The following page explains B1 Thiamine. IV League provides B1 Thiamine IV Therapy.
Vitamin B1 is thiamine. Foods including cereals, entire grains, meat, nuts, beans, and peas all contain thiamine. The conversion of food’s carbohydrates into the substances the body needs is facilitated by thiamine. Vitamin B1 deficiency is treated or prevented using thiamine.
Beriberi is a dangerous disorder brought on by a protracted deficiency of vitamin B1 and is treated by thiamine injection. The body can use carbohydrates as fuel thanks to vitamin B1, often known as thiamine. It is crucial for the metabolism of glucose and is important for the health of the heart, muscles, and nerves.
Due to its water-soluble nature, vitamin B1 dissolves in cooking liquid. It was the first vitamin B family member to be isolated in 1926. Thiamine, a cofactor of vitamin B1, is essential for the health of the heart, muscles, and nerves. It also makes it possible for our body to use carbs as fuel. The half-life of thiamin is brief.
Because the liver only stores a little amount of thiamin, our bodies require a regular intake of thiamin-rich meals. The physiologically active form of thiamin is thiamin diphosphate or thiamin pyrophosphate. Thiamine is used by every living thing, but only plants, bacteria, and fungi are able to produce it.
Thiamine is a vitamin that is destroyed by heat, hence cooking reduces the amount of thiamine in the food. Additionally, some dietary practices, such as excessive coffee or tea consumption and consumption of uncooked fish and shellfish, might lower the body’s capacity to utilize thiamine, leading to inadequate thiamine intake.
Even though thiamin insufficiency symptoms were first mentioned in ancient Chinese medical books, it wasn’t until the late 19th century that they were linked to food. A Japanese doctor observed in 1884 that Japanese sailors who consumed a restricted diet of nothing but rice for months at sea had extremely high rates of disease and mortality.
Rates of disease and death almost completely disappeared when they were fed a more varied diet that included entire grains, meats, beans, and vegetables. The same period saw the discovery by two Dutch researchers that birds fed white polished rice experienced leg paralysis whereas those given brown unpolished rice did not.
Their research revealed that thiamin was present in the outer layers of rice that were polished off. A lack can cause a number of issues in the heart and brain that need a constant flow of energy.
Three of the most important physiological pathways involving thiamine are as follows: the body’s conversion of carbs into energy, and Neurotransmitter synthesis, including that of acetylcholine the defense of the nervous system and the brain.
Thiamin is absorbed by the small intestine through active transport at nutritional dosages and through passive diffusion at pharmacologic concentrations when it is consumed through food and dietary supplements.
The majority of dietary thiamin is found in phosphorylated forms, and before the vitamin is absorbed, intestinal phosphates hydrolyze these forms to produce free thiamin. Dietary thiamin that is still present is in a free (absorbable) form. Although in extremely minute concentrations, thiamin is largely stored in the liver in humans.
Due to the vitamin’s brief half-life, humans need to consume it continuously through their diets.
The predominant metabolically active form of thiamin is thiamin diphosphate (TDP), which accounts for around 80% of the about 25–30 mg of thiamin found in an adult human body.
Although it is also known that bacteria in the large intestine produce free thiamin and TDP, it is not yet understood how much of an impact they may have on thiamin nutrition. Five enzymes involved in the metabolism of glucose, amino acids, and lipids require TDP as a cofactor in order to function.
Blood thiamin levels are not accurate predictors of thiamin status. By comparing the activity of the TDP-dependent transketolase enzyme in erythrocyte hemolysates in the presence and absence of additional TDP, thiamin status is frequently indirectly assessed.
The outcome, also referred to as the “TDP effect,” displays how much transketolase was created when TDP was present. The outcome ranges from 0% to 15% in healthy individuals, from 15% to 25% in those who have a minor insufficiency, and from more than 25% in those who have a deficiency.
