Competing paradigms of obesity pathogenesis: energy balance versus carbohydrate-insulin models

Abstract

The obesity pandemic continues unabated despite a persistent public health campaign to decrease energy intake (“eat less”) and increase energy expenditure (“move more”). One explanation for this failure is that the current approach, based on the notion of energy balance, has not been adequately embraced by the public. Another possibility is that this approach rests on an erroneous paradigm. A new formulation of the energy balance model (EBM), like prior versions, considers overeating (energy intake > expenditure) the primary cause of obesity, incorporating an emphasis on “complex endocrine, metabolic, and nervous system signals” that control food intake below conscious level. This model attributes rising obesity prevalence to inexpensive, convenient, energy-dense, “ultra-processed” foods high in fat and sugar. An alternative view, the carbohydrate-insulin model (CIM), proposes that hormonal responses to highly processed carbohydrates shift energy partitioning toward deposition in adipose tissue, leaving fewer calories available for the body’s metabolic needs. Thus, increasing adiposity causes overeating to compensate for the sequestered calories. Here, we highlight robust contrasts in how the EBM and CIM view obesity pathophysiology and consider deficiencies in the EBM that impede paradigm testing and refinement. Rectifying these deficiencies should assume priority, as a constructive paradigm clash is needed to resolve long-standing scientific controversies and inform the design of new models to guide prevention and treatment. Nevertheless, public health action need not await resolution of this debate, as both models target processed carbohydrates as major drivers of obesity.

Body Fat Reduction Effect of Bifidobacterium breve B-3: A Randomized, Double-Blind, Placebo Comparative Clinical Trial

“…The recent obesity development theory is explained by the “carbohydrate-insulin model” (CIM) based on the hormonal response to highly processed carbohydrates rather than the “energy balance model” (EBM) theory, which posits that obesity occurs because energy intake is less than consumption [ 1 , 2 ]. In 2015, 107.7 and 603.7 million children and adults, respectively, were identified to be obese.…”

Embracing complexity: making sense of diet, nutrition, obesity and type 2 diabetes

“…The debate between these mechanistic processes continues [45][46][47]. However, it is increasingly clear that a focus on energy intake does not account for the impact that diet quality has on long-term weight gain and type 2 diabetes through diverse physiological processes.…”

Eating, diet, and nutrition for the treatment of non-alcoholic fatty liver disease

“…Hypotheses discussing explanations for additional beneficial effects of an LCD on top of a hypocaloric diet be generated from the current discussion on two theories trying to explain energy metabolism in obesity: the carbohydrate-insulin-model and the energy-balance-model [ 48 , 49 ].…”

“…By further stimulating glucose uptake, suppressing the release of fatty acids from adipose tissue, and promoting fat and glycogen production, hyperinsulinemia following carbohydrate intake induces a vicious cycle that “offers an explanation for why average BMI in many countries increased in the late 20th century as public health guidelines recommended replacement of dietary fat with carbohydrates, and consumption of high-glycemic-load foods increased substantially” [ 51 ] . Thus, the carbohydrate-insulin-model considers the high glycemic load as the starting point promoting anabolism including an anabolic hormonal profile, leading to “deposition” of substrates, leaving less energy for the brain (especially in the late postprandial period [ 52 , 53 ]) in turn inducing hunger and appetite [ 48 ].…”