Vitamin B1 Thiamin
Definition: Thiamin (also spelled thiamine) is a water-soluble B vitamin, also known as vitamin B1 or aneurine. Isolated and characterized in the 1930s, thiamin was one of the first organic compounds to be recognized as a vitamin. Thiamin occurs in the human body as free thiamin and in various phosphorylated forms: thiamin monophosphate (TMP), thiamin triphosphate, adenosine thiamin triphosphate, and thiamin pyrophosphate (TPP), which is also known as thiamin diphosphate.
- 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. (
- Severe thiamin deficiency leads to beriberi, a disease that affects multiple organ systems, including the central and peripheral nervous systems.
- 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 encephalopathy-related symptoms.
- Thiamin deficiency can result from poor dietary intake, inadequate provision of 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.
- Alteration in glucose metabolism has been associated with decreased plasma thiamin concentrations in patients with diabetes. Correction of thiamin deficiency may reduce the risk of vascular complications in these patients.
- Alzheimer’s disease has been associated with altered glucose metabolism and thiamin deficiency. Although some promising results have been observed in animal models, it is not known whether supplementation with thiamin or benfotiamine (a synthetic precursor of thiamin) might slow the cognitive decline in patients with Alzheimer’s disease.
- A recent study found decreased levels of thiamin in the brains of patients with Huntington’s disease. Clinical trials are needed to evaluate whether vitamin supplementation might be a potential therapy.
- 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.
- Intravenous thiamin has been studied as a potential treatment for sepsis, either as a monotherapy or in combination with other agents like vitamin C and corticosteroids. Large-scale clinical trials are needed to determine its efficacy.
- Contraceptives, oral: Use of oral contraceptives may cause mild thiamine deficiency.
- Diuretics, loop: Some, but not all, studies have found that treatment with loop diuretics can induce thiamine deficiency by increasing urinary thiamine excretion. Correction of diuretic-induced thiamine deficiency may improve cardiac function in patients with heart failure.
- Lysergic acid diethylamide (LSD): Administration of 3 g of thiamine 1–2 hours before taking LSD has been found to prolong the action of LSD for up to 24 hours.
- Magnesium is required for the conversion of thiamine to its biologically active form. Furthermore, some thiamine-dependent enzymes also require magnesium. In patients who are deficient in both thiamine and magnesium, symptoms of thiamine deficiency may not respond to thiamine supplementation unless magnesium deficiency is also corrected. In addition, administration of large doses of thiamine can exacerbate magnesium deficiency. Magnesium supplementation should therefore be considered for patients being treated with thiamine.
- Vitamin B6. Of 16 children with attention deficit-hyperactivity disorder who had improved while taking thiamine (100 mg 4 times per day), 9 became markedly worse while taking pyridoxine (100 mg 3 times per day or more). Conversely, of 10 children who had improved while taking pyridoxine, 6 became markedly worse while taking thiamine.
- Alpha-lipoic acid. Alpha-lipoic acid (ALA) was lethal when administered intraperitoneally at a dose of 20 mg/kg of body weight to thiamine-deficient rats. ALA toxicity was not seen in thiamine-sufficient rats, and toxicity could be prevented in thiamine-deficient rats by administering thiamine prior to treatment with ALA.36 For patients who may be thiamine-deficient, thiamine should be administered prior to starting ALA treatment. For patients at risk of developing thiamine deficiency, ALA treatment should be accompanied by a thiamine (or vitamin B-complex) supplement.
- Good food sources of thiamine include whole grains, legumes, nuts, meat, and enriched flour.
- Significant losses of thiamine may occur with high-temperature cooking, and substantial amounts are lost in discarded cooking water.
Dosage and administration
- The dosage of thiamine used for different conditions has varied widely, usually in the range of 10–200 mg/day, although larger dosages have been used in some instances. For the treatment of severe acute deficiency, thiamine is usually given parenterally in doses of 50–100 mg/day for several days.
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