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| Recommended daily allowances (RDAs) were instituted by the U.S. Food & Nutrition Board as a standard for the daily amounts of vitamins needed by a healthy person. Unfortunately, the amounts they came up with give us only the bare minimum required to ward off deficiency diseases such as beriberi, rickets, scurvy, and night blindness. They do not account for are the amounts needed to maintain maximum health, rather than borderline health. The proper balance of vitamins and minerals is also important to the proper functioning of all vitamins. Scientific research has proved that an excess of an isolated vitamin or mineral can produce the same symptoms as a deficiency. The B vitamins should always be taken together, but up to two to three times more of one B vitamin than another can be taken for a particular disorder. Although the B vitamins are a team, they are listed individually starting today with B1 -InnerSelf Magazine |
RDA: 1.5 mg
Researched Supplement Range: 50 mg to 200 mg
Notes: excess amount does no good or harm, but is simply excreted from the body.
Important Notes: A water-soluble vitamin that enters and leaves the body each day so for optimum health you should consume it each day. thiamine helps burn carbohydrates for energy, so having optimal body uptake is important in a weight management program.
Vitamin B1 goes by the names Thiamin, thiamine, and Aneurine. B1 is a water-soluble B-complex vitamin. B1 was discovered in the early 1930's. thiamine was one of the first organic compounds to be recognized as a vitamin.
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| Thiamin occurs in the human body as free thiamin and its phosphorylated forms: thiamin monophosphate (TMP), thiamin triphosphate (TTP), and thiamin pyrophosphate (TPP), which is also known as thiamin diphosphate. Function Coenzyme function: Thiamin pyrophosphate (TPP) is a required coenzyme for a small number of very important enzymes. The synthesis of TPP from free thiamin requires magnesium, adenosine triphosphate (ATP), and the enzyme thiamin pyrophosphokinase. Pyruvate dehydrogenase, a-ketoglutarate dehydrogenase, and branched chain ketoacid (BCKA) dehydrogenase each comprise a different enzyme complex found within cellular organelles called mitochondria. They catalyze the decarboxylation of pyruvate, a-ketoglutarate, and branched-chain amino acids to form acetyl-coenzyme A, succinyl-coenzyme A, and derivatives of branched chain amino acids, respectively, all of which play critical roles in the production of energy from food. English Translation - you need Thiamin to convert food biochemically (especially Carbohydrates) into energy. In addition to the thiamin coenzyme (TPP), each dehydrogenase complex requires a niacin-containing coenzyme (NAD), a riboflavin-containing coenzyme (FAD), and lipoic acid. Once again English translation - Vitamin B1 needs other B vitamins such as B6, and B12 to function correctly. Niacin is needed as is Riboflavin - this allows the B1 to bind and function within your body as it should. Transketolase catalyzes critical reactions in another metabolic pathway known as the pentose phosphate pathway. One of the most important intermediates of this pathway is ribose-5-phosphate, a phosphorylated 5-carbon sugar, required for the synthesis of the high-energy ribonucleotides, ATP and guanosine triphosphate (GTP), the nucleic acids, DNA and RNA, and the niacin-containing coenzyme NADPH, which is essential for a number of biosynthetic reactions (see Niacin) . Because transketolase decreases early in thiamin deficiency, measurement of its activity in red blood cells has been used to assess thiamin nutritional status. Once again Niacin is required for Vitamin B1 (Thamin) to properly be used during energy conversions in cells and during digestion. Non-coenzyme function: Thiamin triphosphate (TTP) is concentrated in nerve and muscle cells. Research in animals indicates that TTP activates membrane ion channels, possibly by phosphorylating them. The flow of electrolytes like sodium and chloride in or out of nerve and muscle cells through membrane ion channels plays a role in nerve impulse conduction and voluntary muscle action. Impaired formation of TTP may play a role in the neurologic symptoms of severe thiamin deficiency. Within Vitamin B1 the muscles can not conduct electrical signals from nerve tissue. If the nerve tissue is not conducting electrical signals from the brain do to lack of Thiamin to regulate the ions (Sodium, Chloride), then impairment of muscles and nerves occurs. Weakness, and will fatigue, problems with organs, the brain, and heart will also become evident. Deficiency Beriberi, the disease resulting from severe thiamin deficiency, was described in Chinese literature as early as 2600 B.C. Thiamin deficiency affects the cardiovascular, nervous, muscular, and gastrointestinal systems. Beriberi has been termed dry, wet, and cerebral, depending on the systems affected by severe thiamin deficiency. The main feature of dry (paralytic or nervous) beriberi is peripheral neuropathy. Early in the course of the neuropathy "burning feet syndrome" may occur. Other symptoms include abnormal (exaggerated) reflexes, diminished