Читать книгу Orthomolecular Medicine for Everyone - Abram Hoffer M.D. Ph.D. - Страница 50

Pellagra is one of the classical diseases of Western civilization. It is a niacin-deficiency disease characterized by dermatitis, gastrointestinal disorders, and mental disturbance. It also causes premature aging, brings on neurological conditions, and decreases immunity to a large number of infectious diseases.

As long as populations lived on a variety of whole foods, pellagra was very rare. But when farmers began to grow single crops as the main source of cash and for food, diseases due to single cultured crops (monocultures) became epidemic. Farmers and poor people in the southern United States and in several countries around the Mediterranean Sea (Spain and Italy) began to depend very heavily on corn. Pellagra is the direct result of excessive corn consumption combined with a lack of other foods. This is not due only to a deficiency of vitamin B₃ in corn, but rather to the fact that the vitamin is so tightly bound chemically that too little is absorbed by the body. Curiously, natives of Central America discovered several thousand years ago that corn consumed as tortillas did not cause pellagra. They treated the crudely ground whole corn with calcium-rich alkali, which liberated the vitamin.

A number of diseases present such a varied set of symptoms and signs that a study of these diseases is almost a study of medicine itself. Syphilis is one such disease and pellagra is probably the one condition that can mimic a larger number of physical and psychiatric diseases. Deficiency of the essential fatty acids (EFAs) is another, perhaps because one of the main functions of vitamin B₃ is to aid in the conversion of EFAs to the hormonelike prostaglandins. Pellagra may be due to a deficiency of EFA substrate in contrast to the corn-induced pellagra.² Both result in a deficiency of prostaglandins.

Classic pellagra has been characterized by the four Ds: dermatitis, diarrhea, dementia, and death. It is, after all, a preterminal disease. If a vitamin B₃ deficiency is diagnosed only after pellagra is obvious, one is playing Russian roulette with the life of the patient. Dermatitis is a symmetrical, reddish brown, sometimes black, discoloration of the parts of the body exposed to the sun. It has the appearance of a chronic suntan or sunburn. This is probably a primary tryptophan deficiency. Diarrhea may alternate with constipation. Of course, it increases malabsorption and aggravates the condition. Dementia is an organic dementia with confusion, disorientation, and memory disturbance. This is the typical terminal psychosis.

Earlier stages are more typically schizophrenic, with perceptual changes, disordered thoughts, and mood changes; psychotic behavior is common. At one time, over 25 percent of spring admissions to mental hospitals in the southern United States were psychotic pellagrins. There was no way of distinguishing them from other schizophrenic syndromes until vitamin B₃ came into clinical use. If these patients responded quickly to the vitamin, they were diagnosed with pellagra; if not, they were diagnosed with schizophrenia. This practical diagnostic test had a very important deleterious consequence—it effectively quenched any interest in using vitamin B₃ as a treatment for schizophrenia until double-blind, controlled studies in the 1950s.³ It would have been more appropriate to recognize the pellagra psychosis as one of the schizophrenia syndromes and to classify these patients as fast or slow responders to small doses or megadoses of vitamin B₃.

The intermediate stage of pellagra is characterized by a variety of syndromes representing any of a large number of psychiatric, nonpsychotic states. Early pellagrologists considered neuroses one of the variants of subclinical pellagra, this in-between state. Another form is the syndrome affecting children that produces the hyperactive or learning-disordered child. The severe forms of pellagra take more of a neurological form (organic psychoses or toxic confusional states) and these may be a main factor in some senile psychoses. Huntington’s disease has been described as one of the expressions of pellagra.⁴

Pellagra has several causes. First, it is caused by a deficiency of tryptophan. Normally, this amino acid is the major precursor of vitamin B₃; about 1–2 milligrams (mg) of B₃ is made from 60 mg of tryptophan. There is evidence that tryptophan deficiency may be the cause of the typical skin dermatitis of pellagra: the dermatitis of pellagrins given tryptophan healed more rapidly than when they were give vitamin B₃ only. Second, pellagra is caused by a deficiency of vitamin B₃, caused by diets that contain too much corn or that depend too heavily on other food which has been processed (such as flour) or which is naturally low in this vitamin. A third cause of pellagra is a deficiency of pyridoxine (vitamin B₆). Pyridoxine must be present before tryptophan can be converted to NAD. Diets deficient in B₆ are as pellagragenic as diets deficient in vitamin B₃.

Fourth, pellagra is caused by excessive loss of vitamin B₃ in urine. NAD is made from tryptophan, niacinamide, and niacin. If too much vitamin B₃ is lost, insufficient NAD will be made. The loss of vitamin B₃ is under the control of the ratio of the amino acids isoleucine and leucine. Isoleucine decreases loss of B₃, while leucine increases it. Ideally, foods should contain more isoleucine, but in most there is slightly more leucine. Excessive leucine causes pellagra and isoleucine is an anti-pellagra factor. Corn is the ideal pellagra-producing food, for it is low in tryptophan, low in vitamin B₃, and too high in leucine compared to isoleucine.