Vitamin Therapy in Diabetes Mellitus

The first account of the successful treatment of hyperglycemia with Vitamin B concentrates was mentioned in these pages (Vol. 2, No. 5, page 29, paragraph 4). Vitamin B caused a slow but definite improvement in a majority of the cases treated. At that time attention was called to the fact that diabetes with attendant hypertension also required Vitamin C concentrate to get the best response according to clinical findings.

Diabetes with hypotension is a more evident case of Vitamin B deficiency. Lack of “B” causes a characteristic loss of vascular tone due to the functional failure of the vascular innervation. In all probability the same functional failure of the pancreatic innervation can prevent the normal release of insulin after the ingestion of carbohydrates. In this case the pancreas may be perfectly intact, as is known to be the case in many diabetics. The administration of Vitamin B in such cases may result in immediate release of insulin (within 30 minutes according to the experience of a number of clinicians who have reported to us), and even symptoms of hypoglycemia–hyperinsulinism–may appear.

Hyperinsulinism after meals in otherwise healthy individuals is a not uncommon phenomenon. Strangely enough, the injection of insulin has proved a successful remedy in that it supplies insulin without arousing the pancreas, while if the pancreas is called on, it overdoes the job.

When Vitamin B administration causes hyperinsulinism, it is probably a similar situation. Indeed, the failure of the nervous control would logically result in a loading up of the pancreas beyond the normal, and result in an abnormal amount being released on the repair of the nervous connection. Again, such loss of nerve control with no demand on the pancreas–or reduced demand–can logically result ultimately in pancreatic atrophy or degeneration. It is known that pancreatic alterations occur in avitaminosis B in test animals.¹

The speed with which the administration of Vitamin B in this type of case causes a resumption of insulin secretion has caused comment. It is no more speedy, however, than the cure of a paralyzed pigeon that has been prepared by withdrawal of Vitamin B from its feed, when the vitamin concentrate is supplied. A bird that can neither stand nor fly is restored apparently to normal in a few minutes. The long continued partial avitaminosis to which human patients may be subjected, however, may not always respond as completely; the degenerations in such cases can be expected to be less easily restored. It is that fact that limits our success in both the nervous tissues as well as in the pancreas. Nothing but a clinical test on each patient will tell the story.

Diabetes accompanied with hypertension is a different matter. The hyperglycemia here may be due to the oversecretion of adrenin, which may also be causing the increased blood pressure. Adrenin has as one of its functions the release of glycogen from the liver. Too much adrenin may be due to avitaminosis C and B, as each of these vitamins are necessary to the proper function of the adrenals, especially the cortex, and in their absence a hypertrophy may result.² This hypertrophy often means a hypersecretion of the medulla with attendant hypertension–and diabetes if the pancreas is unable to take the extra load. The well-known effect of Vitamins B and C (as “Catalyn”) to reduce hypertension in these cases depends on the effect on the adrenal gland. If the diabetic condition is due to adrenal stimulation, it also responds to this treatment.

The amount of adrenin that will cause hyperglycemia is less than that necessary to cause a rise in blood pressure.³ Therefore, it is important to supply the Vitamins B and C together in all cases, to see that Vitamin C is tested in those cases where “B” alone fails to be of benefit. Under treatment with vitamin concentrates the average diabetic patient improves so much in his general “sense of well being” that he is inclined to depart from his rigid diet, and that is the important thing to warn him against. A long continued schedule of increased vitamin and low carbohydrate intake is necessary for permanent benefit.

We must accept as a basic fact that most endocrine unbalance is a result of vitamin starvation. The outstanding feature of any chart of vitamin deficiency consequences is an appalling list of endocrine changes–atrophy or hypertrophy–parenchymatous death or “compensatory” enlargement.

Because the pancreas is often intact in severe diabetes, and because It has been found that the pituitary (both anterior and posterior) secretes hormones that cause hyperglycemia,⁴ it has recently been suggested that pituitary disorder may be responsible for diabetes mellitus, and a control of the oversecretion of the diabetogenic hormones by means of X-ray treatments directed to the pituitary has been proposed, and some benefit reported in a few test cases.

