Vitamin B1

Overview

Vitamin B1, also known as thiamine, was the first of the B vitamins to be discovered. It was isolated in 1926 as a water soluble, crystalline yellowish white powder with a salty, slightly nutty taste. In 1936 the nutritionist Roger Williams, Ph.D., synthesized it and determined the chemical formula.

Vitamin B1 plays a vital role in the conversion of blood sugar (glucose) to energy in the Krebs cycle and is involved in the synthesis of acetylcholine. Its metabolic activities primarily affect the nerves, muscles, and cardiovascular system.

Because it is water soluble, thiamine is not stored in the body and must be supplied daily. Vitamin B1 must be phosphorylated in order to be metabolically active. It combines with two molecules of phosphoric acid to form the important co-enzyme thiamine pyrophosphate (TPP).

Beriberi is the classical vitamin B1 deficiency syndrome. It is more prevalent in Asian countries where polished rice is the staple diet. When beriberi occurs in the United States, it is most commonly seen in severely malnourished infants or elderly people. In adults, alcoholism, hemodialysis or peritoneal dialysis, malabsorption syndromes and diets consisting primarily of highly processed, refined foods can be causes of vitamin B1 deficiency. (1)

Two lipid-soluble forms of vitamin B1 are available. One is named thiamine propyl disulfide (TPD). The second is thiamine tetrahydrofurfuryl disulfide (TTHF), which is sometimes called fursulthiamine. There is some indication that these compounds are more efficiently absorbed and utilized than water-soluble thiamine hydrochloride and some companies are beginning to include them in product formulations. (2)

Dosage Info

Dosage Range

1.5-100mg daily, depending on the presence and severity of a deficiency. Doses of 300mg or more per day have been used therapeutically for neurological conditions such as Kearns-Sayre syndrome and Leigh's disease. (3) , (4)

Most Common Dosage

5mg daily.

Dosage Forms

Tablets, capsules, liquids, liposomal sprays, effervescent tablets, and injectable (Rx only).

Adult RDI

1.5mg

Adult ODA

5-10mg

RDA

  • Infants <6 months: 0.2mg (Adequate Intake, AI)
  • Infants 7-12 months: 0.3mg (AI)
  • Children 1-3 years: 0.5mg
  • Children 4-8 years: 0.6mg
  • Children 9-13 years: 0.9mg
  • Males >14 years: 1.2mg
  • Females 14-18 years: 1.0mg
  • Females >19 years: 1.1mg
  • Pregnancy: 1.4mg
  • Lactation: 1.4mg

Interactions and Depletions

Interactions

Depletions

Active Forms

Thiamine hydrochloride, thiamine mononitrate, and tetrahydrofurfuryl disulfide (TTFD).

Absorption

Thiamin is primarily absorbed in the acid medium of the proximal duodenum (jejunum and ileum). The conversion of thiamine to thiamine pyrophosphate takes place in the mucosa of the jejunum. Conditions causing intestinal inflammation such as milk or wheat food allergies can inhibit the body's ability to convert thiamine to its active form, TPP.

Toxicities & Precautions

General

There are no known toxicities associated with vitamin B1.

Functions in the Body

Co-enzyme Activity

Oxidative decarboxylation reactions (removal of CO2 or carboxyl groups) when pyruvic acid is converted to acetyl coenzyme A in the Krebs cycle. This is the primary pathway for energy production in the body and thiamine plays an essential role in energy production.Transketolation reactions (transfer of 2-carbon or keto groups) in the hexose monophosphate shunt.

Carbohydrate Metabolism

Plays a role in conversion of blood sugar (glucose) into biological energy.

Nerves

Role in maintenance of nerve tissues, nerve function, and nerve transmission. Involved in the synthesis of acetylcholine in nerve cell membranes.

Muscles

Important in the maintenance of muscular function, especially the heart.

Fatty Acid Conversion

Involved in conversion to hormones such as cortisol and progesterone.

Amino Acid Conversion

Involved in converting into proteins, hormones and enzymes.

Clinical Applications

Neurological Conditions

Such as sensory neuropathy, (5) sciatica, trigeminal neuralgia, and Bell's palsy. (6)

Alcoholism

Thiamine, which is a cofactor in the metabolism of alcohol is depleted in alcoholics. (7)

Alzheimer's Disease

Improvement with tetrahydrofurfuryl disulfide (TTFD) (8) and thiamine facilitates the production and release of acetylcholine. (9)

Congestive Heart Failure

Loop diuretic drugs used to treat CHF deplete thiamine. (10)

Insomnia

EEG studies show that thiamine deficiency causes sleep disturbances. (11)

Diabetes Mellitus

Diabetics were shown to have low thiamine levels. (12)

Psychiatric Patients

30 percent of patients in psychiatric wards are thiamine deficient. (13)

Symptoms and Causes of Deficiency

Thiamine deficiency tends to be quite rare in the United States. Most adult Americans acquire the Recommended Daily Allowance from fortified and enriched food sources in their diet. These foods include bread, bread products, grains, and prepared cereals. With the exception of lactating females, fewer than 5% of all individuals in the United States had dietary intakes lower than the Estimated Average Requirement. (14)

Several possible causes of a vitamin B1 deficiency are as follows:

