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Nutrient Details For : Thiamin

A nutrient is any element or compound necessary for or contributing to an organism's metabolism, growth, or other functioning. Click name for details Arsenic Biotin Boron Calcium Carbohydrates Carnitine Carotenoids Chloride Choline Chromium Copper Energy Fiber Fluoride Folate Iodine Iron Lipids Magnesium Manganese Molybdenum Niacin Nickel Pantothenic acid Phosphorus Phyto-chemicals Potassium Protein Riboflavin Selenium Silicon Sodium Thiamin Vanadium Vitamin A Vitamin B 12 Vitamin B 6 Vitamin C Vitamin D Vitamin E Vitamin K Zinc Further Trace Elements

Thiamin, also called vitamin B1, is used in many different body functions and deficiencies may have far reaching effects on the body, yet very little of this vitamin is stored in the body, and depletion of this vitamin can happen within 14 days.

Thiamin is also a miraculous nutrient, somebody suffering from beriberi, scarcely able to lift their head from their pillow, will respond quickly from injected thiamin, and will be on their feet within a matter of hours.

Thiamin (Vitamin B-1) is a water-soluble substance, consisting of thiazole and pyrimidine rings joined by a methylene bridge.

Thiamin is found in high concentrations in skeletal muscle, the heart, liver, kidneys and brain. The total amount in an adult is about 30 mg and the biologic half-life in the body is about 15 days. It is not surprising that a state of severe depletion can be seen in patients on a strict thiamin-deficient diet in 18 days.

Similarly, the rate of flux of thiamin across the blood-brain barrier in rats is equivalent to the turnover in brain, indicating no spare thiamin capacity for the brain.

Thiamin diphosphate (ThDP) is the active form of thiamin. ThDP serves as a cofactor for several enzymes involved in carbohydrate catabolism, including pyruvate dehydrogenase, transketolase, and a-ketoglutarate, and for the branched-chain a-keto acid dehydrogenase complex that is involved in amino acid catabolism.

The former enzymes play crucial roles in the tricarboxylic acid cycle and the pentose phosphate pathway. They are important in the biosynthesis of a number of cell constituents, including the neurotransmitters acetylcholine and gamma-aminobutyric acid (GABA), and in the production of reducing equivalents (NADPH) for biosyntheses and pentoses for nucleic acid synthesis. Because of its involvement in the synthesis of precursors of DNA, thiamin utilization is increased in tumors. Limiting thiamin can inhibit tumor cell proliferation. A neurochemical role for thiamin triphosphate (ThTP) has been postulated; ThTP is localized to neuronal cells and is implicated in neuronal conduction.

Thiamin uptake by the small intestines and by cells within various organs is mediated at physiological concentrations by a saturable, high affinity transport system. The requirement for cellular energy (ATP) for thiamin uptake is a secondary event and results from the rapid diphosphorylation of imported thiamin by thiamin diphosphokinase. Alcohol affects various aspects of thiamin transport/uptake, and these effects may contribute to the prevalence of thiamin deficiency in alcoholics. Alcohol also reduces cellular thiamin diphosphokinase activity.

Deficiencies:

The major manifestations of thiamin deficiency in humans involve the cardiovascular (wet beriberi) and nervous (dry beriberi, or neuropathy and/or Wernicke-Korsakoff syndrome) systems. Common findings in beriberi heart disease include peripheral vasodilation, biventricular myocardial failure, and sodium and water retention resulting in high-output state, edema, and potentially acute fulminant cardiovascular collapse (soshin beriberi). Administration of thiamin rapidly restores peripheral vascular resistance, but improvement in myocardial function may be delayed.

The predominant features of cerebral beriberi are confusion, disordered ocular motility, ataxia of gait, and neuropathy. Treatment with thiamin can rapidly reverse some of these acute signs while leaving significant clinical sequelae including memory and other cognitive deficits and residual neurologic signs (called Korsakoff's syndrome, or the chronic phase of Wernicke-Korsakoff syndrome) with characteristic neuropathologic findings.

Recently, amyloid-precursor protein-like immunoreactivity, similar to findings in Alzheimer's patients, have been demonstrated in the brains of thiamin deficient rats consistent with earlier suggestions of a relationship between thiamin deficiency and Alzheimer's disease.

Recommendations:

The Recommended Dietary Allowance is as follows: 0-5 month infants, 0.2 mg/day; 6 to 11 months, 0.3 mg/day; 1-3 years of age, 0.5 mg/day; 4-8 years, 0.6 mg/day; 9-13 years, 0.9 mg/day; males 14 years old and older, 1.2 mg/day; females 14-18 years of age, 1.0 mg/day; and females 19 years and older, 1.1 mg/day. During pregnancy, the RDA is increased to 1.4 mg/day, and during lactation, 1.5 mg/day.

The RDAs are based on the Dietary Reference Intakes of the National Academy of Sciences.

Thiamin is destroyed in cooking, and intake may be low if the diet is high in refined foods. Do not add soda if you are boiling green vegetables since soda is alkaline and will destroy thiamin.

Food sources:

Thiamin is present in many dietary products, but is found in large amounts in lean pork, legumes and yeast. Whole grain products, breads and cereals are the major dietary contributors.

Toxicity:

Thiamin toxicity is uncommon; as excesses are readily excreted, although long-term supplementation of amounts larger than 3 gram have been known to cause toxicity.

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