Urinary thiamin excretion is another frequently used indicator of thiamin status; it gives information on dietary intakes but not tissue storage. Adults who excrete less than 100 mcg of thiamin per day and less than 40 mcg per day have extremely low levels of thiamin intake.
The databases Medline, PubMed, and Embase were electronically searched for original publications published in peer-reviewed journals. We looked for published thiamine compound analysis techniques using MethodsNow. The terms “thiamine and its phosphate esters,” “thiamine technique,” and words referring to critical disease were used as keywords across all databases.
Additionally, inquiries on the inclusion of thiamine measurement were addressed to six external quality assurance (EQA) programme organizations.122 of the 777 recognized published articles were used in this review. HPLC with florescence detection is the most often used documented method. Of the six EQA organizations, two solely measure whole-blood thiamine pyrophosphate as part of their thiamine measurement programmes (TPP).
There was no established standard measurement technique for quantifying thiamine compounds. In general, measuring techniques for thiamine in clinical care are not standardized. As a result, because there are numerous variations in method practices, it is impossible to compare study outcomes because they cannot be linked to any higher order reference.
To offer a link between investigations and aid in reaching agreement on the therapeutic significance of thiamine, traceability of verified reference materials and reference measurement techniques is required.
Benefits of B-1 Thiamine IV Therapy
The body’s most crucial metabolic activities include thiamine (protein, fat and water-salt). It restores the neurological, cardiovascular, and gastrointestinal systems to normal function. Blood production, brain function, and circulation are all influenced by vitamin B1. Taking thiamine increases hunger and tones the heart and intestines.
B1 Thiamine IV aids in the battle against improper metabolism
Thiamine enhances brain function, memory, attention, and thinking. It also improves mood, increases learning capacity, stimulates bone and muscle growth, normalizes appetite, slows the ageing process, reduces the negative effects of alcohol and tobacco, maintains digestive tract muscle tone, eliminates motion sickness and seasickness, and soothes toothaches. IV Vitamin B1 is essential for nerve function, as well as for having healthy skin, hair, muscles, and the brain.
B1 Thiamine IV prevents heart diseases
This vitamin aids in the synthesis of the neurotransmitter acetylcholine, which is necessary for the healthy functioning of the heart and for transmitting signals between the nerves and muscles. As a result, vitamin B1 insufficiency may cause abnormal heart functioning. People with congestive heart failure exhibited significant improvements on their echocardiograms after receiving vitamin B1 intravenously for seven days, demonstrating its potential to prevent heart disease.
B1 Thiamine prevents lactic acidosis, gastrointestinal dysfunction & Delirium
For four enzymes involved in the creation of vital cellular components and the production of energy (ATP), thiamine is a crucial cofactor. Thiamine deficiency can occur in individuals as a result of poor nutrition, alcohol use problems, increased urine excretion, and acute metabolic stress because the overall amount of thiamine in the body is relatively low. Thiamine deficiency can occur in people having surgery and is frequently present in sepsis patients. Congestive heart failure, peripheral neuropathy, Wernicke’s encephalopathy, Korsakoff’s syndrome, and gastrointestinal beriberi can all result from this insufficiency. Additionally, issues associated with intensive care units include disorientation, critical care neuropathy, gastrointestinal dysfunction, and unexplained lactic acidosis can be exacerbated by thiamine deficiency.
Vitamin B1 acts as an energy booster
Vitamin B1 and sugar combine to create energy that your body can utilize. B1 supports the other enzymes while speeding up this process.
Vitamin B1 prevents depression
Combining vitamin B1 pills and an antidepressant is beneficial for treating depression. Mood stabilization and speedier symptom relief are both benefits of vitamin B1. Low moods have also been connected to vitamin B1 deficiency.
Vitamin B1 prevents sepsis
If your vitamin B1 levels are low, sepsis, a serious reaction to an infection, could be fatal. Thiamine can lessen sepsis’s effects in addition to vitamin C.
