Mito
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- Dec 10, 2016
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European Journal of Clinical Nutrition - A review of the carbohydrate-insulin model of obesity
The carbohydrate–insulin model of obesity theorizes that diets high in carbohydrate are particularly fattening due to their propensity to elevate insulin secretion. Insulin directs the partitioning of energy toward storage as fat in adipose tissue and away from oxidation by metabolically active tissues and purportedly results in a perceived state of cellular internal starvation. In response, hunger and appetite increases and metabolism is suppressed, thereby promoting the positive energy balance associated with the development of obesity. Several logical consequences of this carbohydrate–insulin model of obesity were recently investigated in a pair of carefully controlled inpatient feeding studies whose results failed to support key model predictions. Therefore, important aspects of carbohydrate–insulin model have been experimentally falsified suggesting that the model is too simplistic. This review describes the current state of the carbohydrate–insulin model and the implications of its recent experimental tests.
The rise in obesity prevalence may be primarily due to increased consumption of refined carbohydrates, but the mechanisms are likely to be quite different from those proposed by the carbohydrate–insulin model. For example, such diets may lead to greater overall energy intake by increasing palatability, increasing appetite or decreasing satiety.
Conflict of interest
I have received funding from the Nutrition Science Initiative to investigate the effects of ketogenic diets on human energy expenditure.
The carbohydrate–insulin model of obesity theorizes that diets high in carbohydrate are particularly fattening due to their propensity to elevate insulin secretion. Insulin directs the partitioning of energy toward storage as fat in adipose tissue and away from oxidation by metabolically active tissues and purportedly results in a perceived state of cellular internal starvation. In response, hunger and appetite increases and metabolism is suppressed, thereby promoting the positive energy balance associated with the development of obesity. Several logical consequences of this carbohydrate–insulin model of obesity were recently investigated in a pair of carefully controlled inpatient feeding studies whose results failed to support key model predictions. Therefore, important aspects of carbohydrate–insulin model have been experimentally falsified suggesting that the model is too simplistic. This review describes the current state of the carbohydrate–insulin model and the implications of its recent experimental tests.
The rise in obesity prevalence may be primarily due to increased consumption of refined carbohydrates, but the mechanisms are likely to be quite different from those proposed by the carbohydrate–insulin model. For example, such diets may lead to greater overall energy intake by increasing palatability, increasing appetite or decreasing satiety.
Conflict of interest
I have received funding from the Nutrition Science Initiative to investigate the effects of ketogenic diets on human energy expenditure.
