Published Science

The current widespread concern with weight reduction rests on at least two assumptions: first, that weight-reduction programs are effective; second, that they are harmless. Recent studies indicate that such programs may be far from harmless.1,2 This report documents their ineffectiveness. The results of treatment, as reported in the medical literature of the past 30 years, are first reviewed. The results of routine treatment of 100 consecutive obese persons in the Nutrition Clinic of the New York Hospital are then reported.Hundreds of papers on treatment for obesity have been published in the past 30 years. Most, however, do not give figures on the outcome of treatment, and of those that do, most report them in such a way as to obscure the outcome of treatment of individual patients. Some authors, for example, report the total number of patients and the pounds lost without making clear

Experiments were undertaken to ascertain whether the previously demonstrated inhibition of the development of experimental aortic atherosclerosis in alloxan-diabetic rabbits fed cholesterol was due to the injection of alloxan per se or to the existence of the diabetic state produced by alloxan. It was established that, by treating the diabetic state with insulin, the diabetic state could be ameliorated and the inhibitory effect obviated. It was therefore concluded that the inhibitory phenomenon was not due to the injection of alloxan per se but that it was associated with one or more factors that characterize the alloxan diabetic state in the rabbit and that are reversible by insulin therapy. In the course of the experiment it was demonstrated that the inhibitory effect was apparent in cholesterol-fed diabetic rabbits whether or not their diet was supplemented with vegetable oil. The previously reported metabolic abnormalities of the diabetic animals were confirmed. It was established that suitable treatment of the cholesterol-fed diabetic animals with insulin would bring all the metabolic aberrations, including those of the serum lipids, into reasonably close correspondence with those observed in non-diabetic rabbits fed cholesterol.

SUMMARY. Restriction of carbohydrate, alone, appears to make possible the treatment of obesity on a calorically unrestricted diet composed chiefly of protein a

SUMMARY. Evidence for a homeostatic regulation of the appetite and of fat storage suggests, as a cause of obesity, some other hypothesis than “simple overfeedi

Three men are commonly considered the outstanding pioneers in modern treatment of diabetes: Bouchardat (1806-1886) in France, Cantani (1837-1893) in Italy, and Naunyn (1839-1925) in Germany. Of the three, Cantani was foremost in his insistence that stopping glycosuria was the major method of controlling the disease. All three men lived at a time when, after centuries of dense ignorance, there occurred an explosive outburst of scientific achievement and enthusiasm which is reminiscent of the similar excitement arising from the primitive beginnings of an atomic technology in our own time. As background for their researches in diabetes these three pioneers had Rollo's “animal food” empiricism; the physiological revelations of Claude Bernard; the discovery of enzymes and also of internal secretions; the foundation of physiological chemistry by Liebig; Pasteur's incredible bacteriology; the new microscopic anatomy opened up by the Schleiden- Schwann cell theory and followed by Virchow's cellular pathology; many metabolic studies capped by the investigation of respiratory metabolism by Pettenkofer and Voit; and—by no means unimportant in themselves— the developmentof methods of sugar analysis both by copper reduction and by polarimetry.

Obesity is one of the commonest physical abnormalities found in the general population. It shortens life, affects health, and impairs prognosis. It is indeed true that fat comes only from food, and those who wish to get rid of accumulated body fat must eat less than is required to meet the energy requirement of the body.1Numerous investigators are not satisfied with this conception as a complete and final answer to the problem of obesity. Normally, there is a nice adjustment between appetite and caloric needs, and the body ordinarily maintains itself in a fairly constant state. Whatever the underlying cause of obesity is, in the last analysis it involves a disturbance in the normal relation of the appetite to the energy expenditure. The mechanism which determines appetite is a primary factor in the development of obesity. There is no satisfactory answer as to what determines appetite satisfaction, but,