    Cooking can easily destroys vitamin B1, because it is heat sensitive and water-soluble. Certain medications: see interactions and depletions GI conditions: such as diarrhea, and malabsorption due to lactose intolerance and celiac disease (gliadin sensitivity) Dry beriberi: a severe deficiency characterized by peripheral neuropathy, tingling, and numbness, especially in the limbs used most frequently. (15) Wet beriberi is a severe thiamine deficiency that results in cardiovascular problems. (16) Alcohol interferes with the absorption of vitamin B1 which is necessary for the metabolism of alcohol. Severe deficiency associated with alcohol consumption produces a condition called Wernicke-Korsakoff syndrome. Symptoms range from mild confusion to severely impaired memory and cognitive function and even coma. (17) Deficiencies of vitamin B1 manifest primarily as disorders of the neuromuscular, gastrointestinal, and cardiovascular systems. Symptoms are caused by increased plasma concentrations of pyruvate, lactate, and alpha-ketoglutarate, as well as decreased activity of erythrocyte transketolase and decreased synthesis of acetylcholine.
      GI symptoms can include anorexia, indigestion, and weight loss. Nerve degeneration can cause muscular weakness, calf muscle tenderness, and fatigue. Cardiovascular symptoms include edema, increased pulse rate, and palpitations.
    Deficiencies in the elderly can produce depression, irritability, and memory loss. Decreased synthesis of acetylcholine causes: polyneuritis (including "pins and needles" and numbness), loss of reflexes in legs, confusion, emotional instability, and depression.

Dietary Sources

All plant and animal foods contain vitamin B1, but only in low concentrations. The richest sources are brewer’s yeast and organ meats. Whole cereal grains comprise the most important dietary source of vitamin B1 in human diets.

References

  1. Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic acid, Biotin and Choline; A Report of the Standing Committee on the Scientific Evaluation of Dietary Reference Intakes and its Panel on Folate, Other B Vitamins, and Choline and Subcommittee on Upper Reference Levels of Nutrients, Food and Nutrition Board, Institute of Medicine. Washington, DC: National Academy Press; 2000:58, 79-80. Available at: http://www.nap.edu/books/0309065542/html/index.html. Accessed August 28, 2001.
  2. View Abstract: Baker H, et al. Absorption, Utilization and Clinical Effectiveness of Allithiamines Compared to Water-soluble Thiamines. J Nutr Sci Vitaminol.(Tokyo). Aug1976;22:63-68.
  3. Lou HC. Correction of increased plasma pyruvate and plasma lactate levels using large doses of thiamine in patients with Kearns-Sayre syndrome. Arch Neurol. Jul 1981;38(7):469.
  4. View Abstract: Kissel JT, Kolkin S, Chakeres D, Boesel C, Weiss K. Magnetic resonance imaging in a case of autopsy-proved adult subacute necrotizing encephalomyelopathy (Leigh's disease). Arch Neurol. May1987;44(5):563-6.
  5. View Abstract: Ishibashi S, Yokota T, Shiojiri T, et al. Reversible acute axonal polyneuropathy associated with Wernicke-Korsakoff syndrome: impaired physiological nerve conduction due to thiamine deficiency? J Neurol Neurosurg Psychiatry. May2003;74(5):674-6.
  6. View Abstract: Skelton WP, 3rd, et al. Thiamine Deficiency Neuropathy. It's Still Common Today. Postgrad Med. Jun1989; 85(8):301-06.
  7. View Abstract: Cook CC, et al. B Vitamin Deficiency and Neuropsychiatric Syndromes in Alcohol Misuse. Alcohol Alcohol. Aug1998;33(4):317-36.
  8. View Abstract: Mimori Y, et al. Thiamine Therapy in Alzheimer's Disease. Metab Brain Dis. Mar1996;11(1):89-94.
  9. View Abstract: Meador K, et al. Preliminary Findings of High-dose Thiamine in Dementia of Alzheimer's Type. J Geriatr Psychiatry Neurol. Dec1993;6(4):222-29.
  10. View Abstract: Seligmann H, et al. Thiamine Deficiency in Patients with Congestive Heart Failure Receiving Long-term Furosemide Therapy: A Pilot Study. Am J Med. Aug1991;(2):151-55.
  11. View Abstract: Crespi F, et al. Sleep and Indolamine Alterations Induced by Thiamine Deficiency. Brain Res. Sep1982;248(2):275-83.
  12. View Abstract: Saito N, et al. Blood Thiamine Levels in Outpatients with Diabetes Mellitus. J Nutr Sci Vitaminol.(Tokyo). Dec1987;33(6):421-30.
  13. Carney MW. Vitamin Deficiency and Mental Symptoms. Br J Psychiatry. Jun1990;156:878-82.
  14. Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic acid, Biotin and Choline; A Report of the Standing Committee on the Scientific Evaluation of Dietary Reference Intakes and its Panel on Folate, Other B Vitamins, and Choline and Subcommittee on Upper Reference Levels of Nutrients, Food and Nutrition Board, Institute of Medicine. Washington, DC: National Academy Press; 2000:58, 79-80. Available at: http://www.nap.edu/books/0309065542/html/index.html. Accessed August 28, 2001.
  15. View Abstract: Zak J, 3rd, et al. Dry Beriberi: Unusual Complication of Prolonged Parenteral Nutrition. JPEN J Parenter Enteral Nutr. Apr1991;15(2):200-01.
  16. View Abstract: Borghi E, et al. A Case of Wet Beriberi. Recenti Prog Med. Nov1989;80(11):588-90.
  17. View Abstract: Butterworth RF, et al. Thiamine-dependent Enzyme Changes in the Brains of Alcoholics: Relationship to the Wernicke-Korsakoff Syndrome. Alcohol Clin Exp Res. Oct1993;17(5):1084-88.