USA History

The general scope of the investigation was outlined in 1926 and 1927 by an advisory committee of scientists of which Dr. Raymond Pearl of Johns Hopkins University, Baltimore, was chairman. The main portion of the work was carried on while the two subjects lived and ate in the metabolism ward of the Russell Sage Institute of Pathology in Bellevue Hospital, New York. The study was a cooperative one and several papers on various phases of the work have already been published. Short reports on the clinical features and general laboratory findings have been made by Lieb (9) and by McClellan (10). The excretion of acetone bodies has been discussed in papers on ketosis by McClellan, Spencer, Falk, and Du Bois (11) and by McClellan and Toscani (12). The chemical studies on the constituents of the blood have been presented by Lieb and Tolstoi (13) and by Tolstoi (14, 15). References to the above papers will be made later in this report. A series of three papers, of which this is the first, will present the observations made in the ward, calorimeter, and laboratories of the Russell Sage Institute of Pathology.

Two normal men volunteered to live solely on meat for one year, which gave us an unusual opportunity of studying the effects of this diet. The term “meat,” as used by us, included both the lean and the fat portions of animals. The subjects derived most of their calories from fat and the diet was quite different from what one, who uses the term “meat” as including chiefly lean muscle, would expect. Rubner called attention to the fact that a man cannot live on meat alone because of the physical limitation of the apparatus of mastication. He was evidently considering only lean meat as fat offers little difficulty. It is well known that the Eskimos have lived on an almost exclusive meat diet for generat.ions. Certain explorers in the North also have subsisted for long periods on meat. Dr. Vilhjalmur Stefansson in particular has demonstrated that it is feasible for travelers in the arctic region to “live off the country,” which means living on meat alone. The experiences of Stefansson and his companions have been given in his book “The Friendly Arctic”. He spent over 11 years in arctic exploration, during 9 years of which he lived almost exclusively on meat. Stimulated by this experience, Stefansson and Andersen, the latter a member of one of the expeditions, voluntarily agreed to eat nothing but meat for 1 year while they continued their usual activities in the temperate climate of New York.

THE NATURE OF OBESITY

L. H. NEWBURGH AND MARGARET WOODWELL JOHNSTON 

(From the Department of Internal Medicine, Medical School, University of Mickigan, Ann Arbor) (Received for publication April 22, 1929) 

The medical profession in general, believes that there are two kinds of obese persons-those who have become fat because they overeat or under-exercise; and those composing a second group whose adiposity is not closely related to diet, but is caused by an endocrine or constitutional abnormality. The first apparently scientific support of the hypothesis that obesity was often of endogenous origin, came with the finding that some obese persons had an abnormally low basal metabolic rate, on the basis of body weight. When, however, it was shown that the expenditure of energy is proportional to the surface area and not the weight, it was found that most such persons have a normal basal metabolic rate. However, it is true that there remains a small group of fat people whose basal rate is definitely low. Later writers maintained that a common cause of endogenous obesity was to be found in a lessened specific dynamic response to food. But the increase in metabolic rate caused by food is relatively small, so that a method possessed of a high degree of accuracy is needed in order to deal quantitatively with this phenomenon. Our prolonged study of this question has convinced us that the inherent error in the method to date, when it is applied to the human subject, is such that it precludes the possibility of making quantitative statements regarding the specific dynamic response to food in man. Other writers have attributed endogenous obesity to a constitutional anomaly of the cells which somehow lowers the rate of intracellular oxidations.

....

These considerations lead to the conclusion that the fundamental cause of endogenous obesity is not to be found in some type of metabolic abberation; but rather, that these individuals, in common with all obese persons, are the victims of a perverted appetite. In normal people there is a mechanism that maintains an accurate balance between the outgo and the income of energy. All obese persons are, alike in one fundamental respect,-they literally overeat.

