Carbohydrate–insulin model

The carbohydrate-insulin model (CIM) posits that obesity is caused by excess consumption of carbohydrate, which then disrupts normal insulin metabolism leading to weight gain and weight-related illnesses. It is contrasted with the mainstream energy balance model (EBM), which holds that obesity is caused by a excess in calorie consumption compared to calorie expenditure. According to the carbohydrate–insulin model, low-carbohydrate diets would be the most effective in causing long-term weight loss. Notable proponents of the carbohydrate–insulin model include Gary Taubes and David Ludwig. The CIM has been tested in mice and humans. Although some experts consider that these studies falsified the CIM, proponents disagree. Available evidence does not support the existence of a long-term advantage in weight loss for low-carbohydrate diets.

Physiology

The rapid absorption of glucose after consuming a high glycemic load meal increases insulin secretion, suppresses glucagon secretion (which has catabolic effects), and triggers a dominant incretin response of glucose-dependent insulinotropic polypeptide (GIP). This highly anabolic state, during the first few hours after eating, promotes avid glucose uptake in the muscles, liver, and adipose tissue, while suppressing ketone formation. It also stimulates lipogenesis in the liver and adipose tissue. Three hours after eating, most nutrients from a high glycemic load meal have been absorbed in the digestive tract. However, the persistent anabolic actions of this hormonal response delay the transition from glucose uptake to glucose release in the liver and from fatty acid uptake to release in adipocytes. As a result, the concentration of total metabolic fuel in the blood (glucose, non-esterified fatty acids, and ketones) rapidly decreases in the late postprandial phase, possibly reaching lower concentrations than in the fasting state.