But the production by the anterior pituitary of another pancreatropic hormone that stimulates the activity and growth of the Langerhansian Islets is known.⁵ So X-ray treatments are thereby ruled out. We know that avitaminosis B causes degeneration of the pituitary, and no doubt interferes with its normal hormone output, so the avitaminosis hypothesis of diabetes is further reenforced. The normal pituitary, no doubt, secretes a balanced output of glycemic regulators, with adrenin as a further factor. Such a set-up can reasonably be disturbed by vitamin deficiency in two ways:

1. Starvation of the endocrines involved.
2. Paralysis or reduced sensitivity of nervous controls.

An interesting news note recently stated that a South American Honey Bear in a zoo developed diabetes, requiring the administration of insulin. That means to us that the refined sweets that were fed the bear in place of his normal diet of honey merely did what could be expected. We know honey is one of the good sources of Vitamin B. So is wheat–if we get it whole. But the use of vast amounts of refined carbohydrate separated from its normally accompanying vitamin that is necessary to insure its proper assimilation can only be expected to result in a rising curve of incidence of diabetes mellitus that exactly parallels the curve of rising volume of consumption of devitalized foods.

Diabetes mellitus is serious, not particularly because of the blood hyperglycemia, but because the lowered metabolism of glycogen brings about an automatic (defensive) reduction in the conversion of fat (normally stored in the liver) into glycogen, with a resultant damming up of fat in the blood and liver. It is this rise in blood fat that causes diabetic coma.

In diabetes mellitus we have this cycle of events:

1. Failure of the pancreas to supply insulin (for one reason or another).
2. Hyperglycemia and glycosuria.
3. An automatic reduction (defensive reaction to compensate for reduced glycogen metabolism) in amount of reserve fat converted into glycogen.
4. Accumulation of fat in liver, as well as in tissues and in blood. (See Vitamin News, Dec. 15. 1935).
5. “Diabetic” coma because of high blood fat.

The susceptibility of the diabetic to infections and to gangrene can be combatted successfully with concentrates of Vitamins C and D. In gangrene cases especially, the use of our Vitamin C concentrate has produced spectacular results. The dosage should be one or two Vitamin D tablets daily, with two to six Vitamin C tablets.

 

References Cited:

1. McCarison, Indian Journal of Medical Research, 6:550-556, 1919.
2. Sherman and Smith, The Vitamins, page 70, Second Edition, 1931.
3. Houssay, B. A. and di Benedetto, E., Rev. Soc. argent. de biol., 9:310, 1933.
   
   The continuous injection of adrenaline into adrenalectomized dogs, in doses corresponding to the amount normally secreted or very slightly higher, simultaneously with injection of posterior pituitary extract, was followed by hyperglycemia…It is deduced that the posterior pituitary hyperglycemia is due to a humoral action of the liver requiring the secretion of adrenaline.
4. Houssay, B. A. and di Benedetto, E., Ibid., 9:300, 1933.
   
   Dogs anaesthetized with chloralose received variable doses (1 to 2.5 and 5 to 10 mg. per kg.) of extract of standard powder of posterior pituitary gland. The injection was made intravenously, lasting 1 hour, 1 cc. of the solution being injected every minute. Blood sugar (Hagedorn and Jensen method) was determined up to 7 hours after the beginning of the experiment. An increase proportional to the dose injected was observed.
   
   Lucke, Arch. f. exper. Path. u Pharmakol., 170:106, 1933. (Abstracted in Phys. Absts., 19:56).
   A hormone produced in the anterior pituitary is specifically concerned with carbohydrate metabolism, acts as an antagonist to insulin, and is therefore so designated. 
5. Anselmino, K. J., Herold, J. and Hoffmann, F., Klin. Wschnschr., 12:1245 1933.
   
   Anselmino, K. J. and Hoffmann, F., Klin. Wschnschr., 12:1435-1436, 1933.
   
   The authors interpret their findings as evidence that the anterior lobe extract has increased the functional activity of the insular tissue.
   
   The authors conclude that the anterior pituitary factor acts by way of the pancreas where it caused an increase in insulin output.
   
   Geiger, E., Arch. f. exper. Path. u Pharmakol., 172:295, 1933.
   The autonomic innervation of the pancreatic islets has been demonstrated and the vagus shown to carry fibers that cause insulin discharge.
   
   Houssay, B. A., Biasatti, A. and Rietti, C. T., Rev. Soc. argent. de biol., 9: 489, 1933.