Vitamin B1 — Nutrition Sources, Health Benefits & Deficiency

by Arpi Gasparyan | Last updated on March 25, 2024

Medically reviewed by Victoria Mazmanyan

Introduction

Vitamin B1 (thiamin, thiamine) is water-soluble and one of the eight B vitamins. It is naturally present in some foods, artificially added to others, and available as a dietary supplement (vitamin B1, B-complex, multivitamins). Vitamin B1 is involved in energy metabolism, thus participating in cell growth, development, and function (1).

Table of contents

Absorption & Metabolism

Vitamin B1 Measurement Methods

Recommended Intakes

Food Sources of Vitamin B1

Vitamin B1 & Human Health: Deficiency & Symptoms

Pathogenesis of Vitamin B1 Deficiency

Beriberi

Wernicke-Korsakoff Syndrome
Heart Failure

Neuropathy & Neuritis

Alzheimer's Disease

Diabetes

Vitamin B1 Deficiency Risk Groups & Causes

Toxicity & Side Effects

Contraindications & Special Considerations

Interactions With Medications

Historical Facts

Summary

References

Absorption & Metabolism

The small intestine absorbs vitamin B1 through active transport (nutritional doses) and passive diffusion (pharmacologic doses).

Most dietary vitamin B1 comes in phosphorylated forms, which are hydrolyzed by intestinal phosphatases to the vitamin’s free form before absorption. Some amounts of vitamin B1 are in its free or absorbable form. After absorption, thiamine is phosphorylated to its three forms: thiamine monophosphate, thiamine diphosphate (thiamine pyrophosphate), and thiamine triphosphate (2, 3).

Around 80% of the organism's vitamin B1 (25-30mg) is its main metabolically active form of thiamine diphosphate (TDP), otherwise called thiamine pyrophosphate. Thiamine diphosphate is an essential cofactor for several metabolic enzymes involved in glucose, amino acid, lipid metabolism, glycolysis, the Krebs cycle, and the pentose phosphate pathway (1, 2).

Vitamin B1, thiamine, is stored primarily in the liver, as well as the heart, kidneys, and brain; however, in small amounts, as it has a half-life of 14-18 days, meaning it can be stored in the body for a short time, and people need a continuous supply from the diet (1).

Vitamin B1 Measurement Methods

Vitamin B1 levels in the body are indirectly determined by measuring the erythrocyte (red blood cell) transketolase enzyme activity, commonly expressed as a ratio or “activity coefficient” (ETKAC). Vitamin B1 is a cofactor of this enzyme, which is why it is used as a biomarker (2).

Another way to measure vitamin B1 status is urinary thiamine excretion; however, it only shows the dietary intake but not vitamin levels in the organism. Urinary excretion of less than 100 mcg of vitamin B1 daily indicates insufficient intake, whereas less than 40 mcg daily indicates an extremely low intake (1).

Recommended Intakes

According to the 2020-2025 Dietary Guidelines for Americans, the recommended daily allowance or value (RDA or RDV) of vitamin B1 or thiamine for adults is 1.1-1.2 mg (4).

The chart below demonstrates the RDVs for different age groups (4):

Ages	2-3	4-8	9-13	14-18	19-30	31-50	50+
Male	0.5mg	0.6mg	0.9mg	1.2mg	1.2mg	1.2mg	1.2mg
Female	0.5mg	0.6mg	0.9mg	1.0mg	1.1mg	1.1mg	1.1mg

As you can see, the vitamin B1 needs in the body grow as you age and stay at the same level in adulthood.

Food Sources of Vitamin B1

While some foods naturally contain vitamin B1, others are fortified with it.

Many brands of breakfast cereals, instant noodles, beverages, infant formulas, and wheat products (i.e., white bread and pasta) fortify or enrich their products with vitamin B1, which can be seen on the “Nutrition Facts” Label.

The chart below shows foods that naturally contain vitamin B1 and the vitamin levels per 100g of each product.