Vitamin B1 treats diabetes
Take additional thiamine into consideration if you have diabetes. Studies have shown that taking vitamin B1 for six weeks lowers insulin and high blood sugar levels. B1 also aids in lowering high blood pressure and cardiac issues in diabetics. B1 and B12 supplements can aid diabetics with nerve discomfort and may lessen the need for medicines.
History of B-1 Thiamine IV
When investigating how rice bran treated beriberi patients, Umetaro Suzuki in Japan made the first discovery of thiamine in 1910. He gave it the name aberic acid. Suzuki failed to ascertain either its chemical make-up or that it was an amine. Jansen and Donath crystallised thiamine for the first time in 1926. (They dubbed it aneurin, after antineuritic vitamin). Robert R. Williams described thiamine’s chemical make-up and synthesis for the first time in 1935. Additionally, he gave it the name thiamin. Thiamine monophosphate (ThMP), thiamine diphosphate (ThDP), thiamine triphosphate (ThTP), and the recently identified adenine thiamine triphopshate are the four natural thiamine phosphate derivatives that are currently recognised (AThTP). The enzymes pyruvate dehydrogenase, -ketoglutarate dehydrogenase, branched-chain alpha-keto acid dehydrogenase, 2-hydroxyphytanoyl-CoA lyase, and transketolase all require the coenzyme thiamine diphosphate (ThDP) or thiamine pyrophosphate (TPP) to function. While the first two of these enzymes work in the metabolism of carbohydrates, transketolase creates NADPH and the pentose sugars deoxyribose and ribose through the pentose phosphate pathway. Similar to how ribose plays similar job in RNA, deoxyribose is the sugar component of DNA (ribonucleic acid). Pyruvate decarboxylase in yeast and a number of bacterial enzymes both require ThDP as a cofactor. TPP serves as a cofactor for enzymes that catalyse the dehydrogenation of alpha-keto acids (decarboxylation and subsequent conjugation to Coenzyme A). Thiamine pyrophosphokinase, an enzyme that produces TPP, needs free thiamine, magnesium, and adenosine triphosphate (ATP). For a long time, thiamine triphosphate (ThTP) was thought to be a particularly neuroactive type of thiamine. Recently, though, it was shown that ThTP is present in bacteria, fungi, plants, and animals, pointing to a far more universal biological function. It appears to be important in Escherichia coli’s response to amino acid deprivation. E has recently been found to contain adenosine thiamine triphosphate (AThTP), also known as thiaminylated adenosine triphosphate. coli, where it gathers as a result of a lack of carbon. In E. coli, AThTP may make up as much as 20% of the total thiamine. Additionally, it can be found in smaller concentrations in yeast, higher plant roots, and animal tissues.
The thiamin deficiency disease that affects the peripheral nervous system, known as beriberi, has been known sporadically for nearly 1300 years. However, in the nineteenth century, when the steam-powered rice mill was invented and highly milled (polished) rice became more widely consumed, beriberi became a significant public health issue in the Far East. It was found that the component of the rejected polishing that prevented the sickness was thiamin. Even though it has been mostly eradicated, beriberi still affects persons whose diets are particularly heavy in carbs in some regions of the world. Thiamin insufficiency also contributes to the Wernicke-Korsakoff syndrome, a separate illness that affects the central nervous system as opposed to the peripheral nervous system. It happens in developed countries, particularly among drinkers and drug users.
Thiamin was the first vitamin to be shown to have a distinct metabolic role as a coenzyme; in fact, experiments conducted by Peters’ group in the 1920s and 1930s laid the groundwork for current metabolic biochemistry as well as neurochemistry. Despite this, the exact mechanism by which thiamin shortage causes lesions in the central and peripheral nervous systems is still unknown. This is despite the fact that thiamin, in addition to its well-known coenzyme function, also controls the activity of a chloride transporter in nerve cells.
