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The Carbohydrate-Insulin Model of Obesity
abstract
This abstract is available on the publisher's site.
Access this abstract nowAccording to a commonly held view, the obesity pandemic is caused by overconsumption of modern, highly palatable, energy-dense processed foods, exacerbated by a sedentary lifestyle. However, obesity rates remain at historic highs, despite a persistent focus on eating less and moving more, as guided by the energy balance model (EBM). This public health failure may arise from a fundamental limitation of the EBM itself. Conceptualizing obesity as a disorder of energy balance restates a principle of physics without considering the biological mechanisms that promote weight gain. An alternative paradigm, the carbohydrate-insulin model (CIM), proposes a reversal of causal direction. According to the CIM, increasing fat deposition in the body-resulting from the hormonal responses to a high-glycemic-load diet-drives positive energy balance. The CIM provides a conceptual framework with testable hypotheses for how various modifiable factors influence energy balance and fat storage. Rigorous research is needed to compare the validity of these 2 models, which have substantially different implications for obesity management, and to generate new models that best encompass the evidence.
Additional Info
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The Carbohydrate-Insulin Model: A Physiological Perspective on the Obesity Pandemic
Am J Clin Nutr 2021 Sep 13;[EPub Ahead of Print], DS Ludwig, LJ Aronne, A Astrup, R de Cabo, LC Cantley, MI Friedman, SB Heymsfield, JD Johnson, JC King, RM Krauss, DE Lieberman, G Taubes, JS Volek, EC Westman, WC Willett, WS Yancy, CB EbbelingFrom MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
A Calorie Is More Than a Calorie
Two papers reviewed this week shine light on new mechanisms that clinicians should pay attention to in understanding and treating obesity. The first by Ludwig and colleagues proposes a hormonal mechanism that perpetuates obesity through eating a high–glycemic load diet.
Highly processed, refined carbohydrates are absorbed quickly (high-glycemic load), increasing insulin spikes that result in the secretion of glucose-dependent insulinotropic peptide (GIP) and a high insulin-to-glucagon ratio. Together these mechanisms increase insulin sensitivity in adipose tissue but create insulin resistance in muscle and brain. Over time, fat accumulates viscerally while less is taken up in the muscle.
Previous research has shown that, when calories are equal, a high-glycemic load diet results in more weight gain than a low-glycemic load diet. The type of food eaten sets up a hormonal process that exacerbates the fat accumulation, bringing us beyond the myopic view that a “calorie is a calorie.” The package the calorie comes in matters.
The second paper by Mengeste and colleagues describes the characteristics of muscle in obese versus lean individuals.2 As obesity progresses, the obese muscle changes its composition to a type 2 muscle fiber that is less able to utilize sugar for energy because the function and number of mitochondria decline. This results in less fat oxidation and glucose catabolism. The type 2 muscle fibers are also more easily fatigued than the dominant type 1 found in lean individuals. Once obesity is present, exercise is important but initially won’t result in quick weight loss because the muscles are less able to absorb and burn energy.
What Does This All Mean?
Not all calories trigger the same mechanism. Carbohydrates that are refined, void of fiber, and absorbed quickly, trigger a hormonal cascade that exacerbates the accumulation of fat. This changes muscle composition and function, making weight loss and exercise more difficult. These papers expand our old view that one should simply eat less and exercise more to one that recognizes the importance of eating higher-quality food.
What Can We Do?
Be patient as this takes time.
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