Brown rice	0.18mg
White rice, enriched	0.163mg
White rice, unenriched	0.02mg
Flour, enriched	0.785mg
Flour, unenriched	0.12mg
Multigrain bread (includes whole grains)	0.24mg
Pork, fresh, loin	0.88mg
Beef liver	0.194mg
Salmon, Atlantic	0.34mg
Trout	0.143mg
Chicken, breast, meat only	0.08mg
Soybean	0.16mg
Almond	0.21mg
Hazelnut	0.64mg
Pistachio	0.87mg
Black Beans	0.244mg
Peas	0.26mg

Other types of red meat, poultry, fish, and nuts also contain vitamin B1 in varying amounts.

Whole-grain products (whole-wheat flour, brown rice) are naturally richer in vitamin B1 than refined products (white flour, white rice, de-germed cornmeal). Refined grains lack the bran and germ layers that pack most B-complex vitamins, iron, and fiber (5).

Vitamin B1 is more heat-sensitive than other water-soluble B vitamins. High heat and long cooking times destroy vitamin B1 in the food. Some amounts of thiamine are also being leached into the water. Therefore, soaking and washing the cooked product will further decrease the vitamin concentrations (6, 7).

Coffee (regular and decaffeinated) and tea, as well as raw fish and shellfish, contain polyphenolic compounds (thiaminases) that inactivate vitamin B1; their heavy use may increase the risk of thiamine deficiency (6, 8).

Vitamin B1 & Human Health: Deficiency & Symptoms

As previously mentioned, vitamin B1 is required for energy metabolism; thus, it participates in cell growth, development, and function. Vitamin B1 is involved in several functions in the body, such as the nervous system (axonal conduction), muscle functioning (electrolyte flow in the cells), carbohydrate, amino acid, and lipid metabolism, glycolysis, the Krebs cycle, pentose phosphate pathway, and production of hydrochloric acid (HCl) (1, 2, 8).

Vitamin B1 (thiamine) deficiency, also known as beriberi, is more prevalent in East Asian countries due to the overconsumption of white rice.

Pathogenesis of Vitamin B1 Deficiency

Vitamin B1 combines with ATP (adenosine triphosphate) in the liver, kidneys, and leukocytes to form TDP (thiamine diphosphate). Low levels of thiamine lead to decreased transketolase activity in red blood cells and increased pyruvic acid in the blood. Pyruvic acid cannot convert to acetyl-CoA and enter the Krebs cycle, leading to its buildup and anaerobic metabolism to lactic acid (8).

Vitamin B1 deficiency leads to impaired carbohydrate and lipid metabolism, altered mitochondrial activity and cellular membrane functions, decreased energy stores, and reduced neurotransmitter synthesis (9).

Beriberi

Beriberi causes peripheral neuropathy and wasting. Symptoms begin with sensory disturbances and progress to motor and reflex disturbances.

Beriberi is divided into wet and dry forms, which usually overlap. The division is made due to the amount of fluid accumulated in the body. Dry beriberi mainly involves the central nervous system or CNS (the brain and spinal cord), whereas wet beriberi involves the cardiovascular system. Both types can lead to pain and paresthesias (1, 8).

Dry beriberi symptoms: confusion, poor memory, irritability, sleep disturbances, muscle weakness (muscle atrophy), muscle cramps, paresthesias (sensation of tingling, burning, and prickling in the hands and feet), and impaired reflexes.
Wet beriberi symptoms: Tachycardia (fast heart rate), chest pain, wide pulse pressure, hypotension, and shock. In some cases, beriberi may cause heart failure, leading to shortness of breath, lower limb edema (swelling), and warm skin (1, 8, 10).
Gastrointestinal and other symptoms: anorexia, abdominal discomfort, constipation, difficulty swallowing, weight loss, and fatigue (1, 8).

Infantile beriberi is seen in breastfed infants; it is caused by inadequate thiamine levels in the mother's breast milk (9). The signs and symptoms are congestive heart failure, loss of voice, and absent deep tendon reflex (10).

Wernicke-Korsakoff Syndrome

Wernicke-Korsakoff syndrome is a manifestation of CNS involvement, mainly seen in people with chronic alcoholism, rarely in those with severe gastrointestinal disorders, rapidly progressing blood cancer, drug use disorders, or AIDS (1, 8).

The first and acute stage is Wernicke’s encephalopathy, requiring emergent treatment to prevent death. It is characterized by a triad of encephalopathy (brain disorder), ataxia (uncoordinated movements), and oculomotor abnormalities (repetitive, uncontrolled movements of eyes or palsies).

