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Thiamine

From Wikipedia, the free encyclopedia
  (Redirected from Vitamin B1)
 
Thiamine
Kekulé skeletal formula of the cation in thiamine
Ball-and-stick model of the cation in thiamine
Names
IUPAC name
3-((4-Amino-2-methyl-5-pyrimidinyl)methyl)- 5-(2-hydroxyethyl)-4-methylthiazolium chloride
Other names
Aneurine
Thiamin
Identifiers
59-43-8 Yes
3581326
ChEBI CHEBI:18385 
ChEMBL ChEMBL1588 Yes
ChEMBL1547 
ChemSpider 5819 Yes
DrugBank DB00152 Yes
ECHA InfoCard 100.000.387
EC Number 200-425-3
318226
Jmol 3D model Interactive image
Interactive image
Interactive image
KEGG C00378 
MeSH Thiamine
PubChem 6042
UNII X66NSO3N35 Yes
Properties
C12H17N4OS+
Molar mass 265.35 g mol−1
Pharmacology
A11DA01 (WHO)
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
Yes verify (what is Yes ?)
Infobox references
   

Thiaminethiamin, or vitamin B1 (/ˈθ.əmn/  thy -ə-min ), named as the "thio-vitamine" ("sulfur-containing vitamin") is a vitamin of the B complex. First named aneurin for the detrimental neurological effects if not present in the diet, it was eventually assigned the generic descriptor name vitamin B1. Its phosphatederivatives are involved in many cellular processes. The best-characterized form is thiamine pyrophosphate(TPP), a coenzyme in the catabolism of sugars and amino acids. In yeast, TPP is also required in the first step of alcoholic fermentation.

All living organisms use thiamine, but it is synthesized only in bacteriafungi, and plantsAnimals must obtain it from their diet, and thus, for humans, it is an essential nutrient. Insufficient intake in birds produces a characteristic polyneuritis. In mammals, deficiency results in Korsakoff's syndromeoptic neuropathy, and a disease called beriberi that affects the peripheral nervous system (polyneuritis) and/or the cardiovascular system. Thiamine deficiency has a potentially fatal outcome if it remains untreated.[1] In less-severe cases, nonspecific signs include malaise, weight loss, irritability and confusion.[2]

The stable and non-hygroscopic salt thiamine mononitrate is the vitamer used for flour and food fortification. Thiamine is on the World Health Organization's List of Essential Medicines, a list of the most important medication needed in a basic health system.[3]

Chemical properties

Thiamine is a colorless organosulfur compound with a chemical formula C12H17N4OS. Its structure consists of an aminopyrimidine and a thiazole ring linked by a methylene bridge. The thiazole is substituted with methyl and hydroxyethyl side chains. Thiamine is soluble in watermethanol, and glyceroland practically insoluble in less polar organic solvents. It is stable at acidic pH, but is unstable in alkaline solutions.[1][4] Thiamine, which is a N-heterocyclic carbene, can be used in place of cyanide as a catalyst for benzoin condensation.[5][6] Thiamine is unstable to heat, but stable during frozen storage.[citation needed] It is unstable when exposed to ultraviolet light[4] and gamma irradiation.[7][8] Thiamine reacts strongly in Maillard-type reactions.[1]

Biosynthesis

 
A 3D representation of the TPP riboswitch with thiamine bound

Complex thiamine biosynthesis occurs in bacteria, some protozoans, plants, and fungi.[9][10] The thiazole and pyrimidine moieties are bioisynthesized separately and then combined to form ThMP by the action of thiamine-phosphate synthase (EC 2.5.1.3). The biosynthetic pathways may differ among organisms. In E. coli and other enterobacteriaceae, ThMP may be phosphorylated to the cofactor ThDP by a thiamine-phosphate kinase (ThMP + ATP → ThDP + ADP, EC 2.7.4.16). In most bacteria and in eukaryotes, ThMP is hydrolyzed to thiamine, which may then be pyrophosphorylated to ThDP by thiamine diphosphokinase (thiamine + ATP → ThDP + AMP, EC 2.7.6.2).

The biosynthetic pathways are regulated by riboswitches. If there is sufficient thiamine present in the cell then the thiamine binds to the mRNAs for the enzymes that are required in the pathway and prevents their translation. If there is no thiamine present then there is no inhibition, and the enzymes required for the biosynthesis are produced. The specific riboswitch, the TPP riboswitch, is the only riboswitch identified in both eukaryotic and prokaryotic organisms.[11]

Nutrition

Occurrence in foods

Thiamine is found in a wide variety of foods at low concentrations. Yeast, yeast extract, and pork are the most highly concentrated sources of thiamine.[citation needed] In general, cereal grains are the most important dietary sources of thiamine, by virtue of their wide use. Of these, whole grains contain more thiamine than refined grains, as thiamine is found mostly in the outer layers of the grain and in the germ (which are removed during the refining process). For example, 100 g of whole-wheat flour contains 0.55 mg of thiamine, while 100 g of white flour contains only 0.06 mg of thiamine. In the US, processed flour must be enriched with thiamine mononitrate (along with niacin, ferrous iron, riboflavin, and folic acid) to replace that lost in processing. In Australia, thiamine, folic acid, and iodized salt are added for the same reason.[12]

The salt thiamine mononitrate, rather than thiamine hydrochloride, is used for food fortification, as the mononitrate is more stable, and does not absorb water from natural humidity (is non-hygroscopic), whereas thiamine hydrochloride is hygroscopic. When thiamine mononitrate dissolves in water, it releases nitrate (about 19% of its weight) and is thereafter absorbed as the thiamine cation.

The few exceptions that are not fortified include organic wholemeal flour (on the assumption that the wholewheat will have kept more of the nutrients).

Some other foods naturally rich in thiamine are oatmealflax, and sunflower seedsbrown rice, whole grain ryeasparaguskalecauliflowerpotatoesorangesliver (beef, pork, and chicken), and eggs.[2]

Dietary Reference Intakes

The Food and Nutrition Board of the U.S. Institute of Medicine updated Estimated Average Requirements (EARs) and Recommended Dietary Allowances (RDAs) for thiamine in 1998. The current EARs for thiamine for women and men ages 14 and up are 0.9 mg/day and 1.0 mg/day, respectively; the RDAs are 1.1 and 1.2 mg/day. RDAs are higher than EARs so as to identify amounts that will cover people with higher than average requirements. RDA for pregnancy equals 1.4 mg/day. RDA for lactation equals 1.4 mg/day. For infants up to 12 months the Adequate Intake (AI) is 0.2-0.3 mg/day. and for children ages 1–13 years the RDA increases with age from 0.5 to 0.9 mg/day. As for safety, the Food and Nutrition Board of the U.S. Institute of Medicine sets Tolerable Upper Intake Levels (known as ULs) for vitamins and minerals when evidence is sufficient. In the case of thiamine there is no UL, as there is no human data for adverse effects from high doses. The European Food Safety Authority reviewed the same safety question and also reached the conclusion that there was not sufficient evidence to set a UL for thiamine.[13] Collectively the EARs, RDAs and ULs are referred to as Dietary Reference Intakes.[14]

For U.S. food and dietary supplement labeling purposes the amount in a serving is expressed as a percent of Daily Value (%DV). For thiamine labeling purposes 100% of the Daily Value was 1.5 mg, but as of May 2016 it has been revised to 1.2 mg. A table of the pre-change adult Daily Values is provided at Reference Daily Intake. Food and supplement companies have until July 28, 2018 to comply with the change.

