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Symptoms of Thiamine Deficiency

Symptoms of Thiamine Deficiency

Symptoms of Thiamine Deficiency : All the tissues in our body requires one essential nutrient which is basically known to be thiamine also called as thiamin or vitamin B1, “reassurance of the spirit” is called as thiamine.

Thiamin vitamin is found in food and is manufactured as a medication and also as a dietary supplement, some of the food sources of thiamin includes legumes, whole grains, some meat products and fish.

The processing of grains removes the most of the thiamine content and many people from many countries prefer to cereals and flours that are completely enriched with thiamine.

Thiamine deficiency :

Thiamine deficiency is one of the most common disease that is found among the people who are substituting on white rice and highly refined foods with rich contents of carbohydrates in developing countries and among alcoholics.

Symptoms for thiamine deficiency may include high output heart failure, diffuse polyneuropathy, and Wernicke-Korsakoff syndrome, thiamin is given to the patient in order to help diagnose and also to treat the deficiency.

Causes of thiamine deficiency:

Etiology is one of the primary deficiencies causes which is the main reason for the inadequate intake of the thiamin content.

It occurs commonly due to the intake of the high refined carbohydrates like preferring mostly polished rice, wheat flour, white sugar and others which are rich in carbohydrates.

It also starts developing due to the intake of other nutrients in inadequate amounts as this may occur in young adults with severe anorexia, which often occurs in deficiencies of vitamin B.

Secondary thiamine deficiency can be due to the increased demand like hypo thyroids, lactation, strenuous exercise, and fever, impaired absorption which is due to the prolonged diarrhea, impaired metabolism which is due to the hepatic insufficiency.

In alcohols many mechanisms can contribute to thiamine deficiency which can include decreased intake of impaired absorption and usage and also due to the increase demand and apoenzyme defect.


Thiamine deficiency leads to degeneration of peripheral nerves, mammillary bodies, thalamus and cerebellum, cerebral blood flow is markedly reduced and increase in vascular resistance can be seen.

The dilation in heart can be seen and muscle fibers becomes swollen, vacuolized and fragmented with the interstitial spaces dilated by the fluid. Edema occurs in legs and feet due to the occurrence of vasodilation.

Arteriovenous shunting of blood increases and gradually high-output failure of heart occurs due to the deficiency of thiamine.

Symptoms and signs of deficiency in thiamine:

Early symptoms are told to be non-specific and irritability, fatigue, poor memory, disturbances in sleep, precordial pains, and abdominal discomfort may occur.

Different forms of beriberi cause different symptoms like dry beriberi which refers to the peripheral neurologic deficits that occurs due to the deficiency of thiamine.

These deficits are generally bilateral and roughly symmetric which can ultimately occur in a stocking-glove distribution, they completely effect on the predominant lower extremities, beginning with the parenthesis in toes and burning feet with muscle cramps in claves and pains in legs with plantar dysesthesias.

Wernicke-Korsakoff syndrome:

This is a combination of Wernicke encephalopathy and Korsakoff psychosis, which occurs in some of the alcoholics who does not consume foods which are to be fortified with the thiamine.

It consists of psychomotor slowing, ataxia, impaired consciousness, and if in case of untreated can result in coma and death.

Cardiovascular beriberi which is a myocardial disease that occurs due to thiamin deficiency and the effects firstly starts from vasodilation, tachycardia and then a wide pulse pressure with sweating, warm skin and lactic acidosis, later the development of heart failure develops causing orthopnea and peripheral edema with pulmonary edema.

Infantile beriberi which occurs in infants usually in the age of 3 to 4 weeks and who are breastfed by the thiamine deficient mothers, sudden heart failure might also occur in these cases and deep tendon reflexes can be seen clearly.

As because thiamine is necessary for the glucose metabolism and infusions of glucose may precipitate and can also worsen symptoms of the thiamine deficient seen in people.

Thiamine deficiency can prove fatal in many cases non-specific signs includes like malaise, irritability, weight loss and also in confusion states, the well-known disorders of thiamine deficiency includes the above-mentioned symptoms and optic neuropathy. Thiamine deficiency can be seen often in alcohol misuse disorder.

History of thiamine:

Thiamin was told to be the first water-soluble vitamins that is to be described leading to the discovery of many other essential nutrients and also to the notion of the vitamin.

Since 1884 the researches are been conducted for thiamine many scientists like Takaki, umetaro, christiaan Eijkman, Gerrit grijns, Casimir funk and many worked on the vitamin B1.

Thiamin was firstly named as “aneurin” which means to be anti-neuritic vitamin by Rudolph peters and introduced thiamine-deprived pigeons which acts as a model for understanding how thiamine deficiency can lead to the symptoms of beriberi and others and what is the food that to be taken without getting effected by the thiamine deficiency.


Thiamine is told to be found in a wide variety of foods and also in processed foods like whole foods, which can contain edible seeds, legumes, rice and processed foods such as cereals breakfast which is having the highest amount of thiamine in it.

Salt thiamine mononitrate is used rather than thiamine hydrochloride for the purpose of food fortification and as the mononitrate dissolves in water it releases the nitrate in the content of about 19% of its weight and can be therefore observed as the thiamine caution.