The second or chronic stage is Korsakoff syndrome or Korsakoff psychosis, which can be with or without previous Wernicke encephalopathy, leading to permanent brain damage. It is described with severe short-term memory loss, disorientation, and confabulations (false memories) (1, 8, 11).

Heart Failure

The chronic form of wet beriberi has three stages. In the first stage, peripheral blood vessels are dilated (vasodilation), leading to a high cardiac output, which, in turn, activates the RAAS system, leading to salt and water retention in the kidneys. Further dilation of blood vessels increases salt and fluid retention, causing edema in the extremities. Before edema appears, the heart has already been exposed to a severely high workload to pump all the fluid and meet the organ requirements. Parts of the heart muscle become injured, causing a fast heart rate, swelling, high blood pressure, and chest pain.

Wet beriberi can also occur rapidly, causing acute fulminant cardiovascular beriberi, or Shoshin beriberi. Shoshin beriberi causes heart injury, leading to the heart muscle’s inability to satisfy the body’s demands. The disease manifests as cyanosis (bluish-purple color) of the hands and feet, fast heart rate, distended neck veins, restlessness, and anxiety due to a shortage of oxygen in the blood (9).

Neuropathy & Neuritis

Vitamins B1, B6, and B12 are considered neurotropic vitamins. Each vitamin protects the nervous system differently; for example, vitamin B1 acts as an antioxidant, whereas vitamin B6 balances neuronal metabolism, and vitamin B12 maintains myelin sheaths.

These vitamins induce neuronal regeneration after nerve injury. Vitamin B1 facilitates carbohydrate usage for energy production, whereas vitamin B12 promotes neuron survival.

Chronic deficiency of vitamins B1, B6, and B12 will increase the risk of permanent neuronal degeneration and pain, leading to peripheral neuropathy (nerve damage) (12).

Alzheimer's Disease

According to animal studies, vitamin B1 deficiency may play a role in the development of Alzheimer’s disease, as its deficiency is associated with oxidative stress in neurons and their death, memory loss, plaque formation, and impaired glucose metabolism. Autopsy studies of brains have shown that transketolase and other thiamine-dependent enzymes have decreased activity in people with Alzheimer’s disease. However, large and well-designed studies are required to determine whether vitamin B1 intake benefits the disease (1).

Diabetes

Several small studies have shown that thiamine supplementation may decrease blood glucose levels in people with type 2 diabetes or impaired glucose tolerance; however, the potential clinical significance of these studies is not assessed (1).

Vitamin B1 Deficiency Risk Groups & Causes

The main groups at risk of vitamin B1 deficiency are people with alcohol dependence, HIV/AIDS, diabetes, older adults, and people who have undergone bariatric surgery (1).

B1 deficiency is most commonly seen in people with chronic alcohol use disorders. Up to 80% of these people develop vitamin B1 deficiency, as ethanol reduces thiamine absorption and phosphorylation to its active form and stores in the liver. These people also tend to eat less, increasing the risk of inadequate vitamin intake.

Generally, vitamin B1 deficiency can be due to several factors (9, 11, 13):

Lack of dietary intake: foods containing a high level of thiaminases (mentioned above), processed foods with high sulfite contents, alcoholism, starvation, gastric bypass surgery (limited food intake), parenteral nutrition, folate, and magnesium deficiency.
Increased metabolic needs: pregnancy, hyperthyroidism, lactation, fever, severe infections, refeeding syndrome.
Decreased absorption: malabsorption syndromes (i.e., celiac disease, Crohn’s disease, ulcerative colitis, tropical sprue), use of diuretics, peritoneal dialysis, hemodialysis, hyperemesis gravidarum (severe nausea and vomiting during pregnancy).
Rare genetic disorders named thiamine metabolism dysfunction syndromes (THMD): THMD-1 (thiamine-responsive megaloblastic anemia syndrome), THMD-2 (type of biotin or thiamine responsive encephalopathy), THMD-3 (Amish-type microcephaly), THMD-4 (type of bilateral striatal degeneration and progressive polyneuropathy), and THMD-5 (type of episodic encephalopathy).