Antagonists

Thiamine in foods can be degraded in a variety of ways. Sulfites, which are added to foods usually as a preservative,[15] will attack thiamine at the methylene bridge in the structure, cleaving the pyrimidine ring from the thiazole ring.[2] The rate of this reaction is increased under acidic conditions. Thiamine is degraded by thermolabile thiaminases (present in raw fish and shellfish[1]). Some thiaminases are produced by bacteria. Bacterial thiaminases are cell surface enzymes that must dissociate from the membrane before being activated; the dissociation can occur in ruminants under acidotic conditions. Rumen bacteria also reduce sulfate to sulfite, therefore high dietary intakes of sulfate can have thiamine-antagonistic activities.

Plant thiamine antagonists are heat-stable and occur as both the ortho- and para-hydroxyphenols. Some examples of these antagonists are caffeic acidchlorogenic acid, and tannic acid. These compounds interact with the thiamine to oxidize the thiazole ring, thus rendering it unable to be absorbed. Two flavonoids, quercetin and rutin, have also been implicated as thiamine antagonists.[2]

Absorption and transport

Absorption

Thiamine is released by the action of phosphatase and pyrophosphatase in the upper small intestine. At low concentrations, the process is carrier-mediated, and, at higher concentrations, absorption occurs via passive diffusion. Active transport is greatest in the jejunum and ileum; but, active transport can be inhibited by alcohol consumption and by folic deficiency.[1] Decline in thiamine absorption occurs at intakes above 5 mg/day.[16] The cells of the intestinal mucosa have thiamine pyrophosphokinase activity, but it is unclear as to whether the enzyme is linked to active absorption. The majority of thiamine present in the intestine is in the pyrophosphorylated form ThDP, but when thiamine arrives on the serosal side of the intestine it is often in the free form. The uptake of thiamine by the mucosal cell is likely coupled in some way to its phosphorylation/dephosphorylation. On the serosal side of the intestine, evidence has shown that discharge of the vitamin by those cells is dependent on Na+-dependent ATPase.[2]

Bound to serum proteins

The majority of thiamine in serum is bound to proteins, mainly albumin. Approximately 90% of total thiamine in blood is in erythrocytes. A specific binding protein called thiamine-binding protein (TBP) has been identified in rat serum and is believed to be a hormone-regulated carrier protein important for tissue distribution of thiamine.[2]

Cellular uptake

Uptake of thiamine by cells of the blood and other tissues occurs via active transport and passive diffusion.[1] The brain requires a much greater amount of thiamine than in other cells of the body. Much of ingested thiamine never reaches the brain because of passive diffusion and the blood brain barrier. About 80% of intracellular thiamine is phosphorylated and most is bound to proteins. In some tissues, thiamine uptake and secretion appears to be mediated by a soluble thiamine transporter that is dependent on Na+ and a transcellular proton gradient.[2]

Tissue distribution

Human storage of thiamine is about 25 to 30 mg, with the greatest concentrations in skeletal muscle, heart, brain, liver, and kidneys. ThMP and free (unphosphorylated) thiamine is present in plasma, milk, cerebrospinal fluid, and, it is presumed, all extracellular fluids. Unlike the highly phosphorylated forms of thiamine, ThMP and free thiamine are capable of crossing cell membranes. Thiamine contents in human tissues are less than those of other species.[2][17]

Excretion

Thiamine and its acid metabolites (2-methyl-4-amino-5-pyrimidine carboxylic acid, 4-methyl-thiazole-5-acetic acid, and thiamine acetic acid) are excreted principally in the urine.[4]

Thiamine phosphate derivatives and function

Thiamine is usually considered as the transport form of the vitamin. There are five known natural thiamine phosphate derivatives: thiamine monophosphate(ThMP), thiamine diphosphate (ThDP), also sometimes called thiamine pyrophosphate (TPP), thiamine triphosphate (ThTP), and the recently discovered adenosine thiamine triphosphate (AThTP), and adenosine thiamine diphosphate (AThDP). While the coenzyme role of thiamine diphosphate is well-known and extensively characterized, the non-coenzyme action of thiamine and derivatives may be realized through binding to a number of recently identified proteins which do not use the catalytic action of thiamine diphosphate [18]

Thiamine diphosphate

No physiological role is known for ThMP; however, the diphosphate is physiologically relevant. The synthesis of thiamine diphosphate (ThDP), also known as thiamine pyrophosphate (TPP) or cocarboxylase, is catalyzed by an enzyme called thiamine diphosphokinase according to the reaction thiamine + ATP → ThDP + AMP (EC 2.7.6.2). ThDP is a coenzyme for several enzymes that catalyze the transfer of two-carbon units and in particular the dehydrogenation(decarboxylation and subsequent conjugation with coenzyme A) of 2-oxoacids (alpha-keto acids). Examples include:

The enzymes transketolasepyruvate dehydrogenase (PDH), and 2-oxoglutarate dehydrogenase (OGDH) are all important in carbohydrate metabolism. The cytosolic enzyme transketolase is a key player in the pentose phosphate pathway, a major route for the biosynthesis of the pentose sugarsdeoxyribose and ribose. The mitochondrial PDH and OGDH are part of biochemical pathways that result in the generation of adenosine triphosphate(ATP), which is a major form of energy for the cell. PDH links glycolysis to the citric acid cycle, while the reaction catalyzed by OGDH is a rate-limiting step in the citric acid cycle. In the nervous system, PDH is also involved in the production of acetylcholine, a neurotransmitter, and for myelin synthesis.[19]

Thiamine triphosphate

Thiamine triphosphate (ThTP) was long considered a specific neuroactive form of thiamine. However, recently it was shown that ThTP exists in bacteriafungiplants and animals suggesting a much more general cellular role.[20] In particular in E. coli, it seems to play a role in response to amino acid starvation.[21]

Adenosine thiamine triphosphate

Adenosine thiamine triphosphate (AThTP) or thiaminylated adenosine triphosphate has recently been discovered in Escherichia coli, where it accumulates as a result of carbon starvation.[22] In E. coli, AThTP may account for up to 20% of total thiamine. It also exists in lesser amounts in yeast, roots of higher plants and animal tissue.[23]

Adenosine thiamine diphosphate

Adenosine thiamine diphosphate (AThDP) or thiaminylated adenosine diphosphate exists in small amounts in vertebrate liver, but its role remains unknown.[23]

Deficiency

Thiamine derivatives and thiamine-dependent enzymes are present in all cells of the body, thus a thiamine deficiency would seem to adversely affect all of the organ systems. However, the nervous system is particularly sensitive to thiamine deficiency, because of its dependence on oxidative metabolism.

Thiamine deficiency commonly presents subacutely and can lead to metabolic coma and death. A lack of thiamine can be caused by malnutrition, a diet high in thiaminase-rich foods (raw freshwater fish, raw shellfishferns) and/or foods high in anti-thiamine factors (teacoffeebetel nuts)[24] and by grossly impaired nutritional status associated with chronic diseases, such as alcoholism, gastrointestinal diseases, HIV-AIDS, and persistent vomiting.[25] It is thought that many people with diabetes have a deficiency of thiamine and that this may be linked to some of the complications that can occur.[26][27]

Well-known syndromes caused by thiamine deficiency include beriberiWernicke-Korsakoff syndrome, and optic neuropathy.

Beriberi

Beriberi is a neurological and cardiovascular disease. The three major forms of the disorder are dry beriberi, wet beriberi, and infantile beriberi.[4] A fourth form, gastrointestinal beriberi, was recognized in 2004.

