THIAMINE (Vitamin B₁)

Thiamine was discovered in 1921 and synthesized in 1936. Thiamine is lost in cooking,
especially when cooking is prolonged or at high temperatures. Alkalis also destroy thiamine.
Thiamine requirements are based on the calorie content of the diet- a high CHO diet
increases the need for thiamine. The heart and brain are the tissues that store, or become
saturated with, thiamine when intake exceeds requirements; thiamine remaining after tissues are
saturated is excreted in the urine

FUNCTIONS
Thiamine is an important component in the coenzyme thiamine phosphate (TPP), which
is involved in converting CHO (glucose) to energy. Thiamine is also necessary for protein and
fat metabolism and normal nervous functioning.

THIAMINE DEFICIENCY
Significant thiamine depletion can develop within 3 weeks on a diet devoid of thiamine.
In the United States, thiamine deficiency is most commonly related to alcohol abuse, which
alters thiamine intake, absorption. And metabolism. Other high risk groups include renal patients
undergoing long-term dialysis, patients receiving long-term parenteral nutrition, people with
chronic fever, and the relatively few people with thiamine-responsive inborn errors of
metabolism.
Severe thiamine deficiency, known as beri-beri, is rare in the United States, although
subclinical deficiencies may be seen. Throughout history, countries in the orient, which rely
heavily on milled rice (refining rice removes much of the thiamine content) and foods with
antithiamine activity, have had a high incidence of beriberi. Food enrichment programs have
virtually eradicated beriberi in Japan and the Philippines.

Clinical Findings
Beriberi which translates literally to “I can’t, I can’t,” is an accurate description of the
weakening disease that primarily affects the nervous and cardiovascular systems. Adult beriberi
produces symptoms of anorexia, fatigue, nausea, vomiting, irritability, mental confusion,
muscular weakness, peripheral paralysis, emotional instability, depression, and general lethargy.
Beriberi may be classified as “mixed,” which is characterized by neuritis and heart
failure, “dry,” of which polyneuritis is the major finding, or “wet,” which is identified by edema
and heart failure. Without treatment, most patients die from sudden heart failure. Symptoms
include restlessness, pallor, inability to sleep, edema, diarrhea, muscle wasting, and breathing
difficulties. Death caused by acute heart failure may occur 1 to 2 days after the onset of
symptoms.

Treatment
Large oral doses of thiamine or a thiamine derivative are administered. Wet beriberi
responds within a few hours after treatment is initiated if the nervous system is not badly
damaged; recovery from dry beriberi is slower. Infantile beriberi is treated by giving thiamine
to both the lactating mother and to the infant. Because thiamine deficiency rarely occurs alone, a
B-complex multivitamin preparation frequently is given.

FOOD SOURCES
Rich sources of thiamine include unrefined and enriched grains, pork, and organ meats,
legumes, seeds, and nuts. Enriched and fortified grains and cereals contribute substantial
amounts of thiamine to the diet.

NUTRIENT/DRUG INTERACTIONS
Supplements of thiamine can enhance the response to peripherally acting muscle relaxants.
Drugs that affect thiamine are as follows:
Antacids destroy thiamine
Barbiturates decrease thiamine absorption
Diuretics, mercurial increase urinary excretion of thiamine
RIBOFLAVIN (Vitamin B₂)
Riboflavin was discovered in 1932 and synthesized in 1935. Although resistant to heat,
acid, and oxidation, riboflavin is quickly destroyed by light.
The RDA listed for riboflavin is a recommend minimum daily intake. Actual riboflavin
requirements are based on calorie intake. As calorie intake increases, the amount of riboflavin
needed also increases. Because small amounts of riboflavin are “stored” in the liver and kidney,
a daily intake is necessary. Riboflavin consumed in excess of need is excreted in the urine
protein-wasting conditions increase riboflavin excretion.

FUNCTIONS
Riboflavin is part of the coenzymes FAD (Flavin adenine dinucleotide)
and FMN (Flavin mononucleotide), which have vital metabolic roles in energy metabolism,
DNA and protein synthesis, and gluconeogenesis. Riboflavin is also involved in the activation of
vitamin B₆, the conversion of folacin to its coenzyme, corticosteroid synthesis, RBC production,
and thyroid enzyme activity.

RIBOFLAVIN DEFICIENCY
Riboflavin deficiency is uncommon in the United States. People with calorie intakes such
as adolescent women, alcoholics, and the elderly, are at risk for riboflavin deficiency, as are
people with malabsorption syndromes and those using certain drugs.
Clinical Findings
Signs of riboflavin deficiency may not appear for several months on a riboflavin-deficient
diet. Early symptoms include oral lesions dermatitis, normocytic anemia, and scrotal and vulval
skin changes.
Cheilosis (fissuring of the lips), angular stomatitis (cracks in the skin at the corners of the
mouth), a purplish swollen tongue, and reddening of the cornea are characteristics of severe
riboflavin deficiency (ariboflavinosis).
Treatment
Riboflavin deficiency is treated with large doses of riboflavin or B-complex vitamins;
severe deficiency may require parenteral administration. Lesions may heal within few days or
weeks.
FOOD SOURCES
Riboflavin is widely distributed in foods but only in small amount. Good sources include
milk and dairy products, followed by meat, poultry and fish. Enriched and fortified grains and
cereals contribute large amount of riboflavin in the diet.

NUTRIENT/DRUG INTERACTIONS
Drugs that affects riboflavin are as follows:
Amitriptyline - interferes with riboflavin metabolism
Chloramphenicol - may increase the need of riboflavin
Chlorpromazine - may interfere with riboflavin metabolism
Imipramine - may interfere with riboflavin metabolism
Probenecid - increases urinary excretion of riboflavin