Toxicity & Side Effects

Vitamin B1 may cause side effects and allergic reactions in some people, such as hives, itching, weakness, sweating, nausea, restlessness, stomach pain, diarrhea, and, in severe cases, mouth and throat swelling, shortness of breath, and anaphylaxis (14, 15).

According to the National Institutes of Health, excess amounts of vitamin B1 are excreted in the urine. Also, dietary intake of more than 5mg of vitamin B1 leads to a rapid decline in absorption. These mechanisms make vitamin B1 overdose and toxicity less likely. However, the Food and Nutrition Board noted that despite the lack of reported adverse events, excessive thiamine intake could still have adverse effects (1).

It is unlikely for thiamin levels to become toxic solely through dietary intake. However, there is no evidence that high thiamine supplement intake causes toxicity either (16).

Contraindications & Special Considerations

Currently, there are no contraindications for thiamine supplementation except for allergic reactions.

The evidence suggests those with vitamin B1 deficiency and hypoglycemia (decreased blood sugar levels) should always be administered vitamin B1 before glucose to prevent the precipitation of acute Wernicke’s encephalopathy (11, 17).

Interactions With Medications

Most diuretics (furosemide and other loop diuretics, mannitol, acetazolamide, chlorothiazide, and amiloride) may lead to thiamine loss through kidney excretion (increased urine flow rate) (1, 9).

Several cases of beriberi and Wernicke’s encephalopathy were reported due to the treatment with fluorouracil (Adrucil), a chemotherapy drug. The drug may increase thiamine metabolism and block the formation of its active TDP form (1).

Several antibiotics, such as azithromycin, clarithromycin, erythromycin, roxithromycin, and patiromer, are more likely to affect vitamin B1 absorption than other antibiotics.

Vitamin B1 interacts with omadacycline, reducing its levels or effects in the organism (18).

Historical Facts

Beriberi, or Kakke, is a disease caused by thiamine deficiency. It has been known for centuries and may be the first disease for which the term “deficiency disease” has been used. The discovery of vitamin B1 in the 20th century led to a decline in the mortality rate from thiamine deficiency, from 30 to 0.5 per 100 people in Japan from the 1920s to 1969 (6).

Takaki, A Japanese navy surgeon, first pointed out the relationship between beriberi and food. In 1882, 61% of a naval vessel’s crew were affected with vitamin B1 deficiency. In 1884, another crew was loaded with dry milk and meat, and after a voyage, only 14 people of the crew showed symptoms. This led to the conclusion that a lack of nitrogenous food intake caused the disease (6).

In 1890, Eijkman found that chickens fed with polished or white rice but not brown rice died soon from paralysis or polyneuritis and had histological changes in peripheral nerves similar to human beriberi (6, 19).

Gradually, it became evident that polished rice consumption caused beriberi, whereas polished rice intake with other crops and beans prevented the disease.

Eventually, Funk isolated a compound from rice bran (rice polishings), thinking it was the anti-beriberi factor, and named it “vitamine.” The early research led to the discovery of thiamine. Jansen and Donath isolated and crystallized the anti-beriberi substance from rice bran in 1926, and Williams first structured and synthesized thiamine in 1936 (6, 19).

Summary

Vitamin B1 (thiamin, thiamine) is a water-soluble vitamin naturally present in some foods, added to others, and available as a dietary supplement.

Vitamin B1 is required for energy metabolism, the nervous system and muscle functioning, macronutrient metabolism, glycolysis, the Krebs cycle, the pentose phosphate pathway, and hydrochloric acid (HCL) production.

Vitamin B1 (thiamine) deficiency, also known as beriberi, may include the central nervous system, cardiovascular system, or both. Beriberi leads to peripheral nerve damage and fatigue. Symptoms begin with sensory disturbances and progress to motor and reflex disturbances.

The main groups at risk of vitamin B1 deficiency are people with alcohol dependence, malabsorption, HIV/AIDS, diabetes, older adults, people taking diuretics for long periods, and people who have undergone bariatric surgery.

References

Author name: Arpi Gasparyan

Education: General Medicine at YSMU

Last updated: March 25, 2024

Medically reviewed by Victoria Mazmanyan