A comparison was made of the effects of cholesterol feeding in normal rabbits and in rabbits rendered persistently diabetic by means of alloxan. In the two groups of animals hypercholesterolemia of comparable degree was induced by the feeding procedure. Nevertheless, the severity of the atherosclerosis of the aorta produced in the diabetic rabbits was much less than in the non-diabetic control animals. Indeed, a large proportion of the diabetic animals presented no atherosclerosis whatever. There was a similar inhibition of the deposit of lipid substances in the liver, spleen, and adrenal glands of the diabetic rabbits. The inhibition of the development of experimental cholesterol atherosclerosis which was associated with the presence of alloxan diabetes was independent of the administration of alloxan per se. It was not dependent on the sex or weight of the animal, nor upon the daily dosage of cholesterol, the form in which it was administered, nor the duration of cholesterol feeding. It was also independent of changes in body weight occurring during the course of our experiments and of the actual degree of hypercholesterolemia induced by the administration of cholesterol. In addition, there was no gross or histological evidence of a morphological basis for the inhibitory effect either in the aorta or in the other organs in which it was observed. Only two factors were observed to be consistently associated with the inhibition of the expected morphological effects of cholesterol feeding, namely, the diabetic state and a degree of visible lipemia considerably greater than that observed in the control animals. The inhibitory effect observed in these experiments would appear to depend upon some as yet undetermined factor or factors implicit in the diabetic state or closely associated with it. The experimental data presented demonstrate clearly that hypercholesterolemia is not the sole factor concerned in the genesis of experimental cholesterol atherosclerosis, but that another factor, or factors, rendered inoperative in our experiments must be essential to the production of the arterial lesions. In view of the inhibitory effect on the development of experimental cholesterol atherosclerosis observed in alloxan-diabetic rabbits, the effect of alloxan diabetes on the retrogression of such arterial lesions was studied in another series of experiments. No effect on retrogression could be demonstrated within periods lasting up to a maximum of 4 months after the cessation of cholesterol feeding. The results of our two series of experiments, considered together, indicate that the process of deposition of lipids in the arterial walls is governed by factors different from those that are operative in the process of removal of lipids after they have been deposited. The inhibition of the development of experimental cholesterol atherosclerosis in alloxan-diabetic rabbits must depend on interference with the process of deposition of lipids and not on a process of removal of lipids as fast as they are deposited. Our experimental results find no direct application to the problem of arterial disease in human diabetes. Nevertheless, the experimental procedures that we have employed provide a new basis for the design of further experiments directed toward the elucidation of the nature of the unknown factors that govern the process of lipid deposition in the walls of arteries.

Factual evidence that is slowly being accumulated both in this country and in Canada, although it is as yet meager, shows that nutritional deficiency disease prevails in many parts of the country.1 Sebrell2 believes that it is no exaggeration to say that at least one third of the American population is eating a diet which is not adequate in all respects. Basing our judgment on the requirements which modern nutritionists consider as optimum nutrition, not mere adequacy, we believe that widespread improvement in health is possible. The evidence of malnutrition is not restricted to low income groups or families on relief but is just as apt to be found in the middle and upper class families.Although it was suspected that the average American diet might be well below the optimum in certain essential nutrients, there was no means of proof available until the classic publication of Stiebeling

BY KETOSIS we understand the occurrence or accumulation in the blood in significant amounts of the so-called ketone bodies, namely beta-hydroxybutyric acid, acetoacetic (or diacetic) acid and, secondarily, acetone. In normal subjects on a general diet ketone bodies are present in the blood in inconsiderable amounts (Barnes and Wick, 1939). They appear in largest quantities in cases of severe diabetes and with normal subjects only when fasting or when the food carbohydrate is greatly restricted. Hirschfeld in 1895 (42) first showed that the factor common to these conditions and responsible for the ketosis is the absence of carbohydrate from the food or, as in the diabetic, from his metabolism. Today there is no question that ketosis is due to carbohydrate lack.Our ideas of how carbohydrate lack produces a ketosis have undergone many alterations. The old idea, first advanced by Geelmuyden in 1909 (39), that the ketone bodies represented incomplete oxidation products of the fatty acids which required the concomitant oxidation of carbohydrate metabolites for their utilization gained many adherents (93, 100, 94, 51) and the so-called ‘ketogenic-antiketogenic’ ratio (Shaffer, 1923) which implied a quantitative relationship between the oxidation of ketone bodies and glucose became widely accepted.

Analysis of the health records of 6438 children in Chicago