  • Dry beriberi is characterized principally by peripheral neuropathy consisting of symmetric impairment of sensory, motor, and reflex functions affecting distal more than proximal limb segments and causing calf muscle tenderness.[25]

However, it has been recently recognized that peripheral neuropathy (tingling or numbness in the extremities) due to thiamine deficiency could also present with axonal neuropathy (partial paralysis or sensory loss). Peripheral neuropathy can present with subacute motor axonal neuropathy mimicking Guillain–Barré syndrome; or as a large fibre proprioceptive central-peripheral axonal neuropathy presenting as a subacute sensory ataxia.[28]

  • Wet beriberi is associated with mental confusion, muscular atrophyedematachycardiacardiomegaly, and congestive heart failure in addition to peripheral neuropathy.[1]
  • Infantile beriberi occurs in infants breast-fed by thiamin-deficient mothers (who may show no sign of thiamine deficiency). Infants may manifest cardiac, aphonic, or pseudomeningitic forms of the disorder. Infants with cardiac beriberi frequently exhibit a loud piercing cry, vomiting, and tachycardia.[4]Convulsions are not uncommon, and death may ensue if thiamine is not administered promptly.[25]
  • Gastrointestinal beriberi is associated with nausea, vomiting, abdominal pain, and lactic acidosis.[29][30]

Following thiamine treatment, rapid improvement occurs, in general, within 24 hours.[4] Improvements of peripheral neuropathy may require several months of thiamine treatment.[31]

Alcoholic brain disease

Nerve cells and other supporting cells (such as glial cells) of the nervous system require thiamine. Examples of neurologic disorders that are linked to alcohol abuse include Wernicke's encephalopathy (WE), Korsakoff's syndrome (alcohol amnestic disorder), Wernicke–Korsakoff syndrome as well as varying degrees of cognitive impairment.[32]

Wernicke's encephalopathy is the most frequently encountered manifestation of thiamine deficiency in Western society,[33][34] though it may also occur in patients with impaired nutrition from other causes, such as gastrointestinal disease,[33] those with HIV-AIDS, and with the injudicious administration of parenteral glucose or hyperalimentation without adequate B-vitamin supplementation.[35] This is a striking neuro-psychiatric disorder characterized by paralysis of eye movements, abnormal stance and gait, and markedly deranged mental function.[36]

Korsakoff's syndrome is, in general, considered to occur with deterioration of brain function in patients initially diagnosed with WE.[37] This is an amnestic-confabulatory syndrome characterized by retrograde and anterograde amnesia, impairment of conceptual functions, and decreased spontaneity and initiative.[25]

Alcoholics may have thiamine deficiency because of the following:

  • Inadequate nutritional intake: Alcoholics tend to intake less than the recommended amount of thiamine.
  • Decreased uptake of thiamine from the GI tract: Active transport of thiamine into enterocytes is disturbed during acute alcohol exposure.
  • Liver thiamine stores are reduced due to hepatic steatosis or fibrosis.[38]
  • Impaired thiamine utilization: Magnesium, which is required for the binding of thiamine to thiamine-using enzymes within the cell, is also deficient due to chronic alcohol consumption. The inefficient utilization of any thiamine that does reach the cells will further exacerbate the thiamine deficiency.
  • Ethanol per se inhibits thiamine transport in the gastrointestinal system and blocks phosphorylation of thiamine to its cofactor form (ThDP).[39]

Following improved nutrition and the removal of alcohol consumption, some impairments linked with thiamine deficiency are reversed, in particular poor brain functionality, although in more severe cases, Wernicke–Korsakoff syndrome leaves permanent damage. (See delirium tremens.)

Optic neuropathy

Optic neuropathy can also occur in thiamine deficiency and is characterized by bilateral visual loss, cecocentral scotomas and impaired colour perception. The ophthalmological findings usually can show a bilateral oedema of the optic disk in the acute phase, followed by a bilateral optic atrophy.[citation needed]

Thiamine deficiency in poultry

As most feedstuffs used in poultry diets contain enough quantities of vitamins to meet the requirements in this species, deficiencies in this vitamin do not occur with commercial diets. This was, at least, the opinion in the 1960s.[40]

Mature chickens show signs 3 weeks after being fed a deficient diet. In young chicks, it can appear before 2 weeks of age.

Onset is sudden in young chicks. There is anorexia and an unsteady gait. Later on, there are locomotor signs, beginning with an apparent paralysis of the flexor of the toes. The characteristic position is called "stargazing", meaning a chick "sitting on its hocks and the head in opisthotonos".

Response to administration of the vitamin is rather quick, occurring a few hours later.[41][42]

Differential diagnosis include riboflavin deficiency and avian encephalomyelitis. In riboflavin deficiency, the "curled toes" is a characteristic symptom. Muscle tremor is typical of avian encephalomyelitis. A therapeutic diagnosis can be tried by supplementing thiamine only in the affected bird. If the animals do not respond in a few hours, thiamine deficiency can be excluded.

Thiamine deficiency in ruminants

Polioencephalomalacia (PEM) is the most common thiamine deficiency disorder in young ruminant and nonruminant animals. Symptoms of PEM include a profuse, but transient, diarrhea, listlessness, circling movements, star gazing or opisthotonus (head drawn back over neck), and muscle tremors.[43] The most common cause is high-carbohydrate feeds, leading to the overgrowth of thiaminase-producing bacteria, but dietary ingestion of thiaminase (e.g., in bracken fern), or inhibition of thiamine absorption by high sulfur intake are also possible.[44] Another cause of PEM is Clostridium sporogenes or Bacillus aneurinolyticus infection. These bacteria produce thiaminases that will cause an acute thiamine deficiency in the affected animal.[45]

Idiopathic paralytic disease in wild birds, fish

Recently, thiamine deficiency has been identified as the cause of a paralytic disease affecting wild birds in the Baltic Sea area dating back to 1982.[46] In this condition, there is difficulty in keeping the wings folded along the side of the body when resting, loss of the ability to fly and voice, with eventual paralysis of the wings and legs and death. It affects primarily 0.5–1 kg sized birds such as the herring gull (Larus argentatus), common starling (Sturnus vulgaris) and common eider (Somateria mollissima). Researches noted, "Because the investigated species occupy a wide range of ecological niches and positions in the food web, we are open to the possibility that other animal classes may suffer from thiamine deficiency as well."[46]p. 12006

In the counties of Blekinge and Skåne (south-most Sweden) mass deaths of especially herring gull but also other species has been observed since the early 2000s. More recently, species of other classes seems to be affected. High mortality of salmon (Salmo salar) in the river Mörrumsån is reported, and the last years mammals like Eurasian Elk (Alces alces) has suffered death in unusual high number. Lack of thiamine is the common denominator where analysis is done. The County Administrative Board of Blekinge did in April 2012 find the situation so alarming that they asked the Swedish government to set up a closer investigation.[47]

Analysis and diagnostic testing

 
Oxidation of thiamine derivatives to fluorescent thiochromes by potassium ferricyanide under alkaline conditions

A positive diagnosis test for thiamine deficiency can be ascertained by measuring the activity of the enzyme transketolase in erythrocytes (Erythrocyte Transketolase Activation Assay). Thiamine, as well as its phosphate derivatives, can also be detected directly in whole blood, tissues, foods, animal feed, and pharmaceutical preparations following the conversion of thiamine to fluorescent thiochrome derivatives (Thiochrome Assay) and separation by high-performance liquid chromatography (HPLC).[48][49][50] In recent reports, a number of Capillary Electrophoresis (CE) techniques and in-capillary enzyme reaction methods have emerged as potential alternative techniques for the determination and monitoring of thiamine in samples.[51] The normal thiamine concentration in EDTA-blood is about 20-100 µg/l.

