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 Below from thethiaminetherapy group. No URL given.
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Vitamin B1Date updated: March 08, 2007 Natural Standard Research Collaboration SynonymsAneurine HCL, aneurine mononitrate, antiberiberi factor, antiberiberi vitamin, antineuritic factor, antineuritic vitamin, anurine, B complex vitamin, beta-hydroxy-ethylthiazolium chloride, thiamin chloride, thiamin diphosphate, thiamin HCL, thiamin hydrochloride, thiamin monophosphate (TMP), thiamin nitrate, thiamin, thiamin pyrophosphate (TPP), thiamin triphosphate (TTP), thiamine chloride, thiaminium chloride HCL, thiaminium chloride hydrochloride. Combination products: Thiamin is frequently used in combination with other B vitamins in vitamin B complex formulations. Vitamin B complexes generally also include vitamin B2 (riboflavin), vitamin B3 (niacin/niacinamide), vitamin B5 (pantothenic acid), vitamin B6 (pyridoxine), vitamin B12 (cyanocobalamin), and folic acid. However, some products do not contain all of these vitamins, and may include others such as biotin, para-aminobenzoic acid (PABA), choline bitartrate, and inositol. Refer to the manufacturer's label for details. Background
Thiamin (also spelled "thiamine") is a water-soluble B-complex vitamin, previously known as vitamin B1 or aneurine. Thiamin was isolated and characterized in the 1920s, and thus was one of the first organic compounds to be recognized as a vitamin. Thiamin is involved in numerous body functions, including: nervous system and muscle functioning; flow of electrolytes in and out of nerve and muscle cells (through ion channels); multiple enzyme processes (via the coenzyme thiamin pyrophosphate); carbohydrate metabolism; and production of hydrochloric acid (which is necessary for proper digestion). Because there is very little thiamin stored in the body, depletion can occur as quickly as within 14 days. Thiamin deficiency (beriberi): Severe chronic thiamin deficiency can result in potentially serious complications involving the nervous system/brain, muscles, heart, and gastrointestinal system. Consequences of thiamin deficiency were described as early as 2600 B.C. in Chinese texts, and have been labeled historically with the term "beriberi." Beriberi has been divided into three subtypes: dry beriberi refers to neuromuscular complications such as peripheral neuropathy and weakness; wet beriberi refers to cardiovascular complications such as heart failure (Shoshin-type beriberi); and cerebral beriberi refers to central nervous system (brain) complications such as Wernicke's encephalopathy (abnormal eye movements, stance/gait abnormalities, mental dysfunction) or Korsakoff's psychosis (apathy, confusion, severe memory deficits/amnesia). Thiamin deficiency may result from inadequate thiamin intake, an increased requirement for thiamin, excessive loss of thiamin from the body, or consumption of anti-thiamin factors in food. People at particular risk for thiamin deficiency include chronic alcoholics, patients receiving intravenous feeding (total parenteral nutrition/TPN) for more than 7 days without multivitamins or dietary thiamin, or those on kidney dialysis. Chronic alcoholism: In alcoholic or chronically malnourished patients, thiamin should always be administered before intravenous glucose solutions in order to avoid causing Wernicke's encephalopathy. All patients treated for alcohol withdrawal should be administered intravenous thiamin. EvidenceMetabolic disorders (Subacute necrotizing encephalopathy, Maple syrup urine disease, Pyruvate carboxylase deficiency, Hyperalaninemia)
Taking thiamin orally helps to temporarily correct some complications of metabolic disorders associated with genetic diseases including subacute necrotizing encephalopathy (SNE, Leigh's disease), maple syrup urine disease (branched-chain aminoacidopathy), and lactic acidosis associated with pyruvate carboxylase deficiency and hyperalaninemia. Long-term management should be under strict medical supervision.
