Where Can I Buy Thiamine
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Vitamin B1: Thiamine Supplement. Su-Per B1 is a concentrated source of the essential B complex vitamin thiamine, also known as vitamin B1, in a powder. B-1 is essential for carbohydrate metabolism. Highly palatable over a wide range of feeding levels. Shown to reduce diarrhea when other methods have failed. Supplies 625 mg of thiamine per ounce. For a more concentrated source (1000 mg per serving), that it is in a flaxseed meal base, consider Vitamin B1 by Horsetech.
Thiamine plays an important role in the body's metabolism of carbohydrates. The horse's body requires thiamine to produce erythrocyte transketolase, an essential enzyme for energy utilization. Thiamine has also been studied for its effect on the maintenance of healthy appetite and nervous system stability and poise. Thiamine is highly vulnerable to the heat generated in feed processing. Bracken fern, yellow star thistle, and horsetail contain substances that promote thiamine deficiency if eaten. Horses should be prevented from grazing these plants whenever possible.
Thiamine is especially important for horses with increased energy needs due to intense exercise demands. The digestive system is also maintained properly by Thiamine, and added thiamine has been shown to reduce diarrhea when other methods have failed.
Thiamine is water-soluble, and the body excretes any excess it does not need. However, individuals with a thiamine sensitivity may experience flushing, nausea, itching, or hives. Individuals should consult with a doctor before taking any new supplements.
The biologically active form of the vitamin, thiamine pyrophosphate (TPP), is best measured in whole blood and is not found in measurable concentration in plasma. Plasma thiamine concentration reflects recent intake rather than body stores; therefore, whole blood is the preferred specimen for thiamine assessment.
Vitamin B1 refers to a group of compounds that include thiamin and its phosphate esters: thiamine monophosphate (TMP), thiamine pyrophosphate (TPP), and thiamine triphosphate.1-5 All living organisms require thiamine, but it is only synthesized by bacteria, fungi, and plants. Thus, thiamine is an essential nutrient for animals that must obtain it from their diets. The principal biologically active form of thiamine is the pyrophosphate, TPP, which serves as a coenzyme for essential decarboxylation reactions by which carbohydrates, fats, and alcohol are metabolized to produce energy. Thiamine serves a role in the biosynthesis of acetylcholine and gamma-aminobutyric acid (GABA). TPP also facilitates the production of reducing substances involved in oxidant stress defenses, as well as for the synthesis of nucleic acid precursors.5 Thiamine triphosphate serves an important role in the regulation of ion channels of the nervous system.2
Primary thiamine deficiency is most common in underdeveloped countries due to poor oral intake or diets consisting of non-enriched grains.1,5-8 The most common causes of thiamine deficiency in more affluent countries are alcoholism or malnutrition in nonalcoholic patients.5 Secondary thiamine deficiency can occur due to impaired gastrointestinal absorption related to disease or bariatric surgery. Consumption of anti-thiamin enzymes found in raw fish, ferns and betel nuts can reduce the absorption of thiamin.6 A relative thiamine deficiency can also occur in patients receiving enteral or parenteral nutrition therapy, in prolonged diarrheas, and in impaired utilization conditions such as in severe liver disease.5 Conditions that increase metabolic requirements for thiamine such as hyperthyroidism, pregnancy, lactation, and systemic infections with or without fever have been associated with thiamin deficiency. Increased gastrointestinal or renal losses, especially for patients on hemodialysis, can be a risk factor as well as advanced age, diabetes mellitus, AIDS, malignancies and any critical illness.5,7
The earliest symptoms of thiamine deficiency are nonspecific and include fatigue, irritation, poor memory, sleep disturbances, anorexia, abdominal discomfort, and constipation.5 Severe thiamin deficiency is rare and can present as congestive heart failure (wet beriberi), peripheral neuropathy (dry beriberi), Wernicke encephalopathy (WE) and/or Korsakoff syndrome.3-5
Dry beriberi is characterized by central and peripheral neuropathy that can be permanent even following thiamin repletion.3,4 Clinical signs of dry beriberi are bilateral and symmetric, predominantly involving the lower extremities and have been well described in the literature.5 The neurological side effects of thiamin deficiency can progress to Wernicke encephalopathy (WE) and Korsakoff psychosis.3,5,7,9 This diagnosis denotes the acute cerebral manifestation of severe thiamine deficiency that can lead to irreversible memory loss and dementia.5,7,9 Patients with WE present with nystagmus, ophthalmoplegia, mental-status changes, and unsteadiness of stance and gait.9,10 Korsakoff psychosis, an irreversible amnestic confabulatory state, can be the initial presentation in some patients, or it may be a sequel to WE.7 These patients present with clinical manifestations that are highly variable that can include oculomotor abnormalities, gait disturbance, and global confusion with retrograde amnesia, cognitive impairment, and confabulation.3
