Diabetes And Hypoglycemia. Scurvy

Is SCURVY one of the trigger point for adult onset diabetes specially of those with diabetic parents?

Irwin Stone’s Entire Book Now Posted
Now Posted: Irwin Stone’s 1972 book: The Healing Factor
Forewords by Linus Pauling and Albert Szent-Gyorgyi…




Diabetes and its opposite counterpart, hypoglycemia, are diseases caused by disturbances in the delicate balance of the sugar chemistry of the body.  The sugar, glucose, is a normal blood constituent and is used by the body as a source of energy.  To utilize this energy the body requires insulin and some 20 enzymatic chemical reactions.

For the normal functioning of the human body, the concentration of glucose in the blood must be maintained within narrow limits (the normal range is 80 to 120 mg %).  The biochemical traffic policeman that controls the level of glucose in the blood is insulin.  Insulin is produced in a part of the pancreas called the Islets of Langerhans, from where it enters the bloodstream.

Since the amount of glucose in the blood may vary, such as after eating, the insulin must be doled out by the pancreas in just the right amounts.  Too little insulin circulating in the blood permits the glucose levels to rise (hyperglycemia) and brings on the diabetic state.  When the blood level of glucose rises above the height of the kidney dam of 170 mg % (kidney threshold) it spills over into the urine and positive urinary sugar tests result.  Too much insulin in the blood is equally bad because it produces the condition of hypoglycemia (low blood sugar) and there are probably as many people suffering from this serious condition as from diabetes.

In the treatment of diabetes, insulin is injected because, if given orally, it is destroyed by the digestive enzymes.  The dosage of insulin requires careful control because if it is too much, low bloodsugar, or “insulin shock,” will result.  A test used to determine whether pancreatic secretion of insulin is normal or not is the so-called glucose-tolerance test.  A large amount of glucose sugar is fed the fasting patient.  The blood glucose values are determined before and at hourly intervals after ingesting the sugar.  From the result obtained it is possible to distinguish normality, diabetes (too little insulin), and hypoglycemia (too much insulin).  If the body has an excess of sugar beyond its immediate needs, it is converted to the insoluble carbohydrate, glycogen, which is deposited in the liver for storage.  Thus a sugar reserve is available and, in times of need, glycogen can be converted back into the soluble sugar, glucose.

An estimated 4 million Americans have diabetes and about 1/2 of these are undiagnosed.  Heredity is important because, in about 50 percent of the cases, there is a familial history of diabetes.  It has also been estimated that about 22 percent of the United States population carries the recessive gene for this disease.  Diabetes ranks eighth as a cause of death in the United States and it is the third leading cause of blindness.  The importance of maintaining the delicate biochemical balance of insulin, therefore, cannot be underrated.  The use of insulin for the treatment of diabetes began in the 1920s and the Canadians, Frederick Banting and John Macleod, received the 1923 Nobel Prize in Biochemistry for its discovery.

Not long after the discovery of ascorbic acid in the early 1930s, tests on guinea pigs indicated that ascorbic acid had a profound influence on the body’s sugar utilization.  In 1934, C.G. King and coworkers (1), at the University of Pittsburgh, showed that guinea pigs maintained on low levels of ascorbic acid developed degeneration of the Islets of Langerhands.  Guinea pigs depleted of ascorbic acid showed a low glucose tolerance which was rapidly regained on feeding them ascorbic acid.  In 1935 and 1937, they also demonstrated that injection of sublethal doses of diphtheria toxin (increased stress) further diminished their tolerance to sugar in proportion to the length of their ascorbic acid deprivation.

These results were confirmed and extended in a comprehensive series of papers from India by Banerjee (2), starting in 1943.  He not only confirmed that guinea pigs with scurvy showed poor sugar tolerance, but indicated that the insulin content of the pancreas of scorbutic guinea pigs is reduced to about 1/8 that of normal guinea pigs. He observed gross  changes in the microscopic appearance of sections of the pancreas from scorbutic guinea pigs.  The appearance returned to normal when the guinea pigs were given ascorbic acid.  He also reported that the normal conversion of excess sugar into glycogen reserves for liver storage is also impaired in scurvy. In 1947, using improved laboratory techniques, he confirmed his earlier results and revised his estimate of the insulin content of the pancreas of scorbutic guinea pigs to one-quarter that of normal.  He also states in this paper:

The disturbed carbohydrate metabolism as seen in scurvy is due to a deficiency of insulin secretion and a chronic deficiency of this vitamin may be one of the etiological factors (causes) of diabetes mellitus in human subjects.

In 1958, he published the results of additional studies which confirmed his earlier work.  His 1964 paper contained the very suggestive results of the work on the intestinal transport of glucose. It was found that the intestinal absorption of sugar was about doubled when the animals were deprived of ascorbic acid and returned to normal when they received ascorbic acid.  If this observation is applicable to humans, it would mean that the intestines of diabetics,who may exist on chronic, low levels of ascorbic acid, would permit much more rapid absorption of sugar after eating.  The blood sugar levels would rise to higher levels faster and put abnormal stress on the already strained insulin production in their pancreas.