Grade: A Thiamin deficiency (Beriberi, Wernicke's encephalopathy, Korsakoff's psychosis, Wernicke-Korsakoff syndrome)Humans are dependent on dietary intake to fulfill their thiamin requirements. Because there is very little thiamin stored in the body, depletion can occur as quickly as within 14 days. Severe chronic thiamin deficiency can result in potentially serious complications involving the nervous system/brain, muscles, heart, and gastrointestinal system. Causes: Thiamin deficiency can result from inadequate thiamin intake (for example in chronic alcoholics, patients receiving intravenous feeding/parenteral nutrition for more than 7 days without multivitamins or dietary thiamin, or those living in countries with principally carbohydrate-based diets); increased body requirements for thiamin (such as with strenuous exercise, malaria, HIV infection, hyperthyroidism, fever, severe liver disease, pregnancy, breastfeeding, or adolescent growth); excessive loss of thiamin from the body (for example in patients with kidney failure on dialysis or those taking diuretics); or consumption of large amounts of anti-thiamin factors in foods (such as coffee, tea, betel nuts, vitamin C, raw freshwater fish, shellfish, ferns, or African silkworms). Effects: Severe chronic thiamin deficiency can result in potentially serious complications involving the nervous system/brain, muscles, heart, and gastrointestinal system. Historically, the consequences of thiamin deficiency have been classified into three subtypes: 1) dryberiberi refers to neuromuscular complications such as peripheral neuropathy and weakness (including burning feet, exaggerated reflexes, diminished sensation and weakness in the legs and arms, muscle pains, and ultimately seizures in severe cases); 2) wetberiberi refers to cardiovascular complications such as rapid heart rate, pulmonary edema (water in the lungs), and heart failure/cardiomyopathy (Shoshin-type beriberi); and 3) cerebralberiberi refers to central nervous system (brain) complications such as Wernicke's encephalopathy (abnormal eye movements, stance/gait abnormalities, mental dysfunction), Korsakoff's psychosis (apathy, confusion, severe memory deficits/amnesia), or the combination of the two (Wernicke-Korsakoff syndrome). Treatment: Patients diagnosed with Wernicke's encephalopathy, Korsakoff's psychosis, or Wernicke-Korsakoff syndrome should be treated immediately with intravenous thiamin. Therapy usually improves eye symptoms, but may not improve memory deficits or motor coordination, depending on the duration or severity of the thiamin deficiency. Lack of treatment may result in permanent neurologic damage or death. Thiamin supplementation should be considered in chronic alcoholics, and all patients treated for alcohol withdrawal should be administered intravenous thiamin. Thiamin should always be administered before intravenous glucose solutions in alcoholic or chronically malnourished patients, in order to avoid causing Wernicke's encephalopathy. It is not clear that thiamin is beneficial to reverse cardiovascular complications (wet beriberi), although thiamin supplementation may arrest the progression of heart damage. If heart failure is present, standard medical therapy for this condition should be administered. Grade: A Acute alcohol withdrawal
Patients with chronic alcoholism or experiencing alcohol withdrawal are at risk of thiamin deficiency and its associated complications, and should be administered thiamin. Thiamin should always be administered before intravenous glucose solutions in alcoholic or chronically malnourished patients (for example, 100mg IM or IV), in order to avoid causing Wernicke's encephalopathy.
Grade: B Total parenteral nutrition (TPN)
Thiamin should be added to TPN formulations for patients who are unable to receive thiamin through other sources (such as a multivitamin) for more than 7 days. There are documented cases of lactic acidosis occurring in patients receiving TPN without thiamin.
Grade: B Alzheimer's disease
Because thiamin deficiency can result in a form of dementia (Wernicke-Korsakoff syndrome), its relationship to Alzheimer's disease and other forms of dementia has been investigated. Whether thiamin supplementation is of benefit in Alzheimer's disease remains controversial. Some improvements in cognitive function have been reported in Alzheimer's patients taking thiamin. Further evidence is necessary before a firm conclusion can be reached.
Grade: C Athletic performance
There is inconclusive scientific evidence in this area.
Grade: C Cancer
Thiamin deficiency has been observed in some cancer patients, possibly due to increased metabolic needs. It is not clear if lowered levels of thiamin in such patients may actually be adaptive (beneficial). Currently, it remains unclear if thiamin supplementation plays a role in the management of any particular type(s) of cancer. A multivitamin including thiamin is generally considered to be reasonable in such patients, particularly in those with decreased dietary intake or anorexia.