sensation and weakness in the legs and arms. Muscle pain and tenderness and difficulty rising from a squatting position have also been observed. Severely thiamin deficient individuals may experience seizures (convulsions). In addition to neurologic symptoms, wet (cardiac) beriberi is characterized by cardiovascular manifestations of thiamin deficiency, which include rapid heart rate, enlargement of the heart, severe swelling (edema), difficulty breathing, and ultimately congestive heart failure. Cerebral beriberi may lead to Wernicke encephalopathy and Korsakoff psychosis. The diagnosis of Wernicke's encephalopathy is based on a "triad" of signs, which include abnormal eye movements, stance and gait abnormalities, and abnormalities in mental function, which may include a confused apathetic state or a profound memory disorder termed Korsakoff's amnesia or Korsakoff's psychosis. Thiamin deficiency affecting the central nervous system is referred to as Wernicke's disease when the amnesic state is not present and Wernicke-Korsakoff syndrome (WKS) when the amnesic symptoms are present along with the eye movement and gait disorders. Most WKS sufferers are alcoholics, though it has been observed in other disorders of gross malnutrition, including stomach cancer and AIDS. Administration of intravenous thiamin to WKS patients generally results in prompt improvement of the eye symptoms, but improvements in motor coordination and memory may be less, depending on how long the symptoms have been present. Recent evidence of increased immune cell activation and increased free radical production in the areas of the brain that are selectively damaged suggests that oxidative stress plays an important role in the neurologic pathology of thiamin deficiency. Causes of thiamin deficiency: Thiamin deficiency may result from inadequate thiamin intake, an increased requirement for thiamin, excessive loss of thiamin from the body, consumption of anti-thiamin factors in food, or a combination of factors. Inadequate intake: Inadequate consumption of thiamin is the main cause of thiamin deficiency in underdeveloped countries. Thiamin deficiency is common in low income populations whose diets are high in carbohydrate and low in thiamin (e.g., milled or polished rice). Breast fed infants whose mothers are thiamin deficient are vulnerable to developing infantile beriberi. Alcoholism, which is associated with low intake of thiamin among other nutrients, is the primary cause of thiamin deficiency in industrialized countries. Increased requirement: Conditions resulting in an increased requirement for thiamin include strenuous physical exertion, fever, pregnancy, breastfeeding, and adolescent growth. Such conditions place individuals with marginal thiamin intake at risk for developing symptomatic thiamin deficiency. Recently, malaria patients in Thailand were found to be severely thiamin deficient more frequently than non-infected individuals. Malarial infection leads to a large increase in the metabolic demand for glucose, as well as increased demand for the disposal of lactate. The stresses induced by malarial infection could exacerbate thiamin deficiency in individuals already predisposed. HIV-infected individuals, whether or not they had developed AIDS, were also found to be at increased risk for thiamin deficiency. The lack of association between thiamin intake and evidence of deficiency in these HIV-infected individuals suggested they had an increased requirement for thiamin. Excessive loss: Excessive loss of thiamin may precipitate thiamin deficiency. Individuals with kidney failure requiring hemodialysis lose thiamin at an increased rate, and are at risk for thiamin deficiency. By increasing urinary flow, diuretics ("water pills") may prevent reabsorption of thiamin by the kidney and increase its excretion in the urine. Alcoholics who maintain a high fluid intake and urine flow rate may also experience increased loss of thiamin, exacerbating the effects of low thiamin intake. Anti-thiamin factors (ATF): The presence of anti-thiamin factors (ATF) in foods also contributes to the risk of thiamin deficiency. Certain plants contain ATF, which react with thiamin to form a product that is oxidized in the body, rendering it inactive. Consuming large amounts of tea and coffee (including decaffeinated), as well as chewing tea leaves and betel nut have been associated with thiamin depletion in humans due to the presence of ATF. Vitamin C and other antioxidants can protect thiamin in some foods by preventing its oxidation to an inactive form. Thiaminases are enzymes that break down thiamin in food. Individuals who habitually eat certain raw freshwater fish, raw shellfish, and ferns are at higher risk of thiamin deficiency because these foods contain a thiaminase, which would normally be inactivated by the heat used for cooking. An acute neurologic syndrome (seasonal ataxia) in Nigeria has been associated with thiamin deficiency precipitated by a thiaminase in African silkworms, a traditional high-protein food for some Nigerians. The Recommended Dietary Allowance (RDA): The RDA for thiamin, revised in 1998 (11), was based on the prevention of deficiency in generally healthy individuals.
