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Nutritional Pathology Online

As a doctor today I prescribe Thiamine (Vitamin B1) rich foods:   

Prevent Beriberi, Wernicke's Encephalopathy, and Korsakoff's Psychosis.


Dr Sampurna Roy MD       


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In my series of diseases related to nutritional deficiency my today's short post is on Thiamine deficiency.

Thiamine deficiency is an important nutritional disorder in Asia and Africa, specially where people mainly consume polished rice.

Thiamine deficiency in humans affects the cardiovascular, muscular, nervous, and gastrointestinal systems.



With increased awareness of the disease and improved nutrition in many countries, this disorder is less common now than in previous generations.

Foods rich in thiamine (Vitamin B1) -  Thiamine is present in wide range of vegetable and animal products.

Yeast is excellent source of thiamine.

Other sources of food are  cereals, seed (sunflower and sesame) peas, bean, bread, egg yolk, liver, kidney, pork, soyabean, brown rice and peanuts.

Milk, vegetable and fruits do not contain adequate thiamine.


Thiamine is found in the thermolabile portion of the Vitamin B Complex.

In thiamine deficiency carbohydrate metabolism is interrupted at the pyruvic acid stage, and pyruvic acid accumulates in the tissues and the blood.

Thiamine hydrochloride, which was synthesized in 1937, is composed of a pyrimidine base united to a nitrogen-carbon-sulfur ring containing a pentavalent nitrogen.

This compound is phosphorylated to form thiamine pyrophosphate, which acts intracellularly as the coenzyme for carboxylase.

The latter enzyme decarboxylates pyruvic acid and participates in the synthesis of fat from carbohydrate.

The lesions of thiamine deficiency are not produced by the simple injection of pyruvic acid, and it is probable that the failure of complete combustion of carbohydrate is the important factor, with the accumulation of pyruvic acid being incidental.

Thiamine is not stored in the body in large amounts. The depletion period before the onset of symptoms is variable  depending on the metabolic rate and other unknown factors.

There have been reports that anti-thiamine factors in food may play a role in the development of beriberi.


Lesions resulting from Thiamine Deficiency:

Human diseases in which thiamine deficiency plays an important role are Beriberi, Wernicke's encephalopathy, and Korsakoff's psychosis.

In fatal cases of beriberi the findings are  variable. On gross examination the most common lesions are emaciation, muscle atrophy, dilatation (with or without hypertrophy) of the right side of the heart, generalized edema, serous effusions, and chronic passive congestion of the viscera.

Death may be caused by high-output cardiac failure, by acute pulmonary edema, or by pneumonia, or other complicating infections.

The edema is caused in part by cardiac failure, but hypoproteinemia is probably a contributory factor in many cases.

This cardiovascular picture is particularly characteristic of the so-called wet type of beriberi, which is usually acute.

Microscopically loss of striation and fatty degeneration of the myocardial fibers are noted.

There is diffuse edema, often with slight lymphocytic infiltration of the intestinal tissue of many organs.

Skeletal muscles show hyaline and fatty degenerative changes.

Degenerative changes in nerves are more characteristic of the dry or chronic form of the disease, which is seen chiefly in adults.

Myelin degeneration and, in severe cases, fragmentation of the axis cylinders are seen in the affected nerves, which may be those of the extremities, the vagus, or the cranial nerves.

In thiamine-deficient pigeons, axis cylinder degeneration begins distally and progresses until the neurons are involved.

If thiamine is given before neuron death , regeneration of axis cylinders occurs at the usual normal rate. In dogs similar degenerative changes have been described in the central nervous system.

Wernicke's Disease:

Wernicke's Disease is associated with chronic alcoholism and is characterized by ganglion cell degeneration and focal demyelinating lesions and hemorrhage in the nuclei surrounding the ventricles and aqueduct, particularly in the nuclei of the extrinsic muscles of the eye.

There is also some reparative proliferation of neuroglial cells.

The picture is often complicated by symptoms of beriberi, scurvy, riboflavin deficiency and pellagra.

An apparently identical lesion may be produced in thiamine-deficient pigeons.

In view of the experimental evidence, thiamine deficiency is now believed to be the most  important etiologic factor in Wernicke's disease and in the pathologically similar Wernicke-Korsakoff?s syndrome.

Adding thiamine to the diet causes prompt clearing of the neurologic symptoms.

Wernicke-Korsakoff's psychosis, the result of brain damage after recovery from coma in Wernicke's syndrome, improves more slowly, and underlying psychotic elements often remain.

MRI plays an important role in the diagnosis of acute Wernicke's Encephalopathy.

Characteristic lesions are present in the mammillary bodies (atrophy) and surrounding areas around the third ventricle.

Clinicopathologic correlation:

The mechanism by which thiamine deficiency produces its characteristic lesions is not clear.

The degenerative changes in the peripheral nerves and central nervous system are perhaps the result of interrupted carbohydrate metabolism as described previously.

This is probably due to the fact that the metabolism of nervous tissue is believed to be totally dependent on carbohydrate oxidation.

The cardiac manifestations may be related to experimental observation that the oxygen uptake in vitro of the auricles of thiamine-deficient rats is significantly lower than that of the control animals.

A diet consisting largely of carbohydrate is an important contributing factor in the development of thiamine deficiency, since thiamine requirements are proportional to carbohydrate combustion.

Symptoms of peripheral neuritis and mental confusion are explained on the basis of nervous tissue degeneration or anoxia, and cardiorespiratory symptoms such as tachycardia, edema, cyanosis, and pulmonary congestion are partially explained by the cardiac lesions.



In the infantile form of beriberi, vomiting, cyanosis, and tachycardia may be followed by death (probably from pulmonary edema) in 24 to 36 hours.

The mortality of beriberi varies from 5% to 50% depending on the severity of symptoms and on the promptness and adequacy of treatment.



Visit: Pathology of Vitamin A deficiency: Importance of Vitamin A in our daily diet

Visit: As a doctor today I prescribe  Riboflavin  (Vitamin B2) rich foods to prevent mucocutaneous and ocular lesions

Visit: As a doctor today I prescribe Niacin (Vitamin B3) rich foods to eradicate Pellagra - Prevent the 4 Ds - Dermatitis ; Diarrhea ; Dementia and Death

Visit: Eat Citrus Fruits everyday and keep Scurvy away- Pathology of Vitamin C Deficiency

Visit: As a doctor today I prescribe Vitamin K to prevent hemorrhage -The most important health problem of Vitamin K deficiency is Hemorrhagic Disease of the Newborn

Visit: As a doctor today I prescribe nutritious food for every hungry child  


Further reading:

The natural history and pathophysiology of Wernicke's encephalopathy and Korsakoff's psychosis

Operational criteria for the classification of chronic alcoholics: identification of Wernicke's encephalopathy.

Thiamine deficiency in patients with congestive heart failure receiving long-term furosemide therapy: a pilot study

Effects of thiamine deficiency on the central nervous system

The role of thiamine deficiency in alcoholic brain disease

Alcoholic neuropathy is clinicopathologically distinct from thiamine‐deficiency neuropathy

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Dr  Sampurna Roy  MD

Consultant Histopathologist (Kolkata - India)






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