Historical Events

Dr Himsworth explains why he thinks high carb diets are good for diabetics - and pays special attention to how carbohydrate sensitizes the pancreas to release more insulin, while also speaking towards insulin resistance. His 11 page science article is pretty interesting.

High Carbohydrate Diets and Insulin Efficiency

Physicians were slow to appreciate that insulin allowed the proportion of carbohydrate in the diet to be increased, for, as Himsworth said, ‘a well-founded theory directs that the carbohydrates in the diabetic’s diet must be curtailed if health is to be preserved’. On the other hand, as he continued, ‘a brilliant piece of clinical empiricism produces irrefutable proof that a liberal allowance of carbohydrate acts favourably on the diabetic’s health’ [17]. This empiricism began in 1926, when a high carbohydrate diet was first shown to improve glucose tolerance in healthy individuals [18].


Himsworth recommended a high-carbohydrate diet to treat diabetes. Professor Edwin Gale has noted:

He demonstrated that injected insulin produced a greater hypoglycaemic response in individuals treated with the high carbohydrate diet, thus demonstrating that diet could influence insulin sensitivity. The high carbohydrate diet worked because it allowed the flow of glucose to the tissues to be maintained at a lower head of pressure by making people more sensitive to their own insulin.[5]



During the last four years the use of diets containing a relatively large quantity of carbohydrate has become more and more common in the treatment of diabetes mellitus. When these diets were first introduced they were received with many theoretical objections, but their undeniable success rapidly compelled their serious consideration and encouraged their increasing acceptance. This divergence between theoretical objection anid practical success is no minor discrepancy capable of easy adjustment after careful revision of the data, but a definite conflict between two diametrically opposed conclusions. 

On the one hand, a well-founded theory directs that the carbohydrates in the diabetic's diet must be curtailed if health is to be preserved; whilst, on the other, a brilliant piece of clinical empiricism produces irrefutable proof that a liberal allowance of carbohydrate acts favourably on the diabetic's health. At present it may be said that the thepretical objections are securely established, not only on a logical sequence of experimental results, but also on the accumulated clinical experience of diabetes mellitus before the introduction of insulin whilst the beneficial effects attending the use of high carbohydrate diets are inexplicable either by any known physiological or pathological mechanism, or on the basis of previous clinical experience. A probable clue as to the nature of the discrepancy is suggested by a consideration of the chronological relation of the conflicting views. The good results following the use of high carbohydrate diets were not discovered until after the introduction of insulin treatment. This suggests that there exists in the body a mechanism capable of stimulating the utilization of carbohydrate, but which cannot exert its action in the absence of an adequate supply of insulin. It was with the object of searching for this mechanism that the present work was undertaken, and the employment of healthy men as subjects for the search was dictated by the supposition that it would only be possible to detect the unknown mechanism in subjects possessing the normal supply of insulin. 

Theoretical Objections to High Carbohydrate Diet 

Before discussing the present research it is first necessary to glance at the work upon which the theoretical objections to the use of high carbohydrate diets in diabetes are based. For a long time it has been known that the excessive consumption of carbohydrate by the diabetic results in deterioration of his clinical condition. It was not, however, -until a few years before the discovery of insulin that light was thrown, by the work of F. M. Allen and his collaborators, on the mechanism of this unfavourable clinical change. Allen studied the effect of diet upon the health of partially depancreatized dogs, and summed up his results by saying:

"Dogs which have lost a certain amount of pancreatic tissue will become diabetic irrespective of diet. Dogs which retain a sufficient amount of pancreatic tissue will never become diabetic irrespective of diet. But between these two groups is an intermediate group. On an Eskimo diet they may be found to live in health. On a Hindu diet they soon go down to fatal diabetes." 

