ESPE Abstracts

Conventional treatment for obesity, founded on the First Law of Thermodynamics, assumes that all calories are alike, and that to lose weight one must ultimately “eat less and move more.” However, this prescription rarely succeeds over the long term. Calorie restriction elicits predictable biological responses – including increased hunger and reduced energy expenditure – that oppose ongoing weight loss. Indeed, the prevailing Energy Balance Model offers no compelling explanation for what environmental factors have so profoundly altered the biological systems that control body weight. Why has average body mass index increased so rapidly among populations worldwide with relatively stable genetic obesity risk? The Carbohydrate-Insulin Model proposes a reversal in causal direction: Overeating doesn’t drive body fat increase over the long term; instead, the process of storing excess body fat drives overeating. High intakes of processed carbohydrate raise the insulin-to-glucagon ratio, shifting substrate partitioning toward storage in adipose and leaving fewer calories available for metabolically active and fuel sensing tissues. Consequently, hunger increases and metabolic rate slows in the body’s attempt to conserve energy. From this perspective, conventional calorie-restricted, low-fat diets amount to symptomatic treatment, destined to fail for most people. A dietary strategy aiming to lower insulin secretion promises to increase the effectiveness of long-term weight management and chronic disease prevention.