Disease Treatment 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 have been investigated. Several investigators found evidence of decreased activity of the thiamin pyrophosphate-dependent enzymes, a-ketoglutarate dehydrogenase and transketolase, in the brains of patients who died of Alzheimer's disease. Such findings are consistent with evidence of reduced glucose metabolism found on PET scans of the brains of Alzheimer's disease patients. The finding of decreased brain levels of thiamin pyrophophosphate (TPP) in the presence of normal levels of free thiamin and thiamin monophosphate (TMP) suggests that the decreased enzyme activity is not likely to be the result of thiamin deficiency, but rather of impaired synthesis of TPP. Presently, there is only slight evidence that thiamin supplements are of benefit in Alzheimer's disease. A double blind placebo-controlled study of 15 patients (10 completed the study) reported no beneficial effect of 3 grams of thiamin/day on cognitive decline over a 12-month period. A preliminary report from another study claimed a mild benefit of 3 to 8 grams of thiamin/day in dementia of Alzheimer's type in 1993, but no additional data from that study are available. A mild beneficial effect in patients with Alzheimer's disease was reported after 12 weeks of treatment with 100 milligrams/day of a thiamin derivative (thiamin tetrahydrofurfuryl disulfide), but this study was not placebo-controlled. A recent systematic review of randomized, double-blind, placebo-controlled trials of thiamin in patient's with dementia of Alzheimer's type found no evidence that thiamin was a useful treatment for the symptoms of Alzheimer's disease. Congestive heart failure (CHF): Severe thiamin deficiency (wet beriberi) can lead to impaired cardiac function and ultimately congestive heart failure (CHF). Although cardiac manifestations of beriberi are rarely encountered in industrialized countries, CHF due to other causes is common, especially in the elderly. Diuretics used in the treatment of CHF, notably furosemide (Lasix), have been found to increase thiamin excretion, potentially leading to marginal thiamin deficiency. A number of studies have examined thiamin nutritional status in CHF patients and most found a fairly low incidence of thiamin deficiency, as measured by assays of transketolase activity. As in the general population, older CHF patients were found to be at higher risk of thiamin deficiency. An important measure of cardiac function in CHF is the left ventricular ejection fraction (LVEF), which can be assessed by echocardiography. In a randomized double-blind study of 30 CHF patients, all of whom had been taking furosemide for at least 3 months, intravenous (IV) thiamin therapy (200 mg/day) for 7 days resulted in an improved LVEF compared to IV placebo (17). When all 30 of the CHF patients in that study subsequently received 6 weeks of oral thiamin therapy (200 mg/day) the average LVEF improved by 22%. This finding may be significant because improvements in LVEF have been associated with improved survival in CHF patients. Conclusions that can be drawn from the studies published to date are limited due to small sample sizes, lack of randomization in some studies, and a need for more precise assays of thiamin status. Presently, the role of thiamin supplementation in maintaining cardiac function in CHF patients remains controversial. Cancer: Thiamin deficiency has been observed in some cancer patients with rapidly growing tumors. Recent research in cell culture and animal models indicates that rapidly dividing cancer cells have a high requirement for thiamin. All rapidly dividing cells require nucleic acids at an increased rate, but some cancer cells appear to rely heavily on the thiamin pyrophosphate-dependent enzyme, transketolase, to provide the ribose-5-phosphate necessary for nucleic acid synthesis. Thiamin supplementation in cancer patients is common to prevent thiamin deficiency, but some investigators caution that too much thiamin may fuel the growth of some