Thus if sufficient pancreas is removed from a dog so that it is on the borderline of pancreatic diabetes the animal lives, if it receives a low carbohydrate diet, and the blood sugar remains low and glycosuria does not occur. But if such an animal is given a diet rich in carbohydrates the full clinical and chemical picture of pancreatic diabetes appears, and the animal rapidly dies. Allen further confirmed the work of other investigators, showing that, as a general rule, once pancreatic diabetes has been induced in these dogs by excessive intake of carbohydrates, then a return to the low carbohydrate diet will not cure the condition. It would appear that ingestion of excess of carbohydrate overstrained the remaining pancreatic tissue so as to produce a permanent degree of degeneration. In the partially depancreatized dogs which died of the diabetes thus induced, histological examination of their pancreatic tissue revealed hydropic degeneration of the ,B cells of the islets of Langerhans, and Allen emphasized that this was also found in the pancreas of the patient dying in diabetic coma. As by this time the probability of the insular tissue's secreting an "anti-diabetic hormone" was generally accepted, conclusions from Allen's work were easily drawn. In the partially depancreatized dog excess of dietary carbohydrate, by producing a raised blood sugar, causes overstrain of the islets in the remaining pancreatic tissue; under this strain the cells break down and eventually are unable to secrete sufficient hormone to prevent the development of pancreatic diabetes. At death the /B cells of the islets are in a state of hydropic degeneration; the pancreas from the diabetic dead of his disease shows similar lesions; therefore to preserve life in the diabetic the islet cells must be guarded against overstrain by maintaining the blood sugar at a low level by restriction of carbohydrates in the diet. The Allen diet--and the theoretical objections-are based on these conclusions.

Clinical Significance of the Results 

The results recorded in this paper carry us on our way towards the explanation of Allen's glucose equivalent of insulin. The reason behind the observation that the more carbohydrate ingested the greater the amount retained in the body by each unit of insulin is that the more carbohydrate eaten the more sensitive the organism becomes to each unit. Hence the paradox of the glucose insulin equivalent. It will be remembered that Allen's experiments were carried out on depancreatized dogs, and thus demonstrate that such a dog under the stimulus of the administration of carbohydrate is capable of developing an increasing sensitivity to insulin. My results show that the giving of carbohydrate raises the efficiency of. both injected and pancreatic insulin in the normal subject. It only remains to prove that carbohydrate has the same action in the diabetic and the explanation of the beneficial effect of high carbohydrate diets in these patients has been achieved. Ellis has recently supplied this proof. To diabetics needing large doses of insulin he gave glucose by mouth and small doses of insulin every hour. A remarkable increase in insulin efficiency resulted. Despite the ingestion of constant large amounts of glucose the dose of insulin required to restrain the blood sugar within normal limits decreased progressively. These results show that some diabetics, though possibly not all, are capable of developing a heightened sensitivity to insulin under the stimulus of carbohydrate ingestion. Thus the improvement of diabetic patients on a high carbohydrate diet is to be ascribed not to the greater stimulation, and consequent overstrain, of their insulin-secreting tissue by the excessive intake of carbohydrate, but rather to the rendering of the diabetic more susceptible both to his pancreatic and the injected insulin. The result is that each unit of insulin available accounts for a greater amount of carbohydrate. This, necessarily, by allowing a more economical utilization of the insulin secreted, reduces the demand of the body for insulin, with a consequent easing of the strain on the diseased islet cells. By thus lighteing the burden on the cells which remain capable of function it is possible that we aid their conservation as healthy tissue, and save rather than squander the patient's own pancreatic resources. If the augmentation of a diabetic's sensitivity to insulln is of importance in the balanced state, it is of much greater importance in the state of coma. It is well known that hundreds of units of insulin may be given in this condition with little effect on the blood sugar, when in the same diabetic after recovery 20 or 30 units will produce hypoglycaemic symptoms. Many comatose and precomatose patients seem to be relatively insensitive to insulin, and any measure directed to raise their sensitivity would appear to be of benefit. To this end glucose should be administered in large doses. The success of treatment based on this principle I have recorded previously, and the method has since been strongly recommended by Lawrence." A growing number of cases of diabetes are being. reported in which the patients for no ascertainable reason are found to be resistant to insulin. In one such case doses as large as 1,600 units of insulin a day had no effect on the blood sugar. It is possible that these cases may be explained by an almost complete absence of the factor making for susceptibility. In contradistinction to' these insulin-resistant diabetics, cases of spontaneous hypoglycaemia in which no hypertrophy or tumour of the islet cells can be found are continually being recorded. In such patients it is theoretically possible that the hypoglycaemia may be the outcome not of hyperinsulinism, but of the development of a state of a greatly heightened susceptibility lo insulin secreted by the pancreas. Finally, I would suggest the possibility of the existence of a type of diabetes due not to diminished secretion of insulin by the pancreas, but to a greater or less impairment of the organism's susceptibility to insulin. In such a case, although the output of endogenous insulin may be normal in quantity, the diminution or absence of the factor which is concerned in rendering the patient susceptible to insulin would produce a result identical with that of impaired production of insulin-namely, the clinical picture of diabetes mellitus.


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