This section is from the book "Practical Dietetics With Special Reference To Diet In Disease", by William Gilman Thompson. Also available from Amazon: Practical Dietetics with Special Reference to Diet in Disease.
Because so much water is eliminated in the urine there is scarcely any perspiration, and the skin becomes dry and wrinkled, the face looks drawn and pinched, and the eyes are hollow. In advanced cases a sweetish, sickening odour is exhaled from the skin and in the expired air. From lack of intestinal secretion the bowels are usually constipated, although diarrhoea may alternate with constipation in the later stages of the disease.
At first the food eaten does not supply the needs of the body and there is constant craving for more.
To obtain the requisite carbon from fats a labourer, taking his ordinary allowance of proteids, would in addition have to eat about three hundred and fifty grammes of fats, which would be manifestly impossible. The diabetic is practically in this position when all carbohydrates are denied him, and a much larger bulk of food is necessary for him than if he could eat food containing more carbon but less protein. This accounts in a measure for the extreme hunger which is felt by many diabetics when suddenly deprived of their accustomed starchy foods.
In the later stages of the disease dyspeptic symptoms are prominent with flatus, sour eructations, and a disgust for all kinds of food. The teeth decay, the gums become tender, and mastication is difficult.
The alimentary canal is frequently the seat of chronic gastric catarrh, with thickening of the mucous lining of the stomach and small intestine. Diarrhoea may be caused by the excretion of sugar from the intestinal mucous surface. Occasionally nausea and vomiting are present, and the ejecta may contain acetone. The secretion of bile is lessened. Emaciation sooner or later becomes extreme and progresses, although the appetite remains normal or may be still increased.
The loss of weight, which is so pronounced a feature of most advanced cases of diabetes, is attributed in part to the non-burning of carbohydrates, and in part to the loss of their albumin-protecting action (Graham Lusk). In health, oxygen is used to consume sugars, which in diabetes, when sugars are withheld, burns the fat of the body instead, so that the quantity of oxygen inhaled and carbon dioxide exhaled may remain nearly identical in the two conditions, while emaciation progresses. In addition to lack of nitrogen of the tissues the wasting is also in part to be accounted for by the drain of fluid from the system which takes place when once over-action of the kidneys is established. Phthisis is often present and increases the rapidity of the emaciation. Exceptionally, early in the disease the patient, owing to the greater appetite and the large amount of fluid drunk, may increase somewhat in weight. Muscular weakness and debility rapidly supervene to a greater extent than is to be accounted for by the usual loss of flesh.
In general, it may be said in the milder forms of diabetes that the sugar in the urine is derived from carbohydrate foods, while in the more serious forms it is also derived from the nitrogenous metabolism. The sugar which is eaten as food or which is formed by starch in the alimentary canal, after absorption is mainly used under normal conditions in the production of force, but in diabetes it is eliminated unaltered from the body, and there is consequent lack of heat production and muscular power.
Since a large amount of heat-producing material passes from the body without complete oxidation, the body temperature is not infrequently subnormal, and it may so remain throughout the disease unless there be some inflammatory complication. The axillary temperature may be 970 or even 950 F. The occurrence of any acute joint or visceral inflammation or of any acute fever causes a reduction in the quantity of sugar eliminated while the pyrexia lasts. The explanation of this fact is by some observers thought to be due to increased combustion of sugar in the body during the pyrexial stage, but Bernard attributed it to an interference with the glycogenic function of the liver. The pulse becomes rapid and feeble and the temperature is subnormal.
When great feebleness compels the patient to become bedridden, bedsores and excoriations from frequent passage of acid and saccharine urine add to his discomfort.
Diabetic coma is the precursor of sudden death in a certain number of cases, and it is also to be regarded as the worst possible symptom which may arise. Many theories have been offered in explanation of this symptom, and the one which is at present in vogue is that it is produced by an acid intoxication produced by accumulation in the system of ß-oxybutyric acid, constituting an acidosis (Nau-nyn). This acid is found in the tissues and blood, and also, in combination with bases, in the urine. The acid is derived from tissue albumins, and possibly fats, and over 200 grammes may be present in the tissues in a fatal case. Gangrene, asthenia, or intercurrent diseases cause a number of deaths.
There are other symptoms affecting the nervous system, the eyes, etc., and there are many complications which may arise in the course of the disease, but a consideration of them would lead too far from the object of the present discussion, which is to deal with those symptoms which bear a more immediate relation to the metabolism of the food.
Some of the complicating diseases with which diabetes may be associated make it impossible to adhere to a rigid regimen without producing more harm than good. Such, for example, are acute gout and chronic nephritis, in both of which a meat diet is injurious, and if carbohydrates are also cut off the patient has little or nothing left to eat. In these cases the diet must be determined by whichever constitutes the graver complication (see p. 505).