Genetic diseases

Genetic diseases of thiamine transport are rare but serious. Thiamine responsive megaloblastic anemia (TRMA) with diabetes mellitus and sensorineural deafness[52] is an autosomal recessive disorder caused by mutations in the gene SLC19A2,[53] a high affinity thiamine transporter. TRMA patients do not show signs of systemic thiamine deficiency, suggesting redundancy in the thiamine transport system. This has led to the discovery of a second high-affinity thiamine transporter, SLC19A3.[54][55] Leigh disease (subacute necrotising encephalomyelopathy) is an inherited disorder that affects mostly infants in the first years of life and is invariably fatal. Pathological similarities between Leigh disease and WE led to the hypothesis that the cause was a defect in thiamine metabolism. One of the most consistent findings has been an abnormality of the activation of the pyruvate dehydrogenase complex.[56]

Mutations in the SLC19A3 gene have been linked to Biotin-Thiamine Responsive Basal Ganglia Disease[57] which is treated with pharmacological doses of thiamine and biotin, another B vitamin.

Other disorders in which a putative role for thiamine has been implicated include subacute necrotising encephalomyelopathyopsoclonic cerebellopathy (a paraneoplastic syndrome), and Nigerian seasonal ataxia. In addition, several inherited disorders of ThDP-dependent enzymes have been reported,[58]which may respond to thiamine treatment.[25]

History

Thiamine was the first of the water-soluble vitamins to be described,[1] leading to the discovery of more such trace compounds essential for survival and to the notion of vitamin.

In 1884, Kanehiro Takaki (1849–1920), a surgeon general in the Japanese navy, rejected the previous germ theory for beriberi and hypothesized that the disease was due to insufficiencies in the diet instead.[59] Switching diet on a navy ship, he discovered that substituting a diet of white rice only, with one also containing barley, meat, milk, bread, and vegetables nearly eliminated beriberi on a 9-month sea voyage. However, Takaki had added many foods to the successful diet and he incorrectly attributed the benefit to increased nitrogen intake, as vitamins were unknown substances at the time. Nor was the Navy convinced of the need for so expensive a program of dietary improvement, and many men continued to die of beriberi, even during the Russo-Japanese war of 1904–5. Not until 1905, after the anti-beriberi factor had been discovered in rice bran (removed by polishing into white rice) and in brown barley rice, was Takaki's experiment rewarded by making him a baron in the Japanese peerage system, after which he was affectionately called "Barley Baron".

The specific connection to grain was made in 1897 by Christiaan Eijkman (1858–1930), a military doctor in the Dutch Indies, discovered that fowl fed on a diet of cooked, polished rice developed paralysis, which could be reversed by discontinuing rice polishing.[60] He attributed beriberi to a nerve poison in the endosperm of rice, from which the outer layers of the grain gave protection to the body. An associate, Gerrit Grijns (1865–1944), correctly interpreted the connection between excessive consumption of polished rice and beriberi in 1901: He concluded that rice contains an essential nutrient in the outer layers of the grain that is removed by polishing.[61]

Eijkman was eventually awarded the Nobel Prize in Physiology and Medicine in 1929, because his observations led to the discovery of vitamins. These compounds were named by Polish biochemist Casimir Funk. In 1911, Casimir Funk isolated the antineuritic substance from rice bran that he called a "vitamine" (on account of its containing an amino group). Dutch chemists, Barend Coenraad Petrus Jansen (1884–1962) and his closest collaborator Willem Frederik Donath (1889–1957), went on to isolate and crystallize the active agent in 1926,[62] whose structure was determined by Robert Runnels Williams (1886–1965), a US chemist, in 1934. Thiamine (“sulfur-containing vitamin”) was synthesized in 1936 by the same group.[63]

Thiamine was first named "aneurin" (for anti-neuritic vitamin).[64] Sir Rudolph Peters, in Oxford, introduced thiamine-deprived pigeons as a model for understanding how thiamine deficiency can lead to the pathological-physiological symptoms of beriberi. Indeed, feeding the pigeons upon polished rice leads to an easily recognizable behavior of head retraction, a condition called opisthotonos. If not treated, the animal will die after a few days. Administration of thiamine at the stage of opithotonos will lead to a complete cure of the animal within 30 min. As no morphological modifications were observed in the brain of the pigeons before and after treatment with thiamine, Peeters introduced the concept of biochemical lesion.[65]

When Lohman and Schuster (1937) showed that the diphosphorylated thiamine derivative (thiamine diphosphate, ThDP) was a cofactor required for the oxydative decarboxylation of pyruvate,[66] (a reaction now known to be catalyzed by pyruvate dehydrogenase), the mechanism of action of thiamine in the cellular metabolism seemed to be elucidated. At present, this view seems to be oversimplified: Pyruvate dehydrogenase is only one of several enzymes requiring thiamine diphosphate as a cofactor; moreover, other thiamine phosphate derivatives have been discovered since then, and they may also contribute to the symptoms observed during thiamine deficiency.

Finally, the mechanism by which the thiamine moiety of ThDP exerts its coenzyme function by proton substitution on position 2 of the thiazoliumring was elucidated by Ronald Breslow in 1958.[67]

