant medication, phenytoin, for long periods of time (82). 5-Fluorouracil, a drug used in cancer therapy, inhibits the phosphorylation of thiamin to TPP (83). Diuretics, especially furosemide, may increase the risk of thiamin deficiency in individuals with marginal thiamin intake due to increased urinary excretion of thiamin (21). Moreover, chronic alcohol abuse is associated with thiamin deficiency due to low dietary intake, impaired absorption and utilization, and increased excretion of the vitamin (1). Chronic alcohol feeding to rats showed a decrease in the active absorption of thiamin linked to the inhibition of thiamin membrane transporter THTR-1 in the intestinal epithelium (84). Alcohol consumption in rats also decreases the levels of THTR-1 and THTR-2 in renal epithelial cells, thus limiting thiamin re-uptake by the kidneys (85).

Linus Pauling Institute Recommendation

The Linus Pauling Institute supports the recommendation by the Food and Nutrition Board of 1.2 mg/day of thiamin for men and 1.1 mg/day for women. A varied diet should provide enough thiamin for most people. Following the Linus Pauling Institute recommendation to take a daily multivitamin/multimineral supplement, containing 100% of the Daily Values (DV), will ensure an intake of at least 1.5 mg/day of thiamin.

Older adults (>50 years)

Presently, there is no evidence that the requirement for thiamin is increased in older adults, but some studies have found inadequate dietary intake and thiamin insufficiency to be more common in elderly populations (79). Thus, it would be prudent for older adults to take a multivitamin/mineral supplement, which will generally provide at least 1.5 mg/day of thiamin.

Authors and Reviewers

Originally written in 2000 by: 
Jane Higdon, Ph.D. 
Linus Pauling Institute 
Oregon State University

Updated in September 2002 by: 
Jane Higdon, Ph.D. 
Linus Pauling Institute 
Oregon State University

Updated in June 2007 by: 
Victoria J. Drake, Ph.D. 
Linus Pauling Institute 
Oregon State University

Updated in June 2013 by: 
Barbara Delage, Ph.D. 
Linus Pauling Institute 
Oregon State University

Reviewed in July 2013 by: 
Christopher Bates, D.Phil. 
Honorary Senior Scientist 
Formerly Head of Micronutrient Status Research 
MRC Human Nutrition Research 
Elsie Widdowson Laboratory 
Cambridge, UK

Copyright 2000-2021  Linus Pauling Institute


1.  Tanphaichitr V. Thiamin. In: Shils M, Olson JA, Shike M, Ross AC, eds. Modern Nutrition in Health and Disease. 9th ed. Baltimore: Williams & Wilkins; 1999:381-389.

2.  Rindi G. Thiamin. In: Ziegler EE, Filer LJ, eds. Present Knowledge in Nutrition. 7th ed. Washington D.C.: ILSI Press; 1996:160-166.

3.  Hutson SM, Sweatt AJ, Lanoue KF. Branched-chain [corrected] amino acid metabolism: implications for establishing safe intakes. J Nutr. 2005;135(6 Suppl):1557S-1564S.  (PubMed)

4.  Brody T. Nutritional Biochemistry. 2nd ed. San Diego: Academic Press; 1999.

5.  Donnino M. Gastrointestinal beriberi: a previously unrecognized syndrome. Ann Intern Med. 2004;141(11):898-899.  (PubMed)

6.  McDowell L. Thiamin. In: Vitamins in Animal and Human Nutrition. 2nd ed. Ames: Iowa State University Press; 2000:265-310.

7.  Yamasaki H, Tada H, Kawano S, Aonuma K. Reversible pulmonary hypertension, lactic acidosis, and rapidly evolving multiple organ failure as manifestations of shoshin beriberi. Circ J. 2010;74(9):1983-1985.  (PubMed)

8.  Doss A, Mahad D, Romanowski CA. Wernicke encephalopathy: unusual findings in nonalcoholic patients. J Comput Assist Tomogr. 2003;27(2):235-240.  (PubMed)

9.  Hazell AS, Faim S, Wertheimer G, Silva VR, Marques CS. The impact of oxidative stress in thiamine deficiency: a multifactorial targeting issue. Neurochem Int. 2013;62(5):796-802.  (PubMed)

