Jonathan Purnell and Damien Fair in the latest issue of JAMA:
The major new finding reported by Page et al is that the hypothalamic brain signal generated in response to fructose ingestion was statistically different from the response following glucose ingestion. The directionality of the difference is not as important as the fact that a difference was found and is accompanied by an increased sensation of fullness and satiety after glucose, but not fructose, consumption. These findings support the conceptual framework that when the human brain is exposed to fructose, neurobiological pathways involved in appetite regulation are modulated, thereby promoting increased food intake. […]
When results of studies manipulating a dietary element show adverse effects on food intake leading to increased body weight, a common counterargument is that it is the excess calories that are important, not the food. Simply put: just eat less. The reality, however, is that hunger and fullness are major determinants of how much humans eat, just as thirst determines how much humans drink. These sensations cannot simply be willed away or ignored. If the addition of a food group is a primary determinant of the weight gain through enhancing appetite, then whether that food contributes to comorbidity directly or indirectly through effects of increased calorie intake becomes moot. The remedy remains eating less, but the means involve reducing the food element, if possible.
