“This alternate hypothesis implies that sugar has unique effects in the human body leading directly to both diabetes and obesity, independent of the calories consumed. By this way of thinking, refined sugars are indeed toxic, albeit over the course of years or decades. We get fat and diabetic not because we eat too much of them – although that is implied tautologically merely by the terms ‘overconsumption’ and ‘overeating’ – but because they have unique physiological, metabolic and hormonal effects that directly trigger these disorders. If all this is right, then thinking of obesity as an energy-balance disorder is as meaningless as calling poverty a money-balance problem (caused, of course, by earning too little or spending too much, or both).”

“A far more parsimonious hypothesis is that the same thing that makes our fat cells fat makes us fat: ‘high blood glucose’ and concomitant elevated levels of insulin and the insulin resistance itself, both caused by the carbohydrate content of our diets. Insulin is secreted in response to rising blood sugar, and rising blood sugar is a response to a carbohydrate-rich meal. Sugar is implicated, in particular, because its chemical structure includes a large proportion of the carbohydrate fructose, and fructose is preferentially metabolised in the liver. As such, it is a prime suspect for the fat accumulation in liver cells that is hypothesised to be the trigger of insulin resistance itself.”