Thiamin (Vitamin B1): Dietary Source, RDA, and Functions

Thiamin, thiamine, or vitamin B1, is an essential water-soluble vitamin. It is an essential micronutrient for energy metabolism and cognitive and neurological health. Thiamin acts as a coenzyme in the metabolism of carbohydrates and branched-chain amino acids.

Alternate nameThiamin
Year of Discovery1897
Discovered byChristiaan Eijkman

Christiaan Eijkman produced beriberi in chicken by feeding polished rice (Nobel Prize, 1929). Adolf Windaus (Nobel Prize, 1928) elucidated the structure of thiamin.

Dietary Sources

Thiamin is found naturally in food sources. Rich natural sources of thiamin are;

  1. Meat, particularly pork (ham)
  2. Fish
  3. Whole grains (brown rice)
  4. Yeasts
  5. Legumes (green peas)
  6. Soy milk
  7. Watermelon
  8. Acorn squash (pepper squash)
  9. Mussel

In many countries, major dietary sources of thiamin are fortified foods such as wheat grains, wheat flour, bread, cereals, and baby formula [1]. 

Aleurone layer of cereal (food grain) is a rich source of thiamin. Therefore, whole wheat flour and unpolished hand-pounded rice have better nutritive value than completely polished refined foods. When the grains are polished, the aleurone layer is usually removed. Thiamin is partially destroyed by high-heat cooking or long cooking times.

Recommended Dietary Allowance

The requirement is 1-1.5 mg/day. The RDA (Recommended Dietary Allowance) of thiamin for adults is 1.1 mg/day for women and 1.2 mg/day for men. For pregnancy and lactation, the amount increases to 1.4 mg daily.[2]

The requirement for thiamin is increased along with a higher intake of carbohydrates. Dietary reference intakes (DRI) for thiamin depend on calorie intake (0.5 mg/1000 calories). There is no known toxicity for thiamin.

Life Stage GroupThiamin
0-6 months0.2 mg/day
7-12 months0.3 mg/day
1-3 years 0.5 mg/day
4-8 years 0.6 mg/day
9-13 years 0.9 mg/day
14-18 years 1.2 mg/day
>19 years 1.2 mg/day
9-13 years 0.9 mg/day
14-18 years 1.0 mg/day
>19 years 1.1 mg/day
≤ 18 years 1.4 mg/day
19-50 years 1.4 mg/day
≤ 18 years 1.4 mg/day
19-50 years 1.4 mg/day
Source: Standing Committee on the Scientific Evaluation of Dietary Reference Intakes (1997, 1998, 2000) [1]


Thiamin absorption occurs mainly in the jejunum of the small intestine. In the blood, thiamin is transported in the erythrocytes and plasma. A small percentage of thiamin is absorbed, while the remainder is excreted in the urine. Thiamin has a short half-life, and only a minimal amount is stored in the liver, so people require a continuous supply of thiamin from their diet.

Thiamin status is measurable via urinary thiamin excretion, erythrocyte thiamin, and erythrocyte transketolase activity. Thiamine status can be impacted by the consumption of thiamine antagonists, such as alcohol, tea, betel nuts, and thiaminase‐containing fish and ferns [4]. 


Thiamin consists of pyrimidine and thiazole rings linked by a methylene bridge. Thiamin exists in a variety of phosphorylated forms. Its main form is thiamin pyrophosphate or TPP. 

The central role of thiamin is in carbohydrate metabolism. The requirement for thiamin is increased along with a higher intake of carbohydrates.

TPP is a cofactor for >20  enzymatic pathways, including the Krebs cycle and pentose phosphate pathway.  Impairment of these enzymes due to a lack of thiamine can impact neuronal and cardiovascular functions. 


Historically, thiamin deficiency manifests as a disease called beriberi (wet beriberi, dry beriberi, infantile beriberi). Symptoms of thiamin deficiency are nonspecific and include anorexia, weight loss, apathy, short-term memory issues, confusion, irritability, muscular weakness, and heart enlargement.

People with alcohol use disorder develop thiamin deficiency because alcohol inhibits thiamin transport through the intestinal mucosal cells. Acetaldehyde produced from ethanol oxidation displaces pyridoxal phosphate from its protein-binding sites, thereby accelerating its degradation.  The thiamin deficiency in chronic alcohol abusers is manifested as Wernicke-Korsakoff syndrome (cerebral beriberi).

  1. Institute of Medicine (US) Food and Nutrition Board. Dietary Reference Intakes: A Risk Assessment Model for Establishing Upper Intake Levels for Nutrients. Washington (DC): National Academies Press (US); 1998. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Available from:
  2. Institute of Medicine (US) Standing Committee on the Scientific Evaluation of Dietary Reference Intakes and its Panel on Folate, Other B Vitamins, and Choline. Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline. National Academies Press (US); Washington (DC): 1998. [PubMed]
  3. Whitfield, K. C., Smith, T. J., Rohner, F., Wieringa, F. T., & Green, T. J. (2021). Thiamine fortification strategies in low- and middle-income settings: a review. Annals of the New York Academy of Sciences, 1498(1), 29–45.
  4. Whitfield, K.C., Bourassa M.W., Adamolekun B., et al. 2018. Thiamine deficiency disorders: diagnosis, prevalence, and a roadmap for global control programs. Ann. N.Y. Acad. Sci. 1430: 3–43. [PubMed]

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