Dietary intake of thiamine:

DRI is the full form of dietary reference intakes which is considered to be a term for a set of reference values which can be used for planning and assessing the nutrient intake of the healthy people to maintain proper health.

In united states the estimated average intake of thiamine that is generally recommended for the dietary allowances for thiamine which were been updated in 1998 by the NAM national academy of medicine.

For women it is told that 1.0 megajoule of thiamine is required to be consumed by women, children and also men the megajoule conversion is like 1 megajoule can be equal to 238.8 kilo calories and an adult can consume 2388 calories should shift and consume only 1.0 mg.

Estimated average requirement of thiamin is to meet 50% of the requirements of healthy individuals and usually used to assess the nutrient intakes of groups of people to plan nutritionally adequate diets for them and can also be used to assess the nutrient content that they are taking in.

Groups at risk of thiamine:

people with alcohol dependence are most likely to have thiamine in inadequate content, in highly industrialized countries it is told that chronic alcohol uses disorders to appear in most common cause with thiamine deficiency.

80% of the people with chronic alcoholism develops thiamin deficiency because due to the ethanol reduction in gastrointestinal absorption of thiamine, which can be stored in liver and also in thiamin phosphorylation, and also people with alcoholism tend to have inadequate intakes of essential nutrients and proteins which can also include thiamine with them.

Older adults:

20-30% of the older adult’s laboratory results tells that they are frequently affected by the thiamine deficiency and possible reasons are included like less intake of needed diet, and also combination of chronic diseases, concomitant usage of the multiple medications and also low absorption of the thiamine in natural result of aging.

People with HIV/AIDS:

People who are suffering with HIV infection are having the more chances of affected with the thiamine deficiency, and is sequel including beriberi, Wernicke-Korsakoff syndrome.

When 380 people with AIDS are tested it is proven that almost 10% are suffering with Wernicke’s encephalopathy and also experts believe that thiamine deficiency is underdiagnosed in this type of population.

The association that is between the thiamin deficiency and HIV/AIDS is due to the malnutrition as a result of the catabolic state associated with the AIDS.

People with diabetes:

Some studies have found that thiamine levels in plasm are up to 76% become lower in people suffering with type1 diabetes than in healthy people and 50-75% lower in people with type2 diabetes and other studies have shown a higher risk of thiamine deficiency in both type 1 and type 2 diabetes based on the tests that are conducted.

People done with bariatric surgery:

Bariatric surgery is done for loosing weight and is associated with some risks which can include severe thiamine deficiency due to the malabsorption of which that can lead to the beriberi and others.

A literature in 2008 reviewed and said that 84 cases of Wernicke’s encephalopathy after the surgery can result in long lasting neurologic impairments.

Health risks:

Body excretes excess of thiamine through urine and because of lack of lack of reports that can tell effects of high thiamine intakes 50mg per day in the form of food and supplements, FNB never established Uls for thiamine and they hypothesize that the apparent lack of toxify may be excessive intake of thiamine resulting in all other adverse effects.

Although thiamine is not known to get into interactions with any medications certain medications in specific have some effects on thiamin levels.

Furosemide which is a loop diuretic and is used to treat edema and hypertension by increasing the urinary output and research has used the link in use of furosemide to decrease in thiamin concentrations mostly to the deficient levels and as a result of urinary thiamin loss then you can completely get into the stage of deficiency of thiamine.

Chemotherapy with fluorouracil:

Fluorouracil is a chemotherapy drug that is generally used to treat colorectal and other cancers, the literature that is published can include several cases of beriberi, possibly because the drug may increase thiamin metabolism and also block the formation of TDP. Sometimes thiamine supplements can reverse these effects.

 Functioning of thiamine :

Thiamine phosphate derivatives are involved in many of the cellular processes and the best form is told to be thiamine pyrophosphate which is a coenzyme in the catabolism of sugars and in amino acids.

All the organisms use thiamine and it is only made in bacteria, fungi and also from plants, animals obtain their thiamine from their diet and for human it is an important and essential nutrient.

Thiamine is considered to be the transport form of the vitamin and there are 5 known natural thiamine phosphate derivatives.

Thiamine diphosphate :

There is no physiological rule for thiamine monophosphate and however the diphosphate is physiologically relevant, the synthesis of thiamine di phosphate which is also known as thiamine pyrophosphate and also carboxylase is catalyzed by an enzyme and is called thiamine phosphokinase.

The enzymes like transketolase, pyruvate dehydrogenase and 2-oxoglutarate dehydrogenase are all very important in carbohydrate metabolism, the mitochondrial PDH and OGDH are part of biochemical pathways that result in the generation of adenosine triphosphate which is a major form of energy for the cell.

Thiamine triphosphate :

THTP is also known to be thiamine triphosphate and is considered to be a specific neuroactive form of thiamine, however recently it was shown that THTP mostly exists in bacteria, fungi, plants and also in animals which suggesting a much more general cellular role and in particular e. coli, it seems to play a role that in response to amino acid starvation.

They are:

  • Thiamine monophosphate
  • Thiamine diphosphate
  • Thiamine triphosphate
  • Adenosine thiamine triphosphate
  • Adenosine thiamine diphosphate

Transport and absorption of thiamine :

Thiamine is usually released by the action of phosphatase and pyrophosphatase in the upper small intestine and in very low concentrations the process is told to be carrier mediated.

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