Other workers have reached similar results.  In fact, there have been so many papers published that a complete review is impossible in a single  chapter.  We will only discuss some very suggestive results on which further research should be expended.  Altenburger, in 1936, showed that guinea pigs deprived of ascorbic acid were unable to convert glucose to glycogen for storage in their livers, but this condition was promptly relieved when ascorbic acid was administered.  A dose of insulin that produced a pronounced decline in blood sugar in normal monkeys had little effect on monkeys deprived of ascorbic acid (Stewart and coworkers, 1952).  The intimate relationship between insulin and ascorbic acid has been noted numerous times.  When insulin is injected, there is a fall in the ascorbic acid levels in the blood serum of man, dogs, and rats, as shown by Ralli and Sherry in 1940 and 1948.  Haid, in 1941, also noted this drop, not only after insulin injection but in patients in insulin shock.  Previously,  in 1939, Wille reported that ascorbic acid is helpful to schizophrenics receiving insulin shock treatments.  She also produced evidence that ascorbic acid acts to raise the blood sugar levels in hypoglycemic attacks and said that prolonged administration of ascorbic acid will prevent these low blood sugar attache(3).

Ascorbic acid potentiates the action of insulin and, therefore makes it possible to derive the same effect with much less insulin.  This was observed in 1939 by Bartelheimer and was accidently confirmed by Rogoff and coworkers in 1944. (4).  Rogoff and his coworkers noted greater sensitivity in two diabetic children to their usual dose of insulin in the diabetic ward of their Pittsburgh hospital.  On checking, they found that the children had also been given ascorbic acid and they believed this fact was responsible for the excessive insulin effect.  In reviewing the literature, they cite a paper by Dienst, Diemer, and Scheer which reported that the ascorbic acid used in their tests on diabetics was equivalent to the effect of twenty units of insulin.  They also mention the work of Pfleger and Scholl (40) who, in 1937, noted that ascorbic acid so improved the action of insulin that a diabetic could control his sugar tolerance with a lower level of insulin.  Such conclusions should have initiated large-scale intensive research to determine how much ascorbic acid is needed to minimize the disagreeable insulin injections and still maintain controlled sugar metabolism and, incidentally, save diabetics millions of dollars.  The combination of ascorbic acid with the oral medications may also be helpful in avoiding some of the undesirable vascular side effects of diabetic treatment(5).

Tests were started in the early 1930s to determine if the administration of ascorbic acid would reduce the blood sugar levels of diabetics and this resulted in a large volume of medical literature.  As in the treatment of other diseases, with the short-term use of ascorbic acid, the more papers that appeared, the more confusion resulted.  Some clinicians reported good results in controlling diabetes and others stated that there was no effect.  The pros and cons are too numerous to be reviewed here.  It was pointed out, in 1935,that the does used may have been insufficient (6).  Whether or not this was true is unimportant; the entire approach to this research work may have been misdirected.  The tests were aimed at the short-term application of ascorbic acid to see whether diabetes, caused by an already damaged pancreas, could be controlled.  A better approach would have been in the area of prevention:  the long-term administration of ascorbic acid to prevent pancreatic damage and the subsequent occurrence of diabetes.  Such a plan is explained in the following paragraphs.

There is an assemblage of facts, scattered in the medical literature like pieced of a jigsaw puzzle, which have lain dormant for decades.  But when put together, they form the picture for research to possibly prevent the millions of cases of diabetes which develop later in life, especially in individuals who carry the recessive gene for this trait.  The pattern of the projected research would be to correct one genetic disease, hypoascorbemia, in order to help prevent the other, diabetes. Here are the facts

1.  There is a substance called alloxan which, when injected into laboratory animals, produces diabetes.  This has long been known and was used as far back as 1943 as a convenient and rapid means for inducing diabetes in laboratory animals for testing purposes.

2.  When ascorbic acid is oxidized, it forms dehydroascorbic acid, a compound similar in structure to alloxan.  The structures of ascorbic acid, dehydroascorbic acid and alloxan are shown in Figure 6.  One doesn’t have to be a chemist to see the similarity between dehydroascorbic acid and alloxan structures to the right of the midline drawn through the molecule and the dissimilarity of ascorbic acid.  The chemical properties of alloxan and dehydroascorbic acid are also strikingly similar, as noted by Patterson in 1950.

3.  Like alloxan, the injection of dehydroascorbic acid into rats produces diabetes as was shown by Patterson in 1949 and also produces diabetic cataracts as he showed in 1951.  That injection of ascorbic acid does not produce diabetes was shown by Levey and Suter in 1946.

4.  Banerjee reported in 1952 that he found no dehydroascorbic acid in the tissues, including the pancreas, of normal guinea pigs but stated, “It was present in considerable amounts in the tissues of scorbutic guinea pigs: (7).

5.  The mammalian genetic disease, hypoascorbemia, prevents us from making the mammalian liver metabolite, ascorbic acid.  The full correction of this genetic disease provides the rationale for the intake of much higher levels of ascorbic acid (8).

The genetically potential diabetics are those who may develop the diabetic state later in life.  During their early years, they have an apparent normal production and secretion of insulin from their pancreas.  As a group, they are likely to be more sensitive to factors which may affect the delicate physiological balance which controls insulin production.  This is indeed a delicate equilibrium.  With too little insulin, diabetes is the result; too much insulin produces the equally serious disease, hypoglycemia.  These genetically sensitive individuals have probably existed all of their lifetime on suboptimal levels of ascorbic acid.  Even the best diet could not supply their individual requirements. Finally, chronic ascorbic acid deprivation and depletion pushes them over the brink into a state of abnormal insulin production. This chronic exposure of their pancreas to the consequent high ratios of dehydroascorbic acid may slowly damage the secretory cells beyond the point where normal function or regeneration is possible, and the abnormal sugar responses result.

Diabetes may be prevented by the long-term ingestion of daily optimal amounts of ascorbic acid to keep dyhydroascorbic acid-ascorbic acid ratios at a minimum.  The long-term research needed to prove or disprove this thesis will be expensive, but preventing diabetes or hypoglycemia in millions of cases would certainly be worth all the costs.



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