Grade: C Cataract prevention
Preliminary evidence from a population study suggests that high dietary thiamin intake may be associated with a decreased risk of cataracts (approximately 10mg thiamin daily). Further evidence is necessary before a firm conclusion can be reached.
Grade: C Coma/hypothermia of unknown origin
Administration of 50-100mg IV or IM of thiamin is often recommended in patients with coma or hypothermia of unknown origin, due to the possible diagnosis of Wernicke's encephalopathy.
Grade: C Crohn's disease
Decreased serum thiamine levels have been reported in patients with Crohn's disease. It is not clear if routine thiamin supplementation is beneficial in such patients generally.
Grade: C Didmoad (Wolfram) syndrome
Didmoad (Wolfram) syndrome is a rare autosomal recessive inherited disease which results in diabetes mellitus, optic atrophy, diabetes insipidus, sensorineural deafness, and occasionally megaloblastic anemia. The defect is believed to cause a decrease in the enzyme that converts thiamin to its active form, thiamin pyrophosphate. Thiamin, at doses between 25-100mg, has been reported as effective in reversing anemia associated with Didmoad syndrome, within 2 weeks. Thiamin may also be effective in reducing or eliminating insulin requirements. Thiamin appears to be beneficial principally in patients with Didmoad syndrome with anemia. Management should be under strict medical supervision.
Grade: C Heart failure (cardiomyopathy)
Chronic severe thiamin deficiency can cause heart failure (wet beriberi), a condition which merits thiamin supplementation. It is not clear that thiamin supplementation is beneficial in patients with heart failure due to other causes. However, it is reasonable for patients with heart failure to take a daily multivitamin including thiamin, because some of these individuals may be thiamin deficient.
Diuretics may lower thiamin levels, particularly high doses of loop diuretics such as furosemide (Lasix) 80 mg/day. Since diuretics are commonly administered to patients with heart failure, patients taking diuretics are at an increased risk of thiamin deficiency. This area remains controversial, and further evidence is necessary before a firm conclusion can be reached.
Grade: C Pyruvate dehydrogenase deficiency (PDH)
There is preliminary evidence of clinical improvements in children with PDH following thiamin administration. Further evidence is necessary before a firm conclusion can be reached.
Grade: C Subclinical thiamin deficiency in the elderly
While typically asymptomatic, the elderly have been found to have lower thiamin concentrations than younger people. There is limited evidence that thiamin supplementation may be beneficial in individuals with persistently low thiamin blood levels, yielding improved quality of life, decreased systolic blood pressure and decreased weight compared to placebo. Further study is necessary before a firm conclusion can be formed in this area.
Grade: C Hip Fracture
Fractures of the hip are an important cause of later ill health and mortality in older people. People with hip fractures are often malnourished at the time of fracture, and have poor food intake in hospital. Preliminary evidence shows that supplemental thiamin is not beneficial for hip fractures.
Grade: D No EvidenceAge-related lens opacification, Bell's palsy, canker sores, chronic diarrhea, circulation enhancement, depression, diabetes, diabetic nephropathy, dysmenorrheal (painful menstruation), epilepsy, erectile dysfunction, fibromyalgia, gastrointestinal disorders, HIV support, high blood pressure, insect repellant, learning, low back pain, memory enhancement, myelodysplasia, optic neuropathy, multiple sclerosis, poor appetite, protection from radiation-induced genetic changes, tissue healing after surgery, ulcerative colitis.