See also

References

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  11. Jump up^  Bocobza, Samuel; Aharoni, Asaph (2008). "Switching the light on plant riboswitches". Trends in Plant Science13 (10): 526–533. doi:10.1016/j.tplants.2008.07.004PMID 18778966.
  12. Jump up^  Food Standards Australia - Addition of vitamins and minerals to food. Also see Standard 2.1.1 - Cereal Products.
  13. Jump up^  Tolerable Upper Intake Levels For Vitamins And Minerals (PDF), European Food Safety Authority, 2006
  14. Jump up^  Thiamine. IN: Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline. National Academy Press. 1998, PP.58-86.
  15. Jump up^  McGuire, M. and K.A. Beerman. Nutritional Sciences: From Fundamentals to Foods. 2007. California: Thomas Wadsworth.
  16. Jump up^  Hayes KC, Hegsted DM. Toxicity of the Vitamins. In: National Research Council (U.S.). Food Protection Committee. Toxicants Occurring Naturally in Foods. 2nd ed. Washington DCL: National Academy Press; 1973.
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  18. Jump up^  Molecular mechanisms of the non-coenzyme action of thiamin in brain: biochemical, structural and pathway analysis : Scientific Reports
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  20. Jump up^  Makarchikov AF, Lakaye B, Gulyai IE, Czerniecki J, Coumans B, Wins P, Grisar T, Bettendorff L (2003). "Thiamine triphosphate and thiamine triphosphatase activities: from bacteria to mammals". Cell. Mol. Life Sci60(7): 1477–1488. doi:10.1007/s00018-003-3098-4PMID 12943234.
  21. Jump up^  Lakaye B, Wirtzfeld B, Wins P, Grisar T, Bettendorff L (2004). "Thiamine triphosphate, a new signal required for optimal growth of Escherichia coli during amino acid starvation". J. Biol. Chem279 (17): 17142–17147. doi:10.1074/jbc.M313569200PMID 14769791.
  22. Jump up^  Bettendorff L, Wirtzfeld B, Makarchikov AF, Mazzucchelli G, Frédérich M, Gigliobianco T, Gangolf M, De Pauw E, Angenot L, Wins P (2007). "Discovery of a natural thiamine adenine nucleotide". Nature Chemical Biology3 (4): 211–212. doi:10.1038/nchembio867PMID 17334376.
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  24. Jump up^  "Thiamin", Jane Higdon, Micronutrient Information Center, Linus Pauling Institute
  25. Jump up to:a b c d e Butterworth RF. Thiamin. In: Shils ME, Shike M, Ross AC, Caballero B, Cousins RJ, editors. Modern Nutrition in Health and Disease, 10th ed. Baltimore: Lippincott Williams & Wilkins; 2006.
  26. Jump up^  Thornalley PJ (2005). "The potential role of thiamine (vitamin B(1)) in diabetic complications". Curr Diabetes Rev1 (3): 287–98. doi:10.2174/157339905774574383PMID 18220605.
  27. Jump up^  Diabetes problems 'vitamin link'BBC News, 7 August 2007
  28. Jump up^  Spinazzi M, Angelini C, Patrini C. Subacute sensory ataxia and optic neuropathy with thiamine deficiency. Nature Reviews Neurology. 2010;6:288-93
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  34. Jump up^  For an interesting discussion on thiamine fortification of foods, specifically targetting beer, see "Wernicke's encephalopathy and thiamine fortification of food: time for a new direction?"Medical Journal of Australia.
  35. Jump up^  Butterworth RF, Gaudreau C, Vincelette J, et al. (1991). "Thiamine deficiency and wernicke's encephalopathy in AIDS". Metab Brain Dis6 (4): 207–12. doi:10.1007/BF00996920PMID 1812394.
  36. Jump up^  Harper C. (1979). "Wernicke's encephalopathy, a more common disease than realised (a neuropathological study of 51 cases)"J Neurol Neurosurg Psychol42 (3): 226–231. doi:10.1136/jnnp.42.3.226PMC 490724Freely accessiblePMID 438830.
  37. Jump up^  McCollum EV A History of Nutrition. Cambridge, MA: Riverside Press, Houghton Mifflin; 1957.
  38. Jump up^  Butterworth RF (1993). "Pathophysiologic mechanisms responsible for the reversible (thiamine-responsive) and irreversible (thiamine non-responsive) neurological symptoms of Wernicke's encephalopathy". Drug Alcohol Rev12(3): 315–22. doi:10.1080/09595239300185371PMID 16840290.
  39. Jump up^  Rindi G, Imarisio L, Patrini C (1986). "Effects of acute and chronic ethanol administration on regional thiamin pyrophosphokinase activity of the rat brain". Biochem Pharmacol35 (22): 3903–8. doi:10.1016/0006-2952(86)90002-XPMID 3022743.
  40. Jump up^  Merck Veterinary Manual, ed 1967, pp 1440-1441.
  41. Jump up^  R.E. Austic and M.L. Scott, Nutritional deficiency diseases, in Diseases of poultry, ed. by M.S. Hofstad, Iowa State University Press, Ames, Iowa, USA ISBN 0-8138-0430-2, p. 50.
  42. Jump up^  The disease is described more carefully here: merckvetmanual.com
  43. Jump up^  National Research Council. 1996. Nutrient Requirements of Beef Cattle, Seventh Revised Ed. Washington, D.C.: National Academy Press.
  44. Jump up^  Polioencephalomalacia: IntroductionMerck Veterinary Manual
  45. Jump up^  Polioencephalomacia: Introduction, "ACES Publications"
  46. Jump up to:a b Balk, L; Hägerroth, PA; Akerman, G; Hanson, M; Tjärnlund, U; Hansson, T; Hallgrimsson, GT; Zebühr, Y; Broman, D; Mörner, T.; Sundberg, H.; et al. (2009). "Wild birds of declining European species are dying from a thiamine deficiency syndrome"Proc Natl Acad Sci U S A106 (29): 12001–12006. doi:10.1073/pnas.0902903106PMC 2715476Freely accessiblePMID 19597145.
  47. Jump up^  Blekinge län, Länsstyrelsen (2013). "2012-04-15 500-1380-13 Förhöjd dödlighet hos fågel, lax og älg" (PDF).
  48. Jump up^  Bettendorff L, Peeters M, Jouan C, Wins P, Schoffeniels E (1991). "Determination of thiamin and its phosphate esters in cultured neurons and astrocytes using an ion-pair reversed-phase high-performance liquid chromatographic method". Anal. Biochem198 (1): 52–59. doi:10.1016/0003-2697(91)90505-NPMID 1789432.
  49. Jump up^  Losa R, Sierra MI, Fernández A, Blanco D, Buesa J (2005). "Determination of thiamine and its phosphorylated forms in human plasma, erythrocytes and urine by HPLC and fluorescence detection: a preliminary study on cancer patients". J Pharm Biomed Anal37 (5): 1025–1029. doi:10.1016/j.jpba.2004.08.038PMID 15862682.
  50. Jump up^  Lu J, Frank E (May 2008). "Rapid HPLC measurement of thiamine and its phosphate esters in whole blood". Clin Chem54 (5): 901–906. doi:10.1373/clinchem.2007.099077PMID 18356241.
  51. Jump up^  Shabangi M, Sutton J (2005). "Separation of thiamin and its phosphate esters by capillary zone electrophoresis and its application to the analysis of water-soluble vitamins". Journal of Pharmaceutical and Biomedical Analysis38 (1): 66–71. doi:10.1016/j.jpba.2004.11.061PMID 15907621.
  52. Jump up^  Slater, PV (1978). "Thiamine Responsive Megaloblastic Anemia with severe diabetes mellitus and sensorineural deafness (TRMA)". The Australian nurses' journal7 (11): 40–3. PMID 249270.
  53. Jump up^  Kopriva, V; Bilkovic, R; Licko, T (Dec 1977). "Tumours of the small intestine (author's transl)". Ceskoslovenska gastroenterologie a vyziva31 (8): 549–53. ISSN 0009-0565PMID 603941.
  54. Jump up^  Beissel, J (Dec 1977). "The role of right catheterization in valvular prosthesis surveillance (author's transl)". Annales de cardiologie et d'angéiologie26 (6): 587–9. ISSN 0003-3928PMID 606152.
  55. Jump up^  Online Mendelian Inheritance in Man (OMIM) 249270
  56. Jump up^  Butterworth RF. Pyruvate dehydrogenase deficiency disorders. In: McCandless DW, ed. Cerebral Energy Metabolism and Metabolic Encephalopathy. Plenum Publishing Corp.; 1985.
  57. Jump up^  Biotin-Thiamine-Responsive Basal Ganglia Disease - GeneReviews® - NCBI Bookshelf
  58. Jump up^  Blass JP. Inborn errors of pyruvate metabolism. In: Stanbury JB, Wyngaarden JB, Frederckson DS et al., eds. Metabolic Basis of Inherited Disease. 5th ed. New York: McGraw-Hill, 1983.
  59. Jump up^  McCollum EV. A History of Nutrition. Cambridge, Mass.: Riverside Press, Houghton Mifflin; 1957.
  60. Jump up^  Eijkman, C. (1897). "Eine Beriberiähnliche Krankheit der Hühner". Archiv für pathologische Anatomie und Physiologie und für klinische Medizin148(3): 523–532. doi:10.1007/BF01937576.
  61. Jump up^  Grijns, G. (1901). "Over polyneuritis gallinarum". I. Geneesk. Tijdscht. Ned. Ind43: 3–110.
  62. Jump up^  Jansen, B.C.P.; Donath, W.F. (1926). "On the isolation of antiberiberi vitamin". Proc. Kon. Ned. Akad. Wet29: 1390–1400.
  63. Jump up^  Williams, R.R.; Cline, J.K. (1936). "Synthesis of vitamin B1". J. Am. Chem. Soc58 (8): 1504–1505. doi:10.1021/ja01299a505.
  64. Jump up^  Carpenter KJ. Beriberi, white rice, and vitamin B: a disease, a cause, and a cure. Berkeley, CA: University of California Press; 2000
  65. Jump up^  Peters, R.A. (1936). "The biochemical lesion in vitamin B1deficiency. Application of modern biochemical analysis in its diagnosis". Lancet1(5882): 1161–1164. doi:10.1016/S0140-6736(01)28025-8.
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  67. Jump up^  Breslow R (1958). "On the mechanism of thiamine action. IV.1 Evidence from studies on model systems". J Am Chem Soc80 (14): 3719–3726. doi:10.1021/ja01547a064.