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The unspoken proposition is that if researchers could only figure out how to induce those of us who eat too much to rein it in, curb our out-of-control appetites, eat smaller portions, and refrain from reaching for the doughnuts, we’d lose weight or not fatten to begin with. This, again, evokes implicit judgments about why we might fail should we have the misfortune to remain fat. It’s not a failure in our bodies, not some hormonal or physiological phenomenon, that’s drove us (but not our lean friends or siblings) to amass fat. Rather it’s some behavioral quirk, whether moral turpitude, lack of willpower, lack of vigilance, or the sin of gluttony and/or sloth. That’s why we’re still fat. It’s not the expert advice or thinking that’s misguided. It’s us. This blame-the-fat-person, look-who’s-reaching-for-the-doughnuts thinking, the moral judgments and fat shaming, has always been embedded within this idea that obesity is caused ultimately by overeating. Here’s one of the many areas in this controversy in which it helps to know the history. This fat-shaming implication was institutionalized as far back as the 1930s by the University of Michigan physician Louis Newburgh, who was largely responsible for convincing decades of physicians and obesity researchers that obesity is indeed caused by eating too much—“a perverted appetite” or a “lessened outflow of energy,” as he put it—and not by some hormonal or physiological defect. Obesity, he and his colleague Margaret Woodwell Johnston wrote in 1930, is “always caused by an overabundant inflow of energy.” The cause is never an “endocrine disturbance”—that is, hormones—that would manifest itself as a tendency to store calories as fat rather than burn those calories as fuel. By Newburgh’s dictate, the cause is always some form of eating too much. This left open, though, the obvious question: What causes this overabundance? Or, rather, why don’t fat people voluntarily curb their appetites, curb the overabundant inflow, and not get fat? Is it only a question of willpower? This too requires an explanation (just as the NIH authority in Nutrition Action still has to explain why some of us eat too much in this food-rich environment and others don’t). Hence Newburgh, and all those who have come after him, transformed a physiological disorder into a character flaw. The overabundant inflow, said Newburgh, is the result of “various human weaknesses such as over-indulgence and ignorance.” My suspicion, and I hope I’m not doing the man a disservice when he’s no longer around to take offense, is that Newburgh’s thinking was strongly influenced by the fact that he appears to have been pencil thin. Even in cases that seemed obviously hormonal—the pounds of fat often gained by women, for instance, when they pass through menopause or after a hysterectomy, the surgical removal of the uterus—Newburgh refused to concede an explanation other than overindulgence and weakness. Endocrinologists who studied this “well known” phenomenon in animals had concluded by the late 1920s that a critical role for female sex hormones—particularly estrogen—in the process of fat accumulation was implied. Secrete less estrogen, as women do during this phase of their lives or after a hysterectomy, and fat will accumulate. It happens to female animals. Maybe it should be no surprise it happens to female humans, too. So this, at least, must be hormonal. Not so, insisted Newburgh. It’s all eating too much: “Probably she [the woman getting fatter as she goes through menopause] does not know or is but dimly aware that the candies she nibbles at the bridge parties which she so enjoys now that she is rested are adding their quota to her girth.” Very scientific, that.

Gary Taubes. The Case for Keto: Rethinking Weight Control and the Science and Practice of Low-Carb/High-Fat Eating (Kindle Locations 635-640). Knopf. Kindle Edition. 

To the editor: It was with dismay that we read in The Journal, August 10, statements of Dr Edward Tolstoi at a conference of "the members of the Departments of Pharmacology and of Medicine of Cornell University Medical College and the New York Hospital, with the collaboration of other departments" regarding the treatment of diabetes. He said:

"We found that our experimental subjects were free from the symptoms of diabetes in spite of glycosuria when they were receiving a diet of 75 grams of protein, 60 grams of fat, and 200 grams of carbohydrate, and protamine zinc insulin in daily doses of 50 units."

Does it make common sense to say that an adult of average body build and activity receiving 1,640 calories, daily in the form of carbohydrate 200, protein 75, and fat 60 grams who is excreting 150 or even 100 grams of sugar in twenty four hours, thus leaving a net balance of 1,040 or 1,240 calories respectively, could maintain body weight and be in nitrogenous equilibrium for a prolonged period? Furthermore, is it sensible or economical to alow the wastage of so large a part of the food eaten?