Mechanisms of Action for B-1 Thiamine IV
Thiamin is a water-soluble vitamin that enters the bloodstream through the digestive system. After then, it travels through the blood and is eventually eliminated through urination. The liver, heart, kidney, and brain all store trace amounts of thiamin, but only temporarily.
Thiamin is transformed into its active form, thiamin pyrophosphate, in the blood by the enzyme thiamin diphosphokinase (TPP). TPP has a variety of functions throughout the Krebs cycle, pentose phosphate pathway, and glycolysis phases of metabolism.
1. TPP interacts with enzyme processes involved in the metabolism of branched-chain amino acids, lipids, and carbohydrates.
2. TPP participates in a number of processes of carbohydrate oxidative decarboxylation and glycolysis as a cofactor.
3. For mitochondrial enzyme complexes like pyruvate dehydrogenase and -ketoglutarate dehydrogenase, TPP functions as a coenzyme. Both the Krebs cycle and the tricarboxylic acid cycle depend heavily on these enzymes. Lack of thiamin affects the ability of these enzymes to convert lactate into pyruvate, which causes a buildup of lactic acid. Lactic acidosis may result in localized damage to specific brain regions, such as the posteromedial thalamus and mamillary bodies, which can be observed on an MRI.
The decreased nicotinamide adenine dinucleotide phosphate from TPP is necessary for numerous synthetic routes and is required by the erythrocyte transketolase enzyme throughout the pentose phosphate pathway of nucleotide synthesis.
Thiamine is considered to affect endothelial cells by a process that reroutes the glycolytic flux to lessen intracellular protein glycation. Thiamine is primarily the vitamin’s transport form, whereas phosphorylated thiamine derivatives are its active forms. Thiamine monophosphate (ThMP), thiamine diphosphate (ThDP), also known as thiamine pyrophosphate (TPP), thiamine triphosphate (ThTP), and thiamine triphosphate (AThTP), are natural thiamine phosphate derivatives that operate as coenzymes in addition to their own biological activities.
How is B-1 Thiamine IV Therapy Used to Treat Medical Conditions?
IV B-1 Thiamine is used to treat Anemia
An additional B vitamin is folic acid, generally known as folate. Megaloblastic anemias include those brought on by a deficiency of folate or vitamin B12, respectively. With these types of anemia, the red blood cells don’t develop normally. They are very large. And they are shaped like an oval, not round like healthy red blood cells. This causes the bone marrow to make fewer red blood cells. In some cases the red blood cells die sooner than normal.
IV B-1 Thiamine is used to prevent Wernicke-Kosakoff’s syndrome or Beriberi
This is a neurological disorder also known as beriberi. Background There are two clinical manifestations of beriberi caused by thiamine (vitamin B1) deficiency. Patients with wet beriberi present with heart failure, with or without neuropathy, while those with dry beriberi present with neuropathy. The most prevalent form of Guillain-Barre syndrome (GBS), an acute inflammatory demyelinating polyradiculoneuropathy, can be confused with dry beriberi (AIDP). Wernicke’s encephalopathy is the result of a severe thiamine shortage. This article comprises a literature review and describes a case of dry beriberi and Wernicke’s encephalopathy brought on by thiamine deficiency. A 56-year-old lady who had had total parenteral nutrition for six months prior to receiving treatment for protein-calorie deficiency and gallstone pancreatitis (TPN).
She initially went to another hospital with paresthesia in her neck, arms, and lower limbs as well as encephalopathy symptoms. Based on the results of the magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) tests, the initial diagnosis of GBS was made.
Her encephalopathy worsened after receiving IVIG treatment for five days, necessitating transfer to our hospital where she needed to be intubated and given vasopressor therapy. Her brain’s second MRI revealed alterations compatible with Wernicke’s encephalopathy. Her mental state improved after receiving therapy with high-dose intravenous thiamine within 48 hours, and by the third hospital day, she was no longer in need of intubation. Conclusion Thiamine deficiency-related dry beriberi symptoms and signs can resemble acute or chronic GBS symptoms. Thiamine repletion, on the other hand, results in quick clinical improvement and can stop permanent neurologic consequences, such as Korsakoff syndrome. Clinicians should take thiamine shortage into account when treating malnourished individuals who exhibit GBS symptoms and indications.