DosingStandardization Dietary sources of thiamin: Beef, Brewer's yeast, legumes (beans, lentils), milk, nuts, oats, oranges, pork, rice, seeds, wheat, whole grain cereals, and yeast. In industrialized countries, foods made with white rice or white flour are often fortified with thiamin (because most of the naturally occurring thiamin is lost during the refinement process). Dosage forms: Thiamin can be administered orally, intramuscularly, or intravenously. Thiamin is available in 5, 10, 25, 50, 100, 250, or 500 milligram tablets; or as 100 or 200 mg/mL parenteral injections. Maximum concentration is reached in 20-120 minutes for oral administration, and in 2 minutes for intravenous administration. Maximum oral absorption is 8-15mg daily. Oral absorption may be increased by dividing doses, but reduced with the administration of food, or in alcoholics and patients with malabsorption or liver cirrhosis. Patients with normal kidney function excrete 80-96% of intravenous doses, while a small amount is excreted from oral doses. Adults (18 years and older): U.S. Recommended Daily Allowance (RDA): The RDA for adults ages 19 years and older is 1.2mg daily for males and 1.1mg daily for females, taken by mouth. The RDA for pregnant or breastfeeding women of any age is 1.4mgdaily, taken by mouth. As a dietary supplement in adults, 1-2mg daily is sometimes used. Wernicke's encephalopathy (prevention/treatment): 100mg of thiamin administered intravenously (up to 1 gram has been used), followed by 50-100mg daily intravenously or intramuscularly until a regular balanced diet is resumed. Thiamin deficiency: For mild thiamin deficiency in adults, 5-30mgdaily by mouth has been used in a single dose or in 2-3 divided doses, over a 1-month period (single doses generally do not exceed 30mg). For severe deficiency, up to 300mg has been administered. Parenteral (injected) thiamine is recommended for prevention and treatment of Wernicke's encephalopathy in critically ill people or in alcoholic patients experiencing withdrawal, for example between 50-100 mg of intravenous thiamin in single or divided daily doses, over a 3-day period (or until a therapeutic response is seen). Up to 1 gram may be necessary during the first 12 hours. Metabolic/genetic enzyme deficiency disorders: For thiamin-responsive genetic enzyme deficiency disorders, 10-20mg daily has been recommended, although up to 600-4000mg daily in divided doses has been used for Leigh's disease. Neuropathy: 10-20mg daily has been used for mild polyneuropathies, and 30-40mg daily has been used for severe/advanced neuropathies, although safety and effectiveness are not clearly established in patients who are not thiamin deficient. Children (younger than 18 years) Adequate Intake (AI) / U.S. Recommended Daily Allowance (RDA): For infants ages 0-6 months the AI is 0.2mg; for infants 7-12 months the AI is 0.3mg; for children 1-3 years the RDA is 0.5mg; for children 4-8 years the RDA is 0.6mg; for children ages 9-13 years the RDA is 0.9mg; for males ages 14-18 years the RDA is 1.2mg; for females ages 14-18 years the RDA is 1mg, taken by mouth. The RDA for pregnant or breastfeeding women of any age is 1.4mg daily, taken by mouth. Thiamin deficiency/beriberi: Oral doses of 10-50mg daily for 2 weeks followed by 5-10mg daily for 4 weeks have been used. Intravenous doses of 10-25mg daily have been used. Treatment should be under strict medical supervision. SafetyAllergies Rare hypersensitivity/allergic reactions have occurred with thiamin supplementation. A small number of life-threatening anaphylactic reactions have been observed with large parenteral (intravenous, intramuscular, subcutaneous) doses of thiamin (25-100mg), generally after multiple doses administered for 7 days or more. Skin irritation, burning, or itching may rarely occur at injection sites. Contact dermatitis may occur with occupational exposure, and may cause sensitization and lead to dermatitis-type reactions after subsequent oral or injected administrations. Side Effects and Warnings Thiamin is generally considered safe and relatively nontoxic, even at high doses. No clear tolerable upper level (UL) of intake has been established. Doses up to 200mg daily for long-term periods or single doses of up to 8 grams have been reported as being nontoxic. Dermatitis or more serious hypersensitivity reactions occur