Vitamin B1 deficiency (thiamine): Description
Vitamin B1 deficiency (thiamine) or thiamine is a water-soluble vitamin (and, therefore, can’t be stored in the body). This vitamin is found in food and used as a dietary supplement and belongs to the group B vitamins. Thiamine as a coenzyme in the form of thiamine pyrophosphate (TPP) is involved in a various cellular processes including the catabolism of sugars and amino acids and is involved in the fermentation of alcohol as well. Thiamine takes part in the production of glucose as a coenzyme in the pentose monophosphate pathway. About 90% of total thiamine in the blood is found in erythrocytes.
Thiamine deficiency results in several disorders such as beriberi, Wernicke-Korsakoff’s syndrome, Korsakoff’s psychosis and optic neuropathy.
The current estimated average requirements for thiamine for women and men ages 14 and up are 0.9 mg/day and 1.0 mg/day, respectively, according to The Food and Nutrition Board of the U.S. Institute of Medicine.
Food that are rich in thiamine are:
- Whole-grain foods;
- Milk and milk products;
- Vegetables (green, leafy vegetables; beets; potatoes);
- Legumes (lentils, soybeans, nuts, seeds);
- Orange and tomato juices;
Causes and risk factors
A lack of vitamin B1 deficiency (thiamine) can be caused by malnutrition, a diet high in thiaminase-rich foods (raw freshwater fish, raw shellfish, ferns, milled rice) and/or foods high in anti-thiamine factors (tea, coffee, betel nuts). Two flavonoids, quercetin and rutin, are also considered to be thiamine antagonists. Sulfites added to foods interferes with thiamine.
As long as the absorption of thiamine is inhibited by alcohol consumption or by folic deficiency excessive alcohol consumption, gastrointestinal diseases and malnutrition, persistent vomiting and pernicious anemia may be accompanied by the thiamine deficiency.
In some cases the consumption of thiamine is increased and therefore the deficit may develop. These conditions include(vitamin B1 deficiency (thiamine)):
- Diets high in carbohydrate or saturated fat intake and refeeding syndrome;
- Pregnancy and lactation;
- Severe infection/sepsis associated with fever;
- Increased physical exercise;
The nervous system is very sensitive to the vitamin B1 deficiency (thiamine) due to the dependence on oxidative metabolism.
Within a week after thiamine intake is stopped, healthy people develop fast heart rate (tachycardia), fatigue, and decreased deep tendon reflexes; some individuals experience a peripheral neuropathy.
See also Vitamin B2 Deficiency
Historically, beriberi has been common in regions where polished or white rice formed a major part of the diet. The side effect of such diet is the lack of the thiamine in such cereals.
Symptoms of the disease also include weight loss, emotional and sensory disturbances, swellings (edema) and pain in the extremities.
Depending on the body system which functioning is mainly impaired and the age of the affected person beriberi is divided into several forms:
- Dry beriberi specifically affects the peripheral nervous system. Individuals experience sensory and motor impairment of the limbs due to the myelin degeneration. The symptoms include difficulties in walking (because of paresis and paralysis), tingling or loss of sensation (numbness) in hands and feet, loss or decreased tendon reflexes, mental confusion/speech difficulties, poor memory, burning pain, especially in the limbs, involuntary eye movements called nystagmus, loss of coordination and equilibrium (sensory ataxia), muscle cramps and atrophy, foot drop.
- Wet beriberi affects the cardiovascular system and results in increased heart rate (tachycardia), chest pain (due to myocardial injury), hypotension, elevated jugular venous pressure, dyspnea (shortness of breath) on exertion, paroxysmal nocturnal dyspnea and peripheral edema (swollen legs). Heart failure is a life-threatening complication of beriberi.
A more rapid form of wet beriberi is known as an acute fulminant cardiovascular beriberi, or Shoshin beriberi characterized by the rapid development of the heart failure. This type of beriberi is presented with the lividity (cyanosis) of the hands and feet, increased heart rate (tachycardia), distended neck veins, restlessness, and anxiety. The death follows soon within several hours or days if the treatment is not available.
- Infantile beriberi affects the children of malnourished mothers and typically occurs when the child is between two and six months of age. The acute form is characterized by the rapid development of the heart failure. Other symptoms include: weight loss, vomiting and diarrhea, tachycardia and swellings, convulsions and aphonia (the inability to produce voiced sound).
- Gastrointestinal beriberi affects the digestive system and is characterized by anorexia, abdominal discomfort and pain, constipation, nausea and vomiting, dysphagia (difficulty swallowing).
Wernicke-Korsakoff’s syndrome (WKS) is the combination of the Wernicke’s encephalopathy (WE) and Korsakoff’s psychosis.Both disorders are tightly connected and usually diagnosed as one condition. The WKS is usually the result of alcohol abuse. Classically WKS presents with the triad of confusion, ataxia (loss of balance and coordination), and nystagmus (involuntary eye movements). Affected individuals experience gait abnormalities, inability to walk or difficulties walking, diplopia (double vision), strabismus, apathy and indifference, hallucinations, confabulations (a person fills in gaps of memory with data that can be recalled at that moment), intellectual impairment, aphasia (an inability to comprehend and formulate language), apraxia (an inability to perform tasks or movements), agnosia (an inability to recognize objects, persons, sounds etc.) and amnesia (Korsakoff dementia), insomnia, anxiety, weight loss and recurrent vomiting. Other symptoms that are associated with WE are stupor, low blood pressure (hypotension), increased heart rate (tachycardia), hypothermia, epileptic seizures and a progressive loss of hearing. Another malnutrion conditions such as pellagra, amblyopia, iron-deficiency anemia etc may also be found.
Measurement of blood thiamine, pyruvate, alpha-ketoglutarate, lactate, and glyoxylate levels as well as urinary excretion of thiamine and its metabolites are performed to confirm the diagnosis. Brain MRI may also be needed.
The treatment of clinical manifestations of thiamine deficiency should be initiated immediately after the suspicion of vitamin B1 deficiency occurs, either intravenously or intramuscularly.
The recommended dose is of thiamine for beriberi is 50 mg given intramuscularly for several days. Maintenance therapy implies 2.5-5 mg per day orally(vitamin B1 deficiency (thiamine)).
WE is treated with a minimum of 500 mg thiamine hydrochloride given by infusion, three times per day for 2 to 3 days. 250 mg thiamine should be given intravenously or intramuscularly daily for 3 to 5 days, or until the clinical improvement.
Sympthomatic measures are required to alleviate the symptoms of the disease.