Diabetes Is Not Always Permanent

No disease can inflict more savage cruelty than diabetes. Invariably there were patients recovering from insulin shock and diabetic coma, and some who never recovered. Others were hemorrhaging from painful kidneys, and mere youngsters were already blinded from diabetic retinitis. Many diabetics had fatty livers, or swollen "stomachs," agonizingly tender to the touch. Arteries plugged with fatty deposits seemed an inevitable part of the disease, resulting in high blood pressure, frequent strokes, and far more heart attacks than among non-diabetics. Such deposits had caused discomfort in the legs years before the feet ulcerated, flesh rotted, and amputation could no longer be postponed. There were amputation stubs that took an eternity to heal; and tragic elderly persons pitifully learning to walk on artificial limbs.

One could not come to know and love these patients without praying that scientists would soon discover how such suffering could be prevented.

Perhaps a Cause Has Been Found

Insulin is a hormone produced by the pancreas, makes it possible for glucose to enter the cells to be converted into energy or, if not needed immediately, to be changed into glycogen or fat; and insulin is also necessary before stored fat can be used.

When too little vitamin B6 (pyridoxin) is obtained, an essential amino acid from complete proteins, tryptophane, is not used normallyand changed into xanthurenic acid. If animals are deficient in vitamin B6, xanthurenic acid in the blood becomes so high that it damages the pancreas within 48 hours and diabetes is produced. The blood sugar rises far above normal, and glucose spills into the urine. The longer animals are kept on a vitamin-B6-deficient diet, the more extensive is the destruction of pancreatic tissue. Injecting animals with xanthurenic acid also causes the pancreas to be so severely damaged that diabetes develops; again the blood sugar soars and urinary loss of sugar is heavy.

As soon as vitamin B6 is supplied, the amount of xanthurenic acid decreases; when the pancreas has not been seriously harmed, and all diabetic symptoms disappear. If the vitamin is not given, the condition grows steadily worse until the animal dies. Magnesium decreases the need for vitamin B6; and if it is increased in the diet, the amount of xanthurenic acid is reduced even though no vitamin B6 is allowed. Furthermore, magnesium is necessary to activate enzymes containing vitamin B6; and blood magnesium is particularly low in diabetics. Diabetes, therefore, may prove to be caused by the combined deficiencies of this vitamin and mineral.

Saturated fats increase the need for magnesium and vitamin B6;hence deficient rats given a high-fat diet excreted many times more xanthurenic acid than animals fed oils or little fat. They also became grossly obese, and the urinary loss of sugar and destruction of the pancreas paralleled their gain in weight. Because high-protein and high-calorie diets increase the need for vitamin B6, they accelerate the harm done to the pancreas if this vitamin is inadequate. Furthermore, injuries to the pancreas occur long before any other symptoms of a vitamin-B6 deficiency appear. Investigators have stated that their studies give "conclusive evidence that xanthurenic acid may cause human diabetes."

Persons who are overweight are especially susceptible to diabetes; and excess calories from any source increase the vitamin-B6 requirement. Diabetes has been produced in cats by prolonged feeding of sugar, although control animals given starch did not develop the disease. Sugar particularly increases the need for both insulin and vitamin B6; and a high incidence of diabetes occurs in persons eating excessive sugar. Conversely, when food has been limited, as during wartime, diabetes has markedly decreased.

A number of drugs cause xanthurenic acid to appear in human urine, a condition that can be prevented if vitamin B6 is taken with the drug. For instance, such large amounts of xanthurenic acid are formed after penicillin is given to rats that the pancreas is quickly damaged.

Persons mildly deficient in vitamin B6 excrete xanthurenic acid long before any other signs of the dietary insult appear. All diabetics, however, appear to excrete large amounts of this acid, which would indicate that the pancreas is being further damaged. Moreover, uncontrolled diabetics and persons with diabetic retinitis excrete far more xanthurenic acid than do individuals receiving insulin or who have no complications.

When diabetics have been given 50 milligrams of vitamin B6 daily, they showed a rapid and marked decrease in urinary xanthurenic acid ; in one case, the quantity dropped almost 97 per cent the first day. If they continued taking 10 to 20 milligrams of this vitamin daily, none of this acid was excreted, showing that none of them was being formed in the body.

The belief that diabetes is hereditary may be merely a high genetic requirement for vitamin B6. Some infants require many times more of this vitamin than do others. In addition, lecithin, which reduces the high blood fat and cholesterol so characteristic of diabetes, cannot be produced unless vitamin B6 and magnesium are adequate ; therefore deficiencies of these nutrients could in part be responsible for many serious cholesterol complications of diabetes.

Although more research must be done before conclusions can be drawn, any person with diabetes or a family history of the disease may be wise to take at least 10 milligrams of vitamin B6 and 500 milligrams of magnesium daily.

By: David I Crawford

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