rarely. Large doses, greater than 100mg, may cause drowsiness or muscle relaxation. Injections of thiamin may cause burning, which typically occurs with rapid injection of 100mg of thiamin hydrochloride. Reactions can often be avoided by slow administration into larger veins. Pregnancy and Breastfeeding: U.S. Food and Drug Administration PregnancyCategory: C. The U.S. Recommended Daily Allowance (RDA) for pregnant or breastfeeding women of any age is 1.4mg daily, by mouth. There is insufficient reliable information available about the safety of using larger amounts during pregnancy or breastfeeding. InteractionsInteractions with Drugs Phenytoin (Dilantin): Reduced levels of thiamin in blood and cerebrospinal fluid have been reported in individuals taking phenytoin for extended periods of time. However, thiamin supplementation beyond the Recommended Daily Allowance is not currently universally recommended in patients taking phenytoin. Antacids: May lower thiamin levels in the body by decreasing absorption and increasing excretion or metabolism. Barbiturates: Barbiturates may lower thiamin levels in the body by decreasing absorption and increasing excretion or metabolism. Diuretics: Loop diuretics, particularly furosemide (Lasix), have been associated with decreased thiamin levels in the body by increasing urinary excretion (and possibly by decreasing absorption and increasing metabolism). Examples of other loop diuretics include bumetanide (Bumex), ethacrynic acid (Edecrine), and torsemide (Demadex). Theoretically, this effect may also occur with other types of diuretics, including thiazide diuretics such as chlorothiazide (Diuril), chlorthalidone (Hygroton, Thalitone), hydrochlorothiazide (HCTZ, Esidrix, HydroDIURIL, Ortec, Microzide), indapamide (Lozol), and metolazone (Zaroxolyn); or potassium-sparing diuretics such as amiloride (Midamor), spironolactone (Aldactone), and triamterene (Dyrenium). Effects may be most pronounced with larger doses (for example Lasix 80mg) taken over extended periods of time. Assessment of thiamin status may be merited in such patients, although prophylactic thiamin supplementation beyond the Recommended Daily Allowance is not universally recommended at this time. Tobacco: Tobacco use decreases thiamin absorption and may lead to decreased levels in the body. Neuromuscular blocking agents (NMBAs): Effects of NMBAs may be enhanced with concomitant (simultaneous) use of thiamin. Antibiotics: Some antibiotics destroy gastrointestinal flora (normal bacteria in the gut) which manufacture some B vitamins. In theory, this may decrease the amount of thiamin available to humans, although the majority of thiamin is obtained through the diet (not via bacterial production). This interaction is likely not clinically relevant, and patients receiving antibiotics are generally not advised to take additional thiamin supplementation. Birth control pills (oral contraceptives/OCPs): Oral contraceptives may decrease levels of some B vitamins, vitamin C, and zinc in the body. Some studies suggest slight decreases in thiamin levels with oral contraceptive use, while other research has found no significant effects. Additional thiamin supplementation beyond the Recommended Daily Allowance is generally not considered necessary in women taking oral contraceptives. Fluorouracil (5-fluorouracil, 5-FU, Adrucil): The cancer chemotherapy drug 5-fluorouracil (5-FU) inhibits the phosphorylation of thiamin to thiamin pyrophosphate (TPP), interfering with activation of thiamine and possibly increasing its breakdown. People receiving fluorouracil-containing chemotherapy regimens may be at risk for developing symptoms and signs of thiamine deficiency. In addition, chemotherapy patients may be at an elevated risk of developing vitamin deficiencies due to decreased dietary intake. There is not enough evidence to routinely recommend thiamin supplementation in patients receiving 5-FU, although a multivitamin including thiamin is generally regarded as being reasonable. Metformin (Glucophage): In theory, metformin may reduce thiamine activity, and based on animal research, taking thiamin and metformin together may contribute to the risk of lactic acidosis. Although there is no conclusive evidence in humans, caution is warranted. Interactions with Herbs and Dietary Supplements Betel nut (Areca catechu