How is the carbohydrate–insulin pathway of metabolic disease different from the carbohydrate

The pathway described here is broader than body weight. It focuses on insulin as a master regulator of energy partitioning, triglyceride handling, inflammation, and metabolic dysfunction across tissues, of which obesity may be one downstream manifestation, not the central or defining problem.

Scientists are currently debating which central mechanism might promote obesity. These include the energy balance model (EBM), the carbohydrate-insulin model (CIM), and the more recently articulated REDOX model. Taken together, the EBM, CIM and REDOX models offer complementary insights into the pathophysiology of obesity, rather than mutually exclusive explanations.

PSGRNZ highlight an under-examined dimension that may drive obesity: addictive eating patterns and a dopaminergic response associated with cumulative refined carbohydrate exposure, including but not limited to ultra-processed foods. These patterns contribute substantially to non-adherence to dietary guidelines, often precede metabolic syndrome and obesity, yet remain poorly integrated into academic and policy frameworks. While fats and proteins have been progressively marginalised within dietary guidance, the EBM model of obesity offers limited insight into how individuals might sustainably manage hunger and satiety through caloric restriction, particularly in the presence of glycaemic volatility and reward-driven, addictive eating behaviours.

How is the carbohydrate–insulin pathway of metabolic disease different from the carbohydrate–insulin model of obesity?

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