malignant tumors. These investigators suggest that thiamin supplementation be reserved for those cancer patients that are actually thiamin deficient. Presently, there is no evidence available from studies in humans to support or refute this theory. However, it would be prudent for individuals with cancer who are considering thiamin supplementation to discuss this issue with the clinician managing their cancer therapy. Food Sources A varied diet should provide most individuals with adequate thiamin to prevent deficiency. In the U.S. the average dietary thiamin intake for young adult men is about 2 mg/day and 1.2 mg/day for young adult women. A survey of people over the age of 60 found an average dietary thiamin intake of 1.4 mg/day for men and 1.1 mg/day for women. However, institutionalization and poverty increase the likelihood of inadequate thiamin intake in the elderly. Whole grain cereals, legumes (e.g., beans and lentils), nuts, lean pork, and yeast are rich sources of thiamin. Because most of the thiamin is lost during the production of white flour and polished (milled) rice, white rice and foods made from white flour (e.g., bread and pasta) are fortified with thiamin. A number of thiamin-rich foods are listed in the table below along with their thiamin content in milligrams (mg). For more information on the nutrient content of foods you eat frequently, search the USDA food composition database. Safety Toxicity: The Food and Nutrition Board did not set a tolerable upper level (UL) of intake for thiamin because there are no known toxic effects from the consumption of excess thiamin in food or through long-term oral supplementation (up to 200 mg/day). A small number of life threatening anaphylactic reactions have been observed with large intravenous doses of thiamin. However, anaphylactic reactions are the result of an overwhelming allergic response rather than a toxic effect of thiamin. Drug interactions: Reduced blood levels of thiamin have been reported in individuals with seizure disorders (epilepsy) taking the anticonvulsant medication, phenytoin, for long periods of time. 5-Fluorouracil, a drug used in cancer therapy, inhibits the phosphorylation of thiamin to thiamin pyrophosphate (TPP). Diuretics, especially furosemide (Lasix), may increase the risk of thiamin deficiency in individuals with marginal thiamin intake due to increased urinary excretion of thiamin. - Linus Pauling Institute & Charles K. Singleton, Ph.D. Department of Biological SciencesVanderbilt University |
- Beriberi,
constipation,
edema,
enlarged liver,
fatigue,
forgetfulness,
gastrointestinal disturbances,
heart changes,
irritability,
labored breathing,
loss of appetite,
muscle atrophy,
nervousness,
numbness of the hands and feet,
pain and sensitivity,
poor coordination,
tingling sensations,
weak and sore muscles,
general weakness,
severe weight loss.
Therapeutic Uses:
- alzheimer's
diarrhea
constipation
diabetes
indigestion
heart disease
congestive heart failure
stress
mental illness
nausea
Benefits:
Vitamin B1 - Enhances circulation and assists in blood formation, carbohydrate metabolism, and the production of hydrochloric acid, which is important for proper digestion, optimizes cognitive activity and brain function, positive effect on energy, growth, normal appetite, and learning capacity, and is needed for muscle tone of the intestines, stomach, and heart, protecting the body from the degenerative effects of aging, alcohol consumption, and smoking.
Sources of Vitamin B1 (Thamine)
- Milk
Brown rice,
egg yolks,
fish,
legumes,
liver,
peanuts,
peas,
pork,
poultry,
rice bran,
wheat germ,
whole grains,
asparagus,
brewer’s yeast,
broccoli,
Brussels sprouts,
dulse,
kelp,
most nuts,
oatmeal,
plums,
dried prunes,
raisins,
spirulina,
watercress
alfalfa,
bladderwrack,
burdock root,
catnip,
cayenne,
chamomile,
chickweed,
eyebright,
fennel seed,
fenugreek,
hops,
nettle,
oat straw,
parsley,
peppermint,
raspberry leaf,
red clover,
rose hips,
sage,
yarrow,
yellow dock.
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