Although definite diseases can be associated with the excess intake of certain vitamins, these are seldom seen on a large scale. Much more common are the deficiencies described below. Pellagra is a disease caused by the deficiency of niacin, one of the B vitamins.

The name is derived from the rough skin characteristically seen crusting around the hands and neck. Painful burning of the mouth, shaking of the body, and less commonly, mental disturbances can result. Pellagra was common in the United States in the early 1900’s. A healthful diet was discovered to be curative.

One of the essential amino acids, tryptophan, is converted into nicotinic acid, a counterpart of niacin. Deficiency of other nutrients sometimes complicates the disease. Individuals subsisting on a diet primarily of corn are predisposed to pellagra, since corn protein is low in tryptophan and most of the milling removes the vitamin.

Classically pellagra is characterized by the “three D’s” — diarrhea, dermatitis, and dementia. Certain earlier symptoms may develop, however, including loss of appetite, indigestion, weakness, burning in the mouth, and insomnia. Pellagra most commonly appears in the spring or early summer, when the dietary deficiencies of winter combines with renewed exposure to the sun seems to precipitate the outbreak.

The skin problems begin to look much like a sunburn. Burning may be intense. Sun-exposed areas, such as the neck, arms, and hands are affected most commonly. Later the skin becomes brownish in color, then rough and scaly. Soreness of the mouth is typical, with inflammation of the tongue. Diarrhea may or may not be present.

Mental disturbances usually begin with episodes of nervousness and tremor. Later there occurs confusion, depression, or even delirium. Early replacement of the B-complex vitamin with high doses of niacinamide is recommended. This related substance does not cause unpleasant vascular flushing like nicotinic acid does.

Most people can take them orally. As symptoms subside, all vitamins should all be obtained from a wellbalanced, varied diet of natural foods. Thiamine Deficiency, called Beriberi, has been known to western medical science since the seventeenth century. Recognized first in the Orient, beriberi has been associated with a deficiency of thiamine.

It commonly appears when the diet exclusively consists of polished rice. Cases are occasionally encountered in the United States, particularly in infants and in alcoholics. Three main types of this disease are identified. A chronic form called “dry beriberi” causes tenderness in the calf muscles and weakness in the legs.

The acute form, “wet beriberi”, is characterized by cardiovascular changes, with edema, congestion of the lungs, and heart failure. In alcoholics, the brain damage may be irreversible. Beriberi in infants continues to be a health problem in the Far East, where a child may lose his voice, develop heart failure, or gastrointestinal changes with vomiting and constipation.

Adequate nutrition for the breast-feeding mother is particularly important for its prevention. The therapeutic response to Thiamine in infants and adults with beriberi involving the heart is dramatic. A rapid transition, however, should be made from vitamin supplementation to a diet containing adequate wheat germ, rice polishings, or whole grain cereals.

This disease is entirely preventable, and reflects one of many conditions following the wake of the industrial revolution. Riboflavin deficiency is still common in many developing countries. In the Unites States there appears to be a correlation between low income and riboflavin intake. Milk and certain vegetables are good sources of riboflavin.

However, when the milk is exposed to direct sunlight a considerable amount of this vitamin is destroyed. Riboflavin is reduced when the food is treated with alkali, such as we find in certain preservatives and the use of soda. Lack of riboflavin usually results in sores, developing at the corners of the mouth, inflammation of the tongue, and sore throat.

Late findings affect the nerves, as well as the blood, with the development of anemia. Replacement of the vitamin rapidly reduces these changes. Vitamin B6 deficiency is seen occasionally in individuals who eat very few plant foods. Seizures occur in babies fed formulas deficient in B6.

This has especially been a problem when a relatively high kidney excretion develops during pregnancy, while a mother was given high dose supplements. A number of drugs interfere with vitamin B6 utilization, such as isoniazid, used in the treatment of tuberculosis. Eating a natural varied diet, it is not difficult to get plenty of pyridoxine.

It is the vegetable source of vitamin B6. Scurvy is another vitamin deficiency with worldwide prevalence as well as a colorful history. This condition is caused by a deficiency of ascorbic acid, also called vitamin C. It was a common cause of mortality in sailors during the fifteenth and sixteenth centuries.