External links

Source: https://en.wikipedia.org/wiki/Thiamine

PRODIGY-5

ALL IN ONE NUTRITIONAL WITH TRANS-ARMOR® NUTRIENT TECHNOLOGY

BREAKTHROUGH TECHNOLOGY IN PRODIGY 5.

THE FIVE UNIQUE ATTRIBUTES

A revolutionary new product featuring five unique attributes that create an all-in-one nutritional experience for everyone, every day. Take advantage of the technology and know-how, and enjoy the benefits of the phytoplankton, antioxidants, vitamins, and energy you can feel in minutes with the new ForeverGreen product: Prodigy-5.

Vitamins in Prodigy-5

We all know that vitamins and minerals are essential to our overall health, yet many of us are left not getting most of the vitamins and minerals we need through our normal eating habits. Prodigy-5 features a unique blend of vitamins and minerals that were each specifically chosen using the best peer reviewed scientific research available to support your general and eye health.  

Technology & Know-how behind Prodigy-5

​Adam Saucedo, M.D., has teamed up with the brilliant mind of Balamurali Ambati, M.D., PhD, MBA to bring you the exclusive TransArmor™ Nutrient Technology, found only in Prodigy-5. The patent-pending TransArmor™ technology increases the transit time of nutrients through the digestive system and primes the body for increased absorption of these nutrients.

Antioxidants in Prodigy-5

Prodigy-5 features natural pomegranate and raspberry for a bold flavor that also delivers powerful antioxidants! Antioxidants help to rid the body of damaging free radicals. Antioxidants become a powerful defense system to these free radicals, which if left unchallenged, can contribute to the cause of a range of health problems. Raspberries and pomegranates, Marine phytoplankton, Curcuma.

Phytoplankton in Prodigy-5

The most fundamental nutrient on the planet, phytoplankton are microscopic plant-based organisms that generate most of the world’s oxygen. Phytoplankton, found naturally in both salt and fresh water, are a viable source of vitamins, minerals, amino acids, and other micronutrients.

Energy of the Prodigy-5

Prodigy-5 features natural green tea extract, which is known to help increase energy and mental focus. It helps provide the alertness associated with caffeine without the jittery side effects! Green tea has a range of health benefits, and also contains powerful antioxidants, making it the perfect way to get a little extra boost with your daily dose of Prodigy-5.

PRODIGY-5 DEVELOPED BY MEDICAL INDUSTRY LEADERS

Prodigy-5 revolutionaly Trans-Armor™ nutrient technology, developed by medical industry leader doctors aids the body in absorbing more of the nutrition than it normally would, thereby increasing efficiencies and overall health.

In addition to this scientifically proven technology, Prodigy-5 is considered an all-in-one nutritional habit.

Dr. Ambati, child prodigy, and ForeverGreen’s own Research Scientist Adam Saucedo have partnered together and developed what is being called the check-mate in the conversation of nutrition, Prodigy-5.

DR. AMBATI

CHILD PRODIGY

Dr. Ambati started calculus at age 4, graduated high school at age 11, pre-med age 13, med-school at 14 and was announced the Guinness Book of World Records holder for youngest doctor at age 17.

DR. ADAM SAUCEDO

RESEARCH SCIENTIST

Dr. Adam Saucedo is ForeverGreen’s own Research Scientist, founder and Chief Medical Adviser of the Center for the Heart and Founder of the New Life Center; the largest eating disorder clinic in the world.

DID YOU KNOW THAT HUMAN STOMACH ACIDS ARE STRONG ENOUGH TO DISSOLVE A RAZOR BLADE?

This means that your stomach acids act like a wall, preventing supplements and nutrients from passing to your blood stream and cells; only a percentage survives. Plain English? Your body gets only a fraction of the nutrients it digests. So, this begs the question, Can it be changed?

Can we use modern science to get more out of the digestive process? The answer is a very exciting yes!

Prodigy-5 with the perfect micro-nutrient formula featuring “Trans-Armor Nutrient Technology” that can quickly deliver the nutrients you need throughout your entire body and has the ability to increase the absorption and utilization of those nutrients to maximize your results. With this ground-breaking technology and formula, Prodigy-5 is the solution to the global problem of malnutrition.

With today’s nutritionally bankrupt foods, and the bodies inability to absorb 100% of even the healthiest whole foods, malnutrition effects every singe one of us. Whether you are healthy, wealthy, poor or starving, every person on this planet needs the nutritional revolution offered in Prodigy-5. It is literally for EVERYONE, EVERY DAY.

Prodigy-5 delivers a new TransArmor™ Nutrition bio-enhancing technology.
See how it works:

Prodigy-5 revolutionaly Trans-Armor™ nutrient technology, developed by medical industry leader doctors aids the body in absorbing more of the nutrition than it normally would, thereby increasing efficiencies and overall health. In addition to this scientifically proven technology, Prodigy-5 is considered an all-in-one nutritional habit.

Prodigy 5 contains the new "Trans-Armor™" delivery technology that provides nutrition and energy at the highest level of absorption to our body's cells, including:

• a micronutrient formula for general health,
• a micronutrient formula for eye health,
• an impressive antioxidant profile,
• an impressive and new bio-enhancing absorption technology


Does not contain artificial sweetners or additives. Sweetened with Pomegranate, Raspberry, and Stevia.

PRODIGY-5 HIGHLIGHT

PHYTOPLANKTON

One of those rare products that contains almost everything you need for life (and the rebuilding of cells) is marine phytoplankton.

Marine phytoplankton are one-cell plants that are too small to be seen individually without the aid of a microscope. Because they are microscopic, the body’s cells can absorb them immediately (bioavailability) and receive all of their valuable nutrients at the same time for maximum effectiveness.

The marine phytoplankton, also known as a “Superfood”, is according to NASA and plenty of scientific researches the most important plant and food in the world as it provides the earth with over 90% of it’s oxygen. Marine phytoplankton is not only an important source of oxygen it is a critical food source for ocean life and apparently, for us too.

There are very few (foods) that provide all, or even most, of the raw materials to make new cells and sustain the existing ones. A complete super food, these amazing plants contain more than 90 nutrients vital for a healthy body.

It contains all nine amino acids that the body cannot make. The essential fatty acids are also present (Omega-3 and Omega-6). Further it contains the most important vitamins and mineral nutrients. For example vitamin C, H, B1, B2, B3, B6, B12, E, selenium, zinc, chromium, magnesium, calcium, nickel, iron and many more. (General informations about vitamins)

These valuable nutrients are essential for the production of healthy new cells. We all have, at one time or another, cellular or energy blockages, whether they be emotional or physical. And, among the functional ingredients identified from marine algae, natural pigments (NPs) have received particular attention.

Some benefits (but not all) of marine phytoplankton include:

Support Cardiovascular Health: The high level of antioxidants, amino acids, and high levels of omega-3 fatty acids are known to support a healthier cardiovascular system.

Promotes Healthy Skin: There are large amounts of bioflavonoids that can remove toxins from skin cells. Marine phytoplankton also contains riboflavin that reduces free radical attacks in skin cells.

Boost the Immune System: Alanine, beta-carotene, bioflavonoids, and vitamin E are all immune system enhancers found in this superfood.

Increase Energy: Marine phytoplankton detoxifies the body, and eliminates toxins from the cells. This will improve your energy and mood levels.