Like many, others, we believe in controlling the hyperglycemia of diabetes (1) because it is fundamentally an abnormal state, (2) because a high blood sugar is a constant stimulus for insulin secretion and allows no opportunity for rest and recuperation such as the pancreas of a healthy person enjoys between meals and at night and (3) because control of hyperglycemia and glycosuria proves utilization of the diet whereas their disregard leads, in our experience, to accessory annoyances such as polydipsia and polyuria, the attendant necessity for extra food to make up for the loss of calories in the urine and the obvious wear and tear on the system for ingestion, assimilation and excretion of this unutilized extra food, quite apart from needless cost and waste. A high percentage of sugar in the blood implies the same in the tissues ; we think it likely that, directly or indirectly, this conduces to lack of normal tissue repair and resistance to infection, predisposes to degenerative phenomena in arteries and nerves and leads to weakness, weariness and impotence, although we freely admit that positive proof is lacking that all these harmful effects are due to hyperglycemia per se. Unhesitatingly we maintain that the blood sugar should approach normal because it is an index of the control of the diabetic condition ; if normal, it is one assurance that the whole disease is being treated well. Hyperglycemia is the red light which the physician should no more disregard, although he cannot always explain its significance, than he should fail to heed the red signal at the railroad crossing because he cannot see the train around the corner. 

Dr. Tolstoi's advice for certain cases of diabetic acidosis follows : 

First, let us consider the one whose condition is not far advanced, the patient as we see him in the clinic. He may report a sore throat. Examination of the urine reveals a 4 plus acetone reaction and diacetic acid. The skin and the tongue are dry, there is dehydration and there are listlessness and the desire to be left alone. We tell the patient "Go home, take a tablet or two of tablé salt (1 Gm. of salt) every hour, and follow that with a glass of water; in addition, take all the hot salt broth you can." We teach him to examine his urine for acetone and tell him to do so every two hours, and as long as acetone is present to give himself insulin (regular soluble) after each urine examination until the acetone bodies disappear. The dosage of insulin is determined by the urine analyses for sugar. He is told to take 25 units if the result of the test is yellow or red, 15 units if the specimen is green, and the juice of an orange if the Benedict solution is unchanged after boiling. This simple rule also protects the patients against insulin overdosage. 

We condemn such advice. In our opinion it is dangerous to send home patients whose urine gives a 4 plus reaction for acetone and diacetic acid. Dr. Tolstoi does not even suggest that they keep under the supervision of their family physicians. If there is one thing we attempt to do as a result of our experience with patients in coma and near coma, with diabetic children and with diabetic patients in general, it is this—to train them, if any unusual symptoms occur, to call the doctor. A patient who exhibits "listlessness and the desire to be alone" is not likely to carry out intelligent, energetic self treatment. We believe in the orthodox treatment of diabetes. We are convinced that our patients and the patients of other physicians do the best who follow the rules. Differences in diets of from 50 to 75 Gm. of carbohydrate a day are immaterial. By no means can we keep all our patients sugar free, but we do strive to maintain them under as good control as possible, thereby, as we believe, protecting them from complications and progression of the disease. Furthermore, as will appear in the forthcoming (October) (seventh) edition of the "Treatment of Diabetes Mellitus," we have endeavored to support our convictions by recording the complications, the causes of death and the duration of life in 5,669 of our fatal cases between 1898 and 1940. Tables show the decrease of deaths due to coma from 64 per cent to 4 per cent, the steady increase in duration of life after onset from 4.9 to 12.5 years and the advance in the average age at death from 44.5 to 64.8 years. 

Elliott P. Joslin, M.D. 

Howard F. Root, M.D. 

Priscilla White, M.D. 

Alexander Marble, M.D. Boston.

(Image is of Edward Tolstoi)

The Sugar Association, Inc. was originally founded as the Sugar Research Foundation (SRF) by members of the U.S. sugar industry during World War II in June 1943. The Foundation included U.S. beet and cane sugar growers and refiners as its members, and was dedicated to the scientific study of sugar’s role in food and communication of that role to the public during a period of war-time sugar rationing.

By 1946, SRF had expanded its focus to include international members, and grew from its six original board members and 29 firms and corporations to 77 members – including the entire Hawaiian sugar industry and the entire raw sugar production industry of Cuba. SRF members praised the foundation saying, “The U.S. sugar industry has finally ‘found a single, authentic voice for the expression of its views.’” SRF carried out its objectives through the funding and sponsorship of scientific research related to sugar and its by-products, as well as the creation and distribution of educational materials in both print and film formats.