10.  Saad L, Silva LF, Banzato CE, Dantas CR, Garcia C, Jr. Anorexia nervosa and Wernicke-Korsakoff syndrome: a case report. J Med Case Rep. 2010;4:217.  (PubMed)

11.  Becker DA, Balcer LJ, Galetta SL. The Neurological Complications of Nutritional Deficiency following Bariatric Surgery. J Obes. 2012;2012:608534.  (PubMed)

12.  Jung ES, Kwon O, Lee SH, et al. Wernicke's encephalopathy in advanced gastric cancer. Cancer Res Treat. 2010;42(2):77-81.  (PubMed)

13.  Greenspon J, Perrone EE, Alaish SM. Shoshin beriberi mimicking central line sepsis in a child with short bowel syndrome. World journal of pediatrics : World J Pediatr. 2010;6(4):366-368.  (PubMed)

14.  Sequeira Lopes da Silva JT, Almaraz Velarde R, Olgado Ferrero F, et al. Wernicke's encephalopathy induced by total parental nutrition. Nutr Hosp. 2010;25(6):1034-1036.  (PubMed)

15.  Francini-Pesenti F, Brocadello F, Manara R, Santelli L, Laroni A, Caregaro L. Wernicke's syndrome during parenteral feeding: not an unusual complication. Nutrition. 2009;25(2):142-146.  (PubMed)

16.  Krishna S, Taylor AM, Supanaranond W, et al. Thiamine deficiency and malaria in adults from southeast Asia. Lancet. 1999;353(9152):546-549.  (PubMed)

17.  Mayxay M, Taylor AM, Khanthavong M, et al. Thiamin deficiency and uncomplicated falciparum malaria in Laos. Trop Med Int Health. 2007;12(3):363-369.  (PubMed)

18.  Muri RM, Von Overbeck J, Furrer J, Ballmer PE. Thiamin deficiency in HIV-positive patients: evaluation by erythrocyte transketolase activity and thiamin pyrophosphate effect. Clin Nutr. 1999;18(6):375-378.  (PubMed)

19.  Stanga Z, Brunner A, Leuenberger M, et al. Nutrition in clinical practice-the refeeding syndrome: illustrative cases and guidelines for prevention and treatment. Eur J Clin Nutr. 2008;62(6):687-694.  (PubMed)

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(2):69-71.  (PubMed)

21.  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(3):238-243.  (PubMed)

22.  Sica DA. Loop diuretic therapy, thiamine balance, and heart failure. Congestive heart failure 2007;13(4):244-247.  (PubMed)

23.  Zenuk C, Healey J, Donnelly J, Vaillancourt R, Almalki Y, Smith S. Thiamine deficiency in congestive heart failure patients receiving long term furosemide therapy. Can J Clin Pharmacol. 2003;10(4):184-8.  (PubMed)

24.  Hung SC, Hung SH, Tarng DC, Yang WC, Chen TW, Huang TP. Thiamine deficiency and unexplained encephalopathy in hemodialysis and peritoneal dialysis patients. Am J Kidney Dis. 2001;38(5):941-947.  (PubMed)

25.  Wilcox CS. Do diuretics cause thiamine deficiency? J Lab Clin Med. 1999;134(3):192-193.

26.  Vimokesant SL, Hilker DM, Nakornchai S, Rungruangsak K, Dhanamitta S. Effects of betel nut and fermented fish on the thiamin status of northeastern Thais. Am J Clin Nutr. 1975;28(12):1458-1463.  (PubMed)

27.  Ventura A, Mafe MC, Bourguet M, Tornero C. Wernicke's encephalopathy secondary to hyperthyroidism and ingestion of thiaminase-rich products. Neurologia. 2013;28(4):257-259.  (PubMed)

28.  Nishimune T, Watanabe Y, Okazaki H, Akai H. Thiamin is decomposed due to Anaphe spp. entomophagy in seasonal ataxia patients in Nigeria. J Nutr. 2000;130(6):1625-1628.  (PubMed)

29.  Food and Nutrition Board, Institute of Medicine. Thiamin. Dietary Reference Intakes: Thiamin, Riboflavin, Niacin, Vitamin B6, Vitamin B12, Pantothenic Acid, Biotin, and Choline. Washington D.C.: National Academy Press; 1998:58-86.  (National Academy Press)