Stabilizes Blood Sugar Levels: Marine phytoplankton is really good for stabilizing blood sugar levels. Chromium helps to prevent and moderate against diabetes. Glutamic acids help to reduce alcohol and sugar cravings. Phenylalanine is a known sugar craving reducer.

Helps with Joint Health: Manganese helps to assist in joint mobility. Omega-6 fatty acids can relieve symptoms of arthritis. Pathogenic acid can reduce morning pain caused by arthritis. It will help a lot with joint mobility, and reducing pain and stiffness.

Liver Support: The arginine is found in this superfood and is known to help detoxify the liver.

Improves Brain Function: The high amount of omega-3 fatty acids improve brain function. The nucleic acids can enhance the memory. Phenylalanine improves mental clarity. Proline increases learning ability. Magnesium helps reduce mood swings.

More information about phytoplankton

PRODIGY-5 HIGHLIGHT

VITAMINS AND MINERALS

MICRONUTRIENT FORMULA FOR GENERAL HEALTH

Vitamin A • Vitamin C • Vitamin D • Vitamin E • Vitamin K • Vitamin B6 • Vitamin B12 • Folate • B1 (Thiamin) • B2 (Riboflavin) • B3 (Niacin)



MICRONUTRIENT FORMULA FOR EYE HEALTH

Lutein • Zeaxanthin • Copper • Zinc

Vitamins have specific role to play in the natural wear and tear of the body. There are many vitamin benefits that have a major impact on our overall health.
Vitamins are divided into two types: fat soluble and water soluble. Fat soluble vitamins (vitamin A, D, E and K) are stored in the fat tissues and liver. They can remain in the body up to six months. When the body requires these, they are transported to the area of requirement within the body with help of special carriers. Water soluble vitamins (B-vitamins and vitamin C) are not stored in the body like the fat soluble ones. They travel in the blood stream and need to be replenished everyday.


Below is a list of the 13 major vitamins and what each does for your body:

Prodigy-5 contains: Vitamin A (Beta-Carotene) is a natural antioxidant. It belongs to a class of pigments known as carotenoids which include the yellow, red and orange pigments that give many vegetables and plants their coloring. Vitamin A has been found to enhance immune system functions by supporting and promoting the activities of white blood cells as well as other immune related cells. It also helps to inhibit free radicals and their damaging effects which have been associated with arthritis, heart disease and the development and progression of malignant cells (cancer). Beta-carotene is a precursor for vitamin A (approximately 6 mg of ß-carotene = 1 mg vitamin A). Beta-carotene is best known for the body’s ability to convert it into retinal, which is essential for good vision and visual health, skin, and immune functions.
Natural sources of beta-carotene include carrots, pumpkin, sweet potato, spinach, kale, collard and turnip greens, and winter squash.

According to the National Institutes on Health, the average adult male should be getting 900mcg of vitamin C each day. Females should be getting 700mg a day. Individuals with special needs (women who are pregnant, smokers) may have different requirements and should consult their health professional.

Prodigy-5 contains: Vitamin B1 (Thiamin) is a water-soluble B-vitamin involved with many cellular functions including carbohydrates metabolism, break down of amino acids, production of certain neurotransmitters and multiple enzyme processes (through the coenzyme thiamin pyrophosphate, or TPP). Thiamin can be found in small amounts in a wide variety of foods. Pork, sunflower seeds, yeast, peas and wheat are a few examples. Very little thiamin is stored within the body and must be consumed on a regular basis. A deficiency may result in weakness, loss of appetite, nerve degeneration and irritability.

Prodigy-5 contains: Vitamin B2 (Riboflavin), like most B-vitamins, is involved in many cellular functions. Riboflavin is important in energy metabolism, folate synthesis, conversion of tryptophan to niacin and acts as important coenzymes (FAD/FMN) involved in many reactions. It can be found in liver, mushrooms, spinach, milk, eggs and grains. Because it is water-soluble, there is minimal storage of riboflavin within the body and when dietary intake is insufficient, deficiency can occur (usually accompanied with other vitamin deficiencies).

Prodigy-5 contains:Vitamin B3 (Niacin), also referred to as nicotinamide and nicotinic acid, is another water-soluble, B-vitamin involved with energy metabolism. The coenzymes of niacin (NAD/NADH/NADP/NADPH) are necessary for ATP synthesis (the body’s main energy source), synthesis of fatty acids and some hormones and the transport of hydrogen atoms. When niacin levels are low, the body can use L-tryptophan (an essential amino acid) to manufacture the vitamin. This process is not ideal, however, as it can rapidly deplete L-tryptophan in the body and take away from its other needs such as maintaining optimal levels of serotonin and melatonin. Niacin can be found in grains, liver, fish and chicken.

Prodigy-5 contains: Vitamin B6 is a water-soluble vitamin which plays a variety of important roles in numerous biological processes. Humans cannot produce vitamin B6 so it must be obtained from the diet. Adequate sources of B6 include meats (salmon, turkey, chicken) and whole grain products, such as spinach, nuts and bananas. There are three forms of vitamin B6: pyridoxal (PL), pyridoxine (PN) and pyridoxamine (PM). Pyridoxal-5′-phosphate (PLP) is the principal coenzyme form and has the most importance in human metabolism. It acts as a cofactor for many enzymatic reactions involving L-tryptophan, including L-tryptophan’s conversion to serotonin, an important neurotransmitter in the brain. Pyridoxal-5′-phosphate is also involved in other enzymatic reactions where other neurotransmitters, such as gamma-aminobutyric acid (GABA), are synthesized. This plays a critical role in the functions of the nervous system.
Regarding cardiovascular health, there is an association between low vitamin B6 intake with increased blood homocysteine levels and increased risk of cardiovascular diseases, which has been documented in several large observational studies. Vitamin B6, along with folic acid, vitamin B5, vitamin B12 and niacin, is involved in cell metabolism, enhances the immune system, supports the functions of the nervous system, aids in carbohydrate metabolism to produce energy and promotes cognitive health. Vitamin B6 is necessary for the conduction of nerve impulses, regulation of steroid hormones, catabolism of glycogen to glucose, heme synthesis, and the synthesis/ metabolism of amino acids and neurotransmitters.

Prodigy-5 contains: Vitamin B12 is a water-soluble vitamin essential for numerous processes in the body. The richest food sources of vitamin B12 include animal products such as meat, poultry and fish. It is not generally present in plant products with the exeption of peanuts and soybeans which absorb vitamin B12 from bacteria-filled nodules growing on the roots of these plants. Cyanocobalamin is the form most commonly used in supplements but it must be converted into methylcoblamin before it can join the metabolic pool and be properly utilized by the body. Vitamin B12 is also available as methylcobalamin, which is the methylated form, allowing it to become active quicker and be more effective. Vitamin B12 is necessary for countless processes within the body; it transfers methyl groups, plays a part in DNA synthesis and regulation, helps facilitate cell synthesis, maturation and division, helps convert homocysteine to methionine playing a role in cardiovascular protection, aids in the proper functioning of the nervous system, participates in the metabolism of carbohydrates, proteins and fats, helps produce SAMe for mood and cognitive health and also helps produce energy.

Prodigy-5 contains: Vitamin C (Ascorbic acid) is a water-soluble antioxidant essential for human health and life. It has been proven necessary for healthy immune responses, wound healing, non-heme iron absorption (coming from grains and vegetables), reduction in allergic responses, development of connective tissue components such as collagen, and for the prevention of diseases. Vitamin C has also been shown to be important for cardiovascular health, reducing free radicalproduction and free radical damage, and good cognitive health and performance.
Due to human’s inability to produce vitamin C, it is essential to ingest sources containing vitamin C on a regular, if not daily basis. Natural sources of vitamin C include oranges, guavas, peppers (green, red, yellow), kiwis, strawberries, cantaloupes, Brussels sprouts, broccoli, and many other fruits and vegetables.

