TABLE 1.

Historical precedents regarding the carbohydrate-insulin model of obesity

Year	Authors	Quotation
1924	Harris (164)	“[O]ne of the causes of hyperinsulinism is the excessive ingestion of glucose-forming foods … It is possible that the hunger incident to hyperinsulinism may be a cause of overeating, and, therefore, the obesity that so often precedes diabetes.”
1938	Wilder and Wilbur (165)	“[It seems that] mobilization of fat from fat depots is resisted in obesity and that deposition is accelerated…. The effect after meals of withdrawing from the circulation even a little more fat than usual might well account both for the delayed sense of satiety and for the frequently abnormal taste for carbohydrate encountered in obese persons. Energy requirements must be satisfied one way or another, and if part of the food is made less available for metabolism, the result, as is the case in diabetes, inevitably is hunger. A slight tendency in this direction would have a profound effect in the course of time.”
1941	Bauer (166)	“The current energy theory of obesity, which considers only an imbalance between intake of food and expenditure of energy, is unsatisfactory…. An increased appetite with a subsequent imbalance between intake and output of energy is the consequence of the abnormal anlage [predisposition] rather than the cause of obesity.”
1942	Hetherington and Ranson (42)	“[High calorie intake and a sedentary life] may be only symptomatic, and not fundamental. It is not difficult to imagine, for example, a condition of hidden cellular semistarvation caused by a lack of easily utilizable energy-producing material, which would soon tend to force the body either to increase its general food intake, or to cut down its energy expenditure, or both.”
1953	Pennington (167)	“[Caloric restriction] reduces the weight of anyone, obese or lean, regardless of metabolic status, by opposing the homeostatic mechanism for maintaining energy balance. A more rational form of treatment, then, would be one which would enable the organism to establish a homeostatic equilibrium between caloric intake and expenditure at a normal level of body weight. In such a case, treatment would be directed primarily toward mobilization of the adipose deposits, and the appetite would be allowed to regulate the intake of food needed…. The use of a diet allowing an ad libitum intake of protein and fat and restricting only carbohydrate appears to meet the qualifications of such a treatment.”
1957	Thorpe (168)	“Restriction of carbohydrate intake removes the stimulus to insulin production, so that the fat storage activity of insulin will be held to a minimum. … Fat will be mobilized from the adipose deposits of the body, oxidized to ketones in the liver, and circulated to the tissues in this easily combustible form…. [F]or it has long been known that, while carbohydrate can be readily converted into fat in the body, fat cannot be converted into carbohydrate in any significant amounts.”
1965	Berson and Yalow (169)	“The precise relationship of obesity to diabetes is not clear. We generally accept that obesity predisposes to diabetes; but does not mild diabetes predispose to obesity? Since insulin is a most potent lipogenic agent, chronic hyperinsulinism would favor the accumulation of body fat.”