30.  Cumming RG, Mitchell P, Smith W. Diet and cataract: the Blue Mountains Eye Study. Ophthalmology. 2000;107(3):450-456.  (PubMed)

31.  Jacques PF, Taylor A, Moeller S, et al. Long-term nutrient intake and 5-year change in nuclear lens opacities. Arch Ophthalmol. 2005;123(4):517-526.  (PubMed)

32.  Thornalley PJ, Babaei-Jadidi R, Al Ali H, et al. High prevalence of low plasma thiamine concentration in diabetes linked to a marker of vascular disease. Diabetologia. 2007;50(10):2164-2170.  (PubMed)

33.  Larkin JR, Zhang F, Godfrey L, et al. Glucose-induced down regulation of thiamine transporters in the kidney proximal tubular epithelium produces thiamine insufficiency in diabetes. PLoS One. 2012;7:e53175.  (PubMed)

34.  Rathanaswami P, Sundaresan R. Effects of thiamine deficiency on the biosynthesis of insulin in rats. Biochem Int. 1991;24(6):1057-1062.  (PubMed)

35.  Rathanaswami P, Pourany A, Sundaresan R. Effects of thiamine deficiency on the secretion of insulin and the metabolism of glucose in isolated rat pancreatic islets. Biochem Int. 1991;25(3):577-583.  (PubMed)

36.  Alaei Shahmiri F, Soares MJ, Zhao Y, Sherriff J. High-dose thiamine supplementation improves glucose tolerance in hyperglycemic individuals: a randomized, double-blind cross-over trial. Eur J Clin Nutr. 2013. May 29 [Epub ahead of print]  (PubMed)

37.  Gonzalez-Ortiz M, Martinez-Abundis E, Robles-Cervantes JA, Ramirez-Ramirez V, Ramos-Zavala MG. Effect of thiamine administration on metabolic profile, cytokines and inflammatory markers in drug-naive patients with type 2 diabetes. Eur J Clin Nutr. 2011;50(2):145-149.  (PubMed)

38.  Tepper OM, Galiano RD, Capla JM, et al. Human endothelial progenitor cells from type II diabetics exhibit impaired proliferation, adhesion, and incorporation into vascular structures. Circulation. 2002;106(22):2781-2786.  (PubMed)

39.  Wong CY, Qiuwaxi J, Chen H, et al. Daily intake of thiamine correlates with the circulating level of endothelial progenitor cells and the endothelial function in patients with type II diabetes. Mol Nutr Food Res. 2008;52(12):1421-1427.  (PubMed)

40.  Rabbani N, Alam SS, Riaz S, et al. High-dose thiamine therapy for patients with type 2 diabetes and microalbuminuria: a randomised, double-blind placebo-controlled pilot study. Diabetologia. 2009;52(2):208-212.  (PubMed)

41.  Babaei-Jadidi R, Karachalias N, Ahmed N, Battah S, Thornalley PJ. Prevention of incipient diabetic nephropathy by high-dose thiamine and benfotiamine. Diabetes. 2003;52(8):2110-2120.  (PubMed)

42.  Hammes HP, Du X, Edelstein D, et al. Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nature Med. 2003;9(3):294-299.  (PubMed)

43.  Varkonyi T, Kempler P. Diabetic neuropathy: new strategies for treatment. Diabetes Obes Metab. 2008;10(2):99-108.  (PubMed)

44.  Kohda Y, Shirakawa H, Yamane K, et al. Prevention of incipient diabetic cardiomyopathy by high-dose thiamine. J Toxicol Sci. 2008;33(4):459-472.  (PubMed)

45.  Lee DC, Chu J, Satz W, Silbergleit R. Low plasma thiamine levels in elder patients admitted through the emergency department. Acad Emerg Med. 2000;7(10):1156-1159.  (PubMed)

46.  Ito Y, Yamanaka K, Susaki H, Igata A. A cross-investigation between thiamin deficiency and the physical condition of elderly people who require nursing care. J Nutr Sci Vitaminol. 2012;58(3):210-216.  (PubMed)

47.  Prvulovic D, Hampel H. Amyloid β (A-β) and phospho-τ (p-τ) as diagnostic biomarkers in Alzheimer's disease. Clin Chem Lab Med. 2011;49:367-374.  (PubMed)