Prodigy-5 contains: Vitamin D is a fat-soluble vitamin essential for normal growth and development, the formation and maintenance of healthy bones and teeth, and influences the absorption and metabolism of phosphorus and calcium. It is necessary for proper muscle functioning, bone mineralization and stability, and multiple immune functions. Primarily the vitamin D used by the body is produced in the skin after exposure to ultraviolet light from sunlight. Lack of exposure to sunlight, reduced ability to synthesize vitamin D in the skin, age, low dietary intake, or impaired intestinal vitamin D absorption can result in deficiency. Deficiency has been associated with rickets (poor bone formation), porous or weak bones (osteopenia, osteoporosis), pain and muscle weakness, increased risk for cardiovascular disease, impaired cognitive health, and the development and progression of malignant cells (cancer).
Natural food sources of vitamin D are few; these foods are eggs from hens that have been fed vitamin D or fatty fish such as herrings, mackerel, sardines and tuna. Due to low vitamin D levels, countries such as the United States and Canada have opted to fortify foods such as milk and other dairy products, margarines and butters, some natural cereal and grain products.
According to the National Institutes on Health, the average adult should be getting 600IU of vitamin D each day. Individuals with special needs (the elderly, women who are pregnant) may have different requirements and should consult their health professional.

Prodigy-5 contains: Vitamin E is one of the most powerful fat-soluble antioxidants in the body. It has been proven to help promote cardiovascular health, enhanced immune system function, aid in skin repair and to protect cell membranes from damage caused by free radicals. Vitamin E contributes to proper blood flow and clotting as well as cognitive health and function.
Natural sources of vitamin E include herbs such as cloves and oregano, whole grains, nuts and seeds, wheat germ, avocado, egg yolks, and vegetables/fruits such as dark leafy greens, peppers (red, yellow, orange, green), tomatoes, and mangos. Other sources are vegetable oils, margarines, and fortified cereals.

Prodigy-5 contains: Folic Acid is water-soluble vitamin important for many aspects of health. Sources of folic acid include dark, green leafy vegetables such as spinach or asparagus, fortified cereals, orange juice and legumes. Folic acid (folate) must go through a series of chemical conversions before it becomes metabolically active to be properly utilized within the body.
Folinic acid is the highly bioavailable, metabolically active derivative of folic acid and does not require the action of the enzyme dihydrofolinate reductase to become active, so it’s not affected by medicines and herbs that inhibit this enzyme. Adequate folate is necessary for proper DNA and RNA synthesis in regards to fetal growth and development. Due to these effects, the U.S. Public Health Service recommends all women capable of becoming pregnant consume 400 mcg of folic acid daily to prevent neural tube defects.
In addition to its clear effects on fetal growth and development, folic acid also plays an important role in cardiovascular health. By aiding in the conversion of homocysteine to methionine, it has been shown to reduce the levels of homocysteine, a sulfur containing amino acid. In the absence of adequate folic acid levels, homocysteine levels increase and high homocysteine levels are associated with atherosclerosis and the reduced circulation of oxygen and nutrients to the heart, ears and other organs. These results have been documented in countless studies. Folic acid, along with vitamin B6, vitamin B5, vitamin B12 and niacin, is involved in cell metabolism, enhances the immune system, supports the functions of the nervous system, aids in carbohydrate metabolism to produce energy and promotes cognitive health.

Prodigy-5 contains: Vitamin K, a generic term for a group of fat soluble vitamins, are involved mostly in the process of blood clotting, but also needed in metabolic pathways of bones and other tissues. The most well known are vitamin K1, also known as phylloquinone, and vitamin K2, known as menaquinone. Vitamin D and vitamin K work together in bone metabolism and development. Vitamin K works against oral anticoagulants such as 4-hidroxikumarin, and excessive vitamin K intake, either through supplementation or a change in diet, can reduce the anticoagulant effect. Vitamin K1 is mainly found in leafy green vegetables (such as spinach, swiss chard and kale), avocado and kiwi fruit; vitamin K2 can be found in meat, eggs, and dairy and is also synthesized by bacteria in the colon.

More information about vitamins

PRODIGY-5 HIGHLIGHT

ANTIOXIDANTS


WHAT ARE OXIDANTS?

Oxidants are free radicals that either our bodies produce or we get from the environment. Our bodies create oxidants as a response to stress or poor diet, or we are exposed to oxidants through environmental factors like pollution. Oxidative damage is a contributing factor to many diseases, including muscle and tissue degeneration, heart disease, diabetes, cancer, and many other health problems.


WHAT ARE FREE RADICALS?

Free radicals are atoms or groups of atoms with an odd (unpaired) number of electrons. They are like bullies that are low in energy and attack healthy cells and steal their energy to satisfy themselves. Free radicals cause damage to our blood vessels, which can lead to deposits of bad cholesterol and block arteries. Free radicals come in many shapes, sizes, and chemical configurations. What they all share is a voracious appetite for electrons, stealing them from any nearby substances that will yield them.

The human body naturally produces free radicals and the antioxidants to counteract their damaging effects. However, in most cases, free radicals far outnumber the naturally occurring antioxidants. In order to maintain the balance, a continuous supplemental source of external antioxidants are necessary in order to obtain the maximum benefits of antioxidants.


WHAT ARE ANTIOXIDANTS AND WHY DO WE NEED THEM?

Antioxidants are the nutrients’ police force! They are free radical scavengers! They get rid of the bullies! Antioxidants are like a million microscopic special ops on a mission to save your body from the inside out. The benefits of antioxidants are very important to good health, because if free radicals are left unchallenged, they can cause a wide range of illnesses and chronic diseases.

WHERE CAN WE FIND ANTIOXIDANTS?

Obtained through our foods and produced by are bodies, antioxidants are a powerful defense system.
Antioxidants can be found in flavonols (found in chocolate), resveratrol (found in wine), Ellagic acid (found in Raspberries and pomegranate), and lycopene (found in tomatoes). Other popular antioxidants include vitamins A (beta-carotene), C, E, and catechins.

GREAT SOURCES OF ANTIOXIDANTS IN PRODIGY-5

Marine phytoplankton, Raspberries, Pomegranates, Curcuma

Raspberries and pomegranates contain one of the most powerful antioxidants known, Ellagic acid. Ellagic acid is a potent natural antioxidant that can be found in raspberries and pomegranates. Ellagic acid has been shown to be an effective anti- mutagen and anti-carcinogen.

Anthocyanins (red flavonoid pigment found in plants) give pomegranates their red color and offer a strong serving of antioxidants. Punicalagins (a type of phenolic compound) specifically support cardiovascular and neurological health. Studies have shown that antioxidants 18. can play a role in reducing the cell damage of free radicals.

ANTIOXIDANTS AND AGING

Antioxidants are powerful molecules that support healthy aging in more ways than one. These potent compounds aid in an overall healthy lifestyle by supporting cellular health. Aging isn’t about your chronological age; it is more about the amount of stress in your life and the the function of your cells!

More information about antioxidants

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PRODIGY 5 PRICES


PRODIGY-5 Single Case
(One case contains 28 serving) prices
$ 75.95
€ 69.11
Prodigy 5 Single DEF small

PRODIGY-5 Double Case 
(One case contains 28 serving) prices
$ 149.95
€ 136.45
Prodigy 5 Double DEF small

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