Wet beriberi refers to a thiamine deficiency condition where impaired cardiac performance leads to systemic symptoms.4,5 In the initial stages of wet beriberi, high cardiac output produces peripheral vasodilation with warm extremities and excessive sweating.5 As the heart starts to fail further symptoms including tachycardia, a wide pulse pressure and lactic acidosis develop, leading to salt and water retention in the kidneys.5 The resulting fluid overload leads to edema of the dependent extremities.5 A more rapidly progressing form of wet beriberi has been referred to as acute fulminant cardiovascular beriberi or Shoshin beriberi, in which vasodilation continues, resulting in shock in a patient with heart failure.5
The signs and symptoms of wet beriberi and similar to those associated with heart failure from other causes. Several studies have shown that the prevalence of thiamine deficiency is increased in heart failure patients relative to the general population.4,7,11-15 It has been postulated that thiamin deficiency may actually exacerbate underlying heart failure symptoms.3,6 Research has shown that correction of thiamin deficiency can improve left ventricular ejection fraction, an indicator of long term prognosis in heart failure patients.3,16-18 Malnutrition, advanced age, frequent hospitalization, and use of diuretic medications have all been shown to increase the risk of thiamin deficiency in patients with HF.4,7
The levels of TPP in plasma or serum are very low relative to the erythrocyte. Plasma contains mainly thiamine and TMP, whereas TPP predominates in erythrocytes.20 TPP accounts for 90% of the thiamine content in whole blood.2 The TPP concentration in erythrocytes correlates with that in whole blood, a characteristic that allows the use of whole blood, rather than washed erythrocytes, for thiamine assessment.2,19,20 Thus, whole blood is the preferred sample type for analysis of thiamine concentration.
Thiamine is not expected to harm an unborn baby. Your thiamine dose needs may be different during pregnancy. Do not take thiamine without medical advice if you are pregnant or plan to become pregnant.
Injectable thiamine is injected into a muscle. You may be shown how to use injections at home. Do not self-inject this medicine if you do not fully understand how to give the injection and properly dispose of used needles and syringes.
The recommended dietary allowance of thiamine increases with age. Follow your healthcare provider's instructions. You may also consult the National Academy of Sciences \"Dietary Reference Intake\" or the U.S. Department of Agriculture's \"Dietary Reference Intake\" (formerly \"Recommended Daily Allowances\" or RDA) listings for more information.
There may be other drugs that can interact with thiamine. Tell your doctor about all medications you use. This includes prescription, over-the-counter, vitamin, and herbal products. Do not start a new medication without telling your doctor.
Most of the studies on thiamine in dogs have been used to determine the correct nutrition recommendations and examine deficiency.One interesting study focused on a pack of sled dogs that were fed only carp during their sledding season.
VITAMIN B1 INJECTION provides the essential vitamin Thiamine. Thiamine (Vitamin B1) plays an important role in the metabolism of carbohydrates, and energy production for all cells. Thiamine is most important in the breakdown of pyruvic acid, a waste product in hard working muscles, along with lactic acid. In any situation where carbohydrates are the major energy source, or when glucose is added to the diet, thiamine requirement is increased significantly. Thiamine is essential as part of the coenzyme which is involved in the breakdown of glucose for energy. Thiamine, in conjunction with Vitamin B6 (Pyridoxine) is essential in the metabolism of proteins and amino acids. Thiamine has effects on all tissues. The most sensitive are nerves, stomach and heart. Free Thiamine cannot be stored in the body, and it is rapidly absorbed from the intestine or blood, as well as from injection sites. Like all B Complex vitamins, Thiamine is water soluble, so it is rapidly absorbed and excreted from the body, and requires regular supplementation, especially in hard working animals when dietary input will probably not be sufficient. Thiamine is found in both meat and cereal products. Small amounts are manufactured in the gut, as long as horses are not under stress. Thiamine in food is destroyed by cooking. Beef loses up to 75% of its Thiamine when cooked. High doses of Thiamine are reported to help calm nervous or over excitable horses. Clinical signs of Thiamine deficiency include fatigue, muscle weakness, loss of appetite and increased heart rate. (This may be an important factor in endurance horses fed high grain diets). Many of these signs can be traced back to increased tissue levels of lactic and pyruvic acids. Nerve cells are particularly dependant on carbohydrate metabolism, and normal nerve function is greatly effected by increased levels of these acids during hard work. 59ce067264
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