48.  Kish SJ. Brain energy metabolizing enzymes in Alzheimer's disease: α-ketoglutarate dehydrogenase complex and cytochrome oxidase. Ann N Y Acad Sci. 1997;826:218-228.  (PubMed)

49.  Langbaum JB, Chen K, Lee W, et al. Categorical and correlational analyses of baseline fluorodeoxyglucose positron emission tomography images from the Alzheimer's Disease Neuroimaging Initiative (ADNI). NeuroImage. 2009;45(4):1107-1116.  (PubMed)

50.  Arvanitakis Z, Wilson RS, Bienias JL, Evans DA, Bennett DA. Diabetes mellitus and risk of Alzheimer disease and decline in cognitive function. Arch Neurol. 2004;61(5):661-666.  (PubMed)

51.  Gibson GE, Hirsch JA, Cirio RT, Jordan BD, Fonzetti P, Elder J. Abnormal thiamine-dependent processes in Alzheimer's Disease. Lessons from diabetes. Mol Cell Neurosci. 2013;55:17-25.  (PubMed)

52.  Glaso M, Nordbo G, Diep L, Bohmer T. Reduced concentrations of several vitamins in normal weight patients with late-onset dementia of the Alzheimer type without vascular disease. J Nutr Health Aging. 2004;8(5):407-413.  (PubMed)

53.  Bender DA. Optimum nutrition: thiamin, biotin and pantothenate. Proc Nutr Soc. 1999;58(2):427-433.  (PubMed)

54.  Mastrogiacoma F, Bettendorff L, Grisar T, Kish SJ. Brain thiamine, its phosphate esters, and its metabolizing enzymes in Alzheimer's disease. Ann Neurol. 1996;39(5):585-591.  (PubMed)

55.  Heroux M, Raghavendra Rao VL, Lavoie J, Richardson JS, Butterworth RF. Alterations of thiamine phosphorylation and of thiamine-dependent enzymes in Alzheimer's disease. Metab Brain Dis. 1996;11(1):81-88.  (PubMed)

56.  Pan X, Gong N, Zhao J, et al. Powerful beneficial effects of benfotiamine on cognitive impairment and beta-amyloid deposition in amyloid precursor protein/presenilin-1 transgenic mice. Brain. 2010;133(Pt 5):1342-1351.  (PubMed)

57.  Karuppagounder SS, Xu H, Shi Q, et al. Thiamine deficiency induces oxidative stress and exacerbates the plaque pathology in Alzheimer's mouse model. Neurobiol Aging. 2009;30(10):1587-1600.  (PubMed)

58.  Zhang Q, Yang G, Li W, et al. Thiamine deficiency increases beta-secretase activity and accumulation of beta-amyloid peptides. Neurobiol Aging. 2011;32(1):42-53.  (PubMed)

59.  Dumont M, Beal MF. Neuroprotective strategies involving ROS in Alzheimer disease. Free Rad Res Med. 2011;51(5):1014-1026.  (PubMed)

60.  Nolan KA, Black RS, Sheu KF, Langberg J, Blass JP. A trial of thiamine in Alzheimer's disease. Arch Neurology. 1991;48(1):81-83.  (PubMed)

61.  Meador K, Loring D, Nichols M, et al. Preliminary findings of high-dose thiamine in dementia of Alzheimer's type. J Geriatr Psychiatry Neurol. 1993;6(4):222-229.  (PubMed)

62.  Mimori Y, Katsuoka H, Nakamura S. Thiamine therapy in Alzheimer's disease. Metab Brain Dis. 1996;11(1):89-94.  (PubMed)

63.  Rodriguez-Martin JL, Qizilbash N, Lopez-Arrieta JM. Thiamine for Alzheimer's disease (Cochrane Review). Cochrane Database Syst Rev. 2001;2:CD001498.  (PubMed)

64.  Hanninen SA, Darling PB, Sole MJ, Barr A, Keith ME. The prevalence of thiamin deficiency in hospitalized patients with congestive heart failure. J Am Coll Cardiol. 2006;47(2):354-361.  (PubMed)

65.  Wilkinson TJ, Hanger HC, George PM, Sainsbury R. Is thiamine deficiency in elderly people related to age or co-morbidity? Age Ageing. 2000;29(2):111-116.  (PubMed)

66.  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(5):485-490.  (PubMed)

67.  Leslie D, Gheorghiade M. Is there a role for thiamine supplementation in the management of heart failure? Am Heart J. 1996;131(6):1248-1250.