IV Vitamin B-1 prevents fatigue (tiredness)
Depending on how severe the deficiency is, fatigue (tiredness) can be a sign of thiamine deficiency and may appear suddenly or develop over time. According to other reports, weariness might start to emerge just a few weeks after a deficiency. Given the function of thiamine in turning food into energy, this symptom makes sense. The body cannot produce as much energy to use as fuel if there is not enough thiamine present. Numerous studies have connected weariness to thiamine deficiency, despite the fact that it is a common symptom that can signify a number of other medical issues. In fact, some studies advise prioritizing weariness when identifying early indicators of thiamine insufficiency in individuals at risk for it.
Intravenous Vs. Oral Supplementation
When the oral form of the drug cannot be used or would not function as effectively as the injection, intravenous medication is used to treat or prevent a shortage of thiamine (deficiency). Thiamine aids in the body’s utilization of carbohydrates as fuel. Additionally, it is crucial for the healthy operation of your heart, muscles, and nervous system. The majority of people consume enough thiamine, although some medical situations (such as drunkenness, poor nutrition, pregnancy, stomach/intestinal illnesses) might result in a thiamine shortage. In accordance with your doctor’s instructions, intravenous medication is injected into a muscle or vein. Your medical condition and treatment response will determine your dosage. Learn all preparation and administration instructions from your healthcare provider before administering this medication to yourself at home. Before using, visually inspect the product for any flecks or discoloration. The liquid should not be used if either is present. Learn proper disposal and storage practices for medical materials.
Thiamin’s RDI for adults is 1.1 mg for women and 1.2 mg for men per day. The recommended daily intake (RDI) of thiamin for children is 0.2 mg/day throughout early infancy and then gradually rises with age. Women who are expecting should up their thiamin intake to 1.4 milligrammes per day. The average daily thiamin consumption for kids in the US is 1.27 mg, 1.54 mg, and 1.68 mg for those who are 2 to 5 years old, 6 to 11 years old, and 12 to 19 years old, respectively.
The average daily thiamin intake for men and women over the age of 20 is 1.95 mg and 1.39 mg, respectively. Adult enteral formula has 2.2 to 2.9 mg of thiamin per 1500 kcal/day of feed, compared to 3 to 3.5 mg in parenteral multivitamins. Thiamine consumption should range from 1.2 mg to a maximum of 10 mg per day, according to the American Society for Parenteral and Enteral Nutrition.
Thiamin can be given intravenously (IV), intramuscularly (IM), or enterally (E). In patients without access to an IV, the oral route is advised. Wernicke encephalopathy has historically been prevented and treated with thiamin hydrochloride (WE). However, there is not enough data to recommend a specific route, dosage, or length of treatment for Wernicke encephalopathy. In clinical practise, parenteral thiamin of 100 mg and 200 mg three times per day, respectively, has been used for individuals who are at risk of deficiency or who have a confirmed deficiency.
It should be administered before to eating, and following the necessary thiamin dosage, a nutritionally sound diet should be started. The supplementation can switch to the oral route with a dose range of 50 to 100 mg per day after the clinical symptoms go better.
Oral intake of vitamin b-1 through natural sources include fish, flax seeds, navy beans, green peas, brown rice, acorn squash, asparagus.
Molecular Structure of B-1 Thiamine IV
The molecular formula of IV Thiamine is C12H17CIN4OS and its molecular weight is 265.36.
The IUPAC name of IV Thiamine is 2-[3-[(4-amino-2-methylpyrimidin-5-yl)methyl]-4-methyl-1,3-thiazol-3-ium-5-yl]ethanol.
The molecular structure of IV Thiamine is given below: