Obesity has traditionally been thought of as a state of caloric imbalance, where the intake of calories exceeds the expenditure or ‘burning’ of calories. However, a more nuanced appreciation for the complex biochemistry and physiology of cellular energy generation suggests that obesity is a state of hormonal imbalance causing increased shunting of food energy into adipose tissue for storage, resulting in decreased satiety and ultimately leading to increased caloric intake. Adding to this hypothesis, we propose that obesity is also a state of nutrient and energy deficit, leading to decreased fatty acid mobilisation and oxidation, the result of which may be a natural disinclination towards physical activity. Added sugars (sucrose, a.k.a. table sugar and high-fructose corn syrup) may provide energy (4 kcal/g) but at current intakes they do not facilitate—and may even hinder—the production of energy. Not only do added sugars displace nutritionally superior foods in the diet, but they may also deplete nutrients from other foods that have been consumed, as well as from body stores, in order to enable their proper oxidation and liberate their calories as energy. Additionally, the consumption of added sugars damages the mitochondria and hence impairs energy generation. Moreover, overconsuming added sugars may result in a kind of ‘internal starvation’ (via leptin and insulin resistance) leading to further hunger signals in the body. Added sugars promote nutrient and energy deficit and through this novel pathway promote obesity.
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