L.): Consumption of betel nuts may reduce thiamine activity due to chemical inactivation, and may lead to symptoms and signs of thiamin deficiency. Horsetail (Equisetum arvense L.): Horsetail contains a thiaminase-like compound that can destroy thiamine in the stomach, and theoretically causes symptomatic thiamine deficiency. Horsetail products are available without this property, and for example, the Canadian government requires that horsetail products be certified free of thiaminase activity. Diuretic herbs: In theory, diuretic herbs may decrease thiamin levels in the body by increasing urinary excretion. Examples of herbs with possible diuretic activity include artichoke, celery, corn silk, couchgrass, dandelion, elder flower, horsetail, juniper berry, kava, shepherd's purse, uva ursi, and yarrow. Interactions with Foods: Alcohol: Alcohol use decreases thiamin absorption and may lead to decreased levels in the body. Carbonated beverages and foods or beverages with citrates may decrease the effects of thiamin in the body. Coffee, tea: Chronic intake of polyphenols such as tannins in coffee and tea may convert thiamin to an unabsorbable and inactive form, and theoretically can worsen or cause thiamin deficiency. However, this interaction does not appear to be clinically relevant in industrialized countries where most individuals consume adequate dietary thiamin and ascorbic acid (which prevents this interaction). This interaction has been described in Asian populations which chew fermented tea leaves. Raw seafood: Raw freshwater fish and shellfish contain thiaminase enzymes that destroy thiamine. Frequent ingestion of raw fish or shellfish can contribute to thiamine deficiency. Cooking destroys these enzymes, and therefore consumption of cooked seafood does not appear to affect thiamine levels. Interactions with Laboratory Tests Theophylline serum levels: Large amounts of thiamine can interfere with Schack and Waxler spectrophotometric determination of serum theophylline concentrations. Uric acid: Thiamine can cause false positive results in the phosphotungstate method for uric acid determination. Urobilinogen: Thiamine can cause false positive results in the urine spot test with Ehrlich's reagent for urobilinogen. AttributionThis information is based on a systematic review of scientific literature, edited and peer-reviewed by contributors to the Natural Standard Research Collaboration ( www.naturalstandard.com). Bibliography- Anon. From the Centers for Disease Control and Prevention. Lactic acidosis traced to thiamine deficiency related to nationwide shortage of multivitamins for total parenteral nutrition--United States, 1997. JAMA 1997;278(2):109, 111.
- Abbas ZG, Swai AB. Evaluation of the efficacy of thiamine and pyridoxine in the treatment of symptomatic diabetic peripheral neuropathy. East Afr Med J 1997;74(12):803-808.
- Avenell A, Handoll HH. Nutritional supplementation for hip fracture aftercare in older people. Cochrane Database Syst Rev 2005;(2):CD001880.
- Benton D, Fordy J, Haller J. The impact of long-term vitamin supplementation on cognitive functioning. Psychopharmacology (Berl) 1995;117(3):298-305.
- Cook CC, Hallwood PM, Thomson AD. B Vitamin deficiency and neuropsychiatric syndromes in alcohol misuse. Alcohol Alcohol 1998;33(4):317-336.
- Duran M, Wadman SK. Thiamine-responsive inborn errors of metabolism. J Inherit Metab Dis 1985;8 Suppl 1:70-75.
- Nakasaki H, Ohta M, Soeda J, et al. Clinical and biochemical aspects of thiamine treatment for metabolic acidosis during total parenteral nutrition. Nutrition 1997;13(2):110-117.
- Nolan KA, Black RS, Sheu KF, et al. A trial of thiamine in Alzheimer's disease. Arch Neurol 1991;48(1):81-83.
- Ranganathan LN, Ramaratnam S. Vitamins for epilepsy. Cochrane Database Syst Rev 2005;(2):CD004304.
- Saif MW. Is there a role for thiamine in the management of congestive heart failure? South Med J 2003;96(1):114-115.
- Seligmann H, Halkin H, Rauchfleisch S, et al. Thiamine deficiency in patients with congestive heart failure receiving long-term furosemide therapy: a pilot study. Am J Med 1991;91(2):151-155.
- Yates AA, Schlicker SA, Suitor CW. Dietary Reference Intakes: the new basis for recommendations for calcium and related nutrients, B vitamins, and choline. J Am Diet Assoc 1998;98(6):699-706.
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