James Lind, a British naval surgeon, developed a simple cure in 1747 by giving the sailors two oranges and one lemon every day. Their swollen gums, weakness, and bleeding tendencies responded dramatically, giving rise to the nickname, “Limeys.” In more recent times scurvy appears more commonly in alcoholics, food faddists, and the impoverished elderly living on a grossly unbalanced diet.

The principal manifestations of scurvy are hemorrhages in the skin, swollen and bleeding gums, aching muscles, fatigue, and emotional changes. These symptoms appear after two months of depletion. Appearing occasionally in children, scurvy produces tenderness and swelling in the legs. Extreme pain may be present.

Finally, after the teeth erupt, swollen gums and bleeding develops. Skeletal changes show signs of growth retardation. In some cases of a vitamin-D deficiency syndrome, rickets, may co-exist. A carefully taken feeding history is helpful for the diagnosis of infantile scurvy.

After 46 months of age any infant fed solely with the bottle, using only boiled cow’s milk or a milk substitute, may develop this disease. Fresh orange juice or another dietary source of vitamin C is rapidly curative. Extremely high supplements of ascorbic acid are seldom necessary.

They may produce an abnormal dependency, based on the development of increased excretion originating in the kidneys to compensate for this superabundance. Large doses of vitamin C can also inactivate vitamin B12. That, at times, unfavorably affects reproduction.

Vitamin A is primarily manufactured by the conversion of dietary betacarotene into the active form, retinol. One of the first symptoms of vitamin A deficiency is inability to see in reduced light (night blindness). A later change in the eye is the presence of dryness, xerophthalmia. The conjunctiva becomes opaque, the secretion of tears decreases, then a sticky secretion appears over the cornea, called the Bitot spot.

This mark has the appearance of a flake of meringue. Further destruction of the cornea may occur, leading eventually to blindness. In treating the acute disease, a supplement of vitamin A is recommended. The prevention of deficiency using a balanced diet containing green and yellow vegetables, fresh fruit, and vitamin-supplemented milk is entirely adequate.

Green and yellow foods such as carrots, cantaloupe, squash, and dark green leafy vegetables are considered excellent sources for this vitamin. A high intake of carotene appears in adults using carrot juice or a similar food concentrate excessively. Carotenemia may color the skin, but should not be confused with jaundice.

It is considered harmless and will subside when the carotene intake is reduced. Hypervitaminosis A, on the other hand, can produce an acute toxicity. In infants, it presents as drowsiness, vomiting, and other signs of increased intracranial pressure. Adults commonly develop a headache within hours after any injection of a toxic dose.

Blurred vision, nausea, vomiting, or drowsiness may also develop. The skin peels and hair loss occurs. With chronic ingestion of high doses, liver changes resembling cirrhosis are seen. Psychiatric side effects manifest themselves, but prognosis is good when vitamin A ingestion ceases.

Vitamin E is the common name of a group of related fat-soluble vitamin, called tocopherols. They vary in their potency, with the alpha form being thought most active. A number of animals develop a Vitamin E deficiency syndrome, with deterioration in the muscle fibers, impaired reproduction, or anemia.

Clinically, these insufficiencies are rare in adults. When the diet contains enough polyunsaturated fatty acids, plenty of dietary vitamin B is usually available. Unfortunately, optimistic expectations of many researchers have been disappointed in spite of the literature proclaiming the miracleworking powers of this vitamin.

We do not know for certain whether vitamin B supplementation can favorably affect physical endurance, cardiac status, sexual potency, or longevity in individuals with normal blood levels of Vitamin B (tocopherols). A number of vitamins affect the production of blood or its proper coagulation.

Vitamin K is present in most edible vegetables, particularly the green leafy ones. A similar vitamin is also produced by intestinal bacteria. The gradual accumulation of vitamin K levels in a newborn baby explains easily why ancient recommendation for an eight-day circumcision was made to the Jews.

Hemorrhagic disease of the newborn as well as in adults is prevented by proper blood levels of this vitamin. Vitamin B12, folic acid, and iron are also closely related to blood production and have been discussed in Chapter 4, dealing with the circulatory system.