Infections in other parts of the body, such as rectal ulcers, ischio-rectal abscesses or fistulae and chronic bone or skin infections must all be looked for and eradicated before the gastrointestinal infection can be permanently influenced.

The question as to whether gastrointestinal infections in themselves may act as foci, causing secondary infections in other parts of the body, is still a mooted one. In a study of 1439 patients with gastrointestinal infection in office and clinic only 73 showed cardiac involvement, only 13 joint symptoms, 57, kidney complications, and 10, eye infections. Of these 153 cases which represented only a little over 10 per cent of the total number of gastrointestinal infections, 68 occurred in patients with peptic ulcer, which has never been spoken of as a primary focus, and only 28 in cholecystitis and 41 in appendicitis. In my experience the instances in which such infections of other parts of the body were present have therefore been very rare, and where present, the removal of focal infection for the purpose of influencing gastrointestinal infection

have in most instances resulted not only in the relief of the gastrointestinal infection, but also in the disappearance of heart-murmurs, a cessation of joint and nerve pains and improvement in the kidney disease.

SUMMARY

1. The relation between focal infections and chronic gastrointestinal infection has been demonstrated, not only experimentally, but clinically.

2. The removal of focal infections is not only of general but specific value in cases of chronic gastrointestinal infection.

3. Thorough eradication of every focus is necessary if results are to be obtained, adverse results being usually due to insufficient care in this respect.

4. The gastrointestinal tract is not frequently a focus for infections in other parts of the body.

5. The eradication of all focal infections is not only a good preparation for operation in chronic gastrointestinal infection, but in many instances will obviate such operation by producing a cure of the gastrointestinal condition.

T

HIS paper is in the nature

of a preliminary report on the completeness of digestion of food in extremely undernourished diabetics. The type of diabetic referred to shows extreme degrees of undernutrition (fig. 1). The weight is from 20 to 40 per cent below the normal for sex, age and height. The severity of the diabetic condition is pronounced and extreme. Other conditions often complicate the picture but usually post-date the onset of diabetes. Such degrees of undernutrition as are here shown predispose to complications other than those associated with diabetes. itself. These complications doubtedly play a rôle in exaggerating the symptoms of undernutrition.

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Insulin has presented an opportunity to study the processes of upbuilding of the body. Every physician has seen diabetics who were 40 to 60 pounds underweight and unable to ingest enough food to support life without glycosuria, gain in strength and weight until able to live comfortably and become useful to society. Some of these patients gain weight very rapidly, while in others it is gained very slowly.

Read before the American Congress on Internal Medicine, St. Louis, February, 1924.

The reasons for the failure of greatly undernourished patients to gain weight has been the subject of our investigations for the past few months. We have been fortunate in being able to keep patients in the hospital long enough (two to six months) so that the ability or failure to gain in weight can be demonstrated (table 2).

The insulin requirement of these undernourished patients is of interest. The fact that the patient presents the picture of great undernutrition leads one to believe that the diabetic condition is of severe degree. One would suppose that rather large doses of insulin would be required from the beginning of treatment in such cases. It is therefore surprising to find that rather small doses will make the patient sugar-free. When one increases the diet the patient may still remain sugar-free or eliminate unexpectedly small amounts of sugar. A small increase in insulin will perhaps again free the urine of sugar. The diet may possibly be raised to 1800 or 2000 calories and the daily insulin dose amount to but 10 to 15 units. One is tempted to doubt at this stage in the treatment whether the disease is as severe as the clinical picture had led one to believe. A few weeks or perhaps

FIG. 1

a month may elapse; then rather suddenly sugar begins to appear in the urine and increases steadily in amount. The diet has remained the same and the first impulse is to assume that the patient has been getting food surreptitiously. The insulin dose is increased to keep the glycosuria under control. Again the

patient may be sugar-free for a time, but after an interval will show sugar and require still more insulin. The picture presented then is of ever increasing amounts of insulin to control glycosuria without having raised the diet proportionately (table 1).

It has been pointed out by ourselves, as well as many other observers, that clinically there seems to be a quantitative relationship between the insulin administered and the sugar that can be utilized. Roughly, for 1 international unit 2 grams of carbohydrate can be utilized by the body. When one applies this rule to these cases of extreme undernutrition, the above relationship does not hold. As before stated, during the first weeks of treatment 1 unit of insulin might apparently enable the body to use anywhere from 3 to 10 grams of carbohydrate. As the doses of insulin must be increased to control glycosuria, the value of the administered insulin becomes less and less (table 1), perhaps falling below 2 grams of sugar per unit. Thus, in the greatly undernourished patient one observes the following facts: first, failure to gain in weight proportional to the calories fed; second, the insulin requirement increases as treatment progresses; third, the insulin requirement is not proportional to the sugar fed. This last fact being particularly true in the early period of treatment.

How are these observations explained? The undernourished diabetic must differ in some respects from the less severe type. The moderately severe case, not so under

nourished, gains weight rapidly and requires insulin directly in proportion to the increase in his diet. Many explanations occur to us, but only a few of the important ones will be discussed.

We have used the high fat, low protein diets. The observations in this paper are true when patients are fed high fat, low protein and low carbohydrate mixtures. Allen has held that fat decreases the patient's tolerance. These high fat diets may have decreased the patient's own insulin production to such an extent that he required larger doses of insulin. It has been our experience in dealing with the less severe diabetics that they are more apt to gain in tolerance while receiving high fat diets than to lose it. Why should high fat diets injure greatly undernourished patients, while patients with a slightly less severe grade of the disease gain in tolerance?

Another possibility is that insulin is less efficient with high fat diets. The carbohydrate to insulin ratios we have obtained are comparable to those obtained by others using, perhaps, less fat in their diets. Nevertheless, it seems quite probable to us that in order that fat be easily absorbed and laid down in the animal's body in the form of the animal's own fat, sugar must be burned. If the burning of sugar be necessary for the deposition of fat in bodily tissues, it is quite possible that when fat is rapidly deposited there is an extra demand for insulin. Such a demand should be present in any diabetic showing a moderately severe grade of the disease.

The obvious explanation for these phenomena shown by undernourished diabetics is that the digestion and absorption of food is incomplete. Such a patient does not gain in weight because his food is not being absorbed; he does not require much insulin at first because his absorption is incomplete. After receiving insulin for some time the patient's general nutrition is improved; his digestive processes share the improvement and more food is absorbed. Sugar appears in the urine because more is being absorbed from the digestive tract. Everyone has seen the emaciated diabetic before receiving insulin-lethargic of mind and body, skin dry and inelastic and parchment-like in color. A few weeks of insulin treatment and he becomes alert, energetic enough to wish to be out of bed; skin moist and elastic and eyes bright and clear. These changes occur long before there is perceptible gain in weight. Is it not reasonable to suppose that the digestive tract has shared in the rejuvenation that is so evident in the changed mental and general physical aspects of the patient?

The examination of the stools of these undernourished patients showed a great deal of fat, starch and muscle fibers (table 3). We set about the quantitative determination of the losses of food stuffs occurring in the stools. Patients whose weights were 40 to 50 per cent below normal passed stools which were so full of undigested food that the starch and fat could readily be estimated. However, as a rule, we were disappointed in our quantitative determinations.