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In the decade before the discovery of insulin, the prominent American physicians Frederick Allen and Elliott Joslin advocated severe fasting and undernutrition to prolong the lives of diabetic patients. Detractors called this "starvation dieting," and some patients did indeed starve to death. Allen and Joslin promoted the therapy as a desperate application of animal experimentation to clinical treatment, and texts still describe it that way. This justification was exaggerated. The public record contains only the briefest account of relevant animal experiments, and clinical experience at the time provided little indication that severe undernutrition had better outcomes than low carbohydrate diets then in use.

Introduction: Changes in dietary habits influence the glycemic level. Preliminary studies using the low-carbohydrate ketogenic diet (LCKD) were found to be quite promising in controlling diabetes mellitus. Therefore, the objectives of this study are to investigate the therapeutic effects of LCKD in experimental diabetic rats following the administration of streptozotocin (STZ)., Materials and Methods: Adult rats were divided into three groups: normal diet, LCKD, and high-carbohydrate diet. Each group was subdivided into normal, sham, and diabetic groups. Diabetes was induced by a single intraperitoneal injection of STZ (55mg/kg). Specific diets were given to each group of animals for a period of 8 wk and then the animals were sacrificed. The rats were monitored daily for food and water intake, whereas body weight, urine output, and blood glucose levels were monitored weekly. The histology of the islets of Langerhans was studied by histochemical methods., Results: The results showed that LCKD was effective in bringing blood glucose level close to normal (P<0.01). Food and water intake and urine output were increased in all groups except the LCKD group (P<0.01). The body weight was significantly reduced in all diabetic animals except in the LCKD group (P<0.01). Histologic studies showed significant decrease in the islet size and number of beta cells in all the diabetic groups., Conclusion: This study indicates that LCKD has a significant beneficial effect in ameliorating the diabetic state and helping to stabilize hyperglycemia.

The effect of dietary sorbose on diabetes after the incidence of the syndrome in the nonobese diabetic mouse was investigated in the animals from 8 to 14 weeks of age. When sucrose (200 g/kg diet) in a control diet was replaced by sorbose, the body weight and the blood glucose concentration were significantly reduced, but the serum insulin concentration was unchanged. The urinary glucose concentration was the same for both sucrose and sorbose diets. It is suggested that after the incidence of diabetes, dietary sorbose could not improve urinary excretion of glucose, even though sorbose could reduce the blood glucose concentration.

The effect of dietary sorbose on the prevention (Experiment 1) and amelioration (Experiment 2) of diabetes was investigated in the genetically diabetic mouse [C57BL/KsJ (db/db)] for 6 wk. When sucrose (200 g/kg diet) in a control diet was replaced by sorbose, the blood glucose concentration was dramatically lower, but the serum insulin concentrations did not differ. When mice were fed the diets before the onset of diabetic symptoms, glucose excretion in urine was prevented in the mice fed the sorbose diet, but mice fed the control diet excreted glucose in the urine, and the concentration increased with age. When dietary treatment began after the development of diabetic symptoms, dietary sorbose greatly reduced the incidence of hyperglycemia and lowered urinary glucose excretion, compared with mice fed the sucrose-containing diet. These results suggest that dietary sorbose might be useful in patients with, or at risk of developing, noninsulin-dependent diabetes, both before and after exhibiting the syndrome.

Sixteen diabetics were studied over six-week periods on two diets--a conventional carbohydrate-restricted diet and a diet which excluded all refined (fibre-depleted) carbohydrate but which allowed unrefined (fibre-intact) carbohydrate freely. On the latter, there was a substantial increase in dietary fibre intake. Despite this, there was no change in 24-h urinary excretion of glucose nor in blood glycosylated haemoglobin concentration, and there was only a modest improvement in post-prandial plasma glucose concentration. We suggest that simply switching from refined to unrefined cereal foods without increasing total carbohydrate intake is unlikely to produce much improvement in diabetic control.

When nine diabetic patients supplemented either their normal home diets (four patients) or metabolic ward diets (five patients) with 25 g guar gum daily for 5 or 7 days their mean urinary glucose excretion fell by 46% (P less than 0-05) and 54% (P less than 0-01), respectively. Gel-forming,, unabsorbable carbohydrate may therefore be a useful adjunct to anti-diabetic therapy, irrespective of the type of treatment or insulin dosage used.