68.  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(15):4177-4182.  (PubMed)

69.  Zastre JA, Hanberry BS, Sweet RL, et al. Up-regulation of vitamin B1 homeostasis genes in breast cancer. J Nutr Biochem. 2013. May 1 [Epub ahead of print]  (PubMed)

70.  Boros LG, Brandes JL, Lee WN, et al. Thiamine supplementation to cancer patients: a double edged sword. Anticancer Res. 1998;18(1B):595-602.  (PubMed)

71.  Naito E, Ito M, Yokota I, Saijo T, Ogawa Y, Kuroda Y. Diagnosis and molecular analysis of three male patients with thiamine-responsive pyruvate dehydrogenase complex deficiency. J Neurological Sci. 2002;201(1-2):33-37.  (PubMed)

72.  Patel KP, O'Brien TW, Subramony SH, Shuster J, Stacpoole PW. The spectrum of pyruvate dehydrogenase complex deficiency: clinical, biochemical and genetic features in 371 patients. Mol Genet Metab. 2012;106(3):385-394.  (PubMed)

73.  Lee EH, Ahn MS, Hwang JS, Ryu KH, Kim SJ, Kim SH. A Korean female patient with thiamine-responsive pyruvate dehydrogenase complex deficiency due to a novel point mutation (Y161C)in the PDHA1 gene. J Korean Med Sci. 2006;21(5):800-804.  (PubMed)

74.  Chuang DT, Chuang JL, Wynn RM. Lessons from genetic disorders of branched-chain amino acid metabolism. J Nutr. 2006;136(1 Suppl):243S-249S.  (PubMed)

75.  Shaw-Smith C, Flanagan SE, Patch AM, et al. Recessive SLC19A2 mutations are a cause of neonatal diabetes mellitus in thiamine-responsive megaloblastic anaemia. Pediatr Diabetes. 2012;13(4):314-321.  (PubMed)

76.  Akin L, Kurtoglu S, Kendirci M, Akin MA, Karakukcu M. Does early treatment prevent deafness in thiamine-responsive megaloblastic anaemia syndrome? J Clin Res Pediatr Endocrinol. 2011;3(1):36-39.  (PubMed)

77.  Alfadhel M, Almuntashri M, Jadah RH, et al. Biotin-responsive basal ganglia disease should be renamed biotin-thiamine-responsive basal ganglia disease: a retrospective review of the clinical, radiological and molecular findings of 18 new cases. Orphanet J Rare Dis. 2013;8:83.  (PubMed)

78.  LeBlanc JG, Milani C, de Giori GS, Sesma F, van Sinderen D, Ventura M. Bacteria as vitamin suppliers to their host: a gut microbiota perspective. Curr Opin Biotechnol. 2013;24(2):160-168.  (PubMed)

79.  Russell RM, Suter PM. Vitamin requirements of elderly people: an update. Am J Clin Nutr. 1993;58(1):4-14.  (PubMed)

80.  US Department of Agriculture, Agricultural Research Service. FoodData Central, 2019.

81.  Thiamin (vitamin B1). In: Hendler S, Rorvik D, eds. PDR for Nutritional Supplements. 2nd ed. Montvale: Physicians' Desk Reference Inc.; 2008:609-615.

82.  Flodin N. Pharmacology of micronutrients. New York: Alan R. Liss, Inc.; 1988.

83.  Schumann K. Interactions between drugs and vitamins at advanced age. Int J Vitam Nutr Res. 1999;69(3):173-178.  (PubMed)

84.  Subramanya SB, Subramanian VS, Said HM. Chronic alcohol consumption and intestinal thiamin absorption: effects on physiological and molecular parameters of the uptake process. Am J Physiol Gastrointest Liver Physiol. 2010;299(1):G23-G31.  (PubMed)

85.  Subramanian VS, Subramanya SB, Tsukamoto H, Said HM. Effect of chronic alcohol feeding on physiological and molecular parameters of renal thiamin transport. Am J Physiol Renal Physiol. 2010;299(1):F28-F34.  (PubMed)